Re: Beta Sitosterol, Bee Honey and Quercetin

John...This is confusing to me. The following quote was taken from a web
site. "Quercetin is a potent antioxidant, providing cardiovascular
protection by reducing oxidative damage to LDL-cholesterol, the underlying
cause of heart disease". If LDL is the bad cholesterol, why does reducing
oxidative damage to it provide cardiovascular protection. It seems the
other way around. I would think you would want to damage the LDL
cholesterol. What is the equivalent amount of cholesterol (in mg) in 1000
mg of quercetin. I did some searching on "quercetin and cholesterol" and
did not find anything indicating what you are saying...Pete

"John Sankey" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Just to note that quercetin is equivalent to cholesterol, so
you in effect are taking 3x the maximum dietary recommendation
of the heart people. Unless you feel it improves your condition,
I'd be cautious about that dose.

Toxicity is about amounts, not about "things." Water is toxic to
humans if consumed in specific quantities in a given period of time,
but this will vary from one individual to another. Selenium in some
forms is indeed to be avoided, as I mentioned. I would also suggest a
zinc supplement.

As for Pete: Thanks for your honesty. This is a big problem. People
have to live in a specific society with certain
obligations/responsibilities (bills to pay), and you can't get coconut
oil at your local quick mart type of store. You may get to the point,
however, that you decide that your health is more important, and if
so, and you try what I recommend, please let me know how things turn
out.

Best of luck.

One of many:

Cancer Res. 2005 Mar 15;65(6):2498-504.

Manganese superoxide dismutase polymorphism, prediagnostic antioxidant
status, and risk of clinical significant prostate cancer.

Li H, Kantoff PW, Giovannucci E, Leitzmann MF, Gaziano JM, Stampfer MJ,
Ma J.

Channing Laboratory, Department of Medicine Brigham and Women's
Hospital and Harvard Medical School, Boston, MA 02115, USA.
[email hidden]

Oxidative stress may enhance prostatic carcinogenesis. A polymorphism
[valine (V) --> alanine (A)] of manganese superoxide dismutase (MnSOD),
the primary antioxidant enzyme in mitochondria, has been recently
associated with prostate cancer. We examined the relationship between
prostate cancer and the MnSOD polymorphism and its interactions with
baseline plasma antioxidant levels (selenium, lycopene, and
alpha-tocopherol) and beta-carotene treatment among 567 cases and 764
controls nested in the prospective Physicians' Health Study. We found
little overall association between MnSOD polymorphism and prostate
cancer risk; however, this polymorphism significantly modified risk of
prostate cancer associated with prediagnostic plasma antioxidants
(P(interaction) > or = 0.05). Among men with the AA genotype, high
selenium level (4th versus 1st quartile) was associated with a relative
risk (RR) of 0.3 [95% confidence interval (CI), 0.2-0.7] for total
prostate cancer; for clinically aggressive prostate cancer, the RR was
0.2 (95% CI, 0.1-0.5). In contrast, among men with the VV/VA genotype,
the RRs were 0.6 (0.4-1.0) and 0.7 (0.4-1.2) for total and clinically
aggressive prostate cancer. These patterns were similar for lycopene
and alpha-tocopherol and were particularly strong when these
antioxidants and selenium were combined; men with the AA genotype had a
10-fold gradient in risk for aggressive prostate cancer across
quartiles of antioxidant status. Men with AA genotype who were randomly
assigned to beta-carotene treatment (versus placebo) had a RR of 0.6
(95% CI, 0.2-0.9; P(interaction) = 0.03) for fatal prostate cancer, but
no significant association was observed in men with the VV/VA genotype.
Both endogenous and exogenous antioxidants play an important and
interdependent role in preventing clinically significant prostate
cancer.

Pete said:

John...This is confusing to me. The following quote was taken from a web
site. "Quercetin is a potent antioxidant, providing cardiovascular
protection by reducing oxidative damage to LDL-cholesterol, the underlying
cause of heart disease". If LDL is the bad cholesterol, why does reducing
oxidative damage to it provide cardiovascular protection.

