Science and Technology news... :: View topic - The New Generation of Physicians are Frauds!

Bill · Guest

In article <6otu1hF5ef7aU1@mid.individual.net>,
"Juhana Harju" <nope@mail.fi> wrote:

[quote]vauxall wrote:
x-no-archive:yes

The cholesterol - heart disease scam: How the medical-industrial
complex is raking in billions at our expense

http://www.opednews.com/articles/The-cholesterol--heart-di-by-Richard-Clark-
081121-736.html

Although a staggering amount of money has been spent on research to
conclusively prove the link between saturated fat, cholesterol and
Coronary Heart Disease (CHD), there exists a massive volume of
scientific evidence published in peer-reviewed journals that
completely absolves dietary cholesterol, saturated fat and elevated
blood cholesterol of any harmful role in CHD.

The Lancet, Volume 370, Issue 9602, Pages 1829 - 1839, 1 December 2007
doi:10.1016/S0140-6736(07)61778-4

Blood cholesterol and vascular mortality by age, sex, and blood pressure: a
meta-analysis of individual data from 61 prospective studies with 55 000
vascular deaths
Prospective Studies Collaboration

SUMMARY

*Background*
Age, sex, and blood pressure could modify the associations of total
cholesterol (and its main two fractions, HDL and LDL cholesterol) with
vascular mortality. This meta-analysis combined prospective studies of
vascular mortality that recorded both blood pressure and total cholesterol
at baseline, to determine the joint relevance of these two risk factors.

*Methods*
Information was obtained from 61 prospective observational studies, mostly
in western Europe or North America, consisting of almost 900 000 adults
without previous disease and with baseline measurements of total cholesterol
and blood pressure. During nearly 12 million person years at risk between
the ages of 40 and 89 years, there were more than 55 000 vascular deaths (34
000 ischaemic heart disease [IHD], 12 000 stroke, 10 000 other). Information
about HDL cholesterol was available for 150 000 participants, among whom
there were 5000 vascular deaths (3000 IHD, 1000 stroke, 1000 other).
Reported associations are with usual cholesterol levels (ie, corrected for
the regression dilution bias).

*Findings*
1 mmol/L lower total cholesterol was associated with about a half (hazard
ratio 0·44 [95% CI 0·42-0·48]), a third (0·66 [0·65-0·68]), and a sixth
(0·83 [0·81-0·85]) lower IHD mortality in both sexes at ages 40-49, 50-69,
and 70-89 years, respectively, throughout the main range of cholesterol in
most developed countries, with no apparent threshold. The proportional risk
reduction decreased with increasing blood pressure, since the absolute
effects of cholesterol and blood pressure were approximately additive. Of
various simple indices involving HDL cholesterol, the ratio total/HDL
cholesterol was the strongest predictor of IHD mortality (40% more
informative than non-HDL cholesterol and more than twice as informative as
total cholesterol). Total cholesterol was weakly positively related to
ischaemic and total stroke mortality in early middle age (40-59 years), but
this finding could be largely or wholly accounted for by the association of
cholesterol with blood pressure. Moreover, a positive relation was seen only
in middle age and only in those with below-average blood pressure; at older
ages (70-89 years) and, particularly, for those with systolic blood pressure
over about 145 mm Hg, total cholesterol was negatively related to
haemorrhagic and total stroke mortality. The results for other vascular
mortality were intermediate between those for IHD and stroke.

*Interpretation*
Total cholesterol was positively associated with IHD mortality in both
middle and old age and at all blood pressure levels. The absence of an
independent positive association of cholesterol with stroke mortality,
especially at older ages or higher blood pressures, is unexplained, and
invites further research. Nevertheless, there is conclusive evidence from
randomised trials that statins substantially reduce not only coronary event
rates but also total stroke rates in patients with a wide range of ages and
blood pressures.

http://www.thelancet.com/journals/lancet/article/PIIS0140673607617784/abstract
[/quote]
Hi Juhana!

Perhaps you have seen this.

Bill
............................

HYPERTENSION
Reducing heart rate in hypertension is harmful‹or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people with
hypertension is associated with an increased risk of cardiovascular
events and death, a new systematic review shows [1]. Furthermore, the
slower the heart rate, the greater the risk, report Dr Sripal Bangalore
(St Luke>s Roosevelt Hospital, New York) and colleagues in the October
28, 2008 issue of the Journal of the American College of Cardiology.

What we show is that in hypertension, when you slow down the heart rate
with a beta blocker, it actually shortens your life.
Senior author Dr Franz Messerli (St Luke>s Roosevelt Hospital) told
heartwire: "Slowing heart rate is known to prolong life expectancy, and
with beta blockers post-MI and in heart failure, the slower you can make
the heart rate, the better. But this new paper goes against the grain.
What we show is that in hypertension, when you slow down the heart rate
with a beta blocker, it actually shortens your life expectancy, it
causes more heart attacks, more heart failure, and more strokes."
Messerli says he and his team believe the likely explanation for this is
"that slowing the heart rate with beta blockers increases the central
pressure, and obviously the latter is one of the determinants of stroke
and heart attack."
Another hypertension expert sees things slightly differently, however.
Dr John Cockcroft (Wales Heart Institute, Cardiff, UK) argues that in
this review, the studies included almost exclusively used
atenolol‹something the authors do point out‹and that it is this drug per
se that is likely the culprit here.
What is vitally important to determine in this setting, he adds, "is
whether it>s atenolol that>s bad or whether it>s reduction of heart rate
that>s bad." This is crucial because there are other drugs that aren>t
beta blockers that lower heart rate, he explained, such as the new agent
ivabradine (Procoralan, Servier). "This issue needs resolving because if
it>s heart-rate reduction [that is the cause], then that>s bad news, and
we need to know about it."

