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Medical Forum / General / Cardiology / February 2007

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Pantethine - an informal poll

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Port@nospam.invalid - 30 Jan 2007 18:33 GMT
Has anyone here, other than Susan, had any luck raising their HDL
using Pantethine?
The studies Susan has cited sound great but, I've been taking 1350mg
per day since early Aug '06 with no results that I can tell.  HDL
level was 30 in Aug and remains at 30 as of the other day.
I'm just wondering what results others may be getting.
And btw Susan, your comments are more than welcome here. I'm just
wondering who else is trying the stuff besides you and me.
Thanks,
Port
Jason Johnson - 30 Jan 2007 20:44 GMT
Has anyone here, other than Susan, had any luck raising their HDL
using Pantethine?
The studies Susan has cited sound great but, I've been taking 1350mg
per day since early Aug '06 with no results that I can tell.  HDL
level was 30 in Aug and remains at 30 as of the other day.
I'm just wondering what results others may be getting.
And btw Susan, your comments are more than welcome here. I'm just
wondering who else is trying the stuff besides you and me.
Thanks,
Port

~~~~~~~~~~~~~~~~~~~~~~~~

This book discusses the supplements that will help you:

WHAT YOU MUST KNOW ABOUT STATIN DRUGS AND THEIR NATURAL ALTERNATIVES
by Jay S. Cohen, M.D.
Susan - 30 Jan 2007 20:55 GMT
> Has anyone here, other than Susan, had any luck raising their HDL
> using Pantethine?
[quoted text clipped - 6 lines]
> Thanks,
> Port

Hi, I know that OldAl on the diabetic group got a nice uptick in his
HDL.  What is your diet like?  My HDL doubled within two weeks of
cutting out starch and sugar years ago.  Then pantethine bumped it up a
few more points to 70.

It had been 34 for at least a decade.

Susan
Jim Chinnis - 31 Jan 2007 02:50 GMT
Susan <nevermind@nomail.com> wrote in part:

>x-no-archive: yes
>
[quoted text clipped - 17 lines]
>
>Susan

My HDL also rose quite significantly when I decreased my carbohydrate intake
and increased fat. With exercise and moderate weight loss added in, I've
raised it from around 32 to 68.
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 31 Jan 2007 04:21 GMT
> Susan <nevermind@nomail.com> wrote in part:
 My HDL doubled within two weeks of
> >cutting out starch and sugar years ago.  Then pantethine bumped it up a
> >few more points to 70.
[quoted text clipped - 8 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

What level of exercise do you do and roughly what are the
carb:protein:fat ratios you consume as a percentage of total calories?

I ask because I try to burn about 3000 calories a week.  If I do not
consume a good deal of carbs I am really beat and cannot sustain it.  

My understanding is that specific genotypes show the response you
describe - it is not necessarily translatable to everybody and could be
bad for the people who do respond to lower levels of fat in their diet.

Lastly, I assume all your other lipids are well controlled?

Roland
Port@nospam.invalid - 31 Jan 2007 13:15 GMT
Not sure if you're asking me, or Jim.
Be that as it may.........

>What level of exercise do you do

High.
Or at least, as high as possible.

>and roughly what are the
>carb:protein:fat ratios you consume as a percentage of total calories?

I've never counted. But I'd say protein is high, fat is lower, and
carbs even lower than fat (no trans fat, not much saturated fat).

>I ask because I try to burn about 3000 calories a week.  If I do not
>consume a good deal of carbs I am really beat and cannot sustain it.  

I know the feeling.
..... but I sustain it anyway   :-(

>Lastly, I assume all your other lipids are well controlled?

LDL = 45
HDL = 30
TC = 92
TRIG = 85

Port
Jim Chinnis - 31 Jan 2007 18:00 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>> Susan <nevermind@nomail.com> wrote in part:
>  My HDL doubled within two weeks of
[quoted text clipped - 13 lines]
>What level of exercise do you do and roughly what are the
>carb:protein:fat ratios you consume as a percentage of total calories?

I do 45 minutes of cardio each day at about 115 watts. (Sorry, physics is my
background... I think that's only around 70 cal, but I did the math in my
aging head.) I also do a fairly strenuous 45 minute workout in the weight
room 3 times a week. Plus I walk a lot, often long distances across town,
and am active, doing home remodeling, cycling, etc.

I looked up my fat/pro/carb ratios from when I was keeping records on
Fitday.  Scanning it shows around 62% fat, 20% protein, 18% carb. I also
have a couple of glasses of red wine most days.

>I ask because I try to burn about 3000 calories a week.  If I do not
>consume a good deal of carbs I am really beat and cannot sustain it.  
>
>My understanding is that specific genotypes show the response you
>describe - it is not necessarily translatable to everybody and could be
>bad for the people who do respond to lower levels of fat in their diet.

I agree. My internist practically was jumping up and down when he called me
with my lipid panel HDL results after I'd started low-carbing/High-fatting.

>Lastly, I assume all your other lipids are well controlled?

Scanning my records, here are my ranges over the past few years after
changing my diet:

Total: 121-146
LDL:  47-65
TGL: 69-130
HDL: 53-70

In 2001, I made the diet changes and the HDL began climbing. I was losing
weight (ultimately losing about 30 lb), so attributing cause isn't
straightforward. Plotting my HDL against my weight gives a very high
correlation, lower weight meaning higher HDL.

After my HDL rose, my internist put me on atorvastatin 10 mg due to a
wretched family history and a bad coronary artery CI scan (calcium score).
That made no change in my HDL, but made a big drop in LDL.

For most of my life, my lipids ran something like: tot 173, ldl 96, tg 226,
hdl 32. I suspect that's what killed all my male relatives early and my
female relatives just a bit later. There is *no* history of any diabetes in
my family (nor do i have it).

>Roland
--
Jim Chinnis   Warrenton, Virginia, USA
Jim Chinnis - 31 Jan 2007 21:32 GMT
Jim Chinnis <jchinnis@SPAMalum.mit.edu> wrote in part:

>I do 45 minutes of cardio each day at about 115 watts. (Sorry, physics is my
>background... I think that's only around 70 cal, but I did the math in my
>aging head.) I also do a fairly strenuous 45 minute workout in the weight
>room 3 times a week. Plus I walk a lot, often long distances across town,
>and am active, doing home remodeling, cycling, etc.

Oops. I checked the cardio machine after my 45 minutes today and it said I'd
burned 370 calories. So 7 x 370 = 2592 cal/week just from cardio in the gym.
I'm 62 and no athlete, had heart valve surgery in 1988, so it looks pretty
easy to burn an extra 10000 cal / week from moderate exercise.
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 01 Feb 2007 02:19 GMT
> Jim Chinnis <jchinnis@SPAMalum.mit.edu> wrote in part:
>
[quoted text clipped - 10 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

Sounds like you are exercising at a fairly vigorous level - 500 calories
per hour.

I probably consume 30-40% fat(mostly mono, low saturated, 2% or so of
omega-3), 40-50% carbs and 20% protein.  I find it interesting that if I
go down in carbs I am physically drained and you are not with roughly
equivalent caloric expenditures.

For my formal sessions I work out at a slightly higher intensity (~ 600
calories/hr about 7.5-8 METS as a base and then go up to ~900
calories/hr about 12.5 METS for about 50-70% of the time depending on
how I am feeling.

Roland
Joe Doe - 01 Feb 2007 04:53 GMT
> I looked up my fat/pro/carb ratios from when I was keeping records on
> Fitday.  Scanning it shows around 62% fat, 20% protein, 18% carb. I also
> have a couple of glasses of red wine most days.

> Scanning my records, here are my ranges over the past few years after
> changing my diet:
[quoted text clipped - 3 lines]
> TGL: 69-130
> HDL: 53-70

> Jim Chinnis   Warrenton, Virginia, USA

The results certainly look good.

