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The Fallacy of Fish Oil Part 2 Posted on July 19, 2014, 0 Comments


Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis by B. S. Peskin

Original Article Found Here:


14. Failure of LDL Cholesterol to Prevent CVD

It is now well known that LDL-C level, in and of itself, is not predictive of a cardiovascular event. This should not be a surprise, as the body has no plasma LDL-C sensor. This is not a “genetic defect” or oversight since the body has numerous sensors, such as for plasma blood glucose levels in nondiabetics, ranging from 70 to 90 mg/dL. This extremely tight tolerance of plasma glucose levels is 1 part in 1,000—approximately 0.1%. Since there is no hormonal-limiting metabolic factor for LDL-C, it must be viewed as a “dependent” variable, determined as a function of many other biological factors—not independent of them—as previously thought.

Studies confirm this fact. A review of a cholesterol/CVD causal effect categorically failed: among 12 populations with similar cholesterol levels clustered around “normal” levels—5.70 to 6.20 mmol per liter (220 to 240 mg per dL), the blood pressure readings and the serum cholesterol levels were not predictive of ischemic heart disease mortality [14]. If there were a causal correlation, then a 10% reduction should have had significant positive effects; it did not. Nothing has changed today regarding LDL-C's dismal success rate in both predicting and lowering patient CVD.

15. Lipids Are Variable in Tissue Composition
The significant variable in tissue is its lipid structure. Although the genetics of a particular species precisely specify cellular structure, its lipid composition can vary significantly—in particular, when suprapharmacologic amounts of long-chain metabolites are consumed, such as the case with fish oil supplements. A pharmacologic overdose cannot completely be oxidized away for energy or otherwise. Consequently, much of “the overdose” is forced into tissue composition, causing an improper structure—often in maintaining a linear relationship as does plasma and liver and as do RBCs [44, 46, 47]. Cellular bilipid membrane structure and its LDL-C structure warrant intense investigation.

Each of the approximately 100 trillion cells in the human body consists of a bilipid membrane. Importantly, PEOs comprise 25–33% of their polyunsaturated lipids [48]. Additionally, every mitochondrion, typically a hundred to thousands per cell, contains them, too [49, 50]. PEOs can be considered the “brick and mortar” of every cell, tissue, and organ, including mitochondria. In contrast, aside from the brain, eyes, and nervous system, most tissue and organs contain few derivatives like EPA/DHA.

16. Variability in LDL-C
The structure of LDL-C is complex. Its cholesteryl ester is key. The structure of cholesterol itself never changes, merely its esterified moiety—the acyl side chain. That is a big difference that many in the medical community may not appreciate. This is a simple condensation reaction, removing the water, catalyzed by the enzyme ACAT (acyl CoA: cholesterol acyl transferase) between a fatty acid and cholesterol. “R” symbolizes the hydrocarbon portion of the fatty acid. For example, if oleic acid were esterified with cholesterol, then R would be –C8H17=CH–C7H14 with the double bond in cis configuration.

Cholesteryl ester.
Lipoproteins transport cholesterol and its esterified PEOs to the tissues via apoprotein B-100 (ApoB100).

Although the molecule itself may become oxidized, including its highly significant protein component (on a weight basis), that likelihood is extremely low. What is primarily oxidized are the fatty acids esterified to LDL-C comprising the majority of the lipoprotein's center. Parent omega-6 quantities of esterified LA are approximately 85% of its overall 50% fatty acid content [51].

16.1. Esterified Cholesterol

The cholesteryl part or cholesteryl moiety is tied to a structure that does change—particularly, its EFA-based variable “R” component (Figure 1). It is well understood that the PEO LA dominates the esterified portion of cholesterol. The majority of the cholesteryl ester component is LA (Parent omega-6) [52].

The cholesterol ester portion is highly significant compared to free cholesterol or phospholipids (Figure 2). Approximately 70% of the cholesterol in the lipoproteins of the plasma is in the form of cholesterol esters attached to apolipoprotein B [53]. Of dietary cholesterol absorbed, 80%–90% is esterified with long-chain fatty acids in the intestinal mucosa [54].

16.2. LDL-C Is Highly Resistant to Oxidation in the Bloodstream

The fact that cholesterol itself is extremely resistant to oxidization is highly underpublicized, whereas its main esterified component, Parent omega-6 (LA), is more easily oxidized, especially ex vivo by food processing. Dietary LA that has already become oxidized prior to ingestion ex vivo is ubiquitous through processing of foods or overheating, since heating in the presence of air enhances peroxidation of PUFA glycerol esters [55, 56]. This insight suggests that looking in a new direction other than merely lowering LDL-C for the prevention of heart disease is warranted.

17. Human Antioxidant Levels Are Naturally Low
Normal antioxidant levels are lower than would be presumed to be adequate and normal if analysis were not performed in healthy patient populations as a control. The results are startling. Experiments show that the sum molar ratio of all antioxidants to PUFA is a mere 1 : 165 (0.61%), with one antioxidant molecule having to protect the large number of 165 PUFA molecules [51].

The total number of fatty acids bound in the different lipid classes of an LDL particle with a molecular mass of 2.5 million is on average 2,700, of which about one-half (1/2) are polyunsaturated fatty acids (PUFAs), mainly linoleic acid (Parent omega-6), with small amounts of arachidonic acid and docosahexaenoic acid (DHA). Furthermore, only minimal physical and chemical changes related to oxidation are produced by even a prolonged storage of LDL with oxygen or by incubation with low concentrations of copper ions.

Clearly, the quantity of naturally occurring antioxidants is too small for oxidation in vivo to be a significant physiologic issue [14, 51]. The sole logical conclusion is that the PUFA, in particular, LA, is being consumed and is entering the body in an already oxidized state caused by ubiquitous food processing.

18. New Insight: LDL-C Transports an Ingested “Poison”
18.1. CVD Explained: Processed Food Is the Culprit

Heating produces toxic products such as cholesterol oxides. If they are consumed—not produced in the body—they cause deleterious effects. Professor Gerhard Spiteller, who is Chairholder of Biochemistry, Institute of Organic Chemistry at the University of Bayreuth, Germany, has investigated EFAs and their degradation products—specifically, the influence of these substances on the physiology of mammals. He, too, concluded that consumption of oxidized PUFA-cholesterol esters is responsible for the initial damage to endothelial cells and that cholesterol oxidation products are incorporated into LDL cholesterol in the liver [57].

Given that both the cholesterol molecule itself is highly resistant to oxidation and Parent omega-6 is relatively resistant, the only acceptable conclusion is that the majority of the oxidized cholesterol damage is from its esterified component, that is, adulterated (oxidized) LA, patients unknowingly consume.

LDL then carries these toxic compounds into the endothelial walls where they cause cell damage. Injury is not caused by an increase in free cholesterol but by an increase in cholesterol esters of processed LA [58]. In atherosclerotic patients, LDL cholesterol is altered ex vivo by oxidation, and this altered LDL is taken up in unlimited amounts by macrophages. Dead macrophages filled with cholesterol's damaged, functionally impaired esters are then deposited in arteries. LDL-C is effectively transmitting a poison, that is, nonfunctional, adulterated, and harmful LA. We can now explain why statins fail.

18.2. Statin's Failure Explained

From the pharmaceutical company's own admission, the number needed to treat (NNT) for statins is no better than 60 over a 5-year period. This means that 60 patients would need to be treated for 5 years to see 1 positive outcome—a 98.3% (59/60) failure rate. Researchers often say that the NNT is much higher (worse). For example, JUPITER had an NNT of 95, meaning a 99% failure rate [59].

By statin's lowering of LDL-C, its esterified PEO component is also lowered, both adulterated (good outcome) and fully functional (bad outcome). This is problematic and precisely explains why statins do not work. By focusing on the ex vivo LA that has already become oxidized prior to ingestion through processing of foods, cooking, or overheating, a solution can be found to mitigate this damage.

19. Investigating Oils with respect to Arterial Health: IOWA Screening Experiment
A seminal screening experiment was conducted in 2010 comparing the effectiveness of PEO in increasing arterial compliance (flexibility) against fish oil [60]. This is a broad-based population screening—the most realistic population to see effectiveness, if any.

Arterial compliance is the most accurate physiologic assessment of a subject's cardiovascular health. Photoplethysmography is utilized with computer analysis of the (volumetric) curve's second derivative obtaining an acceleration curve. This output is compared to the database consisting of prior population scans grouped by age. The highly statistically significant results and excellent NNTs of IOWA confirm the theoretical predictions of both the failure of fish oil to increase arterial compliance and the significant (predictable) success of PEOs to improve arterial compliance across all populations.

19.1. Marine Oils Decrease Arterial Compliance: A Bad Outcome

The most remarkable finding was that subjects taking fish oil prior to PEOs obtained the most improvement. This was anticipated since those subjects started at a greater vascular deficit caused by the fish oil consumption.

Compared to PEOs, fish oil users had an “11-year-older” cardiovascular system as measured by arterial compliance population scans—more than a decade's additional “hardening of the arteries” compared to their physical age.

Ceasing fish oil use allowed the arterial system to revert to “normal” [45]. Once the vascular system was back to “normal,” the expected improvement from PEOs, as shown by the other groups, was also achieved, which translated to an even greater decrease in biological age based on where they had started. Clearly, fish oil accelerates vascular aging [60]. Marine oils are an anti-antiaging substance.

20. PEOs in Plasma, Lipids, and Esterified Cholesterol
It is necessary to analyze the Parent and derivative content of plasma lipids (lipoproteins, triglycerides, and esterified cholesterol) to determine the specific “bad actor” in CVD and cancer—every country's number 1 and number 2 killers—and confirm LA's prime importance. LDL's esterified linoleic acid is the major source for lipid peroxidation products, yet linoleic acid is highly resistant in LDL against oxidation [61]. This is critically important to understand.

With all the focus on omega-3 series fatty acids, both Parent and derivative, it is significant to note that the free Parent fatty acids (nonesterified) in human plasma, although minute in quantity, are ordinarily composed of about 15% LA (linoleic acid, Parent omega-6) and just 1% ALA (alpha-linolenic acid, Parent omega-3) [61].

Derivatives such as EPA/DHA are naturally much less significant in quantity than LA. In sharp contrast to the high amounts of n-6 series PUFAs, n-3 series PUFAs account for only 1.8% of the fatty acids in triglycerides, 3.5% in the phospholipids, and only 1.7% (ALA is 0.5%) in cholesterol esters. This high preponderance of LA is pervasive throughout: the LA/ALA ratio in triglycerides is 23 : 1; n-3 PUFA makes up only 1-2% of fatty acids in plasma [62]. Even in the brain, LA/ALA uptake is 100 times greater in favor of that of LA [62]. In the brain, AA, an omega-6 long-chain metabolite, comprises a significant 10% of the brain's long-chain fatty acids. Of particular importance is that the triglyceride stores concentrate the important Parent omega-6 fatty acid.

20.1. Importance of Parent Omega-6 and Prostaglandin Metabolites

In human lipid physiology, Parent omega-6 and its long-chain metabolites dominate over Parent omega-3 and its long-chain metabolites. The majority of the plasma fatty acids are LA (Parent omega-6) as are the triglyceride stores (adipose tissue). The metabolites of LA—in particular, prostaglandins PGE1 and PGI2 (prostacyclin)—are significant vasodilators. PGE1 is also the body's most potent anti-inflammatory. If functional LA bioavailability is lowered, the potential for inflammation will rise, leading to atherosclerosis. Weiss, for example, has noted that PGE1 (produced from functional Parent omega-6) reduces the fibrin deposition associated with the pathogenesis of atherosclerosis [63]. Membrane fluidity increases when more functional (undamaged) polyunsaturated fatty acids—in particular, linoleic acid—are available to incorporate into the membrane lipid bilayer.

Because LDL cholesterol is the transport vehicle for PEO delivery into the cell, LDL cholesterol will transport any LA into cells—defective or not—such as oxidized or trans entities. Mitigating the damage caused by extensive ex vivo intake of already oxidized LA is possible by supplemental ingestion of fully functional, unadulterated, nonoxidized LA.

21. Physiologic Excess of Omega-3 Series Fatty Acids Is Harmful, Decreasing Critical Omega-6 Series: Increases in CVD, Diabetes, and Cancer Are Expected
It was understood decades ago that consumed physiologic excess of omega-3 series PUFA is detrimental. Burns and Spector showed that the capacity of endothelial cells—relevant to carcinomas—and macrophages to release prostaglandins is reduced when they accumulate n-3 polyunsaturated fatty acids [64]. This is important because prostaglandins produced from PUFAs—in particular, Parent omega-6 (LA)—reduce the adhesion of tumor cells to microvascular endothelium. Most importantly, fish oil is known to decrease critical anti-inflammatory PGE1 output in proportion to the amount of EPA/DHA consumed [65].

21.1. Marine Oils Raise Resting Blood Glucose Levels and Blunt the Insulin Response Causing Insulin Resistance

Diabetes has become the world's number 1 epidemic. China has recently surpassed the USA in percentages of diabetics. Spontaneous autooxidation of blood glucose is a significant cause of diabetic patients' elevated increased risk of CVD. China has recently surpassed the USA in percentages of diabetics, and their consumption of marine oils keeps rising [66]. The negative impact marine oils have on diabetes, both Type I and Type II, is staggering.

