I am principal director of research at the Gaia Research Institute and in response to a request for comment from an associate who received a newsletter from Sally-Ann Creed that maligns flaxseed oil with the sole purpose of promoting a competing Omega-3 fish oil product in which she has a direct commercial interest, I am compelled to oblige, primarily in the service of exposing unfair commercial competition practice and fraud by way of deliberate scientific misreporting on a matter of natural health, which are precisely what I accuse the Greeds of as a direct result of their maliciously mischievous statements and ‘summary’ of a published study, which ironically does not specifically mention flaxseed oil at all. I consider it appropriate to declare my own possible conflict of interest in flaxseed, which I advocate as a health optimising food and also supply as a service for the funding arm of my Institute in the form of two flaxseed-oil and two defatted flaxseed-cake foods. The oils are specially obtained from the day’s first 25kg cold-pressing of seed and the bottles are flushed with liquid nitrogen to purge oxygen and are frozen and chilled during the entire distribution chain.

Sally-Ann Creed wrote (General Health Newsletter, August 2004 ~ 1.2): “My sweet husband, Bill, has kindly ‘summarised’ an article from the American Journal of Clinical Nutrition, on prostate cancer and the ‘dangers’ of taking ‘ALA, as found in flaxseed oil’, on a regular basis if you wish to protect your prostate! Prostate cancer is on the increase, like all cancers, and the particular one referred to in this article is one which ‘kills’ as it spreads rapidly to bone and surrounding organs. Men everywhere are waking up to the knowledge that this is something that can be avoided. ‘Fish oil instead of flaxseed oil is a first line of defence for men’” (Note: Emphasis always mine – Stuart)

It is clear to me that the Greeds are on a selfish mission to promote their fish oil sales and have set out to first attempt to eliminate alternative Omega-3 options, of which flaxseed is the most viable contender. What may not be clear to reader’s of this scientifically compromised newsletter is just how bad the pseudo-scientific presentation is that is so unashamedly used to hoodwink health seekers into abandoning one perfectly healthy food source for another highly questionable one. The ‘study’ that Bill refers to (Leitzmann M et al, Am J Clin Nutr, 80(1), 2004), discusses apparent relationships between various dietary n-3 fatty acids (ALA, EPA and DHA) and prostate cancer, as perceived from the perspective of a questionnaire of dietary habits. The study makes no specific mention of flaxseed, which may be the richest, but is also the healthiest plant source of Alpha Linolenic Acid (ALA), in that it is an exceptionally rich repository of nutrients, phytoestrogens and other healthful phytochemicals, many of which have significant anti-cancer properties. Given the already considerable issues here, I shall refrain from a discussion of the multiple health benefits of flaxseed.

This study treated all dietary sources of ALA as one, irrespective of how unhealthy some are. This is significant since ALA rich plant oils include those most often extensively processed, including margarines and shortenings, often thermally damaged in baking or extensive frying and which not only are, but also are generally associated with junk foods. Worse still, also included are animal sources of ALA, such as butter, fatty red meat, bacon, hamburgers, frankfurters etc, iro which the same extensive frying and junk food associations apply. Fish, on the other hand, the main source of EPA and DHA, is generally associated with more health conscious diet and lifestyles and it is significant that these and other confounding factors were not evaluated and hence do not allow firm conclusions to emerge regarding any specific source of nor form of ALA in relation to prostate cancer. The causes of prostate cancer are unknown, but ageing is the most significant known risk factor to date (Grover P, Martin F, Carcinogenesis, 23(7), 2002).

This study was not a shoot-out between flaxseed oil and fish oil, as the Greeds would have us believe, but merely served to differentiate between fish-sourced n-3 fatty acids on the one hand and all other sources of n-3 fatty acids on the other hand. There are considerably more variants of and also considerably more is consumed of the latter group, which encompasses both plant and animal sources and includes the good, the bad and the ugly alike, with the bad undisputedly dominating consumption levels. Furthermore, the study related only to group consumption and this only as these appear to relate to prostate, not other cancers. It is well known that perceived benefit from one habit or intervention often entails a shift of risk from one parameter to another. Indeed, nowhere is this better demonstrated than in cancer therapies (eg Tamoxifen), so I would advise that not too much be read into the limited insights emerging from this study, let alone what precious little remains of the fish oil hype after I have dissected the Greed’s abuse of it.

Bill Creed in his ‘summary’ of this study not only makes additions of that which does not exist, but also makes omissions of that which does exist, all illegitimately in the interests of his fraudulent attempt to scare people away from perfectly safe natural flaxseed to potentially highly toxic unnatural fish oil. Besides mischievously adding the names ‘flaxseed oil’ and even “fish oil” to the text (even though flax is not specifically mentioned in the entire study and fish oil is only implied) as possible causes and preventives respectively of advanced prostate cancer, where no evidence for such an assertion exists; he also takes the irregular liberty of adding the word “deadly” to the text, where no such scary emotive adjective appears in the original, again in service of a masked agenda. To ‘summarise’ is not to add something that is not otherwise there. More correctly, the Greeds selectively edited the study, added strategic misleading comments and omitted some of the author’s to manipulate the import thereof in service of their own perverted end.

Further to this, not only does ‘sweet’ Bill fail to correctly contextualise the comparative parameters of the study, as I have done above, he also fails to accurately convey the author’s purposely broad and specifically vague conclusion, namely that “Increased dietary intakes of ALA ‘may’ increase the risk of advanced prostate cancer and in contrast, EPA and DHA intakes ‘may’ reduce the risk of total and advanced prostate cancer”. What Bill also omits to relay, from that which does in fact appear in the study summary, but is mischievously so selectively edited, is the author’s pertinent comment that “ALA intake was unrelated to the risk of total prostate cancer”. Bill strategically fails to mention the wide spectrum of sources and varying qualities of ALA, mentioning only vegetable sources, and this as though vegetable sources were exclusively related to all the recorded advanced cancers, which is not at all correct.

