Four ways to fight cancer 
Author Message
 Four ways to fight cancer

I sent what's below to another newsgroup that I frequent (a music ng) and
thought it appropriate it go to this one too.  The information is all for
real and backed up by hundreds of papers found on Pubmed.


There's four things that I know of that slow and sometimes stop and
sometimes eliminate cancer in humans (though hopefully this is all moot to
you if they got it all).  They can be used, I believe, with most if not all
chemotherapy but always confirm this with your doctor (and do a search on
Pubmed, which I'll discuss briefly below, to see if the effects of the {*filter*}
you're taking are effected, either positively or negatively, by you taking
these substances).

Before I mention the four cancer fighting substances, I'll mention a couple
of quick tips.  Don't let your {*filter*} sugar level get high as cancer cells
are sugar feeders (whereas noncancer cells rely more on fat for their
energy).  This will slow proliferation (if any cancer cells are still
present) of the cancer cells.

Get exercise and plenty of sleep.  Both are very helpful to your immune

Okay here's four potent things to fight cancer.  Each one of them has been
shown in human studies to be effective cancer fighters and can be used
together to fight cancer.


"Cox 2" is short for an enzyme whose actual name  is "cyclo-oxygenase 2."

[Definition of enzyme: An enzyme is a protein molecule that either puts two
molecules together to form a new molecule or it takes apart a molecule
resulting in the creation of component molecules.  For example, one enzyme
may attach molecule A to molecule B to form molecule AB.  Another enzyme may
break apart molecule AB resulting in molecule A and molecule B.  Enzymes
don't get changed in doing this. Each enzyme works on only a few specific
molecules - since there's thousands of different molecules taking part in
chemical reactions in the human body, there's thousands of different kinds
of enzymes in each body.]

There's two "cox" enzymes: the good cox 1 enzyme and the bad cox 2 enzyme.
Cox 1 is always present in the body and is beneficial while cox 2 is
normally only present during inflammation and disease and aids cancer cells
by increasing angiogenesis (angiogenesis is the growth of new {*filter*} vessels
which a growing tumor needs to get larger).

Angiogenesis inhibitors are the hottest topic in cancer research right now
and a lot of the new {*filter*} coming to the market are angiogenesis inhibitors.

There's {*filter*} that inhibit the cox 2 enzyme and thus prevent the cox 2
enzyme from helping cancer cells.  An old cox 2 inhibitor is ibuprofen (but
not aspirin - aspirin only inhibits the cox 1 enzyme).  The downside to
using ibuprofen (and all of the old cox 2 inhibitors) is it also inhibits
the beneficial cox 1 enzyme so a small minority of people who use ibuprofen
(and aspirin) have problems because of this (the main problem being ulcers).
The upside is they are a lot less expensive than the new cox 2 inhibitors.

The new cox 2 inhibitors are called "selective cox 2 inhibitors" better they
only inhibit the bad cox 2 enzyme, not the good cox 1 enzyme so they're
safer.  The  downside is they are still under patent (no generics)
so they are a lot more expensive than ibuprofen and other nonselective cox 2

But cox 2 inhibitors have been shown in many animal and in vitro studies to
fight cancer.  Using Pubmed, you can find a lot of good info on cox 2
inhibitors and cancer.

Pubmed is run by the United States's National Institutes of Health (a
federal agency) so no one's making any money off of it.  I'd start using
Pubmed immediately because the Bush administration might eliminate it anyday
just like they just did to Pubscience (which had been free and in existence
since 1949 - of course this will hurt science knowledge in this country -
pretty shrewd political move by Bush - make the country as a whole dumber
resulting in more Republican voters).

Here's a link to Pubmed:


When you put in words in the Pubmed search box and click on the "Go" button
to the right of the search box, you'll get links to all the articles that
have those words.  Multiple words in the Pubmed search box default to an
"AND" boolean operator in the search.

When you click on an article, you (usually) can't read the entire article,
just the abstract (summary) of the article.  I've gotten the full text of
the articles I wanted whose abstract I had read at Pubmed, by going to the
University of California, San Francisco library (in person, not online).
There you can copy a lot of the articles you find at Pubmed.

To see if UCSF has an article you're interested in, put the journal in the
UCSF searchbox at this link:


When I put in "cox 2 inhibitors colon cancer" (without the quotes) in the
Pubmed search box, I got 143 articles.

CANCER FIGHTER #2: LOVASTATIN (and other statin {*filter*} and anything that
reduces cholesterol)

Cancer cells need lots of cholesterol for their daughter cells.  Every cell
(including a cancer cell) is encapsulated by a covering called a cell
membrane.  The cell membrane is made up of fatty acids but the skeleton
support structure of the cell membrane is made from cholesterol.  Thus fatty
acids and cholesterol are important components of any new cells.

Unlike liver cells which reduce the making of cholesterol when there's lots
of cholesterol in the {*filter*} (from eating a high cholesterol meal), cancer
cells don't slow down their production of cholesterol no matter how much
cholesterol is in the {*filter*}.  In addition to making their own cholesterol,
cancer cells can also use LDL (low density lipoproteins) cholesterol in the
{*filter*} for new membranes.

