| 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.
Sincerely
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.
Regards
Stuart
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