Spontaneous autooxidation of blood glucose is a significant cause of diabetic patients' elevated increased risk of CVD, and marine oils increase plasma glucose levels. Both fish oil supplements and even “oily fish” itself are highly problematic for diabetics. In 2011, researchers looked at the effects on Type II diabetic patients consuming more fish. Only from nonfatty fish, containing more Parent omega-6 and much less EPA/DHA, did the experiment show significantly decreased blood sugar (good outcome). Further, those who ate “fatty” fish saw a decreased insulin output of 21% (bad outcome) compared to those not eating “fatty” fish [67].

“Fatty” fish (containing more EPA/DHA), not a supplement, caused the elevated blood glucose. EPA/DHA fish oil supplements cause elevated blood glucose and blunt the insulin response in diabetics. This deleterious finding was known years ago [68, 69]. Since “fatty/oily” fish caused the same deleterious effects as those of the supplement, the only logical conclusion is that fish oil—in any form—is harmful to any diabetic. Diabetes is America's number 1 epidemic and both oily fish and fish oil supplements exacerbate the condition. Furthermore, marine oils negatively impact the cellular membrane causing elevated insulin resistance. Because marine oils are known to displace critical Parent omega-6 in the cell membrane, this harmful effect is predictable. This issue impacts all tissue as shown below. Furthermore, it is well known cancer cells utilize glucose as their prime metabolic substrate (fuel). Oily fish and marine oil supplements—by allowing much greater blood glucose levels—both exacerbate patients' existing cancer metabolism and metastatic potential [40]. This effect is the opposite of any treatment's desired outcome.

21.2. Potential Brain Developmental Issue: Fish Oil Displaces Critical Omega-6 Metabolites Harming Tissue Structure

Importantly, fish oil potentially damages the brains of both infants and adults because critical omega-6 series metabolites are displaced [46]. This is another reason why fish oil failed to help Alzheimer's victims in a monumentally disappointing 2010 study [70]. The medical journal's authors specifically warned against feeding fish oil to human infants. This experiment was performed in rodents, but the results are applicable to humans because EFA metabolism is similar and applicable to both mammals and rodents [47]. Systemic rises in fish oil's EPA are largely compensated by decreased Parent omega-6 [42].

21.3. Fish Oil Causes Decreased Prostacyclin Production, Increasing CVD

Prostaglandins (hormone-like substances with extremely short half-lives not entering the bloodstream) are capable of both limiting thrombosis and reversing thrombosis in atherosclerotic patients [71].

Prostaglandin PGE1 is the body's most powerful anti-inflammatory and vasodilator and prostacyclin (PGI2) is a vasodilator and prevents both platelet adhesion and aggregation. These are both omega-6 metabolites.

Fish oil increases endothelial platelet aggregation in heart patients [72]. In patients with atherosclerosis, prostacyclin (produced in endothelial tissue) biosynthesis fell by a mean of 42% during the fish-oil period (extremely bad outcome). Synthesis of the platelet agonist thromboxane A2 (produced in the platelets) declined by 58% (good outcome). This may first appear to be a reasonably successful intervention, but that analysis would be incorrect for the following reason: atherosclerotic patients require increased intimal PGI2 output, as vessel wall thrombogenicity, and not reduced platelet adhesion, is a much more significant factor for minimizing thrombosis [73]. Furthermore, template-bleeding times were significantly prolonged in all fish-oil-consuming patients (bad outcome).

22. Association of Increased Marine Oils and Multiple Pathophysiologic Diseases
22.1. Skin Cancer Has Become Epidemic as Fish Oil Supplement Consumption Increases and Results in Epidemics of Pathophysiologic Incorporation of DHA into Epithelial Tissue

The following associative speculation about marine oil's deleterious effects in the development of epithelial-based skin cancers requires confirmation. However, the physiologic/biochemical metabolic pathways detailing this conclusion are strong. Fish oil produces a pathophysiology in epithelial tissue, potentially leading to skin cancer. Likewise, adenocarcinoma of the prostate develops from aberrant epithelial cells. Are these conditions related? Logic tells us they are. We know there are no Parent omega-3 or omega-3 derivatives like EPA/DHA naturally occurring in epithelial tissue [12, 13]; therefore, any incorporation is supraphysiologic. Epithelial tissue's long-chain fatty acid composition is exclusive to Parent omega-6 (LA).

22.2. Increased Carcinoma with Increased Marine Oil Consumption: A Causal Relationship

A very strong melanoma/fish oil consumption association warrants attention. Skin cancer rates and fish oil consumption are both increasing. This is a very troubling (worldwide) association that must be addressed. Based on established physiology, it is predictable that the countries consuming the most fish-oil supplementation will contract skin cancer and prostate cancer the most—and they do, as will be shown later in this section. There are three quantitative EFA physiologic facts that must be understood in determining the definitive cause-effect relationship with fish oil use and cancer contraction. (A) There is neither Parent omega-3 (ALA) nor omega-3 long-chain metabolites (EPA/DHA) in epithelial tissue [12, 13]. (B) Each of the body's 100 trillion cells is comprised of a lipid bilayer with very little EPA/DHA, but significant LA and ALA (25–33%)—excepting those in epithelial tissue which is exclusively comprised of Parent omega-6 only (LA) [48, 49, 74, 75]. The same is true for the mitochondrion, except containing less ALA. Again, there is a physiologically negligible amount of EPA/DHA [49, 50]. We know excess EPA/DHA displaces the main fatty acid in the membrane, Parent omega-6 (LA) [46]. Is the (forced) incorporation of the derivatives EPA/DHA—by consumed supraphysiologic amounts—into epithelial tissue a direct cause of the increased skin cancer and therefore all epithelial-related cancers? The logical answer is yes.

Dermatologists are at a loss to explain the increase in skin cancer regardless of recommendations to their patients that they have less exposure to the sun. Human physiology strongly suggests that fish oil is a significant culprit. A seminal study in Norway revealed that fish oil significantly increased the risk of skin cancer. This is highly underpublicized, but reported in the International Journal of Cancer in 1997. Meticulous study (confirmed by pathology and cancer registry) of over 50,000 Norwegian men and women showed approximately a 3-fold increase in melanoma in women using cod liver oil (considered a superb fish oil supplement). The study was particularly strong, based on its unbiased approach, high participation and response rate, the fact that dietary data was collected prior to the onset of cancer, and the fact that each participant had a complete followup regarding occurrences of cancer, death, and emigration. In fact, all physicians and medical professionals in Norway are required to report malignant diseases to the Cancer Registry, and 98% of these cases are confirmed with microscopic tissue analysis [76]. In Norway, where fishing is a principal industry, they did not want to see a negative finding and it was not publicized. This study shows fish oil causing or associated with an increase in cancer—not prevention of cancer.

22.3. Epithelial (Skin) Cancers

The countries with the greatest skin cancer contraction rates, after Australia, are Scandinavia, Canada, and the United States [66]. Why is this? Marine/fish oil sales have constantly increased over the past 15 years and it has become America's number 1 supplement, and the rest of the world quickly follows America's dietary recommendations. Are these correlations mere coincidence? No. Based on the above science, they are predictable. Given that people are in the sun less and use sunscreen more, there are few valid reasons why skin cancer rates should be increasing worldwide and, in particular, these countries.

In 2010, Cancer Research published a historic article linking fish oil and increased colon cancer risk, as well as increased colitis [77, 78]. The researchers had hypothesized that “feeding fish oil enriched with DHA to mice would decrease the cancer risk,” but they found the opposite to be true. Instead, they discovered that the mice developed deadly, late-stage colon cancer when given high doses of fish oil. They observed increased inflammation and that, as a result, it only took just four weeks for the tumors to develop. This was true for mice that received the highest doses of DHA as well as those receiving lower doses. The researchers stated, “Our findings support a growing body of literature implicating harmful effects of high doses of fish oil consumption in relation to certain diseases.”

The researchers were shocked because they had relied on prior “studies,” not lipid (medical) science, to anticipate the effects of fish oil. Of particular importance was that these researchers even found low doses of fish oil to be harmful. In 2009, another significant journal article uncovered more problems with fish oil use, ultimately forcing the researchers to clearly state, “The particularly high pro-metastatic effect of dietary n-3 PUFA on S11 cells rules out the generalisation that dietary n-3 PUFA inhibit tumour growth and progression” [79].

22.4. Fish Oil Destroys Critical Mitochondrial Physiologic Functionality

Oncologists understand that mitochondrial functionality is a prime factor in the prevention of cancer. Yet, fish oil negatively impacts mitochondrial functionality. A seminal experiment appearing in Cancer Cell in 2006 is critical to the understanding of how fish oil causes such alarming mitochondrial damage, emphasizing that the connection is between fish oil consumption and cancer [80]. This test was conducted on live animals, not in a petri dish. Rats were fed fish oil or beef tallow. The scientists then examined the activity of critical mitochondrial enzymes from their kidney cells. The fish-oil-fed animals suffered an incredible 85% enzyme loss, while the beef-tallow-fed animals suffered only a 45% enzyme loss.

Fish oil caused a 40% net additional reduction in critical mitochondrial enzyme production; that is, cellular respiration in the mitochondria is highly diminished. Why would this be expected with supraphysiologic amounts of marine oils? Cardiolipin structure is highly compromised, as described next.

22.5. A Key Finding: All Tumors Suffer (Often Irreversible) Respiratory Damage

In remarkable research sponsored by the National Cancer Institute and published in 2008 and 2009, researchers found major abnormalities in content or composition of a complex lipid called cardiolipin (CL), stating these abnormalities are “found in all tumors, linking abnormal CL to irreversible respiratory injury” [81]. 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 functionality and membrane integrity. It is used for ATP (energy) synthesis and consists roughly of 20% lipids [82]. Nobel Prize-winner Otto Warburg, MD, PhD, first discovered the mitochondrial impairment/cancer causation link [40, 83–85].

With dietary marine/fish oil supplementation and its EPA/DHA modification of membrane fatty acid composition, which accelerates unnatural lipid peroxidation, significant effects of oxidative damage to many and varied cellular macromolecules occur. For example, peroxidized cardiolipin in the mitochondrial membrane can inactivate cytochrome oxidase by mechanisms similar to those of hydrogen peroxide as well as mechanisms unique to organic hydroperoxides. Dr. Hulbert warns, “Lipid peroxidation should not be perceived solely as ‘damage to lipids,' but should also be considered as a significant endogenous source of damage to other cellular macromolecules, such as proteins and DNA (including mutations)” [18].

Furthermore, the noncharged structure of aldehydes allows their migration with relative ease through hydrophobic membranes and hydrophilic cytosolic media, thereby extending the migration distance far from the production site. On the basis of these features alone, these carbonyl compounds can be more destructive than free radicals and may have far-reaching damaging effects on target sites both within and outside membranes.

Dr. Hulbert makes the importance of mitochondrial functionality clear with his statement, “The insight that the exceptionally long-living species, Homo sapiens, potentially provides for understanding the mechanisms determining animal longevity, is that the fatty acid composition of mitochondrial membranes may be much more important than the composition of other cellular membranes” [17]. A pharmacologic overdose of ALA metabolites exacerbates a shorter lifespan by altering the lipid (mitochondrial) membranes [23].

Mitochondrial cardiolipin molecules are targets of oxygen free radical attack, due to their high content of fatty acids—normally containing negligible long-chain omega-3 metabolites like DHA—unless pharmacologically overdosed as with marine/fish oil. Mitochondrial mediated ROS generation affects the activity of complex I, as well as complexes III and IV, via peroxidation of cardiolipin following oxyradical attack to its fatty acid constituents [18].

Most importantly, there is neither Parent omega-3 nor its metabolites in cardiolipin. Its main substrate is Parent omega-6 [18]. Alteration of mitochondrial structure by fish oil was known in 1990 and published at that time in an article in the Proceedings of the National Academy of Science, as follows: “Phospholipase A2 activity and mitochondrial damage are enhanced when mitochondrial membranes are enriched with n-3 fatty acids [from marine/fish oil]” [86].

Any cancer therapy not taking into account mitochondria efficiency and physiologic structural integrity is deficient and will fail in the long term, as Nobel Prize-winner Otto Warburg, MD, PhD, clearly demonstrated [83–85]. Others have expanded on his seminal discovery with a focus on cellular oxygenation [10, 40]. As confirmation of this fact, it is well supported that hypoxia in the prostate tumor causes greater tumor aggressiveness [87].

23. Furan Fatty Acids: Are Furan Fatty Acids Cardioprotective and Responsible for Any Positive Effects of Fish Consumption?
In addition to abundant n-3 long-chain fatty acids, marine oil/fish oil contains furan fatty acids. Furan fatty acids (F-acids) are heterocyclic lipid components with a furan moiety in the center of the molecule, the predominate acid being F6 (C22H38O3). They are a large group of fatty acids characterized by a furan ring, which carries at one α-position an unbranched fatty acid chain with 9, 11, or 13 carbon atoms and at the other α-position a short straight-chain alkyl group with 3 or 5 carbon atoms. In most cases, two β-positions of the furan ring are substituted by either one or two methyl residues or other group. However, F-acid without any substitutions in both β-positions of the furan ring has also been found (in certain seed oils). They are labeled F1 to F8 with F3 and F4 being isomers. Algae, plants, and other microorganisms which produce furan fatty acids. There are only small amounts of these and they are often quite difficult to separate from other long-chain fatty acids.