LDL is a normal, essential part of the body's function. If it gets
oxidised, however, two things happen:

1) It becomes stickier and can end up stuck in the artery wall

2) It begins to look foreign to the body's immune system and scavenger
white cells will consume it. Unfortunately these white cells don't stop
eating when they're full, so if enough oxidised LDL is around they will
eventually burst releasing the even more damaged LDL, making things
worse (this is what a fatty plaque is).

Quoted message said:

It seems the
other way around. I would think you would want to damage the LDL
cholesterol.

Cholesterol and LDL are supposed to be there and aren't harmful unless
damaged.

MattLB

montygram said:

Toxicity is about amounts, not about "things."

It's absolutely about "things", whatever you mean by that. Some
substances have a negative biochemical effect, some don't. The degree
of that effect depends on how much there is, of course. Just because
something in great excess has a negative effect of some sort, doesn't
mean it's a toxin. The term toxin would be meaningless if everything
was a toxin.

Quoted message said:

Water is toxic to
humans if consumed in specific quantities in a given period of time,
but this will vary from one individual to another.

I see this is another area you don't understand properly. Water isn't
toxic. If you drink too much water you will be in trouble, but not
because the water has poisoned you, rather you will disrupt blood and
EC fluid volumes and salt concentrations.

A toxin in the strictest use of term is a molecule made by a living
organism (usually a microorganism or plant) that causes disease if
introduced into another organism. Poison and toxin aren't therefore the
same thing.

MattLB

montygram said:

One of many:

One of many what? Papers about something the original poster doesn't
have?

Quoted message said:

Cancer Res. 2005 Mar 15;65(6):2498-504.

Manganese superoxide dismutase polymorphism, prediagnostic antioxidant
status, and risk of clinical significant prostate cancer.

<snip>
Prostate cancer isn't the same thing as prostatis or BPH.
MattLB

Matt...thank you for all three of your informative responses. I can see
that you are an intelligent person and know what you are talking about. I
admire that in person. I have studied the immune system for 100's of hours
(its like black magic and highly research orientated and hypothetical) due
to my serious T-4 cell deficiency I mentioned (non HIV-cause unknown -docs
can't help me). I was curious when you said "they will eventually burst"
when describing the WBC's consuming the stuck LDL. I assume you meant the
scavenger white cells. I guess there not smart enough to quit when they can
and thus tend to defeat one of their functions if they burst. If they don't
burst does the stuff they consume end up getting absorbed into the lymphatic
system or does it go somewhere else for storage and dissolution. Very
interesting.

Matt, is your e-mail address legitimate, so I could write you directly, if
you agreed to that. Please let me know either in here or by writing me
directly by taking out the "nospam."out of my address. Thanks....Pete

"MattLB" <[email hidden]> wrote in message
news:[email hidden]...

Quoted message said:

Pete said:

John...This is confusing to me. The following quote was taken from a web
site. "Quercetin is a potent antioxidant, providing cardiovascular
protection by reducing oxidative damage to LDL-cholesterol, the
underlying
cause of heart disease". If LDL is the bad cholesterol, why does
reducing
oxidative damage to it provide cardiovascular protection.

LDL is a normal, essential part of the body's function. If it gets
oxidised, however, two things happen:

1) It becomes stickier and can end up stuck in the artery wall

2) It begins to look foreign to the body's immune system and scavenger
white cells will consume it. Unfortunately these white cells don't stop
eating when they're full, so if enough oxidised LDL is around they will
eventually burst releasing the even more damaged LDL, making things
worse (this is what a fatty plaque is).

Quoted message said:

It seems the
other way around. I would think you would want to damage the LDL
cholesterol.

Cholesterol and LDL are supposed to be there and aren't harmful unless
damaged.

MattLB