Of 47,866 subjects, there were 448 advanced prostate cancers (1.6%). The relative risks in terms of these advanced cancers was in fact attributed to three groups as follows:

  • Relative risk from all non-animal (vegetable) ALA sources: 2.02
  • Relative risk from all animal (meat and dairy) ALA sources: 1.53
  • Relative risk from combined marine EPA and DHA sources: 1.63

This breakdown of comparative relative risk clearly shows a completely different perspective to that which the Greeds have attempted to portray as scientific fact. In fact, the risk from marine sources of n-3 fatty acids is greater than that from meat and dairy and not that much lower than that of vegetable sources, which is especially significant given the abuse to which the vegetable sources are subjected, especially by way of extended heating, often for days, even weeks on end. It gets even worse. An immediately prior questionnaire study of the very same follow-up project clearly identified eating fish ‘more than’ three times per week as being associated with the reduced risk of prostate cancer, with the researchers stating that the marine fatty acids may account for part of the effect, but that other factors in fish may also play a role. Participants in the highest intake category of fish were also found to more often be users of multivitamin and other supplements. Significantly this study also clearly stated that “use of fish oil supplements, as compared with no use, was not associated with a decreased risk of prostate cancer” and “our findings suggest that the beneficial effect associated with eating fish may not necessarily be achieved by fish oil supplements” (Augustsson K et al, Cancer Epidem Biomarkers Prev, 12(1), 2003). So much for Greed’s holier than thou fish oil hype.

[Sally-Ann Creed ends her editorial of Bill’s propaganda by telling her own stinking lie: “Now you know why people who follow the latest cutting edge studies coming out, are so vehemently anti-flaxseed oil, and so pro fish oil!” She then proceeds to promote her book thus: “See my book ‘Let Food Be Your Medicine’, - the chapter on Fats & Oils – for a thorough, scientific investigation of the comparison between the two”. “Scientific investigation”? – what a joke. If hubby Bill the scientist can’t tell the truth and wifey can’t trip him up, but rather, under her editorship, uncritically publishes this crap in her corny newsletter, I really do pity the unsuspecting readers of Sally-Ann Creed’s book and all her other so-called health communications as well as the other junk she sells in the name of health and whose mission, it appears is driven by greed, sadly, no madly, to the exclusion of due consideration of the health rights of those gullible victims exposed to such calculated and fraudulent misinformation. I will be keeping an eye on Sally and Bill. Perhaps Jesus should too, seeing as the Greeds quote New Testament scripture along with this bullshit as part of their scam. Perhaps the Health Professions and Medicines Control Councils too, should keep an eye on the Greeds. That’s my rant over.]

Sally-Ann, further on in said newsletter states: “EPA and DHA is found in pharmaceutical grade fish oil. Contact us if you can’t find it – if it doesn’t say “pharmaceutical grade” – it’s not”! Incidentally, the term “pharmaceutical-grade fish oil” is not an officially recognised industry or regulatory standard. The use of the term signifies a desire to disassociate the fish oil supplement industry from its shocking history of supplying fish oils contaminated with some of the worst manmade oil-soluble toxins known, namely DDT, dioxins and polychlorinated biphenyls, which bio-accumulate in the fat of fish, and are especially concentrated in fish oil, even more so in cold-water fish such as salmon (both sea and pond-raised) and as such have been the major source of these toxins in humans. Can these potentially ‘deadly’ toxins be removed from fish and fish oils? The answer is no in the former and yes in the latter instance, but not without damaging the vast majority of n-3 fatty acids in the process, to the extent that hundreds of times the amount of fish oil is needed to process and reconstitute a near PCB-free artificial n-3 oil. Whereto the damaged more toxic concentrate? Fish oil is not the only source of EPA and DHA, which are synthesised in animals, including humans. In this case, the theft just happens to be from the innocent fish, with a terrible waste to ensure toxin free oil, if indeed this is even the case. We, as humans, are fearfully and wonderfully made to produce our own eicosanoids and do not have to kill to steal them. Incidentally, another source of EPA and DHA is snake oil, which would really be appropriate to the Greeds.

If a particular species of fish is used (eg salmon oil), it is so-called ‘food grade’, usually sold in capsules because of poor taste. Another grade is ‘concentrate’, consisting of ethyl esters of the fish oil that has been subjected to fractional cooling, which solidifies the more saturated fats, leaving behind a more concentrated solution of long-chain omega-3 fatty acids, marketed as containing higher levels of EPA and DHA. Neither of these involves removing toxic contaminants nor the long-chain monoene fatty acids that can give rise to gastric distress. So-called ‘pharmaceutical-grade’ is thermally fractionated and distilled into long-chain omega-3 fatty acids, low in long-chain monoenes. These fractions need to be heavily refined to minimise resultant considerable thermally oxidised and polymerised lipids and also to reduce concentrated environmental toxins to about half the concentration in the crude fish oil. The individual fractions are then combined to provide an appropriate balance of EPA and DHA for the finished oil. All this processing and final re-esterification reduces the stability of the surviving lipids against toxic oxidation, requiring fortification with antioxidants and introduces thermal changes to the oil, which is nevertheless now characterised as tasteless. (Vijai K, Perkins E, The Presence Of Oxidative Polymeric Materials In Encapsulated Fish Oils, Lipids, 26(1), 1991); (Hilbert G et al, Chemosphere, 37(7), 1998); (Tom Saldeen MD, PhD, Fish Oil and Health, Positive Health Publications, 2002)