Bradycardia not synonymous with cardioprotection in hypertension

In the new review, Bangalore et al included nine randomized controlled
trials evaluating beta blockers for hypertension that also reported
heart-rate data, including 34 096 patients taking beta blockers, 30 139
taking other antihypertensives, and 3987 receiving placebo. Of the
patients in the beta-blocker arms, 78% received atenolol, 9% took
oxprenolol, 1% propranolol, and 12% received
atenolol/metoprolol/pindolol or hydrochlorothiazide.
Paradoxically, a lower heart rate (as attained in the beta-blocker group
at study end) was associated with a greater risk for the end points of
all-cause mortality (r=-0.51; p<0.0001), cardiovascular mortality
(r=-0.61; p<0.0001), MI (r=-0.85; p<0.0001), stroke (r=-0.20; p=0.06),
or heart failure (r=-0.64; p<0.0001).
"In contrast to patients with MI and heart failure,
beta-blocker-associated reduction in heart rate increased the risk of
cardiovascular events and death for hypertensive patients," the
researchers conclude.
Messerli told heartwire: "In the past, the term cardioprotection was
synonymous with bradycardia. The more you had bradycardia, the better
the heart was protected. This is not the case in hypertension. This may
be okay post-MI and in heart failure, but it>s not okay in hypertension."
In an editorial accompanying the review, Dr Norman M Kaplan (University
of Texas Southwestern Medical Center, Dallas) agrees [2]: "With this
addition to the evidence, beta blockers will surely remain as indicated
for heart failure, for after MI, and for tachyarrhythmias, but no longer
for hypertension in the absence of these compelling indications."

Difficult to extrapolate findings beyond atenolol

Messerli and his colleagues do state in their discussion, however:
"Further studies are needed to establish causation. It should also be
noted that the beta blocker used in the studies was mainly atenolol, and
hence, any meaningful extrapolation of these results to other beta
blockers, including the newer vasodilating beta blockers, should be done
with caution."

Any meaningful extrapolation of these results to other beta blockers,
including the newer vasodilating beta blockers, should be done with
caution.
Cockcroft contends that because this new review contains studies almost
exclusively using atenolol, "this doesn>t move the argument forward very
much." Atenolol, he says, "has been tried and found guilty, and yet
around 40% of prescriptions for beta blockers in the UK and in the US
are still for atenolol. Atenolol should not be given to anybody. Nobody
disagrees that atenolol is guilty, and yet we are still using it."
He says that people think lowering heart rate is good, "because it
reduces the amount of cyclical stress on the aorta, but if at the same
time you are putting the central aortic pressure up, these things may
cancel each other out." Atenolol has been compared in this respect with
one of the newer vasodilating beta blockers, nebivolol (Bystolic,
Forest/Mylan), and it was found that atenolol increases the central
aortic pressure but nebivolol does not [3], he notes.
"The newer vasodilating beta blockers may well not have any of these
detrimental effects. Because they are vasodilatory, they may well offset
the slowing of heart rate by decreasing wave reflection from the
periphery and, in the case of nebivolol, by releasing nitric oxide, an
endogenous vasodilator with antiatherogenic activity," he adds.

To beta block or not, that is the question

Regarding the role now of beta blockers in hypertension, Messerli
commented to heartwire: "Beta blockers in hypertension are not very
useful, and you probably should use any other single drug first before
you add a beta blocker, and if you want to add a beta blocker, please
use a vasodilating one such as carvedilol or nebivolol."

Atenolol should not be given to anybody. Nobody disagrees that atenolol
is guilty, and yet we are still using it.
Cockcroft agrees with much of this, but maintains that beta blockade is
still very important. "Beta blockade is vital. A large number of
patients with hypertension have angina as well, so they>ve got to have a
beta blocker. Furthermore, there is now evidence that younger subjects
with hypertension (<50 years of age) may well be better treated with a
beta blocker than older hypertensives, as they have a different
hemodynamic form of hypertension. It>s what beta blocker you give them
that counts, and it shouldn>t be atenolol."
He believes the continued obsession with atenolol is "partly due to
cheapness and habit, but also due to the failure of the people with good
beta blockers to disseminate information on the deleterious effects of
atenolol."

Most important issue still not resolved; central pressure should be the
focus

Cockcroft says the more vital issue "that still needs resolving is
whether it>s atenolol that is bad or heart-rate reduction that is bad
news. If it>s the latter, we need to know about it, because there are
other drugs that lower heart rate, such as ivabradine, and if you look
at the BEAUTIFUL trial with this new drug, it was very negative."
He believes a trial directly comparing ivabradine with atenolol in terms
of central aortic pressure is needed, "and then you look at the effects
on hemodynamics in terms of central pressure."
Another way of examining this issue could be to give atenolol to people
who have pacemakers in to slow their heart rate down and then switch the
pacemaker back on and bring the heart rate back up to the baseline
level‹still with them having atenolol on board‹and "if the detrimental
hemodynamics go away, then it>s all heart rate, and if it doesn>t, then
atenolol has some effect beyond heart-rate reduction that is bad.
"These are very, very important mechanistic experiments that need to be
done now that we have other drugs that lower heart rate that aren>t beta
blockers, and we clearly need to be doing these studies," Cockcroft
stresses.
"I personally think that it>s the atenolol that is bad and that it has
some effects beyond heart-rate reduction that are bad, but we don>t know
from this Messerli review. If half [the trials they included] had used
another beta blocker, then you would know for sure."
"It>s central pressure that the pharmaceutical industry should be
focusing on," he adds, "because different drugs, especially beta
blockers, have differential effects on central pressure, and we know
from the Strong Heart Study that central aortic pressure is a better
predictor of outcome than pressure in the arm."
Messerli is a member of the speakers' bureau for Abbott,
GlaxoSmithKline, Novartis, Pfizer, AstraZeneca, Bayer, Boehringer
Ingelheim, Bristol-Myers Squibb, Forest, Sankyo, and Sanofi and has
received research funding/grants from GlaxoSmithKline, Pfizer, Novartis
and CardioVascular Therapeutics. Cockcroft is on the advisory board of
Forest, which markets nebivolol, and has received research funding from
the company.