What prompted you to raise your fat levels so much?  Do you know you
have a high triglyceride response to carbs?  Some other reason?

Secondly, are you concerned that the high fats themselves may be a risk
factor with respect to endothelial function etc.  For example people
report lots of symptoms of endothelial dysfunction post high fat meals
(even "good" fats).  I have not followed this too carefully but a search
for "postprandial lipaemia" will pull out a lot of the relevant research.

Lastly, for people being inspired to move in your direction it is clear
that some people are very sensitive to fat & cholesterol levels in diet.  
Specifically if you are homozygous for the E4 variant of ApoE gene
(about 5% of the population) high fat will be very bad for you.  ApoE4
attaches to VLDL particles and when these particles return to the liver
signals the liver to stop metabolizing lipids and high levels can
accumulate in circulation.  It also enhances fat absorbtion by the gut.  
ApoE2 (1% of the population) acts in the opposite way - a person
homozygous for this absorbs fat poorly and the fat absorbed is cleared  
from circulation because this variant does not shut down liver
metabolism of fat. The majority of the population have ApoE3 which is
intermediate in behaviour.  Heterozygotes ApoE3/2(10% of population) or
ApoE 3/4 (20% of population) tend towards the behaviour of the
homozygote.  So at least 25% of the population will benefit from a low
fat diet.

In general, trial with low fat and monitoring triglyceride response will  
clue you into how low you can go (If triglycerides do not rise with low
fat, high carb then low fat is better for you or if triglycerides do
rise with low fat you can raise your fat level (with "good" fats) to a
level where the triglyceride response is muted.  The triglyceride
response is followed because it can influence LDL particle size &
subclass & having them low is beneficial.  As Jim indicated raising fat
levels with good fats has the potential to not influence LDL levels
substantially but could raise HDL levels improving your ratios.  Raising
with saturated fat will increase both LDL and HDL and not improve your
ratio.

Roland
Jim Chinnis - 01 Feb 2007 16:59 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>> I looked up my fat/pro/carb ratios from when I was keeping records on
>> Fitday.  Scanning it shows around 62% fat, 20% protein, 18% carb. I also
[quoted text clipped - 14 lines]
>What prompted you to raise your fat levels so much?  Do you know you
>have a high triglyceride response to carbs?  Some other reason?

For years I had tried to lose weight by reducing fat (and quantity, of
course). Any losses were always shortlived and my lipids were bad in terms
of HDL and triglycerides.

I simply tried reducing carbs, mostly by eliminating refined carbs and
things like potatoes and rice. Since I still had to eat, my fat and protein
rose accordingly. I didn't want to pump the meat up a lot, so i tended to
eat more salads, hence more olive oil.

I lost weight fairly effortlessly, and it has mostly stayed off, even though
I have reduced the fat and increased (low-glycemic) carbs over the past year
or so.

>Secondly, are you concerned that the high fats themselves may be a risk
>factor with respect to endothelial function etc.  For example people
>report lots of symptoms of endothelial dysfunction post high fat meals
>(even "good" fats).  I have not followed this too carefully but a search
>for "postprandial lipaemia" will pull out a lot of the relevant research.

I'm aware of the issue, but I suspect you know at lot more about it from the
you are writing. I decided that weight loss trumped everything else. Until
research shows that I am better off with 35 extra pounds, mostly around the
middle, and lower fat intake, I'll keep on doing what I am doing.

>Lastly, for people being inspired to move in your direction it is clear
>that some people are very sensitive to fat & cholesterol levels in diet.  
[quoted text clipped - 11 lines]
>homozygote.  So at least 25% of the population will benefit from a low
>fat diet.

Wouldn't the fact that my fasting triglycerides were always high, even on
relatively low-fat diets, pretty much rule out my being ApoE4/4 or maybe
even ApoE4/3?

My family heart disease problem affected most strongly my paternal
grandfather and his 10 children, including my father. But it has extended to
a good fraction of the grandchildren. My father's heart disease advanced
rapidly although he was on an extremely low-fat diet. Neither he nor any of
his siblings had any problem with weight. I seem to have gotten that (in
very mild form) from my mother's side.

Too bad we can't have genetic testing done cheaply.

>In general, trial with low fat and monitoring triglyceride response will  
>clue you into how low you can go (If triglycerides do not rise with low
[quoted text clipped - 7 lines]
>with saturated fat will increase both LDL and HDL and not improve your
>ratio.

Thanks for the great discussion.

>Roland
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 02 Feb 2007 21:07 GMT
> Joe Doe <None@mail.utexas.edu> wrote in part:
> Heterozygotes ApoE3/2(10% of population) or
[quoted text clipped - 5 lines]
> relatively low-fat diets, pretty much rule out my being ApoE4/4 or maybe
> even ApoE4/3?

I think too many other markers (sedentary lifestyle, obesity, diabetes
etc. + ? genetic factors) will influence all these so it is not easy to
come to any conclusions based on one fact in isolation.  I was not
suggesting you were at risk - just trying to let people get fully
informed before they went to any extreme - either very low fat or very
high fat.  

> Too bad we can't have genetic testing done cheaply.

Genetic testing raises other ethical, psychological and practical
issues:  ApoE4 is also a marker for susceptibility to Alzheimer's.  Many
people will not want this information and be unable to cope with it
(even though it is just a marker not a cause or guarantee that you will
get it).  Second if your insurance company pays for  this test it will
go on your record and might adversely affect future choices.  Lastly,
knowing this you may be better able to  plan for the future (buy long
term care insurance for example).

> Thanks for the great discussion.
nd
> --
> Jim Chinnis   Warrenton, Virginia, USA

I have enjoyed it too - we all have to make real time choices with
incomplete and changing data and this is no easy task.   I have actually
benefited from your posts too.  Your general questioning of the sat fat
question has forced me to try and pay more attention to it.  I am more
cautious by nature and stick to the party line on this but am
nonetheless open to changing my opinion.  

Roland
Susan - 02 Feb 2007 21:38 GMT
> Genetic testing raises other ethical, psychological and practical
> issues:  ApoE4 is also a marker for susceptibility to Alzheimer's.  Many
> people will not want this information and be unable to cope with it
> (even though it is just a marker not a cause or guarantee that you will
> get it).

Why not?  More of the current literature indicates that it's preventable
by avoiding high glucose.  Since high insulin levels also promote
inflammation which is also implicated in AD, folks might want to know
that low carb and exercise can prevent, delay or slow progression of AD.
Glucose is the single biggest contributor to dementia, it now appears.

Susan
Jim Chinnis - 02 Feb 2007 23:38 GMT
Susan <nevermind@nomail.com> wrote in part:

>x-no-archive: yes
>
[quoted text clipped - 11 lines]
>
>Susan

Citations?  ;-)
--
Jim Chinnis   Warrenton, Virginia, USA
Susan - 03 Feb 2007 15:18 GMT
> Citations?  ;-)
> --

You can so readily google up the glucose/AD/dementia connection that I
don't feel compelled to dig out my other stuff.

I'll explain more about the insulin/inflammation connection, which is
very well established (we've discussed the many abstracts I have on this
in the past) but I never understood the mechanisms til my recent and
continuing adrenal crisis.

Insulin inhibits cortisol binding globulin; this means that even if
one's cortisol is adequate (in my case, way too high), one can
experience sx and signs of adrenal insufficiency (in my case, Addisonian
crisis).  This will be more pronounced in those with any form of
glucocorticoid resistance.  My Addisonian crisis evolved during my year
on an insulin sensitier, metformin.  The longer I took it, and finally,
with a higher dose, the more adrenally insufficient I became, until
finally, I was in full blown crisis.

Obviously, this isn't going to happen to everyone or to most to this
degree, but you will find that insulin does inhibit cortisol transport
to cells, thus raising inflammation (and cortisol levels and glucose,
ast the body tries to compensate.  Thus a vicious cycle is born.

