You need to know exactly what is present in the that you literally have
in front of you. Olive oil, for example, can vary greatly, from being
"healthy," provided you don't damage it, to being very unhealthy (to
the point that it's used in rancidity testing because it is so
suceptible to free radical degradation). Usually, It's about double
bonds, antioxidant cover, and refining, storing, cooking, though peanut
oil contains other substances that are problematic (see below).
I will respond to anyone who posts something like, "Montygram: why
are the nutritional experts, in general, so lacking in understanding
about their own area of experise?" However, I don't have the time
to follow every new post to every old thread. What's going on here
most of the time is that there are new people who have never read some
crucial posts, and there are a few people who have been here a while
and who seem to want to make the same criticisms without being helpful.
To sum up much of what I've posted briefly:
Dr. Hans Selye recognized many decades ago that "stress" was the
key to what we call "chronic diseases," such as heart disease,
cancer, diabetes, AD, etc., but he only understood in physiologically.
Denham Harman proposed the "free radical theory of aging" in the
1970s. This supplies the underlying biochemical mechanism of the
"stress" that Selye noted.
In the last decade or so, the evidence has mounted to the point that
there really is no other hypothesis that makes sense outside of free
radical activity. Even Dr. Stein of the AHA recently acknowledged this
in the heart disease context (oxidized, not normal, cholesterol, is the
problem). The homocysteine revolution, another example, is nothing to
worry about without the oxidative stress.
In the 1980s, JoAnn Braganza and others began to realize just how
dangerous a diet rich in unsaturated fatty acids can be, especially
considering the typical Western diets, low in antioxidant and usually
involving high heat cooking. The way the highly unsaturated oils are
refined is also usually a major problem.
Recently, biochemist Ray Peat has pointed out that so-called essential
fatty acids are more dangerous than helpful, except perhaps for
pregnant women for a short period of time. I've pointed out that my
grandparents (mid-80s/early 90s) have no source of omega 3 PUFAs and
never have. They rarely go to restaurants, never consume soybean or
canola oil, flax seeds, oily fish (hardly any fish, but always white)
or any other source of omega 3s beyond the tiniest traces, and yet they
are in pretty good shape, with no "chronic diseases." If omega 3s
and 6s are essential, they are required in such small amounts that
nobody should ever go out of their way to consume these potentially
very dangerous substances.
My main point is that it is much better to have the Mead acid as the
PUFA that your body uses to create metabolites used in inflammation and
other processes (rather than the omega 6 arachidonic acid).
Those who have criticized me in the past continue to do so, now
resorting to talking about obvious typographical errors, the cost of
the use of a dog as an experimental animal, and other such nonsense.
They are unable to stay on point. It is true that some experiments
that should be done have not, but that is not my fault. If someone
wants to fund an experiment that I am capable of administering, such as
feeds one group of dogs fresh coconut oil while the other group gets
large amounts of fish oil and safflower oil, I will consider it
strongly. However, the points I make are scientific, that is, they are
consistent with known chemical laws as well as the experimental data.
On the other hand, when a study done on rats (which metabolize fatty
acids differently) is cited as the reason for the essentiality of omega
3 and 6 PUFAs, when in fact, it was done in 1930, before all truly
essential vitamins were known, there is a basic logical problem, let
alone several scientific ones. Yet in some of the massive nutritional
textbooks that I own (recent ones), this citation is still made (Burr &
Burr). The Mead acid is a PUFA, so there is no debate about PUFAs
specifically. My point is that arachidonic acid, which your body packs
away when your diet goes beyond trace amounts of omega 6s, is too
dangerous. I've cited recent studies which make this point
explicitly in previous posts.
Remember the greatest experiment you've never heard about, that is,
hundreds of millions of peoples have lived with a highly saturated
fatty acid diet, and yet have hardly any "chronic disease," whereas
in countries like the USA, with very high omega 6 PUFA consumption, we
are hearing about "epidemics" of various chronic diseases in the
mainstream media almost constantly these days. Some oils high in omega
6 PUFAs seem to have the opposite effect, due to the antioxidant
substances they contain. The best example seems to be sesame oil
(assuming it's high quality and unrefined). These substances inhibit
the creation of arachidonic acid in the body (as well as AA
metabolites). Again, the key is the free radical activity, that is,
antioxidants can lessen the problem, whereas an unstable molecule like
AA leads to too much (often resulting in long term, chronic
inflammatory conditions, such as arthritis, but also cancer, etc.).
The specifically atherogenic qualities of peanut oil have been
established (see below), and the lectins are to blame. However, even
without the lectins, restaurants that use such oils usually reuse them
(and the oils are usually low quality to begin with). Doing this is
undeniably dangerous, and I've posted recent evidence that makes this
point explicitly (see below). Scientists who specialize in this area
have concluded that these oils, used this way, are incredibly toxic.
You should be glad that you only get fat, rather than drop dead on the
spot, because your body has antioxidant mechanisms that deal with it
for a while. But most people will develop some "chronic disease"
on such a diet - it's only a matter of how long it will take. Why
anyone would want to do something so dangerous when there is a tasty,
healthy alternative (fresh coconut oil, or even just butter isn't
much of a problem, though I skin the yellowed sides off the sticks
before using them), is not something that makes any sense.
Lipids. 1998 Aug;33(8):821-3.