Sources
1. Bangalore S, Sawhney S, and Messerli FH. Relation of beta-blocker
induced heart rate lowering and cardioprotection in hypertension. J Am
Coll Cardiol 2008; 52: 1482-1489.
2. Kaplan NM. Beta-blockers in hypertension. Adding insult to injury.
J Am Coll Cardiol 2008; 52: 1490-1491.
3. Dhakam Z, Yasmin, McEniery CM, et al. A comparison of atenolol and
nebivolol in isolated systolic hypertension. J Hypertens 2008; 26:
351-356.

Related links
€ BEAUTIFUL for some: No overall advantage of ivabradine, but
high-heart-rate patients may benefit
[Clinical cardiology > Clinical cardiology; Aug 31, 2008]
€ New review "beats the drum" for not using beta blockers in
uncomplicated hypertension
[Lipid/Metabolic > Lipid/Metabolic; Aug 08, 2007]
€ Central aortic pressure readings seen as more prognostic than
standard brachial pressure
[Prevention > Prevention; Jun 18, 2007]
€ Cochrane review: Beta blockers should not be first line for
hypertension
[HeartWire > News; Feb 02, 2007]
€ New UK hypertension guidelines omit beta blockers for routine use
[HeartWire > News; Jul 06, 2006]
CAFE published: Amlodipine/perindopril combo reduces central aortic BP
[Hypertension > Hypertension; Feb 21, 2006]

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

: J Am Coll Cardiol. 2008 Sep 23;52(13):1062-72.
Links

Beta-blockers for primary prevention of heart failure in patients with
hypertension insights from a meta-analysis.
Bangalore S, Wild D, Parkar S, Kukin M, Messerli FH.
Department of Medicine, Division of Cardiology, St Luke>s Roosevelt
Hospital and Columbia University College of Physicians and Surgeons, New
York, New York 10019, USA.
OBJECTIVES: This study sought to evaluate the efficacy of beta-blockers
(BBs) for primary prevention of heart failure (HF) in patients with
hypertension. BACKGROUND: The American College of Cardiology/American
Heart Association staging for HF classifies patients with hypertension
as stage A HF, for which BBs are a treatment option. However, the
evidence to support this is unknown. METHODS: We conducted a
MEDLINE/EMBASE/CENTRAL search of randomized controlled trials that
evaluated BB as first-line therapy for hypertension with follow-up for
at least 1 year and with data on new-onset HF. The primary outcome was
new-onset HF. Secondary outcomes were all-cause mortality,
cardiovascular mortality, myocardial infarction, and stroke. RESULTS:
Among the 12 randomized controlled trials, which evaluated 112,177
patients with hypertension, BBs reduced blood pressure by 12.6/6.1 mm Hg
when compared with placebo, resulting in a 23% (trend) reduction in HF
risk (p = 0.055). When compared with other agents, the antihypertensive
efficacy of BBs was comparable, which resulted in similar but no
incremental benefit for HF risk reduction in the overall cohort (risk
ratio: 1.00; 95% confidence interval: 0.92 to 1.08), in the elderly (>
or =60 years) or in the young (<60 years). Analyses of secondary
outcomes showed that BBs confirmed similar but no incremental benefit
for the outcomes of all-cause mortality, cardiovascular mortality, and
myocardial infarction but increased stroke risk by 19% in the elderly.
CONCLUSIONS: In hypertensive patients, primary prevention of HF is
strongly dependent on blood pressure reduction. When compared with other
antihypertensive agents, there was similar but no incremental benefit of
BBs for the prevention of HF. However, given the increased risk of
stroke in the elderly, BBs should not be considered as first-line agents
for prevention of HF.
PMID: 18848139 [PubMed - in process

--
Garden in shade zone 5 S Jersey USA

Juhana Harju · Guest

Bill wrote:
[quote]In article <6otu1hF5ef7aU1@mid.individual.net>,
"Juhana Harju" <nope@mail.fi> wrote:

The Lancet, Volume 370, Issue 9602, Pages 1829 - 1839, 1 December
2007 doi:10.1016/S0140-6736(07)61778-4

Blood cholesterol and vascular mortality by age, sex, and blood
pressure: a meta-analysis of individual data from 61 prospective
studies with 55 000 vascular deaths
Prospective Studies Collaboration - -

*Findings*
1 mmol/L lower total cholesterol was associated with about a half
(hazard ratio 0·44 [95% CI 0·42-0·48]), a third (0·66 [0·65-0·68]),
and a sixth (0·83 [0·81-0·85]) lower IHD mortality in both sexes at
ages 40-49, 50-69, and 70-89 years, respectively, throughout the
main range of cholesterol in most developed countries, with no
apparent threshold. The proportional risk reduction decreased with
increasing blood pressure, since the absolute effects of cholesterol
and blood pressure were approximately additive. Of various simple
indices involving HDL cholesterol, the ratio total/HDL cholesterol
was the strongest predictor of IHD mortality (40% more informative
than non-HDL cholesterol and more than twice as informative as total
cholesterol). - -

*Interpretation*
Total cholesterol was positively associated with IHD mortality in
both middle and old age and at all blood pressure levels. - -

http://www.thelancet.com/journals/lancet/article/PIIS0140673607617784/abstract

Hi Juhana!