Susan
Andrew B. Chung, MD/PhD - 03 Feb 2007 17:52 GMT
> > Citations?  ;-)
>
[quoted text clipped - 19 lines]
> to cells, thus raising inflammation (and cortisol levels and glucose,
> ast the body tries to compensate.  Thus a vicious cycle is born.

One can't help but wonder if your Addisonian crisis is a consequence
of your unwise decision to low-carb.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

> Susan
William Wagner - 03 Feb 2007 22:20 GMT
> x-no-archive: yes
>
[quoted text clipped - 24 lines]
>
> Susan

My Wife ingrid takes Metformin.  What is a Addisonian Crisis.  Sort of
sounds like some folks can't handle statins ( me) and your post  
confuses me. (Offers  potential understanding.)

This in particular.....
>The longer I took it, and finally,
> with a higher dose, the more adrenally insufficient I became, until
> finally, I was in full blown crisis.

Sounds like me with incremental statin titration.

Susan.. What did you do?

Signature

S Jersey USA Zone 5 Shade  
http://www.ocutech.com/  High tech Vison aid
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.

Susan - 04 Feb 2007 16:49 GMT
>  My Wife ingrid takes Metformin.  What is a Addisonian Crisis.  Sort of
> sounds like some folks can't handle statins ( me) and your post  
> confuses me. (Offers  potential understanding.)

You can easily google up what Addisonian crisis is.  I'll share with you
that the onset for me was gradual and insidious, beginning with fatigue
on the drug. progressing to worsening energy, vague aches and pains,
loss of appetite that became intense nause, and the end stage involved a
LOT of muscle cramps/spasms.

> This in particular.....
>
[quoted text clipped - 5 lines]
>
>  Susan.. What did you do?

I quit the drug and was able to eat a meal and sleep at night for the
first time the next day.

I don't think what happened to me is common; I think it unmasked
familial glucocorticoid resistance syndrome.

Susan
William Wagner - 04 Feb 2007 17:27 GMT
> x-no-archive: yes
>
[quoted text clipped - 7 lines]
> loss of appetite that became intense nause, and the end stage involved a
> LOT of muscle cramps/spasms.

Sounds like what lipitor did to me minus the Nausea and a issue with  
aching joints. Took about 3 years to notice a decline the an increase in
dosage and I saw the light.  Enough!

> > This in particular.....
> >
[quoted text clipped - 8 lines]
> I quit the drug and was able to eat a meal and sleep at night for the
> first time the next day.

 Such a fast acknowledge of a side effect.  Great!
My healing is taking years.  After CABG I did not know what to think  
would be normal. Still do not.

> I don't think what happened to me is common; I think it unmasked
> familial glucocorticoid resistance syndrome.

 I don't think what happened to me is common either but I am
documenting it all for my extended family.
> Susan

Best !

Bill

Signature

S Jersey USA Zone 5 Shade  
http://www.ocutech.com/  High tech Vison aid
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.

Joe Doe - 04 Feb 2007 01:45 GMT
> Susan <nevermind@nomail.com> wrote in part:
>
[quoted text clipped - 17 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

A few examples of evidence  to the contrary:

For the layman:

http://news.bbc.co.uk/2/hi/health/830289.stm

Or:

Dement Geriatr Cogn Disord. 2006;22(1):99-107

Laitinen MH, Ngandu T, Rovio S, Helkala EL, Uusitalo U, Viitanen M,
Nissinen A,Tuomilehto J, Soininen H, Kivipelto M.
Aging Research Center, Division of Geriatric Epidemiology, Neurotec,
Karolinska Institutet, Stockholm, Sweden.
BACKGROUND: Lifestyle and vascular factors have been linked to dementia
and Alzheimer's disease (AD), but the role of dietary fats in the
development of dementia is less clear. METHODS: Participants were
derived from random, population-based samples initially studied in
midlife (1972, 1977, 1982, or 1987). Fat intake from spreads and milk
products was assessed using a structured questionnaire and an interview.
After an average follow-up of 21 years, a total of 1,449 (73%)
individuals aged 65-80 years participated in the re-examination in 1998.
Altogether 117 persons had dementia. RESULTS: Moderate intake of
polyunsaturated fats at midlife decreased the risk of dementia even
after adjustment for demographic variables, other subtypes of fats,
vascular risk factors and disorders, and apolipoprotein E (ApoE)
genotype (OR 0.40, CI 0.17-0.94 for the 2nd quartile vs. 1st quartile),
whereas saturated fat intake was associated with an increased risk (OR
2.45, CI 1.10-5.47 for the 2nd quartile). The associations were seen
only among the ApoE epsilon4 carriers. CONCLUSIONS: Moderate intake of
unsaturated fats at midlife is protective, whereas a moderate intake of
saturated fats may increase the risk of dementia and AD, especially
among ApoE epsilon4 carriers. Thus, dietary interventions may
potentially modify the risk of dementia, particularly among genetically
susceptible individuals.
Jim Chinnis - 04 Feb 2007 02:31 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>> Susan <nevermind@nomail.com> wrote in part:
>>
[quoted text clipped - 53 lines]
>potentially modify the risk of dementia, particularly among genetically
>susceptible individuals.

This suggests that the genetically increased risk of Alzheimers (from ApoE4)
is due to ApoE4 gene effects on fat metabolism. (Yeah, getting a little off
topic.)
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 05 Feb 2007 22:44 GMT
> This suggests that the genetically increased risk of Alzheimers (from ApoE4)
> is due to ApoE4 gene effects on fat metabolism. (Yeah, getting a little off
> topic.)
> --
> Jim Chinnis   Warrenton, Virginia, USA

A proposed mechanism is outlined in this review:

Apolipoprotein E Recycling Implications for Dyslipidemia and
Atherosclerosis.  Arteriosclerosis, Thrombosis, and Vascular Biology.
2006;26:442.  I have full text access but I do not believe it is
universal.  Too much material to cover succinctly.

Roland
Jim Chinnis - 06 Feb 2007 16:13 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>> This suggests that the genetically increased risk of Alzheimers (from ApoE4)
>> is due to ApoE4 gene effects on fat metabolism. (Yeah, getting a little off
[quoted text clipped - 10 lines]
>
>Roland

I have a copy, but it is outside any areas of expertise I have. I notice the
authors refer to the effect of statins on reducing onset of AD:

"A direct connection between the development of AD and cholesterol
metabolism arises from the observation that treatment with cholesterol
lowering drugs remarkably reduced the onset of AD.72"

Ref 72 is Jick H, Zornberg GL, Jick SS, Seshadri S, Drachman DA. Statins and
the risk of dementia. Lancet. 2000;356:1627–1631.

I think that (2000) result has not panned out.
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 07 Feb 2007 03:19 GMT
> I have a copy, but it is outside any areas of expertise I have. I notice the
> authors refer to the effect of statins on reducing onset of AD:
[quoted text clipped - 9 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

Yes I know there is controversy about the mechanism of statin effects in
AD.

I do not follow the AD literature closely (I usually forget it anyway ;).

Since you have easy full text access you might also want to look at a
review by Ordovas that is more closely linked to the topic at hand
raising HDL.  In this review he discusses a few other loci that
depending on the gene have differential effects on HDL levels when you
raise PUFA intake.

Ordovas JM. Proc Nutr Soc. 2004 Feb;63(1):145-52
The quest for cardiovascular health in the genomic era: nutrigenetics
and plasma lipoproteins.

Roland
Jim Chinnis - 07 Feb 2007 16:20 GMT
Joe Doe <None@mail.utexas.edu> wrote in part:

>> I have a copy, but it is outside any areas of expertise I have. I notice the
>> authors refer to the effect of statins on reducing onset of AD:
[quoted text clipped - 24 lines]
>The quest for cardiovascular health in the genomic era: nutrigenetics
>and plasma lipoproteins.

This is available free on the web from the link on the PubMed page.

Very interesting. And Ordovas is into a lot of fascinating areas.