Analysis of health outcomes of 23,693 postmenopausal women from the prospective study "Diet, Cancer and Health", showed that higher intakes of fish were significantly associated with higher incidence rates of breast cancer (Stripp C et al, J Nutr, 133(11), 2003). Epidemiological studies of raw and deep fried fish consumption revealed absence of anti-cancer effects (Takezaki T et al, Nutr Cancer, 45(2), 2003). Analytic case-control or cohort design epidemiologic studies have not yielded clear conclusions regarding a protective effect for even fish against cancer (Severson R et al, Cancer Res, 49:1857, 1989); (Vatten L et al, Int J Cancer, 46:12, 1990); (Bidoli E et al, Int J Cancer, 50,223, 1992); (Peters R et al, Cancer Causes Control, 3, 457–1992); (Giovannucci E, et al, J Natl Cancer Inst, 85(19), 1993); (Toniolo P et al, Epidemiol, 5:391, 1994); (Giovannucci E et al, Cancer Res, 54:2390, 1994); (Kampman E et al, Cancer Causes Control, 6, 225–1995); (Gaard M et al, Eur J. Cancer Prev, 5, 445, 1996); (Chajes V et al, Int J Cancer, 83:585, 1999); (Holmes M et al, JAMA, 281:914, 1999); (Schuurman A et al, Br J Cancer, 80:1107,1999); (Gertig D et al, Int J Cancer, 80:13, 1999); (Kampman E et al, Cancer Epidemiol Biomarkers Prev, 8:15, 1999); (European Prospective Investigation into Cancer and Nutrition, European Conference on Nutrition and Cancer, Lyon 21-24 June, 2001, British Nutrition Foundation 2001); (Terry P et al, Cancer Epidemiol Biomarkers Prev, 11(1), 2002); (Hirose K, Int J Cancer, 107(2), 2003); (Hjartåker A, Scandinav J Nutr, 47(3), 2003); (Sieri S et al, Cancer Epidemiol Biomarkers Prev, 13(4), 2004); (Wirfalt E et al, Eur J Clin Nutr, 58(5), 2004); (Astorg P, Cancer Causes Control, 15(4), 2004).

It remains to be established whether fish oil, let alone the artificial ‘pharmaceutical grade fish oil’ retains any of the health benefits attributed to fish, as seems unlikely given the existing scientific data. Epidemiologic evidence indicates that fish oil consumption is not associated with decreased risk of prostate cancer (Kolonel L et al, J Natl Cancer Inst, 91(5), 1999); (Augustsson K et al, Cancer Epidem Biomarkers Prev, 12(1), 2003); (Terry P et al, Am J Clin Nutr, 77(3), 2003). In fact, researchers have found that the inhibitory effects of fish oil on the growth of tumours in vitro are abolished by the concurrent addition of vitamin E (Lhuillery C et al, Cancer Lett, 114:233,1997); (Bougnoux P, Curr Opin Clin Nutr Metab Care, 2:121, 1999); (Dommels Y et al, Carcinogenesis, 24:385, 2003) or even vitamin C (Dommels Y et al, Carcinogenesis, 24:385, 2003); (Larsson S et al, Am J Clin Nutr, 79(6), 2004) which, as opposed to synthetic phenolics, are the anti-oxidants most commonly used by the so-called health food industry. Those recklessly extrapolating from epidemiological fish consumption health data to claim actual health benefits for unproven fish oil conveniently ignore factors such as these. Furthermore, the potential processing damage and the toxic environmental contaminants bio-accumulated in the fat of fish and hence in fish oil, are likewise conveniently ignored, if not falsely dismissed by claiming the product to be ‘pharmaceutical grade’, as though this ensured quality, safety and efficacy. Since no such industry or regulatory standard exists, only a current, local, comprehensive certificate of analysis for each product sold should suffice as assurance to the public, that at the very least, the product is safe for consumption.

Although it is widely recognised that lipophilic organic chemicals, particularly persistent organic pollutants (POPs), are ubiquitous in the marine environment and can accumulate in fish oils, dietary supplements are not routinely considered when estimating average daily intakes for these contaminants. A survey of levels of organochlorine residues in hundreds of fish oils, from dozens of countries purchased over the counter as dietary supplements has demonstrated that despite controls on the use of persistent organochlorine substances and significant reductions in some cases, appreciable quantities, especially of polychlorinated biphenyls (PCBs), are still to be found in oils sold as n-3 fatty acid rich fish oil dietary supplements. (Jacobs M, Johnston P, Organochlorine pesticides and PCB residues in pharmaceutical and industrial grade fish oil, Greenpeace Research Laboratories, Technical Note, 4th May 1995); (Jacobs M et al, Chemosphere, 37(9-12), 1998); (Di Muccio A et al, Food Addit Contam, 19(12), 2002); (Jacobs M et al, J Agric Food Chem, 52(6), 2004); (Clemens R et al, Polychlorinated biphenyls (PCBs) in dietary fish oil supplements, Session 49I, Toxicology & Safety Evaluation, IFT Annual Meeting, Las Vegas, July 14, 2004)

Several persistent organic pollutants accumulate in animal fat, particularly in the breast and prostate tissues of humans at the top of the food chain, where they are known to increase the risk of cancer (Bertazzi P et al, Epidemiol, 8(6), 1997); (Liljegren G et al, Eur J Cancer Prev, 7(2), 1998); (Guttes S et al, Arch Environ Contam Toxicol, 35(1), 1998); (Moysich K et al, Cancer Epidemiol Biomarkers Prev, 7:181, 1998); (Porta M et al, Lancet; 354, ISS 9196, 1999); (Romieu I et al, Am J Epidemiol, 152(4), 2000); (Millikan R et al, Cancer Epidemiol Biomarkers Prev, 9(11), 2000); (Stellman S et al, Cancer Epidemiol Biomarkers Prev, 9(11), 2000); (Holford T et al, Intl J Epidemiol, 29(6), 2000); (Aronson K et Al, Cancer Epidem Biomarkers Prev, 9(1), 2000); (Bertazzi P et al, Am J Epidemiol, 153(11), 2001); (Lucena R et al, Eur J Cancer Prev, 10(1), 2001); (Laden F et al, Cancer Epidemiol Biomarkers Prev, 11(12), 2002); (Lopez-Carrillo L, Eur J Cancer Prev, 11(2), 2002;) (Calle E, CA Cancer J Clin 52(5), 2002); (Demers A, Am J Epidemiol 155(7), 2002); (Negri E et al, Eur J Cancer Prev, 12(6), 2003); (Paris-Pombo A et al, Arch Environ Health, 58(1), 2003); (Mc Elroy J et al, Environ Health Perspect, 112(2), 2004).