Perhaps you have seen this.

Bill
...........................

HYPERTENSION
Reducing heart rate in hypertension is harmful or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people
with hypertension is associated with an increased risk of
cardiovascular events and death, a new systematic review shows [1].
Furthermore, the slower the heart rate, the greater the risk, report
Dr Sripal Bangalore (St Luke>s Roosevelt Hospital, New York) and
colleagues in the October 28, 2008 issue of the Journal of the
American College of Cardiology.

What we show is that in hypertension, when you slow down the heart
rate with a beta blocker, it actually shortens your life.
[/quote]
Hi Bill,

No I had missed it. Thanks for posting it, it was interesting.

Hope you are fine.

--
Juhana

E.P. Uum · Guest

So long as peoples worship diverse gods, and each worshipper claims
his/her own god to be the one and only god, those who worship none of
them are well out of those foolish disputes over whose "god" is "God".

A little old man shuffled slowly into "Kilwins", an ice cream parlor in
Spanish Springs-The Villages, and pulled himself slowly, painfully, up
onto a stool.

After catching his breath he ordered a banana split.

The waitress asked kindly, "Crushed nuts?"

"No," he replied, arthritis.

Andrew B. Chung, MD/PhD · Guest

Juhana Harju wrote:
[quote]convicted neighbor Mack wrote:
aineecumi@gmail.com> wrote:

yes it is true that egg may cause a diabetes to people..
better take it less like 1egg for 2days..

xoxo,
aineecumi

false.

Higher intake was associated with higher risk of heart failure in the
Physicians' Health Study.

http://www.ncbi.nlm.nih.gov/pubmed/18195171

I agree with the previous poster that ~ 3 eggs per week might be close to
the optimal intake.

http://www.ajcn.org/cgi/content/abstract/87/4/964
[/quote]
Even that would be excessive for any one person if it causes a loss of
hunger.

<><

http://groups.google.com/group/sci.med.cardiology/msg/3558812d72ab4e17?

Juhana Harju · Guest

Màck©® wrote:
[quote]On Sun, 23 Nov 2008 23:47:05 -0800 (PST), "aineecumi@gmail.com"
aineecumi@gmail.com> wrote:

yes it is true that egg may cause a diabetes to people..
better take it less like 1egg for 2days..

xoxo,
aineecumi

false.
[/quote]
Higher intake was associated with higher risk of heart failure in the
Physicians' Health Study.

http://www.ncbi.nlm.nih.gov/pubmed/18195171

I agree with the previous poster that ~ 3 eggs per week might be close to
the optimal intake.

http://www.ajcn.org/cgi/content/abstract/87/4/964

--
Juhana

Matti Narkia · Guest

Juhana Harju wrote:

[quote]Màck©® wrote:
On Sun, 23 Nov 2008 23:47:05 -0800 (PST), "aineecumi@gmail.com"
aineecumi@gmail.com> wrote:

yes it is true that egg may cause a diabetes to people..
better take it less like 1egg for 2days..

xoxo,
aineecumi

false.

Higher intake was associated with higher risk of heart failure in the
Physicians' Health Study.

http://www.ncbi.nlm.nih.gov/pubmed/18195171

I agree with the previous poster that ~ 3 eggs per week might be close
to the optimal intake.

http://www.ajcn.org/cgi/content/abstract/87/4/964

In this study egg consumption up to 6 per week was safe for[/quote]
non-diabetic. It does not address the consumption of 1 egg/d (7
eggs/week), because the consumption of 7 or more eggs per week was
lumped together.

Here>s an earlier study, which addressed also the consumption of 1 egg
per day:

Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner
BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC.
A prospective study of egg consumption and risk of cardiovascular
disease in men and women.
JAMA. 1999 Apr 21;281(15):1387-94.
PMID: 10217054
<http://jama.ama-assn.org/cgi/content/full/281/15/1387>

"Conclusions These findings suggest that consumption of up to 1
egg per day is unlikely to have substantial overall impact on the
risk of CHD or stroke among healthy men and women. The apparent
increased risk of CHD associated with higher egg consumption among
diabetic participants warrants further research."

So available evidence seems to suggest that 1 egg/d does not raise
CVD risk in non-diabetic persons.

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

Guest · Posted: Tue Nov 25, 2008 6:07 am Post subject: Re: Now ..... It>s eggs :-(

Nothing wrong with eggs, just don>t cook them while exposed to air,
which can oxidize the cholesterol in them.

ironjustice · Guest

On Nov 3, 6:45 am, ironjustice <teamtan...@hotmail.com> wrote:
"Oral ascorbic therapy decreased ferritin levels and
erythropoietin dose" <<

IV Vitamin C May Help to Prevent Erythropoietin Resistance and Iron
Overload in Hemodialysis Patients

Purpose of Review: Parenteral ascorbic acid has been frequently used
to overcome problems of Vitamin C deficiency in haemodialysis
patients. The benefits of Vitamin C supplementation in clinical
studies have been controversial and did not consider toxicological
aspects. The review summarizes recent findings of the effects of
parenteral ascorbic acid and discusses toxicological effects.