Statin {*filter*} such as lovastatin inhibit the production of cholesterol by
both cancer and noncancer cells.  They do this by inhibiting an enzyme with
the extremely strange name of "3-hydroxy 3-methylglutaryl coenzyme A
reductase" though you'll see it shortened to "HMG-CoA reductase" in papers.
I recommending just calling it "hr" which is what I'll call it from here on.

The "hr" enzyme is essential for the making of cholesterol (in both cancer
and noncancer cells).  The "hr" enzyme takes a molecule and makes a few
changes to it resulting in a molecule called "mevalonate" (aka "mevalonic

Mevalonate then (via other enzymes) becomes a series of other products with
the last product being cholesterol. Some of the other products made prior to
cholesterol are also needed by the cancer cell.

So by inhibiting the "hr" enzyme, not only is the cancer cell being deprived
of cholesterol, but it also is deprived of other needed products of the
mevalonate pathway.

Another substance which works like lovastatin (by inhibiting the "hr"
enzyme) is something called a "tocotrienol" which chemically is very similar
to vitamin E (alpha tocopherol).  But though it is very similar to vitamin
E, the difference between the two is crucial since vitamin E has no effect
on the "hr" enzyme while tocotrienols inhibit it.

The richest source of tocotrienols are in barley meal so start eating lots
of barley meal (it will also keep your {*filter*} levels steady) if you still
have cancer.

When I entered "lovastatin mevalonate colon cancer" in the Pubmed search
box, 12 articles came up.  When I entered "lovastatin mevalonate cancer" 128
articles came up.

CANCER FIGHTER #3: EGCG (green tea component)

Green tea contains a substance called "epigallocatechin gallate" which is
abbreviated EGCG.  The tea must be green tea to contain significant
quantities of EGCG.  EGCG is a potent angiogenesis inhibitor in
concentrations achievable in human {*filter*} from drinking green tea (at higher
concentrations, it kills cancer cells but it's hard to get such high
concentrations in human {*filter*}).

After 2 or 3 cups of green tea are dranken (at the same time), your {*filter*} is
saturated with EGCG.  But it doesn't stay in your body long.  After 8 hours,
the concentration of EGCG in the {*filter*} has diminished greatly.  Therefore,
you should drink 2 or 3 cups of green tea every four hours during waking
hours to keep the EGCG concentration in your {*filter*} high.

The easiest way to do this is to make a bunch in the morning and then put it
in a container (such as a thermos) so that you have enough for the day. Then
use it for your drinking fluid (since most of it is water).  You can use
either caffeinated or noncaffeinated green tea.

When I put in "epigallocatechin gallate cancer" in the Pubmed search box,
215 articles came up while 19 articles came up for "epigallocatechin gallate
colon cancer."

CANCER FIGHTER #4: gamma linolenic acid (GLA)

GLA is a fatty acid.  It's a polyunsaturated fatty acid (PUFA).  There's
three types of fatty acids: 1) saturated fatty acids, 2) mono-unsaturated
fatty acids and 3) poly-unsaturated fatty acids.

A fatty acid is, for the most part, a horizontal chain of carbon atoms with
each carbon atom bonded to a pair of hydrogen atoms (one above and one below
each carbon atom).

Each carbon atom has four "bonds" to (respectively) four other atoms (two to
the carbon atoms on each side of it and two to the hydrogen atoms above and
below it).  At least this is the case for saturated fatty acids (they're
called "saturated fatty acids" because every carbon atom is "saturated" with
two hydrogen atoms).

A mono-unsaturated fatty acid has one pair of carbon atoms (in the chain of
carbon atoms) where each of the two carbon atoms has only one hydrogen atom
attached to it (instead of two).

Like all carbon atoms, each of the two carbon atoms must still have four
bonds to other atoms but with one of the hydrogen atoms gone, each of these
two carbon atoms "double bond" to each other (instead of the usual single
bond) so that each still has four bonds to other atoms.

Since each carbon atom of this pair of carbon atoms has only one hydrogen
(instead of two), these two carbon atoms are not "saturated" with hydrogen
atoms.  Thus it's called a "mono" unsaturated fatty acid because there is
one (mono) pair of unsaturated fatty acids.

In "poly" unsaturated fatty acids (PUFAs), there are several (or "poly")
pairs of unsaturated (double-bonded) carbon atoms.

Among the class of polyunsaturated fatty acids, there are two subclasses.
The two subclasses are the "omega 3" fatty acids (called w-3 or n-3 in
papers) and the "omega 6" fatty acids (called w-6 or n-6 in papers) .  An
omega 3 fatty acid has its first pair of double bonded carbon atoms starting
on the 3rd carbon atom (the 3rd and 4th carbon atoms are double bonded to
each other) in the horizontal chain of carbon atoms.

