Oxidation / small dense LDL

"montygram" <[email hidden]> schrieb im Newsbeitrag
news:[email hidden]...

Quoted message said:

I made this point on this NG more than a year ago, because one guy was
saying that only small LDL was a problem, but I made the point that the
free radical reactions were causing there to be more of this form.
It's amazing how these "researchers" keep discovering the same things
and claiming that it's something new. They don't seem to read the
literature that they like to claim they are experts in.

you don't seem to understand the difference between: thinking it so and
_prooving_ it is so.

montygram said:

I made this point on this NG more than a year ago,

What point? What are you referring to? Try quoting what you're
commenting on.

Quoted message said:

because one guy was
saying that only small LDL was a problem, but I made the point that the
free radical reactions were causing there to be more of this form.

So you're actually agreeing with him. I couldn't find the post you're
referring to, but given the various names you've had and your tendency
to break threads and start new ones just to reply, it's perhaps not
surprising. This thread seems pertinent though:

http://groups-beta.google.com/group/sci.med.nutrition/browse_frm/thread/3e781dfb998cc67c/5e9b11766fa1a745?q=nick+small+LDL&rnum=3&hl=en#5e9b11766fa1a745

Quoted message said:

It's amazing how these "researchers" keep discovering the same things
and claiming that it's something new. They don't seem to read the
literature that they like to claim they are experts in.

At least they research things directly, rather than picking and
choosing other people's work to fit their own viewpoint. You're always
going on about scientific method, yet don't seem to realise that most
scientific "truth" is the result of incremental increases in supporting
evidence rather than one big idea.

MattLB

Yes, the theory of relativity is a "little thing."

All the evidence points to free radical damage, in one form or another,
being the root cause of "chronic disease." If I didn't see the
evidence for myself, I would not have believed it. Perhaps you should
remove your head from you hind quarters and take a look for yourself.

Yes, the theory of relativity is a "little thing."

All the evidence points to free radical damage, in one form or another,
being the root cause of "chronic disease." If I didn't see the
evidence for myself, I would not have believed it. Perhaps you should
remove your head from you hind quarters and take a look for yourself.

I didn't do the experiment, but it has been done. Instead of
auditioning for a role on the Sopranos, perhaps you should actually do
some research. I will involve typing in www.pubmed.com and then a few
more words, and then hitting the enter key, but I've got a lot of
confidence it you. Just keep saying to yourself, "I think I can, I
think I can..."

Took me about a minute to find this one:

Ann Med. 2002;34(1):48-54.

Susceptibility of LDL to oxidation in vitro and antioxidant capacity in
familial combined hyperlipidemia: comparison of patients with different
lipid phenotypes.

Liu ML, Ylitalo K, Vakkilainen J, Nuotio I, Valkonen M, Lahdenpera S,
Viikari J, Taskinen MR.

Department of Medicine, Helsinki University Central Hospital, Finland.

BACKGROUND: There is increasing evidence that oxidation of low-density
lipoprotein (LDL) plays an important role in atherogenesis. AIM: To
explore the LDL oxidizability and its determinants in familial combined
hyperlipidemia (FCHL) patients with different phenotypes. METHOD: The
study included 59 FCHL family members with different lipid phenotypes,
39 non-affected relatives, and 30 spouses as healthy controls. RESULTS:
The lag time for LDL oxidation was significantly shorter in FCHL
patients with different lipid phenotypes as compared to healthy
controls. There were no significant differences in the propagation rate
and conjugated diene formation and alpha-tocopherol content in LDL
between the FCHL groups and healthy controls. Plasma concentrations of
alpha-tocopherol in all FCHL patients and uric acid in FCHL patients
with IIB and IV phenotypes were significantly higher than in healthy
controls. Plasma total peroxyl radical trapping capacity measured
(TRAPmea) and TRAPcalc tended to be higher in affected FCHL groups, but
the difference was significant only for IIB phenotype. The peak LDL
particle size in the combined group of FCHL patients was significantly
smaller than in healthy controls. The lag time for LDL oxidation
correlated significantly with LDL size both in the group of FCHL family
members (r = 0.477, P<0.001) and in the healthy controls (r = 0.482,
P<0.01). CONCLUSIONS: LDL from FCHL patients irrespectively of lipid
phenotypes is more susceptible to oxidation in vitro than LDL from
healthy controls. This increased susceptibility of LDL to oxidation in
vitro seems to be attributed to the abundance of small dense LDL
particles and not to the defect of antioxidant capacity in FCHL.

It doesn't matter whether you are "genetically predisposed" to small
LDL, so long as you stay away from unsaturated fatty acids, except in
trace amounts, such as that found in coconut oil.

montygram said:

Took me about a minute to find this one:

Ann Med. 2002;34(1):48-54.

Susceptibility of LDL to oxidation in vitro and antioxidant capacity in
familial combined hyperlipidemia: comparison of patients with different
lipid phenotypes.

Liu ML, Ylitalo K, Vakkilainen J, Nuotio I, Valkonen M, Lahdenpera S,
Viikari J, Taskinen MR.

Department of Medicine, Helsinki University Central Hospital, Finland.

