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Medical Forum / General / Cardiology / October 2006

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Atenelol and weight loss

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Guy Scharf - 19 Oct 2006 22:20 GMT
Can atenelol inhibit weight loss?

Background to my question: I am 63, 6 ft tall, currently weigh 208 lb.  
I have Type 2 diabetes, diagnosed 11 years ago.  Two years ago I had
angina.  Treatment was angioplasty and three stents in LCX, which was
described as completely blocked.  This summer, after more angina,
another angioplasy and three more stents -- two in LCX to fix
renarrowing and one in RCA.

I take Metformin, Actos, Lisinopril, Plavix, Aspirin, Zetia, and was
taking Atenelol (25 mg, twice a day).

I had lost about 30 lb since Spring but my weight loss had been stuck
at a plateau for about three months.  Concurrent with the weight loss,
I had been having increasing problems with light headedness and very
cold hands and feet.  

I tapered off the Atenelol two weeks ago.  This solved the light-
headedness and cold extremities problems.  At the not unexpected cost
of higher heart rate--resting pulse increased from about 65 to 80,
which is where it was several years ago.  Exercise that used to push my
HR to 112 when I was taking the atenelol is now pushing it to 134.  
Overall, my HR speeds up at the slightest exertion compared to when I
was on the atenelol.  I do feel some angina pain when HR reaches 150
(max HR was measured as 160 this summer).  Blood pressure remains low
(e.g., 105/65; it was borderline high two years ago before the first
stents were put in).

To my surprise, I've also found that weight loss -- on the same diet --
has resumed at its previous rate after stopping the Atenelol.

Could the Atenelol have been partially responsible for the plateau?

It occurs to me that the light-headedness and ability to concentrate
could also have hampered my ability to maintain the diet, so that could
also be an explanation.

A second question: is it to be expected that BP would be dramatically
lowered, without any significant change in HR, after angioplasty and
stents and without any additional medications?

I'll be taking a stress echocardiogram and talking to my cardiologist
in two weeks.  I'll be talking with him about these issues of course
but wanted to arm myself with any questions or information I might find
here.

Thanks!

Guy
Susan - 19 Oct 2006 22:29 GMT
> To my surprise, I've also found that weight loss -- on the same diet --
> has resumed at its previous rate after stopping the Atenelol.
[quoted text clipped - 4 lines]
> could also have hampered my ability to maintain the diet, so that could
> also be an explanation.

Atenolol promotes weight gain:

(Hypertension. 2001;37:250.)
© 2001 American Heart Association, Inc.
Scientific Contributions
Hypothesis: ß-Adrenergic Receptor Blockers and Weight Gain
A Systematic Analysis
Arya M. Sharma; Tobias Pischon; Sandra Hardt; Iris Kunz; Friedrich C. Luft

From the Franz Volhard Clinic and Max Delbrück Center for Molecular
Medicine, Medical Faculty of the Charité, Humboldt University, Berlin,
Germany.

Correspondence to Arya M. Sharma, MD, Franz Volhard Clinic,
Wiltbergstrasse 50,13125, Berlin, Germany. E-mail sharma@fvk-berlin.de

One of the arguments put forward against the primary use of ß-blockers
has been concern about adverse metabolic effects, such as unfavorable
effects on lipids or insulin sensitivity. Another less-appreciated
potential drawback is their propensity to cause weight gain in some
patients. In 8 evaluable prospective randomized controlled trials that
lasted >=6 months, body weight was higher in the ß-blocker than in the
control group at the end of the study. The median difference in body
weight was 1.2 kg (range -0.4 to 3.5 kg). A regression analysis
suggested that ß-blockers were associated with an initial weight gain
during the first few months. Thereafter, no further weight gain compared
with controls was apparent. There was no relationship between
demographic characteristics and changes in body weight. Based on these
observations, the first-line use of ß-blockers in obese hypertensive
patients should be reviewed. Obesity management in overweight
hypertensive patients may be more difficult in the face of ß-blocker
treatment.

Key Words: obesity • ß-blockers • body weight • hypertension, obesity

I'm a type 2 DM, too, with a strong family history of CVD.  I've been
able to keep my bg tightly controlled and my lipids dramatically
improved  with diet alone.  I've found a couple of very well studied
supplements that also promote insulin sensitivity and lipid
improvements, and without unfortunate side effects.