Recent Findings: Vitamin C deficiency in haemodialysis patients, which
has been frequently described, cannot be improved with oral
supplementation due to limited absorption of high dosages. To avoid
consequences of Vitamin C deficiency, parenteral Vitamin C solutions
should be administered because this intervention is the only way to
guarantee a sufficient supply to the cells.

A beneficial consequence of parenteral Vitamin C on the recombinant
human erythropoietin resistance is an additional therapeutic effect,
which contributes to the prevention of iron deficiency anaemia in
haemodialysis patients. Thus, large amount of supplemental Vitamin C
are required for extended periods of time (up to 500 mg three times a
week). To avoid hyperoxaluria, plasma oxalate levels should be
monitored on a regular basis, for example, once a week.

Summary: Parenteral administration of ascorbic acid may be an approach
that can overcome problems of Vitamin C deficiency in haemodialysis
patients - in particular problems of iron overload, erythropoietin
resistance, and chronic inflammation.

Biesalski, Hans K. Parenteral ascorbic acid in haemodialysis
patients. Current Opinion in Clinical Nutrition & Metabolic Care.
2008;11(6):741-746.
--------------------------------------------------------------------------------

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

[quote]
This study shows thevitaminCfrees up iron **already there** and NOW
allows it to be used.
Showing CLEARLY not all .. anemia .. is as it .. appears.

There is plenty of iron just like in day care centers.

VitaminCcures anemia in day cares .. and .. in ..dialysis.. care.

"VitaminCimproved responsiveness to Epo by iron mobilization"

Effect of intravenous ascorbic acid in hemodialysis patients with
anemia and hypeferritinemia.
Shahrbanoo K, Taziki O
Saudi J Kidney Dis Transpl 2008 Nov; 19(6):933-6.

Hemodialysis (HD) patients with functional iron deficiency (FID) often
develop resistance to recombinant human erythropoietin (Epo).
The contributory role of chronic infla-mmation and oxidative stress in
its pathogenesis is poorly understood.
We assessed the effect ofvitaminC, an antioxidant, on Epo-
hyporesponsive anemia in hemodialysis patients with un-explained
hyperferritinemia levels.
Thirty-one of 132 with Hb 15 patients received standard care and 300
mg of intravenousvitaminCwith eachdialysissession (group 1) and
15 patients received standard care (group 2).
After 3 months, Hb and transferrin saturation levels significantly
increased in group 1 but not in group 2 (p < 0.05%).
Hemoglobin content in reticulocyte and serum ferritin decreased
significantly in group 1 but not in control group.
In conclusion, hemodialysis patients with refractory anemia and
adequate iron stores,vitaminCimproved responsiveness to Epo by
augmenting iron mobilization and possibly via antioxidant effect.

Saudi journal of kidney diseases and transplantation : an official
publication of the Saudi Center for Organ Transplantation, Saudi
Arabia [Saudi J Kidney Dis Transpl]

--------------------------------------------------------------------------------

Who loves ya.
Tom

Jesus Was A Vegetarian!http://tinyurl.com/634q5a

Man Is A Herbivore!http://tinyurl.com/4rq595

DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk

On Oct 22, 4:13 pm, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
increase of IR in end-stage chronic renal
failure patients on hemodialysis could be related to anemia and
particularly to iron overload

Soo the coclusion was iron overload AND anemia **together** .. found
to be related closely to insulin resistance indialysispatients.
This study finds by givingvitaminCto people WITH kidney disease
decreases the anemia and decreases the iron overload.
Theoretically then .. that would be a good thing.
Saves ya some cash too.
Epo is expensive stuff.

"Oral ascorbic therapy decreased ferritin levels and erythropoietin
dose"
--------
Beneficial hematologic effects of daily oral ascorbic Acid therapy in
ESRD patients with anemia and abnormal iron homeostasis: a preliminary
study.
Ren Fail 2008; 30(9):884-9.
Sirover WD, Siddiqui AA, Benz RL

Aim.
To determine the efficacy and effects of the oral administration of
ascorbic acid on anemia management in ESRD patients with
hyperferritinemia.
Methods.
Twenty-one anemic hemodialysis patients with ferritin levels greater
than 350 ng/mL had received oral daily ascorbic acid at a dose of 500
mg/day and were retrospectively studied. Hemoglobin, hematocrit, EPO
dose, ferritin, and transferrin saturation were recorded at baseline
and after three months of treatment. EPO dose/hematocrit was
calculated. Serum oxalate levels were also measured.
Results.
Hb increased 9% from 11.4 to 12.2 gm/dL (p = 0.05), HCT increased 10%
from 33.3 to 36.7% (p = 0.05), but EPO dose requirement decreased 33%
from 26,229 to 17,559 U/week (p = 0.03). Ferritin levels decreased 21%
from 873 to 691 ng/mL (p = 0.004). Mean oxalate level during therapy
was 87 umol/L (normal <27). Patients with oxalate levels >27 umol/L
were instructed to stop ascorbic acid treatment, and mean levels
decreased from 107 to 19 umol/L (p = 0.01) over a mean time of 71
days.
Conclusion.
In this study, daily oral ascorbic therapy decreased ferritin levels
and EPO dose requirements while raising hemoglobin and hematocrit
level. This beneficial profile of effects of ascorbic acid therapy is
consistent with improvement of EPO resistance and cost savings in this
population.