For xenobiotics such DDT/DDE, polychlorinated biphenyls (PCBs) and dioxin (TCDD) there is unequivocal (clear) evidence of carcinogenicity and this appears to be directly linked to their toxicity. The potential carcinogenic risk to humans of xenobiotic chlorinated compounds, which may act as endocrine disruptors, has been covered in great detail by a number of International Agency for Research on Cancer (IARC) workshops, where the overall conclusions drawn were that TCDD is an unequivocal human carcinogen and whereas PCBs and DDT possible humans carcinogens. (IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs, Volumes 1–42, (Suppl. 007): IARC Lyon, France 1997); (Tsuda H et al, Japan J Clin Oncol, 33(6), 2003) It has been estimated that eating a lot of fish that have accumulated just one xenobiotic, dioxin, will increase lifetime risk of cancer death by as much as 1% to a total of 13% (Steenland K, Deddens J et al, Ind Health, 41(3), 2003).

PCBs have also been associated with several non-cancer health effects, including immune dysfunction and liver, reproductive and endocrine abnormalities. Prenatal exposures have been associated with neurodevelopmental deficits. (US Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, Toxicologic Profile for Polychlorinated Biphenyls (PCBs) (Update). US Department of Health and Human Services, Public Health Service; ATSDR, 2000) Fish can contain the toxins methyl mercury and PCBs and other by-products of our industrial age that gravitate into water. These are lipophilic (fat loving) and being present in fish oils, tend to accumulate in our fat depots when consumed. This is a special consideration for dieters since the lipophilic toxins in fat stores that are being rapidly melted away can flood the body, creating a toxic shock. This is also of particular concern for pregnant and nursing mothers, since these toxins can transfer to and accumulate in the foetus, increasing the risk of abnormalities, disease and weakness. One can estimate that PCB intake parallels fish consumption. Fish oil supplements can also contain mercury and PCBs, the concentration of PCBs ranging from 2% to 43% of recommended safe levels, based on supplement surveys. Supplements should be chosen (very, very) carefully. (Shim S et al, J Food Sci, 68(8), 2003)

The environmental contaminants in fish and fish oils that can affect the neurobehavioural development of the foetus include mercury, DTT, dioxins and polychlorinated biphenyls (PCBs). Most, being semi-volatile, can travel in the air around the world, resisting degradation and persisting in the environment for as long as a century. People who regularly eat large amounts of fatty fish may be at risk of high exposure. Epidemiological studies reveal that the developing brain and nervous system are most vulnerable. Exposed children of mothers who ate fish have done more poorly in a range of skills and development tests, including deficits in general intellectual functioning, short- and long-term memory, and attention span. (Jacobson J, Jacobson S, N Engl J Med, 335(11), 1996); (Food quality. In: “Health and the environment: The health and environment handbook for health professionals”. Health Canada, Ottawa, 1998) (Patandin S et al, J Pediatr, 134(1), 1999); (Stewart P et al, Teratol, 22:21, 2000); (Lonecker M, Rogan W, Pediat Res, 50(3), 2001); (Walkowiak J et al, Lancet, 358:160, 22001); (Woodruff T et al, Pediatr, 113(4), 2004).

The predominant sources of n-3 fatty acids in the diet are vegetable oils and fish. Clearly fish and fish oils carry considerable risks from contaminants. Fish are the major source of EPA and DHA, whereas vegetable oils are the major source of ALA. Other sources include nuts and seeds, vegetables and some fruit. Flaxseed oil is a particularly rich source of ALA n-3 fatty acids. Purslane, a vegetable used in salads along the Mediterranean basin and in the Middle East, is the richest source of ALA of any green leafy vegetable examined and is one of the few plants known to be a source of even EPA. Even a vegetarian source of DHA derived from algae is now available, albeit unnecessary. (Simopoulos A. “Terrestrial sources of n-3 fatty acids: purslane”, In: Quebedeaux B, Bliss F, Eds, Horticulture and human health: contributions of fruits and vegetables, Prentice-Hall, NJ, 1988); (Raper N et al, J Am Coll Nutr, 11:304, 1992); (Simopoulos A et al, J Am Coll Nutr, 11:374, 1992); (Norman H et al, Profiles of omega-3 fatty acids and antioxidants in common purslane, In: Simopoulos A, Pavlou K, Eds, World Rev Nutr Diet, 1992); (Mantzioris E et al, Am J Clin Nutr, 59:1304, 1994); (Simopoulos et al, Purslane in human nutrition and its potential for world agriculture, World Rev Nutr Diet, 1995); (Palaniswamy U, Enhancement of naturally occurring chemopreventive compounds in salad greens through environmental manipulation during crop growth, PhD dissertation, University of Connecticut, 1998); (Simopoulos A, Overview of evolutionary aspects of w3 fatty acids in the diet, In: Simopoulos A, Ed, The Return of w-3 Fatty Acids into the Food Supply, World Rev Nutr Diet, 1998); (Ezekwe M et al, Plant Foods Human Nutr 54(3), 1999); (Simopoulos A, Am J Clin Nutr, 70(3 Suppl), 1999); (Lui L et al, J Chromatogr A, 893(1), 2000); (Crawford M et al, Ann Nutr Metab, 44:263, 2000); (Mc Avoy R et al, J Am Soc Hort Sci, 125(2), 2000);