An omega 6 fatty acid has its first pair of double bonded carbon atoms
starting on the 6th carbon atom (the 6th and 7th carbon atoms are double
bonded to each other) from the start of the chain.

There are several fatty acids in the omega 6 fatty acid category.  Normally
when you eat a vegetable, most of the fat will be an omega 6 fatty acid
called "linoleic acid" or LA for short.  An enzyme converts LA to another
omega 6 fatty acid called (drumroll) GLA (gamma linolenic acid).

Another enzyme converts GLA to DGLA (di-homo gamma linolenic acid).  Finally
DGLA is converted to a fourth omega 6 fatty acid called AA (arachidonic
acid) via yet another enzyme.

By the way, it's the AA fatty acid that the cox 2 enzyme converts to
substances that are beneficial to the cancer cell.  Cox 2 inhibitors keep AA
from being changed to these substances.

To summarize, here's what happens to the LA fatty acid in our vegetables
after we eat them:  LA > GLA > DGLA > AA.

All polyunsaturated fatty acids can become "oxidized" where the double
bonded carbon atoms are.  This means oxygen atoms can attach to these carbon
atoms.  When you leave a polyunsaturated fatty acid out of the  refrigerator
for too long and it's exposed to air, it becomes rancid which means it has
become "oxidized" (or undergone "oxidation").

Because saturated fatty acids don't have any double bonded carbon atoms,
they don't become oxidized which is why they can be used in cooking since
the high heat (which promotes oxidation) doesn't change them.
Mono-unsaturated fatty acids, with only one unsaturated pair of carbon
atoms, are much harder to oxidize than polyunsaturated fatty acids.

It is the ability of polyunsaturated fatty acids to become oxidized which is
the key to their very potent anti-cancer properties.

I mentioned above that cell membranes are made from fatty acids.  Fatty
acids in cell membranes can be oxidized which then can become toxic to the
cell.  Too many oxidized fatty acids in a cell membrane are lethal to cells
(both cancerous and noncancerous cells).  You may have heard of "free
radicals" - well that is what oxidized fatty acids are.

Normal cells have anti-oxidant enzymes (catalase, glutothione peroxidase)
which prevent fatty acids in cell membranes from becoming oxidized.  And
when they do become oxidized, the anti-oxidant enzymes convert the now-toxic
fatty acid to a harmless substance.

But cancer cells do not have the ability to protect fatty acids in their
membranes from becoming oxidized and from oxidized fatty acids doing damage
themselves to anywhere near the extent that normal cells do.  It is this
which makes certain polyunsaturated fatty acids toxic to cancer cells but
harmless to noncancer cells.

The polyunsaturated fatty acids that have these properties are, in the omega
6 class, GLA, DGLA, and AA, and in the omega 3 class, EPA.  GLA (and DGLA)
have the greatest toxicity to cancer cells while having the least toxicity
to normal cells.

So how does one get the cancer cells to use these fatty acids in their
membranes?  Well it turns out that cancer cells use the fatty acids that is
eaten by the host to form their membranes.  Thus if one consumes GLA in
his/her diet, the GLA becomes part of the cancer cell membrane, lots of
toxic products get produced, and the cancer cell dies.

You'll see the word "apoptosis" which means the cancer cell commits suicide
because of too much damage from the toxic products from the oxidized fatty
acids in the cell membrane.

Cancer cells are not very good at converting the fatty acid LA to GLA
because the enzyme that does this is in low supply in cancer cells (but not
normal cells).  This results in cancer cells having a higher concentration
of LA and a lower concentration of GLA (and its downstream products: DGLA
and AA) than do normal cells.

LA, it turns out, is not as easily oxidized as the other three fatty acids
(GLA, DGLA, and AA) so by not converting LA to GLA, the cancer cell protects
itself from the toxic products of an oxidized GLA (or GDLA or AA).

So where does one get GLA?  The two main sources are evening primrose oil
(9% GLA) and borage oil (24% GLA).  Borage oil is clearly preferable because
of the higher GLA content (and lower LA content).  Both evening primrose oil
and borage oil are available in health">food stores and online.

I have a journal article that described an experiment where human volunteers
consumed up to 6 grams of GLA (via borage oil) per day without any side
effects.  The concentration of GLA starts to decrease significantly after 12
hours so the best thing IMO would be to take 3 grams of GLA at, say, 7 am
and then 3 grams at 7 pm.

There is a limit to the amount of polyunsaturated fat the body can handle
(especially heart cells) so don't go hogwild in your intake but as I said, 6
grams per day had no side effects in healthy human volunteers (they took it
for 6 months).

When I put in "gamma linolenic acid cancer" in the Pubmed searchbox, 171
articles came up while "gamma linolenic acid colon cancer" produced 12

If you are going to use the fatty acid approach, I'd recommend taking a cox
2 inhibitor to prevent the cox 2 enzyme from converting AA into
angiogenesis-promoting products.

I wish you the best.


Wed, 25 May 2005 14:40:35 GMT
 [ 1 post ] 

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