Both marine and land animals consume F-acids, thereby incorporating these fatty acids into their phospholipids and cholesterol esters. These particular fatty acids are radical scavenging and may contribute to possible beneficial properties of fish consumption [88].

Recently, it was shown that this class of fatty acids efficiently rescues brain cell death induced by oxidative stress [89]. While the protective effect was strong, it was limited to an effective range only within the cell membrane. Regardless, this is still a significant effect and furan fatty acids should help reduce the risk of Alzheimer's disease.

Although promising, furan acids' effectiveness has been confirmed only in limited human controlled studies [90]. The significant issue to address is whether their effectiveness is countered by the inherent ability of supraphysiologic amounts of marine oil to spontaneously oxidize—per radical induced oxidation—as discussed in prior sections. We think so. Furthermore, furan fatty acids do not negate fatty fish's deleterious effects of elevating blood glucose and blunting the insulin response [67–69]. That is why, overall, the effectiveness of fish/marine oil in the amounts typically recommended is harmful; in particular, by elevating blood glucose levels in cancer victims. However, if the amount of marine/fish oil consumption is reduced significantly to normal physiologic levels as detailed per this review, there may be a positive role for marine oil.

24. Discussion
As demonstrated in cultures that consume fish, its consumption is fine. However, there are many cultures with excellent health and longevity that do not consume fish—the Hunza in Pakistan, the Vicambamba high in the Andes in Ecuador, the Abhasia of the Caucasus Mountains, and—in the United States—fully vegetarian 7th Day Adventists. This review speaks solely of marine oil/fish oil supplements and the concentrated pharmaceuticals of concentrated DHA or EPA like Lovaza and Vascepa. The medical profession is unaware or is not acknowledging the lipid science that unequivocally shows the great harm that marine/fish oil's recommended yet supraphysiologic amounts of EPA/DHA cause. This review gives the medical community many underpublicized physiologic facts that must be known and understood as the healthcare community revisits the practice of prescribing prophylactic marine oil to patients.

Fish oil cannot work, based on human physiology and biochemistry. Humans do not live in frigid waters where an “anti-freeze” is required, that is, EPA/DHA. These so-called active components spontaneously oxidize (radical induced oxidation) at room temperature and are even more problematic at physiologic body temperatures, causing numerous deleterious aldehyde secondary/end products regardless of antioxidant levels.

It has been clearly shown that the general population does not suffer impairment of delta-6/-5 desaturation enzyme impairments, as previously thought in the 20th century.

Prostate and other cancers along with CVD are predicted to increase in patients consuming fish oil on purely theoretical grounds, utilizing known physiology and biochemistry—and they do—in particular, epithelial cancers and impaired arterial intima.

Fully functional, Parent omega-6, LA, has been shown to be critical to both cellular oxygenation and mitochondrial function. Not distinguishing an adulterated (processed) EFA against a fully functional unprocessed EFA—in particular, LA—is the prime cause of confusion leading to inconsistent clinical trials on cardiovascular disease and cancer. The criticality of distinguishing between the effects of adulterated versus unadulterated forms of LA is obvious. Failure to do so has led to the incorrect and misleading conclusion that dietary intake of LA increases CVD risk, when it is only the adulterated LA that does [91]. The Parent EFAs are key; food processing is the root cause of EFA-related issues. Fish-oil supplementation has nothing to do with solving this issue. Although furan fatty acids found in fish oil are strongly radical scavenging, their quantities are too limited to counter the deleterious effects of supplemental marine/fish oils.

25. Conclusion
Marine/fish oil, in the supraphysiologic, prophylactic amounts often consumed, is harmful, possibly even more harmful than trans fats [3]. If proper physiologic amounts were utilized (<20 mg EPA/DHA), perhaps their furan acid content would be a significant positive factor; the concern of rampant oxidation is alleviated. Otherwise, given today's high quantities of fish oil recommendation, we see that their furan acid component is rendered ineffective. The medical profession needs to thoroughly review highly quantitative 21st century lipid physiology and biochemistry and offer the appropriate patient warnings. It is sincerely hoped that future researchers will approach the fish oil controversy with a more comprehensive grasp of the lipid biochemistry and physiology involved. Science must take precedence over “studies” which are often open to (mis)interpretation, leading to continual reversals and inconsistent results in clinical trials.

Using the most direct and effective physiologic measure, fish oil in the doses suggested is unequivocally shown to be an anti-antiaging substance, increasing vascular “biologic aging” by over a decade—causing “hardening of the arteries”—compared to PEO consumption. Compared to taking nothing, fish oil decreased subjects' arterial compliance (a bad outcome), by nearly four years [60].

Prophylactic marine oil consumption given its supraphysiologic EPA/DHA amounts—both theoretically and in clinical use—leads to increased inflammation, increased CVD, and increased cancer risk.

The Fallacy of Fish Oil Part 1 Posted on July 19, 2014, 0 Comments

Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis by B. S. Peskin

Original Article Found Here:


The medical community suffered three significant fish oil failures/setbacks in 2013. Claims that fish oil's EPA/DHA would stop the progression of heart disease were crushed when The Risk and Prevention Study Collaborative Group (Italy) released a conclusive negative finding regarding fish oil for those patients with high risk factors but no previous myocardial infarction. Fish oil failed in all measures of CVD prevention—both primary and secondary. Another major 2013 setback occurred when fish oil's DHA was shown to significantly increase prostate cancer in men, in particular, high-grade prostate cancer, in the Selenium and Vitamin E Cancer Prevention Trial (SELECT) analysis by Brasky et al. Another monumental failure occurred in 2013 whereby fish oil's EPA/DHA failed to improve macular degeneration. In 2010, fish oil's EPA/DHA failed to help Alzheimer's victims, even those with low DHA levels. These are by no means isolated failures. The promise of fish oil and its so-called active ingredients EPA / DHA fails time and time again in clinical trials. This lipids-based physiologic review will explain precisely why there should have never been expectation for success. This review will focus on underpublicized lipid science with a focus on physiology.

1. Introduction
The object of this review is to show how there could be no possible expectation of general patient benefit with prophylactic fish oil use. It will be shown that the amount of EPA/DHA from routine fish oil recommendations is 20Xs–500Xs more than the body would naturally produce on its own from alpha-linolenic acid (ALA)—Parent omega-3.

Advances in quantitative analysis have been made in the 21st century which are not yet disseminated in the medical community; that is, the delta-6/-5 enzymes are not impaired in the general patient population, and the amount of EPA/DHA required on a daily basis by the brain is now known to be less than 7.2 mg/day. Neither extremely important fact was known in the 20th century.

Lipid physiology makes the following clear: (a) Marine oil's EPA/DHA spontaneously oxidizes at room temperature and more rapidly at normal body temperature—no level of antioxidants can stop this deleterious effect. (b) Fish oil blunts the insulin response and raises resting blood glucose levels. (c) Fish oil decreases critical prostacyclin (PGI2) in patients with atherosclerosis—a very bad outcome. (d) Fish oil rapidly decreases arterial compliance—increasing “hardening of the arteries.” (e) In contrast to researcher's expectations, fish oil accelerates metastases in animals. (g) Fish oil's EPA/DHA do nothing to increase cellular and tissue oxygenation; to the contrary, marine oils increase inflammation. (h) Marine oil consumption impairs mitochondrial functionality, making it an anti-antiaging substance.

The medical profession is unaware of or is not acknowledging the lipid science unequivocally showing the great harm that marine/fish oil's supraphysiologic amounts of EPA/DHA cause. As will be shown, the claim that prophylactic use of marine oil produces positive patient results is completely counter to 21st century lipid science.

2. Fish Oil Fails Extensively in Clinical Trials, but These Failures Are Often Underpublicized: Three Significant 2013 Fish Oil Failures
Since many medical professionals are under the wrong impression that fish oil incontrovertibly works, it is instructive to make clear there are numerous recent and not so recent marine oil/fish oil failures occurring across all clinical areas. There are more (underpublicized) failures than (supposed) successes. These failures should cause great pause.

Three highly significant fish oil failures occurred in 2013. In May 2013, The Risk and Prevention Study Collaborative Group (Italy) released a conclusive negative finding regarding fish oil for those patients with high risk factors but no previous myocardial infarction. Fish oil failed in all measures of cardiovascular disease (CVD) prevention—both primary and secondary [1]. This study was so conclusive that Eric Topol, MD, Editor-in-Chief of Medscape and Medscape's Heartwire for cardiologists, issued a new directive to patients to stop taking fish oil, that is, long-chain EFA metabolites of EPA/DHA [2]. The July 2013 landmark article published in the Journal of the National Cancer Institute entitled “Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial” [3] confirmed prior post-2007 findings of increased prostate cancer risk among men with high blood concentrations of long-chain metabolites of ω-3 fatty acids from fish oil studies [4, 5]. The authors warned, “The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis. Recommendations to increase LCω-3PUFA (marine oil's EPA/DHA) intake should consider its potential risks.” The May 2013 trial [6] showed that macular degeneration victims were not helped by fish oil's significant DHA content. The year 2013 was very bad for fish oil findings. Why the failures?

3. Pre-2007 Studies Were Poorly Conducted and Inconsistent with the Science
In a 2012 meta-analysis regarding cardiovascular disease, reviewing 1,007 articles, only 14 studies met the criteria of randomization, double blindness, and placebo control [7]. Clearly, an enormous number of poorly conducted studies in the journals have conclusions that cannot be relied on and are misleading physicians and researchers worldwide. Studies should be used to confirm the physiologic, lipid science, not to be counter to it as many pre-2007 studies were.

In researchers' haste to offer patients a new, effective treatment, fish oil “successes” were highlighted and its failures downplayed. However, post-2007 “studies” of fish oil show significant accumulated failure [8]. When well-controlled studies and experiments are performed, as was done in Harvard Medical School's 1995 experiment giving one group of patients fish oil and a control group olive oil, CVD progression did not lessen with fish oil [9]. Fish oil fails; it has to as the science below confirms.

4. EFAs: Parent Essential Oils (PEOs) and Derivatives
There are only two true 18-chain carbon essential fatty acids (EFAs): linoleic acid (LA) with two double bonds and alpha-linolenic acid (ALA) with three double bonds. Neither can be manufactured in the body; both must come from food.

Longer-chain metabolites are synthesized from LA and ALA. These long-chain metabolites—not essential and often incorrectly termed “EFAs”—are correctly termed “derivatives.” For example, common derivatives of the omega-3 series are EPA (eicosapentaenoic acid) with five double bonds and DHA (docosahexaenoic acid) with six double bonds. To clarify the issue, I term LA and ALA “Parent Essential Oils” (PEOs) or “Parents.” I properly term all of their long-chain metabolites “derivatives.” The body makes these important derivatives from Parents “as needed” in naturally minute amounts. The literature often fails to clearly distinguish these two vastly different substances.

4.1. Most Parents Stay as Parents

A major mistake was made in the 20th century, which misdirected researchers. It was wrongly assumed that the vast majority of “Parents” would be converted into “derivatives.” This did not occur, causing the medical research community to proclaim that there were ubiquitous metabolic deficiencies impacting the delta-6 and delta-5 desaturase enzymes in the general population. This has been shown to be categorically false by advanced 21st century quantitative methods (described later). In humans, no more than one percent (1%) of Parents are naturally converted into derivatives. Fish oil mania wrongly (and hazardously) assumes the converse.

5. Fish Oil Impairs Normal Cellular Physiology: Pathophysiologic Disorders Are Expected
Theoretically (and in clinical experiments) fish oil supplements, in their “normal” although supraphysiologic amounts (calculated below), cause changes in membrane properties that impair oxygen transmission into and through the cell [10]. Physicians and other health professionals often prescribe these supraphysiologic amounts, deleteriously altering phospholipids of cell and mitochondrial membranes.

As will be detailed later, nonfunctional LA-based trans fats, oxidized LA entities, and inappropriate omega-6/omega-3 ratios (caused in part from normally recommended, yet supraphysiologic, marine oil supplementation) are all potential sources of unsaturated fatty acids—in particular, LA (Parent omega-6)—that can disrupt the normal membrane structure, significantly increasing the potential for cancer [11]. All of the supraphysiologic, excess EPA/DHA cannot be beta-oxidized away. Thus a significant amount of the excess will be physiologically incorporated into all cell membranes, detrimentally.

6. Arterial Intima: Endothelial Tissue Comprised of Epithelial Cells—CVD Explained
The innermost lining of arterial intima is endothelial tissue, comprised of epithelial cells containing significant LA, but no alpha-linolenic acid (ALA) [12, 13]. A significant biologic effect of oxidized LDL is its cytotoxic effect on cultured endothelial cells directly lining the arterial wall [14]. Dietary LA becomes adulterated (peroxidized) from food processing (described later) and deposited in arterial intimal cell membranes and leads to abnormal oxidation at the vascular injury site, thus causing injurious inflammation.