The precursor to EPA and DHA in the n-3 fatty acid synthetic pathway is ALA (18:3n-3), which is especially rich in flaxseed (Conner W, Am J Clin Nutr, 74(4), 2001). DHA is synthesised by humans from ALA. DHA is transferred across the placenta to the foetus during pregnancy and is always present in human milk along with other n-3 fatty acids, including ALA (Ruyle M et al, Proc Natl Acad Sci, U S A, 87:7902, 1990). An imbalance in proper ratio of dietary n-6 to n-3 fatty acids can accentuate an n-3 fatty acid deficiency state. Diseases that may be prevented or ameliorated with n- fatty acids include cancers of the breast, colon, and prostate. (Conner W, Am J Clin Nutr, 71 (1), 2000) Humans can convert ALA to EPA, which can be further elongated and desaturated to DHA, the efficiency of this conversion and desaturation varying with physiological need, individual component fat profile and the total quantity of fat consumed, with low fat diets and diets with low exogenous levels of EPA and DHA resulting in the greatest synthesis (Emken E et al, Biochim Biophys Acta, 1213:277, 1994); (Jones P, Kubow S, Lipids, sterols, and their metabolites, In: Shiels M et al, Eds. Modern Nutrition in Health and Disease, Williams and Wilkins, Baltimore, 1999); (Vermunt S et al, Lipids, 35:137, 2000); (Pawlosky R et al, J Lipid Res, 42:1257, 2001); (Burdge G et al, Br J Nutr, 90:311, 2003).

Whilst clearly only a very weak case can be made for so-called “pharmaceutical grade” fish oils, a stronger case can be made for cold-pressed, high lignan flaxseed oil, neither of which were the specific focus of the Greed’s fraudulently abused summarised study (Leitzmann M et al, Am J Clin Nutr, 80(1), 2004). Even the benefits attributable to fish oil are as a result of its EPA and DHA content, which humans efficiently synthesise from ALA when other fats are in balanced proportion. The ratio of n-3/n-6 has an important association with the benign or malignant state of prostatic disease (Newcomer L et al, Prostate, 47(4), 2001) and other cancers (Chajes V, Bougnox P, World Rev Nutr Diet, 92:133, 2003); (Goodstine S et al, J Nutr, 133(5), 2003). In a nutritional epidemiologist's view: “An emphasis is on the dietary ratio of LA to ALA, rather than the absolute amounts of ALA, is what is critical for disease prevention, due to the competition between these two essential PUFAs for their entry into the elongation and desaturation pathways leading to the synthesis of their respective eicosanoids” (Khor G, Asia Pac J Clin Nutr, 13(S22), 2004). The well-known Budwig cancer therapy’, which daily utilises several tablespoons of high quality flaxseed oil is a case in point, without even needing to call on the considerable scientific data supporting the anti-cancer properties of flaxseed. ‘Pharmaceutical grade fish oil’ is a suspect artificial industrial product. Properly cold-pressed flaxseed oil remains a healthy natural food.

An animal carcinogen study that compared vegetable oils and fish oil determined that fish oil, but not vegetable oils enhanced carcinogenesis (Appel M, Woutersen R, Nutr Cancer, 47(1), 2003). Animal studies comparing vegetable oils and fish oil on tumour growth and metastasis have determined beneficial effects on these indexes for flaxseed oil, but not for other vegetable oils (Witek R et al, Arch Immunol Ther Exp (Warsz), 25(6), 1977); (Witek R et al, Pharmazie, 39(7), 1984); (Yam D et al, Br J Cancer, 62(6), 1990); (Thompson L et al, Carcinogenesis (Lond.), 17:1373, 1996); (Cognault S et al, Nutr Cancer, 36(1), 2000); (Thuy N et al, J Nutr Sci Vitaminol (Tokyo), 47(5), 2001); (Jelinska M, Biochim Biophys Acta, 1637(3), 2003); nor for fish oil (Fritsche K, Johnston P, J Nutr, 120(12), 1990). There are no known studies where flaxseed oil caused prostate (or any other) cancer. There are no known studies where flaxseed caused prostrate (or any other) cancer. Conversely, it is known that a diet supplemented with flaxseed inhibits the growth and development of prostate cancer in animal models (Lin X et al, Urology, 60(5), 2002), experiments with human cells (Yang Y et al, Clin Biochem, 32(6), 1999); (Lin X et al, Anticancer Res, 21:3995, 2001) and in studies with humans (Gann P et al, J Natl Cancer Inst, 86(4), 1994); (Morton M et al, Cancer Lett, 114(1-2), 1997); (Yan L et al, Cancer Lett, 124(2), 1998); (Tou J, et al, J Toxicol Environ Health, 56(8), 1999); (Denis L et al, Eur Urol, 35(5-6), 1999); (Demark-Wahnefried W et al, Urology, 58(1), 2001); (Demark-Wahnefried W et al, Urology, 63(5), 2004).

Flaxseed, the richest source of mammalian-specific lignans, of which there are 75 to 800 times more than in any other food (Thompson et al, Nutr Cancer, 27:26, 1997), has been extensively studied and both with and without its n-3 oil component, has been found to possess diverse anti-cancer properties (Hirano T et al, Cancer Invest, 8:595, 1990); (Serraino M, Thompson L, Cancer Lett. 60:135, 1991); (Thompson L et al, Nutr Cancer, 16:43, 1991); (Serraino M et al, Cancer Lett, 60:142, 1992); (Serraino M, Thompson L, Nutr Cancer, 17:153, 1992); (Serraino M, Thompson L, Cancer Lett., 63:159, 1992); (Schweigerer L et al, Eur J Clin Invest, 22:260, 1992); (Serraino M, Thompson Nutr Cancer, 17:153, 1992); (Obermeyer W et al, FASEB J, A863, 1993); (Phipps W et al, J Clin Endocrinol Metab, 77:1215, 1993); (Wang C et al, J Steroid Biochem Mol Biol, 50:205, 1994); (Cunnane S, Thompson L, Eds, Flaxseed in Human Nutrition, AOCS Press, Champaign, IL 1995); (Thompson L et al, Carcinogenesis, 17:1373, 1996); (Jenab M, Thompson L, Carcinogenesis (Lond), 17:1343, 1996); (Thompson Let al, Carcinogenesis (Lond), 17:1373, 1996); (Thompson et al, Nutr Cancer, 27:26, 1997); (Thompson L et al, Nutr Cancer, 26:159,1996); (Nesbitt P, Thompson L, Nutr Cancer, 29(3), 1997); (Prasad K, Mol Cell Biochem, 168(1-2), 1997); (Thompson L, Baillieres Clin Endocrinol Metab, 12:691,1998); (Orcheson L et al, Cancer Lett, 125(1-2), 1998); (Sung M et al, Anticancer Res, 18:1405, 1998); (Yan L, et al, Cancer Lett, 124(2), 1998); (Nesbitt P et al, Am J Clin Nutr, 69: 549, 1999); (Brzezinski A, Debi A, Eur J Obstet Gynecol Reprod Biol, 85(1), 1999); (Jenab M et al, Nutr Cancer, 33(2), 1999); (Rickard S et al, Nutr Cancer, 35(1), 1999); (Li D, et al, Cancer Lett, 142(1): 91, 1999); (Janet C et al, Carcinogenesis, 20(9), 1999); (Haggans C et al, Nutr Cancer, 33(2) 1999); (Rickard S et al, Cancer Lett, 161(1), 2000); (Ward W et al, Nutr Cancer, 37(2), 2000); (Hutchins A et al, Nutr Cancer, 39(1), 2001); (Chen J et al, Nutr Cancer, 43(2), 2002); (Dabrosin C et al, Cancer Lett, 185(1), 2002); (Chen J et al, Exp Biol Med (Maywood), 228(8), 2003); (Trentin G et al, Mutat Res, 551(1-2), 2004).