Renal failure [Ren Fail]

Who loves ya.
Tom

Jesus Was A Vegetarian!http://tinyurl.com/634q5a

Man Is A Herbivore!http://tinyurl.com/4rq595

DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk

The effect of nutritional status, body composition, inflammation and
serum iron on the developement of insulin resistance among patients on
long-term hemodialysis.
Rasiæ-Milutinoviæ Z, Peruniciæ G, Pljesa S, Gluviæ Z, Iliæ M, Stokiæ
E
Med Pregl 2007.:33-8.

We investigated the effect of body composition, nutrition,
inflammation and iron status on insulin resistance in patients with
long-term hemodialysis.
We selected 43 stable end-stage chronic renal failure patients, on
maintenance hemodialysis.
We evaluated the nutritional status, body composition by subjective
global assessment (SGA), anthropometric measurements (BMI and waist
circumference), bioelectrical impedance analysis and biochemical
parameters measurements [serum albumin, cholesterol, HDL-cholesterol,
triglyceride, hematocrit, hemoglobin, iron, ferritin, calcium,
phosphorus, intact parathormone (i-PTH), TNF-alpha, IL-6 and high
sensitivityC-reactive protein].
All parameters were evaluated by comparisons between HOMA-IR tertiles,
and after simple regression analysis, by backward multivariate
regression analysis we identified independent variables for IR.
As the tertile of HOMA-IR increased, serum level of glucose, insulin,
and waist increascd, whereas HDL-cholesterol level decreased, or the
prevalence of the metabolic syndrome increased across the tertiles of
HOMA-IR.
After adjustment for gender, age, hemodialysis duration, ferritin,
phosphorus, waist and total fat percentages, multivariate regression
analysis was performed and the association with HOMA-IR was still
strong only for serum levels of iron and TNF-alpha.
That explains 16% of the total variation in HOMA-IR.
Our results suggest that the increase of IR in end-stage chronic renal
failure patients on hemodialysis could be related to anemia and
particularly to iron overload.
Moreover, chronic inflammatory status with over-production of
adipokine TNF-alpha participate in the pathogenesis of IR too.
The present study demonstrated that adipokine TNF-alpha and serum iron
participated as independent predictors in the pathogenesis of insulin
resistance on long-term hemodialysis patients.

Medicinski pregled [Med Pregl]

Who loves ya.
Tom

Jesus Was A Vegetarian!http://tinyurl.com/634q5a

Man Is A Herbivore!http://tinyurl.com/4rq595

DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk-Hide quoted text -

- Show quoted text -- Hide quoted text -

- Show quoted text -[/quote]

Andrew B. Chung, MD/PhD · Guest

http://groups.google.com/group/sci.med.cardiology/msg/9c5c55fcace06864?

<><

May dear neighbors, friends, and brethren have a blessedly wonderful
2008th year since the birth of our LORD Jesus Christ as our Messiah,
the Son of Man ...

.... by being hungrier:

http://groups.google.com/group/sci.med.cardiology/msg/f891e617d10bd689?

Hunger is wonderful ! ! !

It>s how we know the answer to the question "What does Jesus
want?" (WDJW):

http://groups.google.com/group/sci.med.cardiology/msg/f43db72a7c5c1da0?

Yes, hunger is our knowledge of good versus evil that Adam and Eve
paid for with their and our immortal lives:

http://groups.google.com/group/sci.med.cardiology/msg/52a3db8576495806?

"Blessed are you who hunger NOW...

.... for you will be satisfied." -- LORD Jesus Christ (Luke 6:21)

Amen.

Here is a Spirit-guided exegesis of Luke 6:21 given in hopes of
promoting much greater understanding:

http://groups.google.com/group/sci.med.cardiology/msg/cc2aa8f8a4d41360?

Be hungrier, which is truly healthier:

http://groups.google.com/group/sci.med.cardiology/msg/991d4e30704307e7?

Marana tha

Prayerfully in the awesome name of our Messiah, LORD Jesus Christ,

Andrew <><
--
http://groups.google.com/group/sci.med.cardiology/msg/3558812d72ab4e17?

trigonometry1972@gmail.co · Guest

On Nov 24, 10:07 pm, monty1...@lycos.com wrote:
[quote]Nothing wrong with eggs, just don>t cook them while exposed to air,
which can oxidize the cholesterol in them.
[/quote]
The worst form of eggs by way of oxysterol content are
those products containing powdered egg yolk.
Also I>d assume any product held along time
on the shelf after being baked with whole egg
would only worsen the situation.
Cutting back on dietary carbs should help the
body to better handle cholesterol by lowering
triglyceride levels. Eggs do have the down side
of having high levels of arachidonic acid.
On the other hand, they are one of
the best sources of methyl group contributors
and good source of sulfur containing amino acids.

Trig

Juhana Harju · Guest

trigonometry1972@gmail.com wrote:
[quote]On Nov 24, 10:07 pm, monty1...@lycos.com wrote:

Nothing wrong with eggs, just don>t cook them while exposed to air,
which can oxidize the cholesterol in them.

The worst form of eggs by way of oxysterol content are
those products containing powdered egg yolk.
[/quote]
I agree that that may be the worst thing in them.