Lectin may contribute to the atherogenicity of peanut oil.
Kritchevsky, et al.
"Peanut oil is unexpectedly atherogenic for rats, rabbits, and
primates. The lesions it produces are more fibrous than fatty. The
mechanism underlying the atherogenicity of peanut oil has been elusive.
Randomization of peanut oil reduces significantly its atherogenic
properties, but native and randomized peanut oils have similar rates of
lipolysis, and rats fed the two oils absorb and transport lipids in a
similar fashion. Peanut oil differs from other oils in having a
relatively high lectin content, and the randomization process markedly
reduces the lectin content as well. The biologically active lectin of
peanut oil has an affinity for glycoproteins found specifically on
arterial smooth muscle cells. Peanut lectin has been shown to stimulate
growth of smooth muscle and pulmonary arterial cells..."
These two are from
www.sciencedaily.com:
5/2/2005
Food Fried In Vegetable Oil May Contain Toxic Compound
MINNEAPOLIS / ST. PAUL -- University of Minnesota researchers A. Saari
Csallany, a professor of food chemistry and nutritional biochemistry,
and graduate student Christine Seppanen have shown that when highly
unsaturated vegetable oils are heated at frying temperature (365 F) for
extended periods--or even for half an hour--a highly toxic compound,
HNE (4-hydroxy-trans-2-nonenal) forms in the oil.
Previously, vegetable oils such as soybean, sunflower and corn were
regarded as heart-healthy because of their high levels of linoleic
acid, a polyunsaturated fatty acid. HNE is incorporated into fried food
in the same concentration as it forms in the heated oil. Also, Csallany
and her colleagues have found three toxic HNE-related compounds (known
as HHE, HOE and HDE) in heated soybean oil. They will present their
work at a poster session from 9 a.m. to 2 p.m. Wednesday, May 4, at the
96th annual meeting of the American Oil Chemists Society in the Salt
Lake City Convention Center.
"HNE is a well known, highly toxic compound that is easily absorbed
from the diet," said Csallany. "The toxicity arises because the
compound is highly reactive with proteins, nucleic acids--DNA and
RNA--and other biomolecules. HNE is formed from the oxidation of
linoleic acid, and reports have related it to several diseases,
including atherosclerosis, stroke, Parkinson's, Alzheimer's,
Huntington's and liver diseases."
Csallany's work underscores the risk of repeated heating, or reusing,
highly unsaturated oils for frying because HNE accumulates with each
heating cycle. In future studies, Csallany and her colleagues plan to
determine how long polyunsaturated oil must be heated at lower
temperatures in order to form HNE and its related compounds. The study
was funded by the University of Minnesota.
6/17/2005
Toxic Substances In The Oxidation Of Fats And Oils
Consumers' food health and safety may be affected by the presence of
micro-organisms and toxic substances in foodstuffs. The cause of the
presence of toxic substances in food is sometimes due to the fact that
these have been subject to processes of degradation. The oxidation or
thermal degradation of food lipids causes deterioration in foodstuffs
and the generation of toxic substances.
At the EHU-UPV (University of the Basque Country) Pharmacy Faculty they
have been studying the process of the oxidative degradation of
foodstuffs. Research was began with oils, given that these are
exclusively (99 %) made up of lipids while, in subsequent stages, the
study was extended to other foods prone to undergoing processes of
oxidative degradation.
Processes of oxidative degradation
Researchers investigated processes of oxidative degradation - notably
that caused at 70ºC with ventilation - of a broad group of oils with
very wide-ranging compositions. Another degradation process studied was
that which is caused by microwave action that does not heat greater
than a temperature of 190 ºC.
In both processes deterioration of the oils takes place. In the first
type of process (70 ºC with ventilation) hydroperoxides are first
produced and subsequently aldehydes. In the second kind of process
(microwave) it is basically aldehydes produced. It has to be pointed
out that both the oxidative conditions and the composition of the oil
determined the velocity of the degradation and both the nature and
concentration of the compounds produced.
These studies have shown, for the first time, that degradation of
lipids in foods can produce toxic oxygenated aldehydes. These
compounds, well-known in medical studies for their geno- and cytotoxic
activity, considered as markers of oxidative stress in cells as well as
being causal agents of degenerative illnesses, had not previously been
detected in foodstuffs.
Researchers have shown that some oils produce these toxic substances in
greater quantities and at a greater rate. Virgin olive oil was, amongst
all the oils studied, that which took longer to produce this type of
compounds and produced a lower concentration of them.
The technique
Researchers carried out this investigation, studying the liquid phase
of the oil by means of Proton Nuclear Magnetic Resonance and Fourier
Transform Infrarred Spectroscopy, and the gaseous phase of the oil with
Solid Phase Microextraccion techniques followed by Gas
Chromatography-Mass Spectrometry. The confirmation of the identity of
the aldehydes detected was carried out with pattern substances and with
proton nuclear magnetic resonance spectra for a number of toxic
aldehydes provided by American researchers who are studying the
presence of these compounds in damaged cells and tissues.
The presence of toxic oxygenated aldehydes in fats and oils subjected
to thermal treatment highlights the need to control the manufacture and
preparation processes of foodstuffs as well as the fatty material
employed, given their capacity to generate these oxygenated aldehydes
responsible for degenerative illnesses. This research opens new lines
of investigation and perspectives in the field of food safety.