The anticancer properties of flax reside more in the seedcake than the oil, which latter as a food source is more specifically beneficial to inflammatory, osteoporotic and cardiovascular conditions, not the topic under discussion here. A logical question at this point would be: “Why not just eat the flaxseeds and so get the best of both sides of the coin”? The answer is simple, yet complex. Flaxseed contains cyanogenic glycosides, that via autohydrolysis, release potentially toxic hydrogen cyanide (the dose makes the poison) in the presence of water (Poulton J, Ciba Found Symp, 140:67, 1988); (Chadha R et al, Food Addit Contam, 12: 527, 1995). Cyanogenic glycosides (linamarin, linustatin, neolinustatin) are highest in the mucilage in the seedcake. Generally, only up to 50 g of flaxseed daily is safe (Cunnane S, et al, Br J Nutr, 69:443, 1993); (Wanasundara P, Shahidi F, Adv Exp Med Biol, 434:307, 1998) and palatable, due to the release of a mass of ever-increasing slimy mucilage that fills the mouth on chewing the seeds, limiting the amount of lignan that can be safely obtained from consumption of flaxseed. Many foods are cyanogenic, (eg wheat, barley and many nuts and seeds, as an evolutionary adaptation to discourage herbivory. Our bodies have a limited capacity to detoxify cyanide through addition of sulphur (from amino acids) to form thiocyanate or reaction with cysteine directly to form beta-cyanoalanine. Thus if the dietary levels of sulphur-containing amino acids are high, the body can tolerate, indeed even benefit from moderate intake of cyanide, but if the diet has low protein or amino acid composition imbalances, then it may be low in the sulphur-containing amino acids and hence be susceptible to toxicity.

Chewing the seeds releases masses of slimy mucilage and initiates the conversion of cyanogenic glycosides to toxic hydrogen cyanide. Grinding the seeds warms the fragile oils and exposes them to oxygen, oxidising and rendering them otherwise toxic, over and above later autohydrolysis in the gut fluid. On my website I addressed this dilemma thus: “New (soft) technologies (as pioneered by Gaia Research) can produce products that extend the nutraceutical properties ascribed to flaxseed while minimizing drawbacks associated with the consumption of whole flaxseed, which are usually consumed associated with baked goods, which damages the EFAs and other healthful components, or suffers from toxicity in excess. Correctly processed raw flaxseed can have reduced levels of the strong laxative/purgative effects normally associated with the high cyanogenic glycoside mucilage component of flaxseed, which otherwise releases toxic hydrogen cyanide via auto-hydrolysis in the presence of water in the gut. Although this is associated with a non-targeted additional laetrile-type of anti-cancer effect, it strongly limits the amount of the most healthful SDG that could otherwise be consumed. A typical concentration of SDG in oil-free flaxseed is around 1.5%. Careful processing can concentrate the SDG, whilst reducing the glycosides, allowing for a much-reduced gastric challenging serving size suitable for an optimal daily quantity”. Flax lignans need to be micronised and acted upon by water and bacteria in the gut to be optimally utilised as human nutrition. Carefully cold-expressing and packaging the oil and defatting, centrifuging-out the mucilage and stabilising the seedcake with antioxidant herbs and spices, to separate the water and oil soluble fractions into two healthy individual foodstuffs, provides a novel modern approach to said limitations to a healthy natural substance so appropriate to humans needs at this troubled time of our evolution.

Being fruit eaters by creation and eons of evolution (we differ genetically less than 2% from frugivorous great apes), humanity remains anatomically, physiologically and biochemically optimally suited to tree- and seed-, not sea- foods. We have and will continue to change this divine design at our own peril and also that of all life on this precious planet.

Stuart Thomson (August 2004)

Further to my report “Does Flaxseed Oil Cause and Fish Oil Prevent Prostate Cancer?”, which I prepared in August 2004 to put to rest the nonsense circulating on Information Highway regarding extrapolations of Alpha Linolenic Acid (ALA) consumption and incidence of prostate cancer to flaxseed oil, a very rich source of ALA, I have undertaken a thorough investigation of the subsequent published scientific literature and can confidently state that my position, that properly cold-pressed and stored Flaxseed oil is not a risk for prostate cancer, is even stronger following the passage of time. Even ALA as a significant factor has now dropped off the scientific radar screen.