BACKGROUND: There is increasing evidence that oxidation of low-density
lipoprotein (LDL) plays an important role in atherogenesis. AIM: To
explore the LDL oxidizability and its determinants in familial combined
hyperlipidemia (FCHL) patients with different phenotypes. METHOD: The
study included 59 FCHL family members with different lipid phenotypes,
39 non-affected relatives, and 30 spouses as healthy controls. RESULTS:
The lag time for LDL oxidation was significantly shorter in FCHL
patients with different lipid phenotypes as compared to healthy
controls. There were no significant differences in the propagation rate
and conjugated diene formation and alpha-tocopherol content in LDL
between the FCHL groups and healthy controls. Plasma concentrations of
alpha-tocopherol in all FCHL patients and uric acid in FCHL patients
with IIB and IV phenotypes were significantly higher than in healthy
controls. Plasma total peroxyl radical trapping capacity measured
(TRAPmea) and TRAPcalc tended to be higher in affected FCHL groups, but
the difference was significant only for IIB phenotype. The peak LDL
particle size in the combined group of FCHL patients was significantly
smaller than in healthy controls. The lag time for LDL oxidation
correlated significantly with LDL size both in the group of FCHL family
members (r = 0.477, P<0.001) and in the healthy controls (r = 0.482,
P<0.01). CONCLUSIONS: LDL from FCHL patients irrespectively of lipid
phenotypes is more susceptible to oxidation in vitro than LDL from
healthy controls. This increased susceptibility of LDL to oxidation in
vitro seems to be attributed to the abundance of small dense LDL
particles and not to the defect of antioxidant capacity in FCHL.

It doesn't matter whether you are "genetically predisposed" to small
LDL, so long as you stay away from unsaturated fatty acids, except in
trace amounts, such as that found in coconut oil.

I'm sorry, I'm having trouble understanding your meaning. Let me
try to rephrase:
Independent of genetics, as long as you keep below some level of UFA,
WHAT?

Something good will result?

There's nothing in the thread about UFA. You're introducing it
here. If you had cited anything in support of whatever you were
trying to say we might have figured it out. There is certainly
nothing about them in the abstract you pasted in.

I'm guessing that you think too much dietary UFA is bad, but what
you think happens when one bite(?) of something with more than
coconut oil is unknown. I expect all will agree that some level
of UFA is too much, but you seem to be trying to make a statement
here about a specific level.

One of the benefits of consuming UFAs may be that they react with
the limited serum oxidizer supply, consuming it so as to reduce
the extent to which it oxidizes LDL.

I could research what you stated if you had said *anything*.

"montygram" <[email hidden]> schrieb im Newsbeitrag
news:[email hidden]...

Quoted message said:

I didn't do the experiment, but it has been done. Instead of
auditioning for a role on the Sopranos, perhaps you should actually do
some research. I will involve typing in www.pubmed.com and then a few
more words, and then hitting the enter key, but I've got a lot of
confidence it you. Just keep saying to yourself, "I think I can, I
think I can..."

I don't doubt that the experiment has been done, I doubt that you know what
a single experiment means when it comes to uncover a certain biochemical
mechanism.

Typing random keywords into a pubmed searchbox is not any kind of
achievement, even though you seem to believe it is- understanding the
principles that these studies are based on and knowing what a study says and
what it really does not say is an entirely different thing.. and you are
very strongly lacking in that part (I just remember that SOD/age study you
posted).

montygram said:

Took me about a minute to find this one:

A pity you didn't take a bit longer to read it and understand it.

Quoted message said:

Ann Med. 2002;34(1):48-54.

Susceptibility of LDL to oxidation in vitro and antioxidant capacity in
familial combined hyperlipidemia: comparison of patients with different
lipid phenotypes.

Liu ML, Ylitalo K, Vakkilainen J, Nuotio I, Valkonen M, Lahdenpera S,
Viikari J, Taskinen MR.

Department of Medicine, Helsinki University Central Hospital, Finland.

BACKGROUND: There is increasing evidence that oxidation of low-density
lipoprotein (LDL) plays an important role in atherogenesis. AIM: To
explore the LDL oxidizability and its determinants in familial combined
hyperlipidemia (FCHL) patients with different phenotypes.

<snip>

Quoted message said:

CONCLUSIONS: LDL from FCHL patients irrespectively of lipid
phenotypes is more susceptible to oxidation in vitro than LDL from
healthy controls. This increased susceptibility of LDL to oxidation in
vitro seems to be attributed to the abundance of small dense LDL
particles and not to the defect of antioxidant capacity in FCHL.

It doesn't matter whether you are "genetically predisposed" to small
LDL, so long as you stay away from unsaturated fatty acids, except in
trace amounts, such as that found in coconut oil.

Clearly you don't have a clue what FCHL is, or you'd realise that
regardless of what they eat or don't eat they will have high LDL and
greatly increased chance of death from atherosclerosis.

MattLB

I'll guess you're replying to something I said, probably this bit:

" At least they research things directly, rather than picking and
choosing other people's work to fit their own viewpoint. You're always
going on about scientific method, yet don't seem to realise that most
scientific "truth" is the result of incremental increases in supporting
evidence rather than one big idea. "

montygram said:

Yes, the theory of relativity is a "little thing."

One: it was/is a theory. If it hadn't been supported by subsequent
experimental evidence/observation that's all it would be.
Two: Einstein is a household name precisely because it wasn't "most"
research. I thought that was rather obvious.

Quoted message said:

All the evidence points to free radical damage, in one form or another,
being the root cause of "chronic disease." If I didn't see the
evidence for myself,

Where exactly did you see free radical damage causing chronic disease?

Quoted message said:

I would not have believed it. Perhaps you should
remove your head from you hind quarters and take a look for yourself.

I don't actually walk on all fours.

MattLB