Thank you!
--
Jim Chinnis   Warrenton, Virginia, USA
William Wagner - 07 Feb 2007 16:35 GMT
> Joe Doe <None@mail.utexas.edu> wrote in part:
>
[quoted text clipped - 36 lines]
> --
> Jim Chinnis   Warrenton, Virginia, USA

I guess my genetic makeup is of import.   Hmmm I always thought so.
Partly.....May ;)) .

Bill

Notice Feb 2004 and the  sort of quiet response only noted here.
Thanks Folks!

..............
"Now, the characterization of individuals who may respond better to one
type of dietary recommendation than another can be begun. Thus, a
low-fat low-cholesterol strategy may be particularly efficacious in
lowering the plasma cholesterol levels of those subjects carrying the
apoE4 allele at the APOE gene. HDL-cholesterol (HDL-C) levels are also
modulated by dietary, behavioural and genetic factors."

"This knowledge should lead to successful dietary recommendations partly
based on genetic factors that may help to reduce cardiovascular risk
more efficiently than the current universal recommendations."

..........................

1: Proc Nutr Soc. 2004 Feb;63(1):145-52.
  Links
The quest for cardiovascular health in the genomic era: nutrigenetics
and plasma lipoproteins.
  €  Ordovas JM.
Nutrition and Genomics Laboratory, JM-USDA-Human Nutrition Research
Center on Aging at Tufts University, Boston, MA 02111, USA.
jordov01@tufts.edu
Nutrigenetics and nutrigenomics are promising multidisciplinary fields
that focus on studying the interactions between nutritional factors,
genetic factors and health outcomes. Their goal is to achieve more
efficient individual dietary intervention strategies aimed at preventing
disease, improving quality of life and achieving healthy aging. Our
studies, and those of many other investigators, using population-based
and intervention studies have found evidence for interactions between
dietary factors, genetic variants and biochemical markers of CVD. Now,
the characterization of individuals who may respond better to one type
of dietary recommendation than another can be begun. Thus, a low-fat
low-cholesterol strategy may be particularly efficacious in lowering the
plasma cholesterol levels of those subjects carrying the apoE4 allele at
the APOE gene. HDL-cholesterol (HDL-C) levels are also modulated by
dietary, behavioural and genetic factors. It has been reported that the
effect of PUFA intake on HDL-C concentrations is modulated by an APOA1
genetic polymorphism. Thus, subjects carrying the A allele at the -75
G/A polymorphism show an increase in HDL-C with increased intakes of
PUFA, whereas those homozygotes for the more common G allele have the
expected lowering of HDL-C levels with increased intake of PUFA.
Variability at the hepatic lipase gene is also associated with
interactions between intake of fat and HDL-C concentrations that could
shed some light on the different abilities of certain ethnic groups to
adapt to new nutritional environments. This knowledge should lead to
successful dietary recommendations partly based on genetic factors that
may help to reduce cardiovascular risk more efficiently than the current
universal recommendations.
PMID: 15070444 [PubMed - indexed for MEDLINE]

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Jim Chinnis - 07 Feb 2007 18:46 GMT
This is a paper with great insights: "These studies should
help to put to rest the heated debate about the suitability
of the traditional approach of recommending low-fat
low-cholesterol diets for the entire population v. other
recommendations based on the fact that some populations
with relatively high intakes of non-saturated fats have very
low rates of CVD and other chronic disorders (Hu, 2003).
Individuals that may respond better to one type of
recommendation than another can now begin to be
characterized under the controlled conditions of scientific
research." It goes on to characterize some of what is known now (2004).

This really underscores how important it is to try different regimes and
then test and try again until you find what works for you.

I was also struck by Fig. 1 (I can't reproduce it here), which shows how
dramatically HDL responds to different amounts of polyunsaturated fatty
acids. In different genotypes, it tends to vary by 50% as the PUFA is
doubled or halved! So why on earth are pharmaceutical firms investing
bazillions on finding a drug to boost HDL?! It looks to me like
cardiovascular disease could be knocked way down by just testing a few
different diets on patients and then having them use the one that produces
the best change in lipids!
--
Jim Chinnis   Warrenton, Virginia, USA
Jim Chinnis - 07 Feb 2007 18:49 GMT
Jim Chinnis <jchinnis@SPAMalum.mit.edu> wrote in part:

>I was also struck by Fig. 1 (I can't reproduce it here), which shows how
>dramatically HDL responds to different amounts of polyunsaturated fatty
>acids. In different genotypes, it tends to vary by 50% as the PUFA is
>doubled or halved!

Correction: The impact is somewhat less than 50%. (It is smallest in those
who have HDL fall with increased PUFA.)
--
Jim Chinnis   Warrenton, Virginia, USA
RArmant - 04 Feb 2007 22:22 GMT
The key fat in the diet to avoiding alzheimer's is DHA -- maybe a gram
or more per day. Do a search on pubmed.gov with keywords:DHA alzheimer's
Speaking of pantethine there is good theory that it can boost BDNF.

Fish oils with a high DHA/EPA ratio are beginning to hit the market. DHA
but not EPA appears to increase lipoprotein particle size.
Both tend to drive down triglycerides.
http://www.iherb.com/store/ProductDetails.aspx?c=Herbs&pid=NWY-15682

>> Susan <nevermind@nomail.com> wrote in part:
>>
[quoted text clipped - 53 lines]
>potentially modify the risk of dementia, particularly among genetically
>susceptible individuals.
Susan - 01 Feb 2007 23:15 GMT
> What prompted you to raise your fat levels so much?  Do you know you
> have a high triglyceride response to carbs?  Some other reason?

Triglycerides are a direct measure of dietary carbs.  They go down very
rapidly once carbs are cut.

Susan
Susan - 31 Jan 2007 22:12 GMT
> What level of exercise do you do and roughly what are the
> carb:protein:fat ratios you consume as a percentage of total calories?
[quoted text clipped - 9 lines]
>
> Roland

I didn't do exercise when I got those results.

Susan
Port@nospam.invalid - 31 Jan 2007 12:35 GMT
jchinnis wrote:
>My HDL also rose quite significantly when I decreased my carbohydrate intake
>and increased fat.

"Increased fat" how? Red meat? (I've been looking for an excuse to eat
a steak).  And which fats? Saturated? Unsaturated? Both?

Port
Jim Chinnis - 31 Jan 2007 18:08 GMT
Port@nospam.invalid wrote in part:

>jchinnis wrote:
>>My HDL also rose quite significantly when I decreased my carbohydrate intake
[quoted text clipped - 4 lines]
>
>Port

I eat red meat about once a week, but I never buy supermarket meat
(sometimes from Whole Foods). I buy locally and get beef from pastured
cattle. The fat content is lower and of a healthier type. Beef, lamb, pork
is probably the order of predominance.

Increased fat is mostly from olive oil, nuts, and cheese (I try to get
sheep/goat cheese and avoid the dairy cow-factory stuff). I don't eat bacon
and pork sausage or such except very rarely, but that's not so much because
of the admonitions to avoid saturated fat, which i find unconvincing. But,
aside from cheeses, most saturated fats come from things I don't eat for
other reasons.
--
Jim Chinnis   Warrenton, Virginia, USA
Joe Doe - 01 Feb 2007 04:14 GMT
> jchinnis wrote:
> >My HDL also rose quite significantly when I decreased my carbohydrate intake
[quoted text clipped - 4 lines]
>
> Port

Monounsaturated would be the safest to increase - olive and canola oil,
nuts, walnuts, avocado.  Omega-3s to about 2% of your total calories.

Roland
Susan - 01 Feb 2007 23:14 GMT
>>jchinnis wrote:
>>
[quoted text clipped - 10 lines]
>
> Roland

All unpolluted fats are healthy and safe, including saturated.  Unless
you eat them with starches and sugar; that causes oxidation an promotes
inflammation.