Alan Gaby M.D. addressing this issue in the December 2004 issue of the widely respected influential independent publication Townsend Newsletter for Doctors and Patients, wrote as follows:

“For at least two reasons, the idea that ALA causes prostate cancer lacks biological plausibility. First, the content of ALA in a typical Western diet has declined considerably as a result of partial hydrogenation of edible oils and less grazing by farm animals on ALA-rich grasses. If anything, the modern diet is marginally deficient in ALA (Rudin D, Med Hypotheses, 8:17-47, 1982). It is difficult to believe that the lower end of the historical range for an essential nutrient is still too much. Second, ALA at a concentration less than 10 microM inhibits the enzyme 5alpha-reductase in vitro (Liang T, Liao S, Biochem J, 285:557-562, 1992). This enzyme catalyzes the conversion of testosterone to its more biologically active metabolite, dihydrotestosterone, believed to play a role in the development of benign and malignant prostate cancer. A substance that inhibits 5alpha-reductase might, therefore prevent, rather than promote, prostate cancer.”

“While it is unlikely that ALA itself is a carcinogen, it is possible certain foods that contain ALA have cancer-causing effects unrelated to their ALA content. One such food might be canola oil. In comparative studies, rodents fed canola oil had androgen concentrations significantly higher than those fed other oils (Gromadzka-Ostrowska J et al, Reprod Biol, 2:277-293, 2002). If canola oil also increases androgen concentrations in humans, it could increase the risk of prostate cancer. Another factor is the unstable nature of ALA, which is highly unsaturated and therefore prone to become oxidized, either spontaneously or in the presence of heat. Cooking with soybean oil or canola oil (the two main plant sources of ALA in most human diets) might lead to the formation of carcinogenic byproducts” (rather than pristine essential ALA itself).

Personally, I do believe that excessive damaged alpha linolenic acid (as is much of it in the modern food chain, including rancid flaxseed oil) is likely to be implicated in cancer etiology, hence Gaia’s extraordinarily high standard of using only the first 25kg seed truly cold-pressed on a given day, nitrogen flushing and hermetically sealing containers, refrigerating and freezing prior to passage between supplier and consumer. We do take responsibility for our customer’s health very seriously.

The principal study addressed in said rebuttal (Leitzmann M et al, Am J Clin Nutr, 80(1), 2004) (May) did not mention flaxseed oil at all, but was seized upon by fish oil marketers to put down their plant kingdom competing source of dietary Omega 3 EFA. My subsequent chronological literature search produced no confirmatory published studies implicating flaxseed oil or even ALA in any cancers. I have summarised the main scientific findings, but unlike the fish oil salespersons, shall refrain from suggesting that the implicated substances, not to mention foods containing them, be avoided. The subsequent findings do however illustrate the absurdity of jumping to conclusions. My new National Library of Medicine (USA) search of diet related prostate cancer causation, including alpha linolenic acid and flaxseed oil, identified only the following subsequent published studies:

a) A detailed ‘review’ of (all) studies on the association between prostate cancer and dietary fat indicated associations between prostate cancer and total fat consumption. The strongest association was for alpha-linolenic acid (ALA), but the studies were extremely inconsistent. In better but fewer studies, monounsaturated fat, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were also risk factors. Associations with advanced prostate cancer were more homogeneous and suggested an association with total and saturated fat, but no associations with polyunsaturated fat, linoleic acid, ALA, EPA, or DHA. (Dennis L et al, Am J Epidem, 160(5), 2004)

b) EPA and DHA, found mainly in fatty fish (marine fatty acids), can both be biosynthesized in humans from ALA sources, which include green leafy vegetables, flaxseed, canola oil, soybeans, and walnuts. Mechanisms by which these fatty acids might ‘lower’ cancer risk is the inhibition of likely cancer initiating and promoting eicosanoid production from Omega-6 fatty acid precursors, which include linoleic acid (LA) in vegetable oils (of which flaxseed oil has the lowest content) and arachidonic acid (AA) in animal products. No clear causative or protective association was found between prostate cancer risk and intake of EPA or DHA. (Terry P et al, J Nutr, 134(12), 2004)

c) A direct association with prostate cancer was found for intake of starch and monounsaturated fatty acids (eg olive oil), whereas an ‘inverse’ (protective) association emerged for polyunsaturated fatty acids, including alpha linolenic acid (ALA) (Bidoli E et al, Ann Oncol, 16(1), 2005).

d) Dairy consumption ‘may’ increase prostate cancer risk through a calcium-related pathway (Tseng M et al, Am J Clin Nutr, 81(5), 2005).

e) Dairy, calcium, zinc at high doses, saturated fat and grilled meats ‘may’ increase prostate cancer risk (Chan J et al, J Clin Oncol, 23(32), 2005).

f) Intake of dairy products and calcium ‘may’ be associated with an increased risk of prostate cancer (Gao X et al, J Natl Cancer Inst, 97(23), 2005).

g) Increased calcium and animal fat consumption ‘may’ increase the risk of prostate cancer (Segev Y, Nativ O, Harefuah, 145(1), 2006).

h) A systematic review of a large body of literature spanning numerous cohorts from many countries with different demographic characteristics does not provide evidence of a significant association between omega-3 fatty acids (eg flax & hemp) and cancer. For prostate cancer, there was 1 estimate of decreased risk and 1 of increased risk for prostate cancer, whereas 15 other estimates did not show a significant association. (MacLean C, JAMA, 295(4), 2006)

i) Investigation of the associations between prudent and Western dietary patterns and risk of prostate cancer demonstrated an effect only in advanced prostate cancer in among older men (Wu K et al, Cancer Epidemiol Biomarkers Prev, 15(1), 2006).

j) Milk and fresh tomato consumption were associated with small elevations in risk of prostate cancer (Chan J et al, Cancer Causes Control, 17(2), 2006).