My rule: if a medicine makes you feel worse, don't take it, it's bad for
you.

Susan
Guy Scharf - 20 Oct 2006 18:09 GMT
>> Could the Atenelol have been partially responsible for the
>> plateau?
[quoted text clipped - 48 lines]
> My rule: if a medicine makes you feel worse, don't take it, it's
> bad for you.

Susan,

Thank you very much for the reference.

Do you know if there is a relationship between atenelol and sleep?  
I've found that since stopping the atenelol that I have been sleeping
more deeply and dreaming a lot more.

I agree completely with your rule about medicines!  I'm very sensitive
to my reactions and stop medicines quickly.  As a result, I have a
growing list of medicines I have allergic or negative reactions to.  
From talking with others, I think some people just suffer through the
reactions.  I have tried three statins, with significant negative
reactions to all of them.

When I get my weight down to into a desirable range, I'm going to re-
evaluate the DM medicines I am taking and reduce dosages or eliminate
them  if possible.  My doctor fully supports my doing that, and has
even recommended stopping meds occasionally to see if they are still
needed.  I recently had to stop the metformin for several days and the
BG readings during that period atest that I'm not ready to eliminate
that medication yet!  :-)

My lipids are now barely within the normal range and I've been able to
partially address the HDL/Trig ratio problem typical of Metabolic
Syndrome with weight loss and exercise.  I expect to continue to
improve as weight loss continues.  I'm not yet down to the recommended
range for people with DM or CVD though.

I've just started Zetia and will retest lipids after being on that for
a while.

After seeing what the Zetia does, I plan to try Bio-Lipotrol.  This
contains Vit B3, Inositol, Guggle Gum extract, Red Yeast Rice extract
and Policosanol.  My wife's naturopath says he has seen significant
cholesterol reduction using this supplement.  What supplement do you
find useful for reducing cholesterol counts?

Thanks again.

Guy
Susan - 20 Oct 2006 21:07 GMT
> Susan,
>
[quoted text clipped - 3 lines]
> I've found that since stopping the atenelol that I have been sleeping
> more deeply and dreaming a lot more.

I'm not an expert, just a person with a number of health issues.  I know
that there's a connection to suppressed adrenal function and sleep,
because it's happened to me, and my sleep gets wrecked, even if I'm
exhausted.  If atenolol works by blocking your adrenal response, that
could play a part in the sleep issue, I suppose.

> I agree completely with your rule about medicines!  I'm very sensitive
> to my reactions and stop medicines quickly.  As a result, I have a
> growing list of medicines I have allergic or negative reactions to.  
> From talking with others, I think some people just suffer through the
> reactions.  I have tried three statins, with significant negative
> reactions to all of them.

Try pantethine: all the benefits, none of the risks of statins, and it
supports adrenals:

1: Minerva Med. 1990 Jun;81(6):475-9.     Related Articles, Links

[Evaluation of the cholesterol-lowering effectiveness of pantethine in
women in perimenopausal age]

[Article in Italian]

Binaghi P, Cellina G, Lo Cicero G, Bruschi F, Porcaro E, Penotti M.

Servizio di Cardiologia, Istitut Clinici di Perfezionamento, Milano.

Cardiovascular diseases are the main cause of death also in women. Their
incidence, rapidly growing in the peri-menopausal period, is related to
serum levels of total cholesterol and its LDL fraction. It was also
shown that the peroxidation of LDL is an additional factor in the
genesis of atherosclerotic vascular disease. As long-term treatments
with synthetic lipid-lowering drugs may cause undesirable side effects,
while pantethine is known to be well tolerated, we treated 24
hypercholesterolemic women (total serum cholesterol greater than or
equal to 240 mg/dl), in perimenopausal age (range: 45-55 years, mean +/-
SD = 51.6 +/- 2.4) with 900 mg/day of pantethine. This is a precursor of
coenzyme A, with an antiperoxidation effect in vivo, and our aim was to
confirm its lipid lowering activity in this particular type of patients.
After 16 weeks of treatment, significant reductions of total
cholesterol, LDL-cholesterol and LDL-C/HDL-C ratio could be observed. No
remarkable changes of the main laboratory parameters (fasting blood
sugar, B.U.N., creatinine, uric acid) were seen. Efficacy percentages of
the treatment were about 80%. None of the patients complained of adverse
reactions due to the treatment with pantethine. In conclusion, we
suggest that pantethine should be considered in the long-term treatment
of lipid derangements occurring in the perimenopausal age.