Susan
Port@nospam.invalid - 02 Feb 2007 02:24 GMT
>unpolluted fats

"Unpolluted" how?
i.e. is that the difference between grass fed vs feed lot beef?

Port
Susan - 02 Feb 2007 16:21 GMT
>>unpolluted fats
>
> "Unpolluted" how?
> i.e. is that the difference between grass fed vs feed lot beef?

Yes, that and between hydrogenated transfats and non hydrogenated.

Susan
Port@nospam.invalid - 31 Jan 2007 12:22 GMT
>What is your diet like?

Limited.... lots of rabbit food.
But it's a sort of Mediterranean diet without the potatoes, bread, and
certain fruits. No sugar, no soft drinks, or that sort of thing. For
meat I eat chicken, turkey, and fish.
That's off the top of my head but there's more .... or maybe I should
say there's more don'ts than do's.

Port
Andrew B. Chung, MD/PhD - 31 Jan 2007 14:06 GMT
> >What is your diet like?
>
> Limited.... **lots** of rabbit food.

**emphasis** added.

> But it's a sort of Mediterranean diet without the potatoes, bread, and
> certain fruits. No sugar, no soft drinks, or that sort of thing. For
> meat I eat chicken, turkey, and fish.
> That's off the top of my head but there's more .... or maybe I should
> say there's more don'ts than do's.

It is clear that your problem is the amount.

See **emphasis** above.

May the following help you lose the visceral adipose tissue (VAT) that
is lowering your HDL by way of systemic vascular inflammation:

http://HeartMDPhD.com/HolySpirit/overweight.asp

Low HDL is classic for metabolic syndrome (MetS).

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Port@nospam.invalid - 31 Jan 2007 16:14 GMT
Port wrote:
>> Limited.... **lots** of rabbit food.

>**emphasis** added.
>It is clear that your problem is the amount.

oh!.... I meant "lots" as a percentage of my total intake.  Not
necessarily "lots" in the total volume sense. However, you're right in
that I may be eating more than 2 pounds/day. I've never actually
weighed my food except as a part of me after I've already eaten it.
Anyhow.... point well taken.

>May the following help you lose the visceral adipose tissue (VAT) that
>is lowering your HDL by way of systemic vascular inflammation:
>http://HeartMDPhD.com/HolySpirit/overweight.asp

I especially like this part: "When you find yourself unable to put up
with your hunger in between smaller meals, it would be wise for you to
find things to do instead of things to eat".

With minor alteration, that could also be good advice for a smoker's
group (find something to do instead of something to smoke).

I don't smoke btw, just thought it a good idea.

>Low HDL is classic for metabolic syndrome (MetS).

yeah, that's what I worry about  :-(

Port
Andrew B. Chung, MD/PhD - 31 Jan 2007 17:18 GMT
> > neighbor Port wrote:
> >> Limited.... **lots** of rabbit food.
[quoted text clipped - 8 lines]
> weighed my food except as a part of me after I've already eaten it.
> Anyhow.... point well taken.

Simply here to help by informing you.

> >May the following help you lose the visceral adipose tissue (VAT) that
> >is lowering your HDL by way of systemic vascular inflammation:
[quoted text clipped - 8 lines]
>
> I don't smoke btw, just thought it a good idea.

Weight gain from overeating is an issue with many folks trying to quit
smoking.  Again, the root problem is the false belief that "Hunger is
bad."

Becoming healthier from quitting smoking necessarily means that folks
will become much hungrier.

Super healthy folks are super hungry.

> >Low HDL is classic for metabolic syndrome (MetS).
>
> yeah, that's what I worry about  :-(

Lose the VAT, cure the MetS.

You now know how.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Port@nospam.invalid - 31 Jan 2007 17:46 GMT
>Weight gain from overeating is an issue with many folks trying to quit
>smoking.

Absolutely agreed.

>Again, the root problem is the false belief that "Hunger is
>bad."

Even without hunger, they have an uncontrollable psychological urge to
occupy their hands and to stuff things in their mouth.  In other
words, picking up food and stuffing it.  Same with drinking.
A "smoker" at a party will, out of habit, do the following:
Puff - slurp - puff -slurp - puff - slurp- puff - slurp - and so on.
But a recent X-smoker, out of habit will, at the exact same rate:
Slurp -slurp - slurp - slurp - slurp - slurp - slurp -  resulting in
twice the alcohol consumption, double the intoxication, both much to
the surprise of the new x-smoker.
(just a little tip for any soon to be x-smokers out there... so watch
it lol!)

Port
William Wagner - 31 Jan 2007 18:16 GMT
> >Weight gain from overeating is an issue with many folks trying to quit
> >smoking.
[quoted text clipped - 17 lines]
>
> Port

We used to say ( Who ever we was) that we all have vices.  The secret
was  to to chose less harmful ones or at least rotate though  them.
Aging hippie stuff.

French Writer Balzac said the only vice was wanting to know every thing.

I smoke on rare occasions when my Moroccan future daughter in-law  
offers.    I drink when I feel like it and cook /garden/ fix house  
every day.  I consider all of this fun.

Tagine  with chicken and preserved lemon heating up now.

Bill

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Andrew B. Chung, MD/PhD - 31 Jan 2007 18:44 GMT
> Andrew, in the Holy Spirit, boldly wrote:
>
[quoted text clipped - 17 lines]
> (just a little tip for any soon to be x-smokers out there... so watch
> it lol!)

Without appetite/hunger, the urge to put things into the mouth would
be gone.

"Hunger is good."

"Blessed are you who hunger now for you will be satisfied." -- LORD
Jesus Christ (Luke 6:21)

Amen.

What is harmful is the false belief that "Hunger is bad."

It is the latter that causes the irrational and uncontrollable
compulsion to overeat.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Susan - 31 Jan 2007 22:12 GMT
>>What is your diet like?
>
[quoted text clipped - 6 lines]
>
> Port

Could you be more specific?  There are a number of meditteranean diets.

Susan
Port@nospam.invalid - 31 Jan 2007 22:47 GMT
>>>What is your diet like?

Port wrote:
>> Limited.... lots of rabbit food.
>> But it's a sort of Mediterranean diet without the potatoes, bread, and
>> certain fruits. No sugar, no soft drinks, or that sort of thing. For
>> meat I eat chicken, turkey, and fish.

Susan:
>Could you be more specific?

Do I have too??  It's making me hungry  :-(

>There are a number of meditteranean diets.

And mine's not exactly like any of them (that's why I said "sort of").
I'm a single guy, hate to cook, so that leaves out anything difficult.
So what I've mentioned up there is most of what I live on. Maybe an
occasional "heart healthy wrap" from SubWay, and Green Salads, lots of
them, with Olive oil & vinegar dressing, almonds or grapes or an apple
for snacks, yolkless eggs for breakfast sometimes or maybe Oatmeal,
Green Tea to drink and decaf coffee. Vegetables are usually Brussell
Sprouts, Broccoli, Green Beans, or similar. And I blend up a smoothie
occasionally with bananas, Soy milk, berries of some sort, and Protein
Powder.
That's about all I can think of offhand. Was there anything in
particular you were wondering about?

Port
William Wagner - 31 Jan 2007 23:28 GMT
> >>>What is your diet like?
>
[quoted text clipped - 25 lines]
>
> Port

Cook this Port!

Cuban  Sandwich

1 loaf French bread ( I use freshest I can get)
Mayonnaise
Dijon mustard (Any)
1/4 pound thinly sliced ham ( I like two different types)
4 slices Swiss cheese
Kosher dill pickles, sliced ( I like bread and Butter)
Butter, for grilling ( Yea I know)


Slice the bread in half lengthwise. Spread one half with mayonnaise and
the other with mustard. Layer the ham and Swiss cheese on 1 half of the
bread. Layer the pickle slices over the cheese. Top with the other bread
half. In a large skillet over medium-high heat, heat enough butter to
coat the cooking surface. Place the sandwich in the pan and weight with
another heavy pan or a brick wrapped in foil and grill until the cheese
is melted. Cut the loaf to make 4 sandwiches.