In my previous report, I touched on the known anticancer properties of flaxseed lignans. I have summarised this research as it relates to the prevention and treatment of prostate cancer:

Asian and vegetarian men both consume high-fibre diets that provide a rich supply of weak dietary phyto-oestrogens. Plant lignans are present in many cereals, grains, fruits and vegetables and give rise to the mammalian lignans enterodiol and enterolactone. The richest source is flaxseed. In addition to their oestrogenic activity, these plant compounds can interfere with steroid metabolism and bioavailability and inhibit enzymes crucial to cellular proliferation and hence may contribute to lower incidences of prostate cancer. (Denis L et al, Eur Urol, 35(5-6), 1999)

Flaxseed ingestion produces large amounts of mammalian lignans with weak estrogenic/anti-estrogenic properties shown to reduce adult relative prostate weight and cell proliferation, suggesting potential protection against prostate disease, without affecting sex hormone levels. (Tou J, et al, J Toxicol Environ Health, 56(8), 1999)

Flaxseed and especially ground flaxseed is known to reduce prostate weight in animal studies (Sprando R, et al, Food Chem Toxicol, 38(4), 2000).

Dietary fat and fiber affect hormonal levels and may influence cancer progression. Flaxseed is a rich source of lignan and omega-3 fatty acids and pilot studies suggest that the consumption of the lignan, along with concomitant fat restriction, may thwart prostate cancer. Further study is needed to determine the benefit of this dietary regimen as either a complementary or preventive therapy. (Demark –Wahnefried W, et al, Eurol, 58(1): 2001)

Enterolactone suppresses the growth of prostate cancer cells, and may do so via hormonally-dependent and independent mechanisms (Lin X et al, Anticancer Res, 21(6A), 2001).

A diet supplemented with 5% flaxseed inhibits the growth and development of prostate cancer in the animal studies (Lin X et al, Urology, 60(5), 2002).

Prostate cancer patients should not smoke, they should reduce their intake of saturated and trans fats, increase their consumption of a diversity of fruit and vegetables, consume moderate quantities of dietary soy or flaxseed, increase their consumption of omega-3 fatty acids, maintain a healthy weight and get at least 30 min/day of physical activity. Clinicians need to constantly emphasize these basic changes in order to truly impact the overall health of any patient following definitive prostate therapy. (Moyad M, Curr Opin Urol, 13(2), 2003)

There is evidence to support epidemiologic studies claiming that male populations who consume high phytoestrogen diets have a reduced risk of prostate cancer development and progression. Flax meal has been shown to favorably influence the PSA level and the free/total PSA ratio in patients with prostate cancer (Dalais F et al, Urology, 64(3), 2004).

Flaxseed is a more potent source of phytoestrogens than soy. The lignans in flax seed are a major component of flax's anti-cancer effects. Some brands of flax seed oil retain some of the seed particulate because of the beneficial properties of the lignans. These lignans are metabolized in the digestive tract to enterodiol and enterolactone, with oestrogenic activity. Ground flax seed may be a very beneficial food for men battling prostate cancer, since intake of the (increased availability) lignan fraction will lower cancer risk. (Donaldson M, Nutr J, 2004; 3:19, 2004)

There is a growing interest in lignans due to applications in cancer chemotherapy and other effects for development of potential new therapeutic agents (Saleem M et al, Nat Prod Rep, 22(6), 2005)

High intake of food items rich in enterolactone (bacterial breakdown of flaxseed) are associated with a decreased risk of prostate cancer (Hedelin M et al, Cancer Causes Control, 17(2), 2006).

Gaia Organics have developed a unique flaxseed lignan product, already mentioned in my above-mentioned report, that removes the interfering fat and toxic cyanide precursors from the seedcake, which micronised lignan particles are them mixed with antioxidant herbs and spices to provide a very convenient and highly bioavailable flaxseed lignan concentrate, without the inconvenience and risks of chewing or grinding flaxseed in an effort to access these rare dietary, yet vital substances.

For prostate (and other) cancers, I have always recommended and supplied green tea. Here is a short summary of the anti- prostate cancer properties of Chinese green tea:

Oral consumption of green tea has been shown to inhibit prostate cancer and metastasis experimentally, resulting in marked inhibition of prostate cancer progression (Saleem M, Clin Cancer Res, 11(3), 2005).

The Prostate Cancer Prevention Trial and other large-scale trials have identified promising agents against prostate cancer, including green tea (Klein E, Crit Rev Oncol Hematol, 54(1), 2005).

Treatment of prostate cancer cells with green tea activates growth arrest and apoptosis (Hastak K et al, FASEB J, 19(7), 2005).

Several epidemiological studies substantiate that green tea has a protective effect against a variety of malignant proliferative disorders, including prostate cancer, attributed to the biologically active catechins that mediate diverse physiological and pharmacological actions in bringing about the regression of the tumors by several mechanisms that antagonize the growth factor-induced proliferative disorders (Doss N et al, J Nutr Biochem, 16(5), 2005).

The medicinal benefits of green tea include of prostate anticancer properties (Cooper R et al, J Altern Complement Med, 11(4), 2005).

Green tea may have a chemopreventive effect against prostate cancer by inducing apoptosis (Sonn G et al, Prostate Cancer Prostatic Dis, 8(4), 2005).

Green tea has a preventive, protective and control effect against prostate cancer (Patel S et al, BJU Int, 96(9), 2005).

Green Tea Catechins administration to mice genetically resistant to prostate cancer has resulted in substantial delay of prostate cancer progression in 80% of the animals. (Scaltriti M et al, Carcinogenesis, 28 Nov 2005 [Epub ahead of print]).

A one-year proof-of-principle study of oral administration of green tea in volunteers with high-grade prostate intraepithelial neoplasia proved to be very safe and effective for treating pre-malignant lesions before prostate cancer even develops and also of help for treating the symptoms of benign prostate hyperplasia (Bettuzzi S et al, Cancer Res, 66(2), 2006).

Geographical and case-control studies are showing that green tea drinking could afford prostate cancer chemopreventive effects in humans (Siddiqui I et al, Mol Nutr Food Res, 50(1), 2006). (Jan)

I trust that this update and recommendation guideline will assist you in definitively countering any nonsense picked up on the Internet and elsewhere with regards to the safety of flaxseed oil relative to prostate cancer and also two means to actively counter the condition of prostate cancer itself.



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