In this case, abnormal oxidation, caused by ex vivo radical induced lipid peroxidation (adulteration) of LA, involves formation of a hydroperoxide from LA by abstraction of a hydrogen atom as a radical from the doubly allylic methylene group between the two double bonds, followed by the addition of oxygen, a diradical, to make a hydroperoxide radical, which can then pick up another reactive hydrogen atom, perhaps from another LA molecule, to form the hydroperoxide. This, in turn, may break the O–O bond to form an alkoxide and a hydroxyl radical, which can continue to make more undesirable oxidized products [15]. Therefore, atherosclerosis can be prevented/arrested if endothelial cells remain fully functional [16].

Although lipid peroxidation can be caused by injury to tissue or aging, it does not have to be initiated in this fashion. Furthermore, a bivalent metal ion can cleave the O–O bond; nonfunctionality can occur from the commercial processing of the linoleic oil (LA).

7. Bis-Allylic Bonds: Fish Oil's Spontaneous Oxidation (Rancidity) at Room Temperature and In Vivo
Polyunsaturated fatty acids including LA contain the system HC=CH–CH2–CH=CH. Long-chain fatty acids contain bis-allylic hydrogens whereby the –C=C– units are separated by a single-bonded –C– (carbon) atom. The hydrogen atoms attached to each of these intermediate –C– atoms are called bis-allylic hydrogens and have the lowest C–H (weakest) bond-energies of the fatty acid chain. The weak bond makes them enormously susceptible to attack by reactive oxygen species (ROS) generated elsewhere in the body [17]. Because of the five double bonds in EPA and six double bonds in DPA, these metabolites are highly sensitive to temperature.

In particular, DHA, with its 6 double bonds, contains 5 bis-allylic bonds and is therefore 320 times more susceptible to oxidative attack, that is, becoming rancid, than monounsaturated oleic acid (18 : 1), which has no bis-allylic hydrogens in its chain. A saturated fat membrane containing just 5% DHA (fish oil) is 16 times more susceptible to peroxidative damage [18]. Fish oil's DHA is 7 times more susceptible to peroxidative damage than LA (Parent omega-6), the most significant fatty acid by both weight and functionality in the cell's bilipid membrane. The shifting of the body's antioxidants required to combat this physiologic insult causes a shortage elsewhere. This fact should cause the medical community great concern. Keeping tissue fluid in frigid waters is not a physiologic concern of humans.

7.1. Marine Oils Keep Membranes of Fish Fluid in Frigid Waters

The following underpublicized medical fact goes a long way toward explaining marine oil's tremendous cancer- causing potential in humans. Fatty, cold-water fish (the type we are told is best) live in temperatures as low as 32°F, but warm-water fish may live in 70°F waters and have 14Xs less EPA/DHA content than their cold-water relatives [19]. At normal human physiologic temperatures, fish oil spontaneously becomes rancid (as the above section detailed).

A human placed in ice-cold, frigid waters would suffer hypothermia, freeze, and likely die. Fish do not freeze because they have significantly higher levels of the EFA derivatives EPA and DHA than those in humans.

Our ambient and physiologic conditions are not similar to that of fish. Marine/fish oil researchers did not consider this important fact. EPA/DHA acts as “biological antifreeze” to fish living in frigid waters. Humans do not require such copious amounts because we have an internal temperature of 98.6°F. The deleterious effects when humans consume supraphysiologic amounts of marine oil's EPA/DHA are described next.

8. Primary and Secondary Lipid Oxidation and Hydroperoxides
There is much to know regarding specific lipid oxidation markers. Oxidative rancidity occurs in 3 distinct stages/phases: initiation, propagation, and ultimately termination. During the initiation stage, molecular oxygen combines with unsaturated fatty acids to produce hydroperoxides and free radicals, both of which are very reactive. Heat and light increase the rate of all phases. Then, the products of this stage react with additional lipids to form other reactive chemical species—often termed “autooxidation.” In the final termination (secondary) phase, relatively unreactive compounds are formed, including hydrocarbons, aldehydes, and ketones. Quantitative measure of all phases is required for a complete picture.

8.1. Malondialdehyde (MDA)/p-Anisidine Increases with Fish Oil/Marine Oil

Supplementation with polyunsaturated fatty acids in particular, EPA/DHA, as opposed to saturated fatty acids, results in a statistically significant increase in lipid peroxidation in the plasma and liver. Fish oil ingestion raises levels of extremely harmful malondialdehyde (MDA) [20]: “Ingestion of CLO [cod liver oil] was associated with an increase in MDA excretion in all six subjects. The mean increase of 37.5%, from 24.5 ± 3.5 μg to 34.7 ± 2.5 μg MDA (mean + SEM), was [statistically] significant and CLO ingestion again was associated with an increase in MDA excretion in all subjects. The mean increase of 54.3%, from 31.7 μg to 49.1 μg MDA/sample was highly significant.” Parent omega-6 (LA) undergoes—like all PUFAs—lipid peroxidation, but the amount of MDA produced is much, much lower than that by oxidation of EPA or DHA because MDA production requires at least 3 or more double bonds in a molecule.

The p-anisidine test measures the aldehyde content generated during decomposition of hydroperoxides. It correlates well with volatile substances. Volatile aldehydes and other later-stage aldehydes leave behind a nonvolatile product that the p-anisidine test measures well (via correlation). “Pristine” fish oil can have an allowable p-anisidine value of 19, clearly showing significant secondary stage oxidation [21], whereas a PEO formulation without fish oil is closer to a p-anisidine value of 4—confirming fish oil's substantial inherent propensity to become rancid at room temperature.

8.2. Thiobarbituric Acid Reactive Substances (TBARS) Increase with Fish Oil/Marine Oil

A 2000 study reported in the American Journal of Clinical Nutrition found that plasma TBARS (substances which react to the organic compound thiobarbituric acid and which are a result of lipid peroxidation) were >21% higher after fish-oil supplementation than after sunflower-oil supplementation (containing Parent LA, not derivatives) and 23% higher than after safflower-oil supplementation (containing Parent LA, not derivatives). The article explored the limitations of the various assays available for the measurement of lipid peroxidation in vivo, including the F2-isoprostane assay's inability to provide direct information about the peroxidation of 20:5n-3 (EPA) and 22:6n-3 (DHA) [22]. Fish oil oxidizes in plasma, producing numerous deleterious products. This long-term damaging effect is cumulative.

8.3. Clinical Proof and Verification of Fish Oil's Harmful Oxidation

Regardless of antioxidant level added to the fish oil supplement, rancidity/peroxidation upon ingestion (in vivo) becomes a very significant and problematic issue. Oxidation of EPA leads to generation of a mixture of aldehydes, peroxides, and other oxidation products. Highly polyunsaturated, long-chained EPA and more so with DHA, due to its additional double bond, is readily oxidized at room temperature even in the absence of exogenous oxidizing reagents. Importantly, in vivo, a large increase in tissue and plasma accumulation of fatty acid oxidation products is noted in subjects consuming fish oil even after addition of antioxidant supplements to the diet—this effect strongly suggests extensive oxidation of omega-3 fatty acids such as EPA in vivo. This deleterious effect is true as evidenced by the trial in which a 14% decrease in life expectancy occurred in those animals fed fish oil [23].

In humans and primates such as the monkey, no quantity of in vivo antioxidants will stop EPA/DHA damage as measured by lipofuscin, the peroxidized “age spots.” Lipofuscin was three-fold (3Xs) greater in the livers of monkeys fed fish oil. Furthermore, another measure of oxidative damage, the levels of basal thiobarbituric acid reactive substances (TBARS), was four-fold (4Xs) greater than that of the monkeys fed corn oil with no EPA/DHA. The researchers found that even a ten-fold (10Xs) increase in alpha-tocopherol, a potent antioxidant, was not fully able to prevent the peroxidative damage from fish oil [24].

9. Inflammation and the Cancer Connection
As per the above details, oxidation of marine oil's EPA/DHA is inherently inflammatory. Inflammation is now seen as causal to cancer as it is to CVD: “The connection between inflammation and cancer has moved to center stage in the research arena” [25]. This rewriting of the textbooks comes from one of the world's most renowned cancer researchers, Robert Weinberg of MIT (originator of the term “oncogene”), causing him to revise his leading textbook, The Biology of Cancer (Garland Science, 2006), to reflect this new understanding.

Prior sections detailed how fish oil causes inflammation in vivo because EPA/DHA spontaneously oxidize at room temperature and much more quickly at body temperature. Their harmful hydroperoxide products become incorporated in esterified cholesterol and it is well known in cardiology that oxidized cholesterol causes the inflammation leading to CVD. Increased cancer is expected with increased consumption of marine oils.

The inflammation/cancer connection is supported with the finding that asbestos causes inflammation, reported in 2010 in Medical News Today. “For the past 40 years researchers have tried to understand why asbestos causes cancer. This research emphasizes the role of inflammation in causing different types of cancer” [26, 27].

Inflammation alone, regardless of initiating conditions, accelerates cancer proliferation. Since 2007, cancer researchers understand and acknowledge that the fundamental, prime cause of cancer is inflammation, not genetics [28–30]. A further inflammation/cancer connection was reported in Cancer Epidemiology, Biomarkers & Prevention in 2005, with the statement that “There is a growing body of evidence supporting the role of chronic inflammation with prostate carcinogenesis and thus the associations of transfatty acids with increased inflammatory response may explain their associations with prostate cancer risk” [31]. The SELECT [3] showed that marine oil's DHA was more inflammatory than trans fats.

10. Parent-to-Derivative Amounts and Metabolism
What percentage of PEOs does become converted (naturally) to long-chain metabolites such as EPA and DHA? This important question must be addressed and answered before their correct supplemental dosage (if any) can be determined. This fundamental research was neglected concerning marine oils, which tragically led to recommendations of haphazard supraphysiologic overdoses of marine oil's EPA/DHA.

New, twenty-first century quantitative research from both NIH and USDA shows considerably lesser amounts of natural DHA conversion/usage from ALA than the medical community has been led to believe. These findings will be upsetting to those health professionals recommending fish oil prophylactically. The conversion amount is much less than the medical field assumes: it is less than 5%—often less than 1%—with at least 95% of PEOs staying in Parent form. This singular mistake of assuming very high conversion amounts, whereas in actuality their conversion amounts are extremely low, led to the irrational fish oil mania.

Contrary to wrong dogma, the enzymes that produce PEO derivatives (the delta-6 and delta-5 desaturase enzymes) are not impaired in the vast majority of patients [32]. Conversion of ALA (Parent omega-3) to DHA is unlikely to ever normally exceed 1% in humans [33].

Research at the United States Department of Agriculture's USDA Food Composition Laboratory (2001) reported a natural net conversion rate of a mere 0.046% of ALA to DHA and 0.2% to EPA—not the highly misleading 15% conversion rate that is often quoted [34]. This is a mistake of nearly 2 orders of magnitude (100-fold). In 2009 NIH researchers determined the amount of DHA utilized in human brain tissue to be a mere 3.8 mg ± 1.7 mg/day. Therefore, based on the variance, brain tissue in 95% of all subjects, allowing for variation in brain size, would consume no more than 0.4 mg–7.2 mg of DHA per day [32].

10.1. No Delta-6/-5 Desaturase Widespread Impairment in (Average) Patients

Highly accurate, quantitative experiments were performed showing that both animals and the average healthy person are quite capable of metabolizing adequate amounts of DHA from Parent omega-3 (ALA).

As will be clearly demonstrated, there is no widespread impairment in the typical patient whatsoever; the normal conversion amounts are simply very low. These conversion amounts are extremely small and naturally limited. This mistake often leads to suprapharmacologic recommendations and can potentially overdose patients by factors of 20-fold to 500-fold, depending on specific supplement and amounts prescribed.

Because the body cannot oxidize away these tremendous overdoses of EPA/DHA, they become incorporated into tissue and organs with deleterious effects as confirmed by the skyrocketing increase in all epithelial-based cancers (described later). Supraphysiologic amounts are forced into tissue, causing gross physiologic imbalance and great potential for harm.

An important experiment measuring plasma fatty acids in 62 fire fighters concluded that the consumption of ALA-enriched (Parent omega-3) supplements over a 12-week period elevated levels of long-chain metabolites EPA and DHA. This experiment unequivocally showed the unimpaired effectiveness of ALA conversion from Parent omega-3. The researchers further stated that the general population could achieve the amounts of ALA required to obtain these effects by modifying their diet, ensuring adequate ALA (Parent omega-3) [35].

10.2. Vegans—Consuming No Fish—Produce Sufficient DHA

Even vegetarians consuming little or no fish had acceptable EPA/DHA levels [36]. This is a group that absolutely would be expected to manifest gross neurological abnormalities, including both visual impairment and cognitive impairment, yet there is no clinical evidence of such neurologic and cognitive abnormalities in vegetarians [36, 37].

Confirmation in 2010 showed that vegetarians with an intake of 0.3% DHA compared to fish eaters produced 85% of the EPA levels and 83% of the DHA levels that consumers of fish did. These amounts are within the “normal” ranges [37].