........

I think this is under two LBS :))

Bill

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Port@nospam.invalid - 01 Feb 2007 00:35 GMT
>Cook this Port!

Sounds scrumptious!

But the bread.... isn't that a starch? Susan says I should substitute
fat for starch. Could y'all work that out amongst yourselves please?

>Mayonnaise

Mayonaise??
I should eat mayonaise??

>Place the sandwich in the pan and weight with
>another heavy pan or a brick wrapped in foil and grill until the cheese
>is melted. Cut the loaf to make 4 sandwiches.
>I think this is under two LBS :))

aha! good. So the brick doesn't count against the weight limit then,
right?  ;-)

Seriously, that sounds great.
Maybe I can get my girlfriend to whip one up when I go over there this
weekend. She's from New Orleans. Those Yats are all born knowing how
to cook over there  ;-)

Port
William Wagner - 01 Feb 2007 11:18 GMT
> Mayonnaise

A little once in awhile.

http://en.wikipedia.org/wiki/Mayonnaise

>But the bread.... isn't that a starch?

A little once in awhile.

My Cuban has a light layer of Mayo  and a light layer of Mustard.  Get
the best quality of Ham possible.  Tear out the FRESH roll's soft parts
some if you must.  But most important enjoy !

My dad and I share one about  twice a month.  He is 86 and likes to add
more mayo to his.  I use a Foreman grill.

Bill

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Susan - 31 Jan 2007 23:36 GMT
> And mine's not exactly like any of them (that's why I said "sort of").
> I'm a single guy, hate to cook, so that leaves out anything difficult.
[quoted text clipped - 10 lines]
>
> Port

Well, it's impossible to say how your diet may be influencing your HDL
or other parameters, since you don't offer ratios or percentages for
macronutrients.

If you're eating 30% fat or below, odds are you could raise your HDL by
substituting fats for starches.  And by eating grass fed meat and dairy
instead of feedlot raised.

Susan
Port@nospam.invalid - 01 Feb 2007 00:20 GMT
Susan:
>you don't offer ratios or percentages for
>macronutrients.

oh! There's a reason for that. I, unfortunately, have no clue what
they are (I operate, more or less, on the seat-o-the-pants method).

>If you're eating 30% fat or below, odds are you could raise your HDL by
>substituting fats for starches.

I think <30% fat would be a good bet. But, what starches?? I don't eat
any bread or potatoes. Is the "wrap" around a Subway sandwich a
starch? I'd hate to give that up. It holds my sandwich together  :-(

>And by eating grass fed meat and dairy
>instead of feedlot raised.

I don't eat feedlot raised beef. In fact I don't eat any beef at all
(unless I cheat.... but that's only once in a blue moon). Where does
one find beef, other than on the hoof in a pasture, that's known to be
grass fed? I'd dearly love a steak once in awhile.

Port
Andrew B. Chung, MD/PhD - 01 Feb 2007 08:48 GMT
> >>>What is your diet like?
>
[quoted text clipped - 8 lines]
>
> Do I have too??  It's making me hungry  :-(

The frown indicates that you still remain brainwashed to falsely
believe that "hunger is bad."

Until you overcome this and know/believe in your heart that 'hunger is
good," you will not be able to eat less down to the optimal amount
that will cause you to lose all the visceral adipose tissue.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Art Deco - 03 Feb 2007 16:53 GMT
>> >>>What is your diet like?
>>
[quoted text clipped - 15 lines]
>good," you will not be able to eat less down to the optimal amount
>that will cause you to lose all the visceral adipose tissue.

Poor Chung, no one pays any attention when he tries his hand at an
on-topic post.

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William Wagner - 30 Jan 2007 21:20 GMT
> Has anyone here, other than Susan, had any luck raising their HDL
> using Pantethine?
[quoted text clipped - 6 lines]
> Thanks,
> Port

Hi port!  Hope all is well!

I use about  600MG Pantethine along with about 1000 MG Niacin each day.
My HDL is about 70. I'd like to exercise more but that will take me time
due to muscle loss.

anyway look at

http://groups.google.com/group/sci.med.cardiology/browse_frm/thread/be254
060f0d84214/b6590fa321e1f191?lnk=st&q=hdl+cholesterol+wagner&rnum=1#b6590
fa321e1f191

or

http://preview.tinyurl.com/39wt43

Bill CABG 4      9/14/01

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Port@nospam.invalid - 31 Jan 2007 12:58 GMT
>anyway look at
>http://groups.google.com/group/sci.med.cardiology/browse_frm/thread/be254
>060f0d84214/b6590fa321e1f191?lnk=st&q=hdl+cholesterol+wagner&rnum=1#b6590
>fa321e1f191
>or
>http://preview.tinyurl.com/39wt43

Yes, thanks, I've long since had that thread saved and locked.

.... and for those who prefer using a Newsreader rather than a Web
Browser/Google, the thread begins with Message-ID:
<PainInAss__williamwag-5C8373.10541522092005@news.supernews.com>

It's worth the read.

Port
Joe Doe - 30 Jan 2007 22:29 GMT
> Has anyone here, other than Susan, had any luck raising their HDL
> using Pantethine?
[quoted text clipped - 6 lines]
> Thanks,
> Port

I do not use it.

Have you tried Niacin?

Roland
Port@nospam.invalid - 31 Jan 2007 12:28 GMT
>Have you tried Niacin?

Yep. Been on 500mg/day for about a year now.
Port@nospam.invalid - 31 Jan 2007 12:43 GMT
Port wrote:
>500mg/day

Ooops... make that 1000mg. Each pill is 500mg, and I take two.
Joe Doe - 01 Feb 2007 01:31 GMT
>  Port wrote:
> >500mg/day
>
> Ooops... make that 1000mg. Each pill is 500mg, and I take two.

I think one of the unfair realities is that for all the interventions
(niacin, exercise etc.) the response is higher for people with already
high HDL levels.  

If you are taking the niacin under medical supervision there is scope to
increase the dose as long as your liver enzymes are monitored.  It has
an effect on lowering Lp(a) and for this application they need quite
high doses (more than 2-3 grams).

Roland
Susan - 01 Feb 2007 23:13 GMT
>> Port wrote:
>>
[quoted text clipped - 12 lines]
>
> Roland

That's just not so.  The folks with the worst numbers are the most
insulin resistant and will get the most benefit from low carb.

My HDL was 34 for at least a decade and went up to 68 within two weeks
of cutting starches and sugar out of my diet.

Susan
Joe Doe - 02 Feb 2007 20:51 GMT
> x-no-archive: yes
>
[quoted text clipped - 11 lines]
> That's just not so.  The folks with the worst numbers are the most
> insulin resistant and will get the most benefit from low carb.

Well I posted about a group of people for whom high fat is not a good
approach (ApoE4 homozygotes).  

Secondly, many factors can influence HDL levels including known genetic
factors and some will be totally unresponsive to any current
intervention diet or otherwise.  For example Hypoalphaproteinemia is in
this class.  

Roland
William Wagner - 02 Feb 2007 21:27 GMT
> > x-no-archive: yes
> >
[quoted text clipped - 21 lines]
>
> Roland

Jim I continue to read Rolands posts.

Hypoalphaproteinemia  however is very difficult  for my little brain.
Still I prefer  to dumb up vs dumb down. I have to ask what does it mean
and why not say in the post  up front?

Bill

Yin Teh Wu Wie.     See I can be obscure  too.
Means trying to do good in the present moment.

...........................................