[quote]Also I>d assume any product held along time
on the shelf after being baked with whole egg
would only worsen the situation.
Cutting back on dietary carbs should help the
body to better handle cholesterol by lowering
triglyceride levels. Eggs do have the down side
of having high levels of arachidonic acid.
On the other hand, they are one of
the best sources of methyl group contributors
and good source of sulfur containing amino acids.
[/quote]
I agree that they have some nutritional benefits also and I agree that it is
good to include some eggs to diet. High amount of sulfur containing amino
acids can also be a disadvantage as they contribute most to the metabolic
acidosis, which is harmful especially in the elderly people. From positive
side I would like to mention the high content of chromium in eggs (in egg
yolks 183 mcg/100 g). Eggs also contain lutein, a carotenoid protecting the
eyes. Although the lutein content is not very high, it is in a form that is
easily absorbed by the body.

--
Juhana

"Aliquando insanire iucundum est."
- Seneca

jay · Guest

[quote]The cholesterol - heart disease scam ...
[/quote]
Below pubmed abstracts indicate that Persistent Organic/Environmental
Pollutants such as PCBs and dioxin distrub lipid metabolism. Nearly
everyone has been exposed to POPs, mostly from animal-based dietary
fats during the past two or three decades. Some people are genetically
more susceptible.

Down regulation of hepatic PPARalpha function by AhR ligand.
Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription
factor that mediates a spectrum of toxic and biological effects of
2,3,7,8-tetrachloro dibenzo-p-dioxin (TCDD) and related compounds.
Peroxisome proliferator activated receptor alpha (PPARalpha) is a
nuclear receptor involved in the maintenance of lipid and glucose
homeostasis. ... Our results suggest that AhR has an inhibitory effect
on PPARalpha function and a new pathway by which AhR ligands could
disturb lipid metabolism. PMID: 15585952

Modification of environmental toxicity by nutrients: implications in
atherosclerosis.
We hypothesize that nutrition can modulate the toxicity of
environmental pollutants and thus modulate health and disease outcome
associated with chemical insult. There is now increasing evidence that
exposure to persistent organic pollutants, such as PCBs, can
contribute to the development of inflammatory diseases such as
atherosclerosis. Activation, chronic inflammation, and dysfunction of
the vascular endothelium are critical events in the initiation and
acceleration of atherosclerotic lesion formation. Our studies indicate
that an increase in cellular oxidative stress and an imbalance in
antioxidant status are critical events in PCB-mediated induction of
inflammatory genes and endothelial cell dysfunction. Furthermore, we
have found that specific dietary fats can further compromise
endothelial dysfunction induced by selected PCBs and that antioxidant
nutrients (such as vitamin E and dietary flavonoids) can protect
against endothelial cell damage mediated by these persistent organic
pollutants. Our recent data suggest that membrane lipid rafts such as
caveolae may play a major role in the regulation of PCB-induced
inflammatory signaling in endothelial cells. In addition, PCB- and
lipid-induced inflammation can be down-regulated by ligands of anti-
atherogenic peroxisome proliferator-activated receptors (PPARs). We
hypothesize that PCBs contribute to an endothelial inflammatory
response in part by down-regulating PPAR signaling. Our data so far
support our hypothesis that antioxidant nutrients and related
bioactive compounds common in fruits and vegetables protect against
environmental toxic insult to the vascular endothelium by down-
regulation of signaling pathways involved in inflammatory responses
and atherosclerosis. Even though the concept that nutrition may modify
or ameliorate the toxicity of environmental chemicals is provocative
and warrants further study, the implications for human health could be
significant. More research is needed to understand observed
interactions of PCB toxicity with nutritional interventions. PMID:
16046791

PPARalpha ligands reduce PCB-induced endothelial activation: possible
interactions in inflammation and atherosclerosis.
Exposure to polychlorinated biphenyls (PCBs) can activate inflammatory
responses in vascular endothelial cells. Activation of peroxisome
proliferator-activated receptors (PPARs) by nutrients or synthetic
agonists has been shown to block pro-inflammatory responses both in
vitro and in vivo. Here we demonstrate that activation of PPARalpha by
synthetic agonists can reduce 3,3>4,4'-tetrachlorobiphenyl (PCB77)-
induced endothelial cell activation. Primary vascular endothelial
cells were pretreated with the PPARalpha ligands fenofibrate or
WY14643 followed by exposure to PCB77. PPARalpha activation protected
endothelial cells against PCB77-induced expression of the pro-
inflammatory proteins vascular cell adhesion molecule-1 (VCAM-1),
cycloxygenase-2 (COX-2), and PCB77-induced expression and activity of
the aryl hydrocarbon receptor (AHR) responsive cytochrome P450 1A1
(CYP1A1). Furthermore, basal AHR expression was downregulated by
fenofibrate and WY14643. We also investigated the possible
interactions between PCBs, and basal PPAR activity and protein
expression. Treatment with PCB77 significantly reduced basal mRNA
expression of PPARalpha and the PPAR responsive gene CYP4A1, as well
as PPARalpha protein expression. Also, PCB77 exposure caused a
significant decrease in basal PPAR-dependent reporter gene expression
in MCF-7 cells. Overall, these findings suggest that PPARalpha
agonists can reduce PCB77 induction of endothelial cell activation by
inhibition of the AHR pathway, and that coplanar PCB induced pro-
inflammatory effects could be mediated, in part, by inhibition of
PPARalpha expression and function. PMID: 17955387

Matti Narkia · Guest

ironjustice@aol.com wrote:

[quote]On Nov 27, 8:29 am, "ironjust...@aol.com" <ironjust...@aol.com
wrote:"RISP Risperidone did not alter omega-3 fatty acid on the ALA-
diet."

http://www.modernforager.com

"Delta-5 desaturase is inhibited by EPA , meaning that the body works
to slow down EPA production when EPA is high. High levels of omega-6
in the diet can also affect the conversions.
Animal fat, transfat and excessive omega 6 fatty acids inhibits the
conversion of ALA into DHA and EPA. Being deficient in certain
vitamins and minerals also inhbits conversion of ALA into DHA and EPA.
Healthy bodies, contrary to popular belief, convert ALA into DHA and
EPA. Some researchers even believe that conversion in many people is
as inefficient as it is because the body will not convert more than is
needed…"

More than is needed .. ?