10.3. Rodents Have a 50-Fold Safety Margin: Would Not Humans?

Rats fed a DHA-free but α-LNA (n-3 PUFA) (Parent omega-3) adequate diet naturally produced from Parent omega-3 (ALA) fifty times (50Xs) more DHA than their brains required [38]—an enormous “safety factor.” Certainly, nature would ensure humans the same margin of safety shown to a rodent. This result in an animal species clearly supports highly quantitative 21st century research from the National Institutes of Health (NIH) finding extremely low—yet adequate—natural conversion rates in humans [32].

11. Amounts of EPA/DHA in Fish Oil Supplements: Pharmacological Plasma Overdoses
Given the above analyses, how much EPA/DHA does the typical marine oil/fish oil supplement provide? An average 1,000 mg health-food-grade fish oil capsule contains approximately 180 mg EPA and 120 mg DHA. Pharmaceutical-grade versions contain higher doses. Furthermore EPA [left and right double arrow ] DHA. This is not the case with PEOs. They are unidirectional. The American Heart Association states that those with documented CHD are advised to consume about 1 gm (1,000 mg) of EPA + DHA per day. Is this advice rational? No.

As an example, using the USDA food composition research formulas covered earlier, if patients consumed a supplement of 600 mg of Parent ALA, they would naturally convert it to EPA by no more than the (generous) factor of 0.25% = 1.5 mg EPA and 1.5 mg × 0.63 × 0.37 = 0.35 mg to DHA in patient plasma. Therefore, just one capsule provides the amounts shown in the analysis below, and many people are overdosing even more by taking 2 to 4 fish oil capsules each day, likely in part because the cardiology and heart recommendations are often “EPA + DHA ranging from 0.5 to 1.8 grams per day.” What overdose does this translate to?

11.1. Potential EPA/DHA Overdoses Are Frequent

Potential Overdose equates to the following plasma overdoses: EPA = 180 mg/1.5 mg = 120 times overdose and DHA = 120 mg/0.35 mg = 340 times overdose. These facts should cause great pause and concern. (Technically, a bit more is required for additional metabolic pathways aside from direct tissue incorporation like prostaglandin production, but it is not a significant amount by weight on a daily basis.) The medical community and most physicians and other health professionals may unknowingly be overdosing patients prophylactically with supraphysiologic supplemental amounts of omega-3 derivatives.

12. The Significant Problem: Radical Induced Lipid Peroxidation—Food Processors Require Long Shelf Life
Radical induced lipid peroxidation (adulteration) of omega-6 fats—in particular, LA—is created by food processors' need for long oil life during frying and baking, especially because their use of saturated fats is avoided. Omega-3 fats are never used in cooking; they are far too reactive.

Abnormal peroxidation of the Parent omega-6 oil (LA), therefore, is the core of the EFA-based deficiency. It has nothing to do with marine oils and everything to do with the adulteration of the plant-based Parent essential oil, LA. For example, trans fats—to some extent—are found in all commercial restaurants, supermarkets' prepared food and frozen food sections, and even in fine-dining restaurants' frying oils. The substrate for trans fats is Parent omega-6 (LA). Just 0.5 grams of a 1% trans fat containing adulterated oil (a conservative amount) is very harmful to humans. Even with the FDA's 2014 ban on trans fats, the FDA allows <0.5 grams/serving to be labeled as zero (0). Yet, this apparently negligible amount contains enough trans fats to overpower each cell in the body by a factor of approximately 3,600 [39].

12.1. Cellular Oxygenation Maximized with Unadulterated LA—Parent Omega-6

Marine/fish oils do nothing to promote cellular oxygenation in the mitochondria—this is a key role exclusive to Parent omega-6 (LA) [10, 40]. Marine oils, due to their inherent inflammatory property in vivo, cause the opposite of the desired effect and are therefore deleterious.

12.2. Pathophysiology Effects from Damaged Cell Membranes Caused by Radical Induced Lipid Peroxidation

With functional LA deficiency there is an enormous increase in permeability of epithelial tissue and an increase in capillary fragility, further explaining the pathophysiology of CVD and how it may be prevented [41]. Oxidation of LDL-C causes significant depletion of LA (Parent omega-6) [14]. Because LDL cholesterol is the transport vehicle for PEO delivery into the cell (described below), LDL cholesterol will transport LA into cells, whether the LA is defective or not (such as oxidized or trans entities).

Of great importance is the fact that with ingestion of marine/fish oil (EPA/DHA) there was a corresponding decrease in tissue's LA, causing pathophysiologic deficiency [42].

13. Tissue Incorporation of Dietary Fats is Proportional to Consumption
The concentration in adipose tissue triacylglycerols is roughly proportional to dietary concentration and is now frequently used as a measure of relative dietary intake. It has been long known that the fatty acid composition of the diet can influence membrane fatty acid composition [43, 44].

Fortunately, tissue alteration caused by supraphysiologic amounts of marine oil consumption can be remedied. Once removed, it takes 18 weeks to fully rid patients of the negative effects of fish oil [45].

Who Sponsors your Experts? Posted on May 14, 2014, 0 Comments

I Went to the Nutritionists' Annual Confab. It Was Catered by McDonald's.

Our national nutrition experts are in bed with Big Food. And we wonder why we're fat.
By Kiera Butler | Mon May. 12, 2014 

Our nutrition experts are in bed with Big Food. And we wonder why we're fat.

McDonald's sponsored the annual conference of the California branch of the nutritionists' professional organization. Kiera Butler
One recent Friday afternoon, in a Mariott Hotel ballroom in Pomona, California, I watched two women skeptically evaluate their McDonald's lunches. One peered into a plastic bowl containing a salad of lettuce, bacon, chicken, cheese, and ranch dressing. The other arranged two chocolate chip cookies and a yogurt parfait on a napkin. "Eww," she said, gingerly stirring the layers of yogurt and pink strawberry goop. The woman with the salad nodded in agreement, poking at a wan chicken strip with her plastic fork.

When I asked how they were liking their lunches, both women grimaced and assured me that they "never" go to McDonald's. So why were they eating it today? Well, they didn't really have a choice. The women were registered dietitians halfway through day two of the annual conference [1] of the California Dietetic Association [2] (CDA). They were hoping to rack up some of the continuing education credits they needed to maintain their certification. McDonald's, the conference's featured sponsor, was the sole provider of lunch. "I guess it's good to know that they have healthier options now," said the woman with the salad.

As I wandered the exhibition hall, I saw that McDonald's wasn't the only food company giving away freebies. Cheerful reps at the Hershey's booth passed out miniature cartons of chocolate and strawberry milk. Butter Buds offered packets of fake butter crystals. The California Beef Council guy gave me a pamphlet on how to lose weight by eating steak. Amy's Naturals had microwave brownies. The night before, Sizzler, California Pizza Kitchen, Boston Market, and other chain restaurants had hosted a free evening buffet for conference-goers: "Local Restaurant Samplings for Your Pleasure."

And that wasn't all. The sessions—the real meat and potatoes of the conference—had food industry sponsors as well. The Wheat Council hosted a presentation about how gluten intolerance was just a fad, not a real medical problem. The International Food Information Council [3]—whose supporters [4] include Coca-Cola, Hershey, Yum Brands, Kraft, and McDonald's—presented a discussion in which the panelists assured audience members that genetically modified foods were safe and environmentally sustainable. In "Bringing Affordable Healthier Food to Communities," Walmart spokespeople sang the praises of (what else?) Walmart.

After lunch, I attended "Sweeteners in Schools: Keeping Science First in a Controversial Discussion." Sponsored by the Corn Refiners Association, whose members produce and sell high-fructose corn syrup, it included a panel composed of three of the trade group's representatives. The panelists bemoaned some schools' decision to remove chocolate milk from their cafeteria menus. Later, one panelist said that she'd been dismayed to learn that some schools had banned sugary treats from classroom Valentine's Day parties, which "could be a teachable moment for kids about moderation." The moderator nodded in agreement, and added, "The bottom line is that all sugars contain the same calories, so you can't say that there is one ingredient causing the obesity crisis." The claim was presented as fact, despite mounting scientific evidence [5] that high-fructose corn syrup prompts more weight gain than other sugars.

The School Nutrition Association has asked Congress to lift the rule that students must take fruits and vegetables on the lunch line.
Later, I asked conference spokeswoman Pat Smith whether she thought it was fair to present such a one-sided discussion. She claimed that the sponsors did not influence any of the content in the program. "We like to think that our dietitians have a thought process and that we are presenting them with what is out there," she said. "They need to make their own decisions on what they have listened to and apply that to their client base."

"But it's hard to make a decision if you're only hearing one side of the story," I countered.

She told me that she hadn't known beforehand that the Corn Refiners panel would be composed entirely of its own representatives. And yet, when I asked her how the panel was chosen, she explained that it was approved by a committee. She also confirmed that the Corn Refiners had paid for the panel, but she declined to say how much. (She had previously declined me press credentials for the conference, explaining that the CDA would have its own journalists covering the event.)

With 75,000 members, the CDA's parent organization, the national Academy of Nutrition and Dietetics [6] (AND), is the world's largest professional association for nutritionists and dietitians. It accredits undergraduate and graduate programs in nutrition science and awards credentials to dietitian degree candidates who pass its exam. In Washington, its lobbying arm is active on issues including childhood obesity, Medicare, and the farm bill.

It also has strong ties to the food industry. In 2013, Michele Simon, a public health lawyer and food politics blogger [7], launched an investigation (PDF [8]) into the academy's sponsorship policies. Simon found that its corporate support has increased dramatically over the past decade: In 2001, the academy listed just 10 sponsors. By 2011 [9], there were 38, including Coca-Cola, PepsiCo, Nestlé, National Cattlemen's Beef Association, Mars, and many others. Corporate contributions are its largest source of income, generating nearly 40 percent of its total revenue.

Simon also learned that in 2012, Nestlé paid $47,200 for its 2,500-square-foot display in the exhibition hall at the annual AND conference, and PepsiCo paid $38,000 for 1,600 square feet. The academy's position papers, she noted, state that its sponsors do not influence its positions on controversial issues. And yet it often takes a pro-industry stance. When New York City was considering a ban on sales of oversized sodas, for example, the academy opposed it.

"No wonder Americans are overweight and diabetic. The gatekeepers for our information about food are getting their information from junk-food companies."
AND is not the only powerful nutritionists' group with strong corporate ties. The sponsors [10] of the School Nutrition Association [11]'s 2013 annual conference included PepsiCo, Domino's Pizza, and Sara Lee. SNA made headlines [12] recently when it asked Congress to lift the rule that students must take fruits and vegetables on the lunch line, and to ease the rules around sodium and whole grains.

Marion Nestle [13], a New York University nutritionist, wrote about nutritionists and corporate sponsorships in her 2007 book, Food Politics: How the Food Industry Influences Nutrition and Health [14]. "I worry a lot about food industry co-optation of my profession," she wrote to me in an email. "Food companies are smart. They know that if they can make friends and help inform dietitians and nutritionists that the people they are supporting or helping will be reluctant to suggest eating less of their products."

Andy Bellatti [15], a dietitian and member of AND, recalls his shock the first time he attended the organization's national conference, in 2008. "I could get continuing education credits for literally sitting in a room and listening to Frito-Lay tell me that Sun Chips are a good way to meet my fiber needs," he says. "I thought, 'No wonder Americans are overweight and diabetic. The gatekeepers for our information about food are getting their information from junk-food companies.'"

Bellatti took photos of the displays in the exhibition hall and posted them on his blog. The post started a conversation among academy members, many of whom were outraged when they learned about the sponsorships. They worried that if word got out that dietitians' professional organization had been bought out by food corporations, the profession would lose credibility. So Bellatti and several other members founded Dietitians for Professional Integrity [16], consisting of academy members who want to change the sponsorship policies. They lobbied the leadership, but nothing changed—except for the rules about photography at the annual conference. The following year, when Bellatti took out his camera in the exhibition hall, he was told that photographs were prohibited.

Simon, the author of the 2013 report, found in a survey of AND members that four-fifths believed "sponsorship implies Academy endorsement of that company." Just as many said that they thought members should have a say in selecting the sponsors, and most said that they would be willing to pay higher dues in order to avoid having so many corporations represented at the annual conference.

I asked AND spokesman Tom Ryan whether the academy has any plans to review its rules for food industry sponsors. He referred me to the academy's corporate sponsorship website [17], which contains no suggestion of forthcoming changes. When I pressed him on it, Ryan replied, "I am not going to respond to that question."

At the CDA conference I attended, most of the dietitians I talked to said that they did not realize the sessions were sponsored by companies. "I hope they're telling us the real science," said one graduate student attendee.

At the McDonald's booth, company spokespeople told conference attendees about McDonald's healthy menu options. 
Toward the end of the day, I spoke to a 65-year-old retired dietitian from Orange County. She told me she'd been attending CDA's annual conferences for 30 years. Shaking her head, she said that she didn't approve of the trend of junk-food sponsors. "I guess they need the money, but this is pathetic," she said, rolling her eyes. She found the McDonald's lunch particularly deplorable. "A dietitian you'd expect to be principled," she said. "But here I feel like we're sleeping with the enemy."