http://content.nhiondemand.com/moh/media/HC1.asp?objID=100227&ctype=hc

Hyperbetalipoproteinemia patients have increased hepatic apolipoprotein
production with acceptable LDL and triglyceride levels, but still have a
positive family history of premature CHD. Hypoalphaproteinemia is a
condition involving the so-called "isolated low HDL" patients. Little is
known about the cause, but it is associated with increased CHD, obesity,
smoking and lack of exercise. Evidence of drug effectiveness is lacking
for these patients; therefore, lifestyle changes that increase HDL and
lower LDL are most often advocated.(2)

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Susan - 02 Feb 2007 21:35 GMT
> Well I posted about a group of people for whom high fat is not a good
> approach (ApoE4 homozygotes).  

I recall requesting such testing a few years ago and I was in the bad
phenotype at the time.

> Secondly, many factors can influence HDL levels including known genetic
> factors and some will be totally unresponsive to any current
> intervention diet or otherwise.  For example Hypoalphaproteinemia is in
> this class.  

I don't believe I saw citations, just assertions.

Susan
Joe Doe - 04 Feb 2007 01:35 GMT
> x-no-archive: yes

.

> > Secondly, many factors can influence HDL levels including known genetic
> > factors and some will be totally unresponsive to any current
[quoted text clipped - 4 lines]
>
> Susan

For my original point:

Does Exercise Increase HDL Cholesterol in Those Who Need It the Most?
Paul D. Thompson; Daniel J. Rader
Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1097.

http://atvb.ahajournals.org/cgi/content/full/21/7/1097 which is an
editorial on a paper that is linked and also has free access.

To illustrate one of many genetic abnormalities that have low HDL see
reviews at bottom. Tangier disease for example which is a physical
mutation a ABCA1 transporter and will not respond to interventions.  
There are many other examples showing how nuanced lipid biochemistry is:
ApoA1 Milano has very low HDL & high triglycerides and no
artheroschlerotic  effect and is in fact protective!!!  The same is true
for LCAT mutants.  You can also find ApoA mutants that are
artheroschhlerotic.  

Your unshakable belief that carbohydrate restriction is the answer to
all life's problems is not shared by me.  I do think it might be wise to
not swing to any extreme (extreme low carb or low fat).  Smoking,
obesity, sedentary lifestyle, steroids, kidney disease, thyroid disease,
beta-blockers are some of the many factors that can affect HDL levels.  
To reduce everything to carbohydrates is too simplistic.  I doubt I can
change your mind and so will not bother to provide citations as proof
for these factors.

1: Curr Opin Cardiol. 2004 Jul;19(4):380-4.

Genetic determinants of low high-density lipoprotein cholesterol.
Miller M, Zhan M.
Department of Medicine, University of Maryland Hospital and Veterans
Affairs Medical Center, Baltimore, Maryland, USA.
mmiller@heart.umaryland.edu

PURPOSE OF REVIEW: High-density lipoprotein cholesterol (HDL-C) has been
well established as an inverse predictor of coronary heart disease
(CHD), and in recent years, investigations have focused on the genetic
regulation of high-density lipoprotein. Although numerous candidate
genes contribute to the low HDL-C phenotype, their impact on CHD is
heterogeneous, reflecting diverse gene-gene interactions and
gene-environmental relationships. This review summarizes recent data
involving HDL regulatory genes and their role in atherothrombosis.
RECENT FINDINGS: The primary genetic determinants associated with
relative HDL-C deficiency states are the ATP binding cassette protein,
ABCA1; apolipoprotein (APO) A1; and lecithin cholesteryl acyl
transferase. Other potentially important candidates invoked in low HDL-C
syndromes in humans include APOC3, lipoprotein lipase, sphingomyelin
phosphodiesterase 1, and glucocerebrosidase. Molecular variation in
ABCAI and APOAI and, in selected cases, lecithin cholesteryl acyl
transferase deficiency have been associated with increased CHD, whereas
two notable variants, APOAIMilano and APOAIParis, are associated with
reduced risk. SUMMARY: Low HDL-C syndromes have generally been
correlated with an increased risk of CHD. However, single-gene
abnormalities responsible for HDL-C deficiency states may have variable
effects on atherothrombotic risk.

Roland
Pramesh Rutajit - 08 Feb 2007 04:39 GMT
>>  Port wrote:
>> >500mg/day
[quoted text clipped - 11 lines]
>
> Roland

I found that every increment of 500 mg from 500 mg to 2500 mg had a positive
effect on cholesterol as monitored by a stranded CBC/CMP+Cholesterol test
as well as the VAP test.  Not only is HDL quantity important but
quality/subfractions are also important and LDL particle size improved with
each 500 mg increase.  I also monitored homocysteine and C-Reactive Protein
at each step since niacin can increase homocysteine. I stopped at 2500
mg/day when LDL particle type moved solidly into the TYPE A category.  
Liver enzymes were monitored at each step and Niacin had no addition affect
over and above the small dose statin I was already taking.

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Pramesh Rutajit - p2976221tongue@newsguy.com - remove tongue to reply.

Joe Doe - 01 Feb 2007 04:10 GMT
> >Have you tried Niacin?
>
> Yep. Been on 500mg/day for about a year now.

One other thing if you are not taking Niaspan or the vitamin Niacin the
form you are taking me be ineffective (many so called "non flushing"
forms sold are not effective).  I am not sure if what you are taking is
a physician recommended form or not.

Secondly the time to kick in may be slow.  For exercise it is reported
frequently (even though the exercise effect can be quite modest).  The
Niacin lag is covered in a blog entry (Jan 19) of Dr. William Davis (a
cardiologist who wrote track your plaque) here:

http://heartscanblog.blogspot.com/

He recommends "Slo-Niacin" as a Niaspan alternative that is cheap and
readily available.  I do not know anything about it, but presume he is
right about safety and efficacy.

The same blog has a link to a recent NYT piece plugging Niacin in
general.

Roland
eml - 04 Feb 2007 15:57 GMT
http://www.medscape.com/viewarticle/551008
By Will Boggs, MD
NEW YORK (Reuters Health) Jan 19 - A decline in total cholesterol
levels precedes the diagnosis of dementia by at least 15 years,
according to an epidemiologic study reported in the January issue of
the Archives of Neurology.
"Studies like this are extremely valuable because they can provide a
'window' on to processes going on early in dementia, allowing
researchers to look back in time at people's health and other
characteristics and compare these between people who develop dementia
and those who do not," Dr. Robert Stewart from King's College London,
UK told Reuters Health.
Dr. Stewart and colleagues used data from the Honolulu-Asia Aging
Study to compare the natural history of cholesterol level change over
a 26-year period between 56 men who were found to have dementia at
examination 3 years after the last cholesterol measurement and 971 men
who did not have dementia.
Total cholesterol levels at the beginning of the study did not differ
by later dementia status, the authors report, but the decline in
subsequent cholesterol levels was significantly steeper among men who
went on to develop dementia.
Adjustment for potential confounding factors strengthened the
association between cholesterol level decline and the development of
dementia, the results indicate.
The cholesterol level decline was most marked in men with dementia and
the APOE epsilon-4 allele and in those with dementia and worse self-
reported general health at the final cholesterol measurement, the
researchers note.
"The observed associations may not represent direct causal pathways,"
the investigators say. "Hypocholesterolemia is recognized to be
associated with frailty and poor general health. It also has been
found to be specifically associated with inflammatory markers and poor
nutritional status."
Rather, they suggest, "It is possible that the decline in cholesterol
levels is a marker for early processes that reflect neurodegenerative
changes and also lead to a decline in general health status."
The drop in cholesterol was not a result of medication. "Very few of
the participants in this study were receiving cholesterol lowering
treatment at the time the decline in cholesterol levels was observed
(there were few cholesterol lowering medications around at that time
in the 1970s), so medication was not responsible for this," Dr.
Stewart explained.
"The drop in cholesterol was instead probably caused by some other
event and was a 'marker' of risk rather than actually increasing the
risk itself," he concluded.
Arch Neurol 2007;64:103-107.