Is THAT the one of the .. keys .. ?

Too much of the OTHER fatty acids PREVENTS the **conversion** of Alpha-
linolenic.

But it is these "other fatty acids" (mainly EPA and DHA) that ALA is[/quote]
being converted to. So if you take them directly, you don>t
need to rely on ALA and on its inefficient and unreliable
conversion to EPA and DHA. Of course ALA may have some other uses than
being a precursor for EPA and DHA. It certainly can be included
in cell membranes and used as fuel, i.e. as a source of energy.

Delta-5 desaturase is also needed in the process of converting linolenic
acid (LA) to arachidonic acid (AA). Threfore EPA also inhibits this
conversion, which is not necessary a bad thing, but in most cases
beneficial, IMHO.

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition

ironjustice@aol.com · Guest

On Nov 27, 9:59 am, Matti Narkia <m...@mbnet.fi> wrote:But it is these
"other fatty acids" (mainly EPA and DHA) that ALA is being converted
to. <<

I don>t really think you have gotten the whole **GIST** of the
thread ..

The thread IS .. too much EPA causes a lack of ALA conversion ..

The thread is .. ALA ..

It seems what you seem to be saying is .. ALA is not that important ..

On a thread in which the ALA has been shown to BE .. that important ..
IE: conversion to the fatty acids to prevent one from having a
schizophrenic episode.

Now one might wonder why you would say that when you don>t seem to
care to include an article which may SHOW the inclusion of fish oil
PREVENTS schizophenia WHEN included with Risperidone .. ?

You don>t think the fact that choline is finding such efficacy in
OTHER brain diseases that it TOO would be involved in ADHD .. bi-
polar .. schizophrenia .. ?

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

[quote]ironjust...@aol.com wrote:
On Nov 27, 8:29 am, "ironjust...@aol.com" <ironjust...@aol.com
wrote:"RISP Risperidone did not alter omega-3 fatty acid on the ALA-
diet."

http://www.modernforager.com

"Delta-5 desaturase is inhibited by EPA , meaning that the body works
to slow down EPA production when EPA is high. High levels of omega-6
in the diet can also affect the conversions.
Animal fat, transfat and excessive omega 6 fatty acids inhibits the
conversion of ALA into DHA and EPA. Being deficient in certain
vitamins and minerals also inhbits conversion of ALA into DHA and EPA.
Healthy bodies, contrary to popular belief, convert ALA into DHA and
EPA. Some researchers even believe that conversion in many people is
as inefficient as it is because the body will not convert more than is
needed…"

More than is needed .. ?

Is THAT the one of the .. keys .. ?

Too much of the OTHER fatty acids PREVENTS the **conversion** of Alpha-
linolenic.

But it is these "other fatty acids" (mainly EPA and DHA) that ALA is
being converted to. So if you take them directly, you don>t
need to rely on ALA and on its inefficient and unreliable
conversion to EPA and DHA. Of course ALA may have some other uses than
being a precursor for EPA and DHA. It certainly can be included
in cell membranes and used as fuel, i.e. as a source of energy.

Delta-5 desaturase is also needed in the process of converting linolenic
acid (LA) to arachidonic acid (AA). Threfore EPA also inhibits this
conversion, which is not necessary a bad thing, but in most cases
beneficial, IMHO.

--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition- Hide quoted text -

- Show quoted text -[/quote]

ironjustice@aol.com · Guest

On Nov 27, 4:37 pm, Matti Narkia <m...@mbnet.fi> wrote:
It probably isn>t. It>s main function is to serve as a precursor to
EPA,
which is a precursor of DPA, which is a precursor of DHA. If you
get enough EPA directly from food or supplements, there is no need
to convert ALA to EPA. That is not so hard to understand, is it?
ALA still possibly can have some other functions, which we are not
aware yet, but if you get enough EPA directly, ALA conversion is
not needed.
<<

This ALA conversion is what produces THE acetylcholine / choline which
you fail to mention ..

Is it somehow hard to understand you CANNOT get your choline from fish
oil .. ?

Choline was mentioned as the "possibly other functions" .. but you
simply REPEAT what you .. said.

The thread SPECIFICALLY says .. ALA .. as the fatty acid .. but it
DOESN>T say .. fish oil .. and THAT is because .. ? .. you don>t get
ALA from fish oil.

In ALA there is ALSO .. choline .. WHICH is showing great efficacy in
the treatment of brain diseases / IE: fifty years of drugs.

Sooo .. as I said .. ALA has shown efficacy .. AND choline or lack
thereof is shown to be involved in brain diseases AND fish oil doesn>t
supply EITHER of those .. but .. ALA does.

Which would make one who might be PRESENTLY experiencing problems that
weighing the two options PRESENTED in this thread .. that fish oil
seems NOT to be indicated IE: no studies presented .. BUT .. Alpha-
lnolenic acid IS indicated because of the PROVEN efficacy of both
choline targeting and fatty acid targeting in seperate studies.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://tinyurl.com/634q5a

Man Is A Herbivore!
http://tinyurl.com/4rq595

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

[quote]--
Matti Narkia

http://ma.gnolia.com/groups/Nutrition[/quote]


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