Source URL:
[9] http://file:///home/chronos/user/Downloads/AnnualReport_2011.pdf

Statins, Cholesterol, and One Medical Professional's Experience Posted on March 28, 2014, 1 Comment

Why I've ditched statins for good

As experts clash over proposals that millions more of us take statins to prevent heart disease and stroke, a vascular surgeon explains why he feels better without them

Dr Haroun Gajraj: 'After looking more closely at the research, I’d concluded that statins were not going to save me from a heart attack and that my cholesterol levels were all but irrelevant.
Dr Haroun Gajraj: 'After looking more closely at the research, I’d concluded that statins were not going to save me from a heart attack and that my cholesterol levels were all but irrelevant.  

When I had a routine health check-up eight years ago, my cholesterol was so high that the laboratory thought there had been a mistake. I had 9.3 millimoles of cholesterol in every litre of blood — almost twice the recommended maximum.

It was quite a shock. The GP instantly prescribed statins, the cholesterol-lowering drugs that are supposed to prevent heart disease and strokes. For eight years, I faithfully popped my 20mg atorvastatin pills, without side effects. Then, one day last May, I stopped. It wasn’t a snap decision; after looking more closely at the research, I’d concluded that statins were not going to save me from a heart attack and that my cholesterol levels were all but irrelevant.

When I informed my GP of my decision three months later, I wasn’t entirely honest. Rather than say I was sceptical about the drugs, I told my doctor I’d quit the statins because they were causing pain in my arm.

He didn’t bat an eyelid. Evidence from the drug industry published this month – evidence I suspect was heavily reliant on data from the drug industry, as Dr James Le Fanu pointed out on these pages last week – may suggest that side effects are uncommon, but previous studies have found that one in five people on statins suffers adverse side effects, from muscle pain and diarrhoea to memory loss and blurred vision.

The GP simply suggested I try another brand of statin. The sooner the better, he said, given that I’d already been off my prescription for three months. “Hang on,” I said. “Could you give me a blood test first?” When the results came back, he was amazed that my total blood cholesterol was lower than when I’d been on statins. After three months without the pills, it was 5.4mmol/l (5.4 millimoles per litre of blood) compared with 5.7 mmol/l a year earlier.

The only major changes I’d made to my lifestyle since coming off statins were eliminating sugar (including alcohol and starchy foods such as bread) and eating more animal fat. Many experts now believe that sugar is emerging as a true villain in the heart-disease story; while after decades of demonisation, saturated fat has been acquitted of causing heart disease by a recent “meta” analysis of 70 studies by Cambridge University.

Typically, I was eating red meat three or four times a week and enjoying butter, full-fat milk and plenty of eggs. You would have thought that after three months on a diet so high in saturated fat, my cholesterol would have shot back up to pre-statin levels — but no, it came down and has stayed down seven months on. Not only that, but my levels of LDL (so-called bad cholesterol) were also lower than when I’d been on statins, and my ratio of HDL (so-called good cholesterol) to LDL was under four for the first time, an excellent sign, according to medical wisdom.

Not that I cared about any of this.

Yes, it was the statins that originally reduced my cholesterol levels so dramatically. But so what? I believe that high cholesterol has been a scapegoat for too long. Yes, it may, in some circumstances, be an indicator of heart disease but there is no evidence of a causal link. In my view, high total blood cholesterol or high LDL levels no more cause heart attacks than paramedics cause car crashes, even though they are present at the scene.

Just lowering cholesterol with drugs without sorting out the dietary and lifestyle factors that actually cause heart disease is nonsensical. Besides, there are plenty of other, more reliable indicators of heart-disease risk. What further astonished my GP was that on these indicators I was now apparently better off in other ways than when I’d been on statins. My blood pressure was down. For the first time in years, I was slimmer, especially around the belly. My triglycerides — a type of blood fat with a causal link to heart disease — were lower than at any time in the preceding eight years. My fasting blood glucose was at the optimum level, whereas a year earlier it had been too high. My total white blood count — a marker of inflammation — was lower.

My blood test for a marker called glycated haemoglobin (A1c), high levels of which are associated with heart disease and overall mortality, were bang on normal. Finally, my level of c-reactive protein (CRP) — a protein that rises in response to inflammation — was extremely low. So, biochemically, I was in excellent shape, better than when I’d been on the statins. “Have you taken up running?” asked my bemused GP.

No, I’d always run. For years, I’d exercised three times a week, eaten plenty of fish, refrained from smoking and tried to keep my stress levels low. The only thing I’d changed was my intake of sugar and animal fat.

That check-up was seven months ago and now, at 58, I’m not on a single tablet. My GP is happy. I feel better than I have in years and, at the same time, deeply concerned about proposals advising even wider use of statins.

Until 2005, statins were prescribed only to those with at least a 30 per cent or greater risk of having a heart attack within 10 years. This was then reduced to a 20 per cent risk. Now, draft NHS guidelines would have them dished out to those with just a 10 per cent risk — in other words, most men over the age of 50 and most women over the age of 60.

I am a vascular surgeon. Before founding a private clinic in Dorset 11 years ago, specialising in varicose veins, I worked in the NHS for 13 years. Back then, I didn’t question medical guidance on cholesterol, and thought statins were a wonder drug. And so they probably are, for men who have heart disease — not necessarily because they lower cholesterol, but because they may cut other risks such as the inflammation-marker CRP. Exercise, weight loss and omega 3 supplements also lower CRP.

But what about other groups — women, the elderly and people like me who have not been diagnosed with heart disease? The evidence that we will benefit from cholesterol-lowering drugs is ambiguous at best. The 2011 Hunt 2 study, one of the most recent and largest, followed 52,000 men and women in Norway aged 20-74 with no pre-existing heart disease, for 10 years.

The results for women were crystal clear. The lower a woman’s total cholesterol, the greater her risk of dying, either of heart disease or anything else, including cancer. This reflects findings in previous studies.

For men, high cholesterol was associated with heart disease and death from other causes. But so, too, was low cholesterol — below 5mmol/l. Again, this is only an association, not a causal link. A range of between 5mmol/l and 7mmol/l was the optimum level. Guess what? This is already the national average. In addition, numerous studies have linked high cholesterol levels with increased longevity in the elderly.

As for me, I have not been diagnosed with heart disease, and nobody in my family has had a heart attack. However, all four of my paternal uncles and my sister have diabetes. Research from Canada, published last year in the BMJ, has shown that statins raise the risk of diabetes, so that gives me little faith. The controversy over these drugs was reignited last week when Prof Sir Rory Collins from Oxford University warned that doctors’ hesitancy about prescribing them to those at risk could cost lives.

GPs are, by definition, generalists. They don’t have time to read and analyse data from every paper on every medical condition. Even so, in a recent survey by Pulse magazine, six in 10 GPs opposed the draft proposal to lower the risk level at which patients are prescribed statins. And 55 per cent said they would not take statins themselves or recommend them to a relative, based on the proposed new guidelines.

If that doesn’t speak volumes, I don’t know what does.

Original article can be found here:

What's So Important about Posture? Posted on February 11, 2014, 2 Comments

"Postural anomalies create fascial tensions, which interfere with visceral function."

- Guy Voyer, The ELDOA

Your Mom Could Be Put in Jail If She Tells You to "Eat Your Veggies" Posted on January 21, 2014, 0 Comments

Original article can be found here:

When it comes to nutrition, it is very important that you have the right to freedom of choice and information. Unfortunately, organizations such as the American Dietetic Association (now calling itself the Academy of Nutrition and Dietetics or AND) are threatening your freedom of choice about health and nutrition.

The AND has pushed state laws to block almost anyone, except their registered dietitians (RDs), from legally giving nutritional advice.

Their mission is to censor the broader nutrition community, which includes many well trained and educated practitioners, such as clinical nutritionists, pharmacists, naturopathic doctors and traditional naturopaths, acupuncturists, herbalists, nurses, mental health professionals, homeopaths, personal trainers, and the like.

Though it may seem incredible that laws have been crafted to create a de facto monopoly for one private group, this is exactly what's happened. Why should you be concerned?

Your most fundamental tool for staying healthy is your ability to pursue different avenues and philosophies of care, and based on that information, decide which are best for you.

If your goal is optimal health, you have to address your nutrition—it's the most fundamental factor. Just as you can choose from a number of different healthcare providers for your medical needs (MDs, DOs, NDs, ANPs, chiropractors, etc.), you should also be free to choose your nutrition practitioner.

The Nutrition Monopoly Is Beginning to Crumble

For decades, the broader nutrition community, which includes a diverse set of practitioners using tools of nutrition integrated into various kinds of practice, was not organized as a cohesive group. Legislators were hearing from only the well organized and heavily funded dietitians.

Dietetic licensure bills, designed to keep everybody else out, have met little resistance and have been signed into law in state after state. With little to no credible evidence, legislators have been sold on scare stories of potential harm to the public and misinformation about other trained and qualified professionals. But the tide is turning!

Over the last two years, no state has passed a law giving dietitians exclusive practice rights. This is largely due to the efforts of Center for Nutrition Advocacy, tirelessly spearheading this work, organizing and advocating for the broader nutrition community. The Center helps build coalitions in any state where a dietetics monopoly needs to be prevented or overturned. Why is such a coalition necessary?

Desperate to protect their monopoly, the well funded AND will stop at nothing to hunt down and push over anyone standing in their way. If you think this is an exaggeration, let's take a look at the evidence.

ANH-USA Uncovers Devious Activity by State Dietetic and Health Boards

The extreme measures the establishment is willing to take to protect their nutrition monopoly is quite shocking. In an exclusive report, the Alliance for Natural Health (ANH-USA) reveals finding government surveillance, undercover sting operations, and investigations of nutrition professionals into the alleged crime of "practicing nutrition without a license."

According to ANH-USA:

"These actions, together with the levying of criminal penalties, have been undertaken by state health departments and state dietetics boards that are enforcing monopolistic laws sponsored by the Academy of Nutrition and Dietetics. More often than not, they are supported by local law enforcement or the offices of state attorneys general.

The AND—formally the American Dietetic Association, or ADA—is not a medical organization, but a trade group that represents the interests of Registered Dietitians (RDs, who are certified by the AND's credentialing arm). The AND has about 74,000 members.

These non-RD nutrition professionals are being targeted by these states' RD monopoly laws, despite the fact that many of them have advanced degrees and a tremendous number of clinical hours to their credit. They are being prosecuted for 'practicing dietetics without a license' or for referring to themselves as 'a nutritionist' in media or marketing materials."

One of AND's key strategies is to create a dietetics board, comprised of RDs, to enforce the law in any state that passes an RD monopoly bill. This board can levy hefty fines against any nutritionist who is not an RD, put practitioners out of business, and even urge state Attorneys General to file criminal charges, allegedly to "protect the public health."

After combing through three years of records, ANH-USA failed to find even one case of an unlicensed nutrition practitioner causing harm to a patient, and not one consumer complaint had ever been filed. In fact, the only complaints were those filed by RD board members themselves.

In other words, no evidence whatsoever could be found that an open and competitive market for nutrition services endangers public health and safety. As of May 2013, only 24 states had passed restrictive nutrition counseling laws. The remaining states realize that this push has nothing to do with protecting the public, and everything to do with eliminating the competition.

The Steve Cooksey Witch Hunt

Organizations like AND are trying to use the legislative system to create an unfair monopoly in the same way physicians have (via the AMA). Their goal is simple: eliminate the competition. Paleo Blogger Steve Cooksey found himself in exactly that position—targeted by the AND because he was considered to be "the competition."

The North Carolina Board of Dietetics/Nutrition launched an attack on Cooksey's blog featuring nutritional principles of the Paleo Diet, accusing the blogger of practicing nutritional counseling without a license. In response, he filed a lawsuit against the board for violating his First Amendment rights. Unfortunately, his story is not unique.

Similar witch-hunts are being conducted across the country. In 2012, the Department of Health devoted 681 hours, at a cost of $19,857, to investigating those practicing nutrition without a license, which represented a 229 percent increase over the previous two years.Telling people to "eat their vegetables" may land you in jail, or hip deep in legal expenses—or worse. And all of this effort is to protect the public from a risk that doesn't even exist.

The AND has even stooped so low as to offer prizes to its members for spying and snitching on the competition. In internal documents leaked to Forbes by outraged AND members, the goal and strategies to limit marketing competition are openly discussed, including spying on private citizens and conspiring to use the monopoly laws against them.

For example, RDs in MI participated in a "Documentation of Harm Contest." Those who completed and submitted the most "Documentation of Harm" forms were eligible to win free registration to Michigan's annual conference. Documentation of Harm forms, used in every state now, are essentially a complaint form filled out by an RD to target unlicensed nutritionists caught in the "dangerous" act of giving dietary advice. In 2012 AND unveiled a program to train RDs to "hunt for harm" and report it. In MA RDs are encouraged to question each client and even the RDs own relatives about non-RD practitioners they have seen, and to "help" the client fill out the complaint forms! These completely unvetted tattle tales are then offered to legislators as evidence.

Continuing Education Brought to You by... Kellogg, Coca-Cola and ConAgra!

The dietary advice provided by the Academy of Nutrition and Dietetics and their minions is quite poor because it's based on information from the processed food industry. You may not be aware that the AND is partnered with and sponsored by junk-food giants, including Coca-Cola, PepsiCo, Mars, and Kellogg. Consequently, dietary advice from many RDs is likely to be heavily biased by information from food-industry bigwigs.