Andrew B. Chung, MD/PhD - 04 Feb 2007 18:03 GMT
> http://www.medscape.com/viewarticle/551008
> By Will Boggs, MD
[quoted text clipped - 42 lines]
> risk itself," he concluded.
> Arch Neurol 2007;64:103-107.

Decreases in serum cholesterol occurs invariably whenever folks eat
less.

In the United States, where most folks have been brainwashed to
falsely believe that being hungry is bad, this generally occurs
primarily when people lose their appetites (ie are no longer hungry).
Clinically, this is called anorexia.

Anorexia is what is truly bad.  Folks with anorexia are dying.

"Hunger is good." -- Holy Spirit

Amen.

"Blessed are you who hunger now for you will be satisfied." -- LORD
Jesus Christ (Luke 6:21)

Amen.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Jim Chinnis - 04 Feb 2007 20:34 GMT
"Andrew B. Chung, MD/PhD" <love10@thetruth.com> wrote in part:

>Decreases in serum cholesterol occurs invariably whenever folks eat
>less.
[quoted text clipped - 5 lines]
>
>Anorexia is what is truly bad.  Folks with anorexia are dying.

Weight loss years before diagnosis of Alzheimer has also been documented.
--
Jim Chinnis   Warrenton, Virginia, USA
Andrew B. Chung, MD/PhD - 04 Feb 2007 22:16 GMT
> Andrew, in the Holy Spirit, boldly wrote:
>
[quoted text clipped - 9 lines]
>
> Weight loss years before diagnosis of Alzheimer has also been documented.

Correct.  This is consistent with years of eating less as a
consequence of anorexia.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Jim Chinnis - 05 Feb 2007 00:42 GMT
"Andrew B. Chung, MD/PhD" <love10@thetruth.com> wrote in part:

>> Andrew, in the Holy Spirit, boldly wrote:
>>
[quoted text clipped - 12 lines]
>Correct.  This is consistent with years of eating less as a
>consequence of anorexia.

That was my point.
--
Jim Chinnis   Warrenton, Virginia, USA
Andrew B. Chung, MD/PhD - 05 Feb 2007 18:11 GMT
> Andrew, in the Holy Spirit, boldly wrote:
> >> Andrew, in the Holy Spirit, boldly wrote:
[quoted text clipped - 15 lines]
>
> That was my point.

Perhaps it would be were this is a debate.

Takes two to debate.

In the interim, GOD's purpose for me here remains to inform and not to
either debate or convince.

Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com

> Jim Chinnis   Warrenton, Virginia, USA
Art Deco - 06 Feb 2007 01:22 GMT
False prophet Andrew B. Chung spammed:

>> Andrew, in the Holy Spirit, boldly wrote:
>> >> Andrew, in the Holy Spirit, boldly wrote:
[quoted text clipped - 22 lines]
>In the interim, GOD's purpose for me here remains to inform and not to
>either debate or convince.

Translation:  "I'm right, everyone else is wrong; no debate is
necessary; if you question my words I'll label you a 'convict' and put
your name in my kooky webshite list, and if you laugh at me I'll label
you a 'demon'".

Signature

"To err is human, to cover it up is Weasel" -- Dogbert

Pramesh Rutajit - 08 Feb 2007 04:33 GMT
>> >Have you tried Niacin?
>>
[quoted text clipped - 20 lines]
>
> Roland

I buy my Niacin in bottles of 200 grams for $6.00 and take 2.5 grams/day in
divided doses.

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Port@nospam.invalid - 08 Feb 2007 08:25 GMT
>I buy my Niacin in bottles of 200 grams for $6.00 and take 2.5 grams/day in
>divided doses.

200 grams??  Is that the whole bottle? How much is in each pill? And
where do you find them for $6? Locally? Internet?
I think I've been buying the "ineffective" kind. I'm about to run out
though so I'm shopping around.

Rick
RArmant - 10 Feb 2007 23:50 GMT
>>I buy my Niacin in bottles of 200 grams for $6.00 and take 2.5 grams/day in
>>divided doses.
[quoted text clipped - 3 lines]
>I think I've been buying the "ineffective" kind. I'm about to run out
>though so I'm shopping around.

This is 125 grams for $6.71 -- 250 tablets 500mg each.
http://www.iherb.com/store/ProductDetails.aspx?c=Herbs&pid=NOW-00482

This type of niacin will cause a painful itchy flush if you are not use
to it. Aspirin if taken about 15 minutes before the niacin can mitigate
the flush.
Port@nospam.invalid - 11 Feb 2007 23:59 GMT
>This is 125 grams for $6.71 -- 250 tablets 500mg each.

I don't even remember what I've been paying but seems like it's more
than $6-$7 per 125grams. Been gettin' 'em at Walmart.

>This type of niacin will cause a painful itchy flush if you are not use
>to it.

I've been taking the non-flush kind and haven't really investigated
the pros/cons. I can deal with a little pain and itchy though, if it
can get my HDL up.

Aspirin if taken about 15 minutes before the niacin can mitigate
>the flush.

Think I might give your kind a go for awhile.
Thanks,
Port
RArmant - 12 Feb 2007 02:30 GMT
>>This is 125 grams for $6.71 -- 250 tablets 500mg each.
>
[quoted text clipped - 14 lines]
>Thanks,
>Port

You might be interested what the heart scan blog has to say on niacin:
http://heartscanblog.blogspot.com/search?q=niacin

This is what Dr. Davis has to say about no-flush niacin:
http://heartscanblog.blogspot.com/search/label/No%20flush%20%3D%20No%20effect
Port@nospam.invalid - 13 Feb 2007 20:47 GMT
>You might be interested what the heart scan blog has to say on niacin:
>http://heartscanblog.blogspot.com/search?q=niacin

>what Dr. Davis has to say about no-flush niacin:
>http://heartscanblog.blogspot.com/search/label/No%20flush%20%3D%20No%20effect

Yep, thanks.
I bought his preferred form.  SloNiacin (Upsher Smith). 100 tablets of
500 mg for $12.44 at Walmart.
I'll post my results in a few months  :-)

Port
RArmant - 15 Feb 2007 13:57 GMT
>>You might be interested what the heart scan blog has to say on niacin:
>>http://heartscanblog.blogspot.com/search?q=niacin
[quoted text clipped - 6 lines]
>500 mg for $12.44 at Walmart.
>I'll post my results in a few months  :-)

Dr. Davis suggests that vitamin D3 deficiency is also a risk factor for
heart disease --
http://heartscanblog.blogspot.com/search?q=%22vitamin+d%22+
Pramesh Rutajit - 12 Feb 2007 19:22 GMT
>>This is 125 grams for $6.71 -- 250 tablets 500mg each.
>
[quoted text clipped - 7 lines]
> the pros/cons. I can deal with a little pain and itchy though, if it
> can get my HDL up.

I don't think either kind of the non-flush variant does anything for HDL or
LDL particle size.

>  Aspirin if taken about 15 minutes before the niacin can mitigate
>>the flush.
>
> Think I might give your kind a go for awhile.
> Thanks,
> Port

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Pramesh Rutajit - 12 Feb 2007 19:21 GMT
>>I buy my Niacin in bottles of 200 grams for $6.00 and take 2.5 grams/day
>>in divided doses.
[quoted text clipped - 5 lines]
>
> Rick

http://www.beyond-a-century.com

It's 200 grams of B3 powder.  I weigh out 1.25 grams in the morning and
evening for a total of 2.5 grams/day.

I prefer to swish my B3 around in my mouth with tomato juice and follow that
with about 12 oz of water.  It usually eliminates any flush.

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Pramesh Rutajit - 08 Feb 2007 04:31 GMT
> Has anyone here, other than Susan, had any luck raising their HDL
> using Pantethine?
[quoted text clipped - 6 lines]
> Thanks,
> Port

It did nothing for me but I had already raised my HDL 31 to mid 60s before
giving it a try.

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