Case in point: the AND's annual conference is often called "the world's largest meeting of food and nutrition experts." Interestingly, these conferences are absent of any true nutritional experts whose knowledge could make a positive impact on Americans' health. But they do showcase numerous representatives from processed food and junk-food giants. Here is a profile of AND's food industry sponsorship:
•In 2001, AND listed 10 food industry sponsors; their 2011 annual report lists 38
•Since 2001, the most loyal AND sponsor is the National Cattleman's Beef Association
•ConAgra and General Mills have been AND sponsors for 10 of the last 12 years; Kellogg and the National Dairy Council for nine of the 12
•At the expo, based on square footage, only about 12 percent of the exhibitor floor space was occupied by fruit and vegetable vendors—the remainder was occupied by processed food representatives
•The credentialing arm of the ANA offers "continuing education" provided by Coca-Cola, Kraft Foods, Nestle, Mars, and PepsiCo—the very companies that make the foods you need to eat LESS of in order to stay healthy and fight obesity, heart disease, diabetes, cancer and countless other chronic diseases!

Nutrition Monopoly Bound to Result in Seriously Flawed Advice

Allowing industry representatives to provide continuing education is problematic on many levels. The food industry is not in the education business—it's in the sell-more-food business. And attaching the name "council" or "academy" does not automatically mean your information is evidence-based. The processed food industry cherry-picks research and spins it to get favorable outcomes—meaning, better sales. More often than not, this has nothing to do with real science.

It's no surprise that the AND claims sugar, artificial sweeteners, artificial colors, and fluoride are safe for children. The organization receives about $1 million a year from the pharmaceutical industry and takes no issue with pharmaceutical companies marketing their drugs at AND events.

Essentially, most RDs are getting the same corporate sponsored education as physicians, much of it riddled with bias, and a good deal of it is just industry propaganda cleverly cloaked as science. A great example of this is the perverted scientific misinformation propagated by the media through agencies like the Science Media Center, which exist for the sole purpose of promoting the industry agenda.

That said, there are some RDs who have banded together to fight for reform. They have formed an organization called Dietitians for Professional Integrity, aimed at pushing for more transparency and independence from industry. When you examine the evidence, it's very clear: the real mission of the AND is to support the processed food and pharmaceutical industries, rather than improve public health. Unfortunately, many people will adopt their nutritional advice, and their health will suffer as a result.

The Tides Are Turning—Michigan Steps into the Lead

Michigan is poised to become the latest state to reverse the dietetics monopoly. On November 13, 2013, the Michigan House passed a bill to repeal Michigan's 2006 Dietetics Nutrition Licensing law, which had erected a de facto monopoly for registered dietitians. CNA coalition members in Michigan expressed a willingness to collaborate with dietitians to engineer a bill that wasn't "RD-centric" and would give much broader practice rights.

However, as the dietitians have been unwilling to make any meaningful concession, repealing the current law is the only option at the moment to protect non-RD nutrition practitioners, retail businesses, and consumers in Michigan. "We will always remain willing to discuss alternatives" said Michigan Nutrition Association Executive Director Judy Stone, "but the current law simply cannot stand because it is clearly in the interests of no one except registered dietitians."

The Michigan Senate has the repeal bill HB 4688 on deck, but first the Chair and members of the Senate Regulatory Reform Committee must be convinced by constituents to hold a hearing on the bill, which hasn't happened yet. If you live in Michigan or know people in Michigan, you can help ensure the passage of this bill, which is one more step in protecting your freedom of choice about your nutrition and healthcare. For information about the Michigan repeal or any other state, check out CNA, where you can also sign up to be among the first to know if something is happening in your state.

Final Thoughts

The Center for Nutrition Advocacy is the clearinghouse for up-to-date information on legislation that affects practice rights and access rights to meaningful nutrition information not sponsored by the junk food giants. It's outrageous to think that only one group—especially one that promotes nutrition practices that are frequently BAD for your health—should control whom you consult for nutrition advice.

CNA will be holding a free webinar tomorrow, Jan 22 at 5pm PT/7pm CT/8pm ET to discuss licensing nationwide and its impact on anyone who uses nutrition in their work.

There is still much work to be done to educate legislators about the differences between dietitians and nutritionists, so that they don't blindly vote for regulations that interfere with practice rights or your right to choose a practitioner. Remember, choose your practitioner carefully—just as you can receive bad advice from a registered dietitian, you can receive equally bad advice from a poorly educated non-RD nutritionist. You need to thoroughly vet ALL of your healthcare providers, and diet/nutrition is no exception.

R.I.P. Nelson Mandela Posted on December 06, 2013, 0 Comments

NYTimes Op-Ed about New Cholesterol Recommendations Posted on November 15, 2013, 0 Comments

Don’t Give More Patients Statins

ON Tuesday, the American Heart Association and the American College of Cardiology issued new cholesterol guidelines that essentially declared, in one fell swoop, that millions of healthy Americans should immediately start taking pills — namely statins — for undefined health “benefits.”

This announcement is not a result of a sudden epidemic of heart disease, nor is it based on new data showing the benefits of lower cholesterol. Instead, it is a consequence of simply expanding the definition of who should take the drugs — a decision that will benefit the pharmaceutical industry more than anyone else.

The new guidelines, among other things, now recommend statins for people with a lower risk of heart disease (a 7.5 percent risk over the next 10 years, compared with the previous guidelines’ 10 to 20 percent risk), and for people with a risk of stroke. In addition, they eliminate the earlier criteria that a patient’s “bad cholesterol,” or LDL, be at or above a certain level. Although statins are no longer recommended for the small group of patients who were on the drugs only to lower their bad cholesterol, eliminating the LDL criteria will mean a vast increase in prescriptions over all. According to our calculations, it will increase the number of healthy people for whom statins are recommended by nearly 70 percent.

This may sound like good news for patients, and it would be — if statins actually offered meaningful protection from our No. 1 killer, heart disease; if they helped people live longer or better; and if they had minimal adverse side effects. However, none of these are the case.

Statins are effective for people with known heart disease. But for people who have less than a 20 percent risk of getting heart disease in the next 10 years, statins not only fail to reduce the risk of death, but also fail even to reduce the risk of serious illness — as shown in a recent BMJ article co-written by one of us. That article shows that, based on the same data the new guidelines rely on, 140 people in this risk group would need to be treated with statins in order to prevent a single heart attack or stroke, without any overall reduction in death or serious illness.

At the same time, 18 percent or more of this group would experience side effects, including muscle pain or weakness, decreased cognitive function, increased risk of diabetes (especially for women), cataracts or sexual dysfunction.

Perhaps more dangerous, statins provide false reassurances that may discourage patients from taking the steps that actually reduce cardiovascular disease. According to the World Health Organization, 80 percent of cardiovascular disease is caused by smoking, lack of exercise, an unhealthy diet, and other lifestyle factors. Statins give the illusion of protection to many people, who would be much better served, for example, by simply walking an extra 10 minutes per day.

Aside from these concerns, we have more reasons to be wary about the data behind this expansion of drug therapy.

When the last guidelines were issued by the National Heart, Lung, and Blood Institute in 2001, they nearly tripled the number of Americans for whom cholesterol-lowering drug therapy was recommended — from 13 million to 36 million. These guidelines were reportedly based strictly on results from clinical trials. But this was contradicted by the data described in the document itself.

For example, even though the guidelines recommended that women between the ages of 45 and 75 at increased risk of heart disease and with relatively high LDL levels take statins, the fine print in the 284-page document admitted, “Clinical trials of LDL lowering generally are lacking for this risk category.” The general lack of evidence for LDL level targets is why they have been dropped from the current guidelines. In fact, committee members noted that cholesterol lowered by drugs may not have the same effect as cholesterol lowered by nondrug methods, such as diet, exercise and being lucky enough to have good genes.

The process by which these latest guidelines were developed gives rise to further skepticism. The group that wrote the recommendations was not sufficiently free of conflicts of interest; several of the experts on the panel have recent or current financial ties to drug makers. In addition, both the American Heart Association and the American College of Cardiology, while nonprofit entities, are heavily supported by drug companies.

The American people deserve to have important medical guidelines developed by doctors and scientists on whom they can confidently rely to make judgments free from influence, conscious or unconscious, by the industries that stand to gain or lose.

We believe that the new guidelines are not adequately supported by objective data, and that statins should not be recommended for this vastly expanded class of healthy Americans. Instead of converting millions of people into statin customers, we should be focusing on the real factors that undeniably reduce the risk of heart disease: healthy diets, exercise and avoiding smoking. Patients should be skeptical about the guidelines, and have a meaningful dialogue with their doctors about statins, including what the evidence does and does not show, before deciding what is best for them.

John D. Abramson, a lecturer at Harvard Medical School and the author of “Overdosed America: The Broken Promise of American Medicine,” serves as an expert in litigation involving the pharmaceutical industry. Rita F. Redberg is a cardiologist at the University of California, San Francisco Medical Center and the editor of JAMA Internal Medicine.

The BIGGEST Loser Posted on October 14, 2013, 0 Comments

“A recent study looking specifically at contestants on The Biggest Loser found that they experienced a significant drop in resting metabolic rate, burning 504 fewer calories on average, thanks to an effect known as “metabolic adaptation.” And perhaps as many as 90 percent of the contestants on the show regain all their lost weight, according to US News.”

Only Joy is Real Posted on August 17, 2013, 0 Comments

I recognize and release the joy within myself.  Love-energy expresses through me to all people and all things.  Any obstacles to my joy are dissolved.  I experience joy by being joyful.

The only real feeling we ever have is joy.  Any part of our lives which we experience as less than joyful is an illusion. 

Then energy of Universal Intelligence is not available to support non-joyful, non-loving illusions.  Such illusions are sustained by our own will of mind and will of emotions.  That is why dealing with illusions is so tiring.

Focus your attention on the quality of your desire.  Quality of life is the feeling that is the setting for the events and the people that pass through our lives.  Most of us have buried the joy beneath layers and layers of illusory feelings.  It is necessary to keep peeling the layers of illusions away until joy is uncovered and allowed to fill our being.

The only obstacle to releasing joy is the unwillingness to feel love for ourselves and others.  

Abundance Posted on July 09, 2013, 0 Comments

Abundance is the natural state of affairs in the Universe; it flows in my life as I release all attachment to it.

I release that which resists the manifestation of abundance in all aspects of my life.  I acknowledge all that I have and express gratitude for it.  I open to receive.

The more joy we focus on the things in life that are working perfectly--joys, health, and harmonies in relationship, the more they increase.  Abundance is truly all around us and only fails to flow into our lives when we resist it.

True abundance is in infinite supply.  We give and receive abundantly.  The more we give and receive love, the more we open ourselves to receive and to give those things which represent love. 

Releasing the Past, Living in the Present Posted on May 28, 2013, 0 Comments

I now let go of all negative or distorted thoughts and memories.  The past no longer exists.  I allow Universal Intelligence to lovingly support me in my present circumstance.  

We hold onto the past by judging it.  We release past judgments by forgiving ourselves and others at a deep feeling level.

Fear of the past, present, or future, is a withholding of love from ourselves and others.  Pain is the manifestation of that fear in our bodies.  Pain and fear are self-created.  When the pain is persistent, practice feeling forgiveness for the persons involved (including one's self) until love and calm are felt.   

No Pain More Gain Posted on May 22, 2013, 0 Comments

“To me, the sign of a really excellent routine is one which places great demands on the athlete, yet produces progressive long-term improvement without soreness, injury or the athlete ever feeling thoroughly depleted. Any fool can create a program that is so demanding that it would virtually kill the toughest Marine or hardiest of elite athletes, but not any fool can create a tough program that produces progress without unnecessary pain.”

-Dr. Mel C. Siff

The Universe Handles the Details Posted on May 17, 2013, 0 Comments

Through my faculty of intuitive knowing, I allow Infinite Intelligence to select the details and variables of my life.  Without efforting, I open to, and focus on, the present.  I do what I love.  The Universe specializes in the details of my life.

Our training in struggle and absorbing discomfort on the path to success encourages us to plan our lives in advance.  Unfortunately, planning tends to keep us out of the present (the only time that ever exists) and forces us to select only from variables of which we have conscious knowledge.  However, there are many variables that, if known, we would eagerly select in place of ones we have chosen.  There is a simple way to locate them.  It is through the use of our intuition--our clear connection to Infinite Intelligence. 

What We Focus on Expands Posted on May 01, 2013, 0 Comments

I see the light of my inner wisdom; and I perceive only light in outer circumstances.  In all situations, regardless of appearances, I see only light.

Our perceived need to deal with our problems only attracts more of them to us.  The key is to release the need to see problems and see only solutions.  Every perceived problem indicates an unwillingness to see the perfection behind the illusion.  We can discipline ourselves to see and feel only abundance, perfection and peacefulness in every situation. 

Define the Ideal Posted on April 23, 2013, 0 Comments

I acknowledge and release views of reality that are less than ideal.  Only ideals of perfection guide my feelings and thoughts in creating the events of my life. 

To the extent we are not satisfied with the life we have, we must define what we prefer.  Changes in our lives result from changing our beliefs.  By defining our ideal on a regular basis, we change our beliefs and this brings about changes in our lives.  

Each one of us can have our life any way we like it.  We must conceive of life in ideal terms before we experience it that way.  When we feel and see everything working perfectly, it does.

Carrageenan Concerns go Mainstream Posted on March 23, 2013, 3 Comments,0,2164837.story

Doubts surface about safety of common food additive, carrageenan

March 18, 2013 - Chicago Tribune

March 18–Sara Baker says the light went on in her head after a cup of hot cocoa set off a storm in her stomach.

“I went back and looked at the package, and there it was: carrageenan,” said Baker, a career services coordinator from Bloomington, in central Illinois.

Baker had been taking medication for ulcerative colitis for years but still suffered debilitating digestive flare-ups without warning. She had read warnings about carrageenan in a natural health newsletter but didn’t take them seriously. After all, researchers haven’t conclusively linked the common food additive to gastrointestinal problems in humans.

This time, though, “it really clicked,” she said. “It took awhile to learn just how many things it’s in, but now that know, I can avoid it, and I no longer have the problems.”

Experiences like Baker’s have led some people with gastrointestinal problems to sidestep mainstream medical advice and avoid carrageenan, a seaweed-derived texturizer found in meat, dairy and other processed foods — including some organic products.

For scientists, however, these are just anecdotes. Though studies on lab animals and human cells have suggested that carrageenan can cause gastrointestinal inflammation, many researchers and physicians say it’s unclear whether the additive has the same impact on people who consume it.

Scientists at the University of Illinois at Chicago and University of Chicago are seeking to address that question with a controlled clinical trial that Baker is participating in.

“I believe it’s worth investigating and doing the science to find out,” said Dr. Stephen Hanauer, a medical professor and chief of gastroenterology and nutrition at University of Chicago Medicine.

His co-researcher, UIC physician and professor Joanne Tobacman, has been looking at the health effects of carrageenan for more than a decade and is concerned enough to have petitioned the U.S. Food and Drug Administration in 2008 to prohibit the use of carrageenan in food.

Her petition cited decades of publicly funded, peer-reviewed science — including her own — on carrageenan-induced inflammation in animals and cells. In June, the FDA responded with a letter of denial.

Tobacman said “it was disappointing that, with such clear evidence about the effects of carrageenan on inflammation, the FDA did not restrict the use of carrageenan, particularly in infant formula.” Europe doesn’t allow the ingredient in formula.

The additive, which lends a uniform, creamy texture to food, can be found in soy milk, yogurt, ice cream, cheeses, some meats, diet soft drinks and even toothpaste.

Michael Adams, deputy director of the FDA’s Office of Food Additive Safety, said the petition didn’t make a compelling case to re-examine the safety of carrageenan. “It has been reviewed repeatedly by FDA scientists and other international organizations, and in the judgment of those experts there hasn’t been a problem,” he said.

Adams called a rat study from 2006 “the gold standard for us because it exactly mimics the exposure consumers are going to get when they eat these carrageenan-containing foods.”

That study was funded and performed by a manufacturer of carrageenan. Adams said he didn’t know that but added: “If you look at the science and you believe it’s well done, it doesn’t matter where the money comes from.”

The Cornucopia Institute, a Wisconsin-based organic industry watchdog group, was expected to release a report Sunday night on carrageenan called “How a Natural Food Additive Is Making Us Sick.”

Charlotte Vallaeys, Cornucopia’s director of food policy, said the group felt “an ethical obligation” to raise awareness. “If government agencies weren’t going to protect consumers, then it seemed we needed to let consumers know about this so they could protect themselves.”

The institute also is challenging the FDA’s denial of Tobacman’s petition. Among other objections, Cornucopia’s letter to the agency asks why officials didn’t consider any studies on carrageenan published in the last four years.

Adams said the FDA’s scientific evaluation in response to the petition was finished in May 2009, after which it spent more than three years in what he calls the “administrative chain.”

Regarding infant formula, Adams said, Europe takes a different approach to food additives than the U.S., sometimes banning a substance when toxicity studies raise concerns but aren’t conclusive. “The Europeans do their business that way, but we don’t,” he said. “We would base it more on the science we have rather than waiting for science to be developed.”

While the Chicago researchers proceed with their work and advocates seek federal action, some consumers and activists have made an impact on their own by lobbying manufacturers directly to phase out the ingredient.

Last month Stonyfield joined a number of manufacturers who have removed or have pledged to remove carrageenan from their organic products. Organic Valley says it has removed the ingredient from most food items but is still working on reformulations for soy milk, chocolate milk and one version of its whipping cream.

A representative of the organic dairy company Horizon Organic and soy milk maker Silk (each majority-owned by Dean Foods) said both view carrageenan as safe and wouldn’t comment on any plans to remove it.

The U.S. National Organic Standards Board reapproved the use of carrageenan in most organic foods last year but decided to prohibit its use in organic infant formula.

Carrageenan manufacturers, the FDA, the United Nations food additives committee and some scientists say it is safe, as evidenced by centuries of use.

Marinalg International, a Brussels-based trade association representing producers of carrageenan, notes in an online statement that the U.N. additives committee has approved the use of carrageenan without a specific limit — with the exception of infant formula.

Among the studies the panel looked at, Marinalg said, was “a valuable, scientifically critical literature review” of carrageenan by Drs. Samuel Cohen and Nobuyuki Ito. The fact that Marinalg funded the 2002 report didn’t influence the “thorough and sound” review, according to Cohen, a physician and professor of medicine at the University of Nebraska.

James McKim, chief scientific officer at the toxicological research firm CeeTox Inc., said industry-funded science is not unusual and should be taken seriously. Marinalg recently hired McKim to review the last 30 years of carrageenan safety studies. His paper hasn’t been published yet, but he says it will affirm carrageenan’s safety.

The Tribune asked Marinalg and McKim if they were aware of any peer-reviewed scientific research that supported the safety of carrageenan but wasn’t performed by industry-funded scientists. They agreed to look but provided no examples after three weeks. The Tribune made a similar request to the FDA, which also provided no immediate examples.

In 2001, Tobacman published a scientific review in a National Institute of Health journal suggesting that consumption of carrageenan in lab animals was associated with “intestinal ulcerations” and tumors. She concluded that the “widespread use of carrageenan in the Western diet should be reconsidered.”

Beyond the acute reaction it triggers in some, Tobacman said in a recent email, carrageenan may also promote low levels of chronic internal inflammation, a factor linked to common chronic disorders such as diabetes, atherosclerosis and arthritis.

Still, many gastroenterologists are not convinced carrageenan is dangerous.

“There are some studies in rats and mice showing that carrageenan exposure can lead to GI inflammation that mimics things like Crohn’s” disease, said Dr. Sunanda Kane, a Mayo Clinic physician and medical adviser to the Crohn’s and Colitis Foundation of America. “But it’s never been shown on human tissue in humans walking around.”

Over the last 50 years, incidence of inflammatory bowel disease has risen as people eat more processed food, Kane said. “But is it carrageenan or that we don’t exercise or have lots of other additives and preservatives or fructose in our food supply?”

In Hanauer and Tobacman’s study, people whose ulcerative colitis is in remission are being put on a carrageenan-free diet, then given either a controlled dose of carrageenan or a placebo.

So far, the research has been hampered by low volunteer rates — currently, fewer than 20 subjects. Hanauer notes that the prospect of re-inflaming one’s inactive ulcerative colitis isn’t particularly attractive.

But Baker, who was one of more than 120 people who responded when Cornucopia asked to hear from those with carrageenan-related digestive problems, said she was willing to go through it to help establish human science on the topic.

“I believe there are people who are as sick as I was, or even worse, who need this information,” she said.

Customers instead of Cures Posted on December 27, 2012, 0 Comments

"It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine." --Dr. Marcia Angell, Past Editor in Chief, NEJM


Some select quotes from Drug Companies & Doctors: A Story of Corruption (  The text in red is what I've highlighted:

"Before a new drug can enter the market, its manufacturer must sponsor clinical trials to show the Food and Drug Administration that the drug is safe and effective, usually as compared with a placebo or dummy pill. The results of all the trials (there may be many) are submitted to the FDA, and if one or two trials are positive—that is, they show effectiveness without serious risk—the drug is usually approved, even if all the other trials are negative."

"A review of seventy-four clinical trials of antidepressants, for example, found that thirty-seven of thirty-eight positive studies were published. But of the thirty-six negative studies, thirty-three were either not published or published in a form that conveyed a positive outcome."

"Clinical trials are also biased through designs for research that are chosen to yield favorable results for sponsors. For example, the sponsor’s drug may be compared with another drug administered at a dose so low that the sponsor’s drug looks more powerful. Or a drug that is likely to be used by older people will be tested in young people, so that side effects are less likely to emerge. A common form of bias stems from the standard practice of comparing a new drug with a placebo, when the relevant question is how it compares with an existing drug. In short, it is often possible to make clinical trials come out pretty much any way you want,..."

"A recent survey found that about two thirds of academic medical centers hold equity interest in companies that sponsor research within the same institution."

"A study of medical school department chairs found that two thirds received departmental income from drug companies and three fifths received personal income."

"Perhaps most important, many members of the standing committees of experts that advise the FDA on drug approvals also have financial ties to the pharmaceutical industry"

"To promote new or exaggerated conditions, companies give them serious-sounding names along with abbreviations. Thus, heartburn is now “gastro-esophageal reflux disease” or GERD; impotence is “erectile dysfunction” or ED; premenstrual tension is “premenstrual dysphoric disorder” or PMMD; and shyness is “social anxiety disorder” (no abbreviation yet)."

"Even when changes in lifestyle would be more effective, doctors and their patients often believe that for every ailment and discontent there is a drug."

In the 1970s, a small group of leading psychiatrists met behind closed doors and literally rewrote the book on their profession. Revising and greatly expanding the Diagnostic and Statistical Manual of Mental Disorders (DSM for short), they turned what had been a thin, spiral-bound handbook into a hefty tome. Almost overnight the number of diagnoses exploded. The result was a windfall for the pharmaceutical industry and a massive conflict of interest for psychiatry at large...


For those interested in learning more:

Side Effects: A Prosecutor, a Whistleblower, and a Bestselling Antidepressant on Trial

Our Daily Meds: How the Pharmaceutical Companies Transformed Themselves into Slick Marketing Machines and Hooked the Nation on Prescription Drugs  

Shyness: How Normal Behavior Became a Sickness

Question from a Client with a Cold Posted on December 13, 2012, 1 Comment

I'm still on if you are.  Out of courtesy need you to know I have nasty head cold.  Let me know how u feel about having me in studio.  ;)


It's not the germ, it's the terrain.
Should be good.
We just shouldn't make out.
See you then.

I stole the first line of my response from Louis Pasteur who recanted the Germ Theory on his death bed.  The line about making out--that's an Andrew Original...

A letter to "Dr." Oz (which we should all sign) Posted on December 11, 2012, 0 Comments

 The original article can be found here:

Gary Null: Letter To Dr. OZ

  • Gary Null, December 3, 2012

For related articles and more information, please visit OCA's All About Organics page.

Dear Dr. Oz,

You may remember when I invited you to appear in a PBS special, Get Healthy Now, along with other medical panelists, in 1999. We have not spoken since, however, my audience and I are very concerned about the inflammatory comments that you made in a recent issue of TIME Magazine. In effect, you stated that there is no basic difference between non-organic, genetically modified produce and organic varieties and that people are wasting their money buying organic foods. You also suggest that individuals who purchase organic foods are taking part in a "snooty" form of "elitism" and that in effect, it's the "99%" just trying to act like the "1%".

This was unexpected as a person with your reputation and resources could easily have found the several hundred to several thousand peer-reviewed articles highlighting the dangers of consuming pesticides, fungicides, herbicides and genetically engineered foods, especially to those people most vulnerable to chemical toxicity or environmentally-induced illnesses, such as children. Also, you could have examined the 40 years of scientific and lay literature on the plight of farm workers who experienced the highest incidence of birth defects and other adverse health consequences as a result of working with toxins in the soil as well as the hundreds of studies confirming the damaging effects of modern commercial meat, poultry and fish production on our health the environment. Additionally, you could have carried out a review of the water and soil conservation literature that shows how the enormous quantities of excess nitrogen released during the production of our commercial, factory farmed foods have contributed to massive fish die-offs and dead zones, the largest of which is at the mouth of the Mississippi river and is larger than the state of New Jersey. And finally, you may want to have a conversation with your wife, who recently used our studios at the Progressive Radio Network along with Jeffrey Smith, the leading critic of GMO foods in the US, to narrate a documentary challenging genetic engineering. Certainly your wife, a dedicated, conscientious and highly educated consumer activist, would be a great resource for you.

My hope is that this information will motivate you to have your staff do their due diligence, research the facts and realize that you are supporting the "1%"- Monsanto, your television network and their sponsors- and that may be a position in need of reevaluation. I will remain optimistic that you will be thoughtful enough to set aside your ego and any special interests that have propagandized you, and that you will seek the truth, speak out and write a rebuttal. I look forward to your communication.


Gary Null