PMID: 2359503 [PubMed - indexed for MEDLINE]
1: Acta Biomed Ateneo Parmense. 1984;55(1):25-42.     Related Articles, Links

[Hyperlipidemia, diabetes and atherosclerosis: efficacy of treatment
with pantethine]

[Article in Italian]

Arsenio L, Caronna S, Lateana M, Magnati G, Strata A, Zammarchi G.

The hypolipidemizing effects of Pantethine were investigated by the
Authors in 37 hypercholesterolemic and/or hypertriglyceridemic patients.
Of these, 21 were also diabetic, in a satisfying glucidic compensation,
in order to verify the action of this drug also in this metabolic
condition. The study was carried out for three months and during this
period the patients were given Pantethine at the dose of 600 mg/die
orally. At the 30th, the 60th, the 90th day of treatment the following
parameters were controlled: cholesterolemia, HDL cholesterol,
apolipoproteins A and B, triglyceridemia, systolic and diastolic
arterial pressure, uricemia, body weight. Thirty days after suspending
the treatment, the parameters were controlled again to detect a possible
"rebound" effect. The results were analyzed on the whole case-record,
subdividing the patients in dislipidemic and diabetic-dislipidemic, and
on the basis of the Fredrickson's classification. Pantethine induced in
all groups a quick and progressive decrease of cholesterolemia,
triglyceridemia, LDL cholesterol and Apolipoproteins B with increased
HDL cholesterol and Apolipoproteins A. After suspending the treatment,
there is a clear inversion of the state of these parameters. The Authors
conclude that the present work shows that Pantethine, a natural and
atoxic substance, an important component of Coenzyme A, is efficacious
in determining a clear tendency towards normalization of the lipidic values.

PMID: 6232801 [PubMed - indexed for MEDLINE]
1: Atherosclerosis. 1984 Jan;50(1):73-83.     Related Articles, Links

Controlled evaluation of pantethine, a natural hypolipidemic compound,
in patients with different forms of hyperlipoproteinemia.

Gaddi A, Descovich GC, Noseda G, Fragiacomo C, Colombo L, Craveri A,
Montanari G, Sirtori CR.

Pantethine (P), the stable disulphate form of pantetheine, major
component and precursor of coenzyme A, was evaluated within a
double-blind protocol (8 weeks for P or for a corresponding placebo) in
29 patients, 11 with type IIB hyperlipoproteinemia, 15 with type IV, and
3 with an isolated reduction of high density lipoprotein cholesterol
(HDL-C) levels. In type IIB patients, P (300 mg t.i.d.) determined a
highly significant lowering of plasma total and low density lipoprotein
(LDL) associated cholesterol (-13.5% for both parameters). In the same
patients, HDL-C levels increased about 10% at the end of treatment.
Switching from P to placebo was associated with a rapid return to the
baseline cholesterolemia. Both in type IIB and type IV patients, plasma
triglyceride levels were reduced around 30%, when P was given as the
first treatment; when it was preceded by placebo, reductions were less
striking (respectively, -17.8% for type IIB and -13.0% for type IV, at
the end of P treatment). HDL-C levels were not increased by P, either in
type IV, and in the patients with low HDL cholesterolemia. In type IV,
LDL cholesterol levels showed a variable response to P: they tended to
increase when below 132 mg/dl, prior to treatment, and to be reduced
when above this level. This study provides evidence for a significant
hypocholesterolemic effect of P, a natural compound free of overt side
effects. It also indicates that P may raise HDL-C levels in type IIB
patients, while moderately reducing triglyceridemia.

Publication Types:
•    Clinical Trial
•    Controlled Clinical Trial

PMID: 6365107 [PubMed - indexed for MEDLINE]
1: Int J Clin Pharmacol Ther Toxicol. 1986 Nov;24(11):630-7.     Related
Articles, Links

Lipoprotein changes induced by pantethine in hyperlipoproteinemic
patients: adults and children.

Bertolini S, Donati C, Elicio N, Daga A, Cuzzolaro S, Marcenaro A,
Saturnino M, Balestreri R.

Following a brief outline of current knowledge concerning
atherosclerosis and its treatment, the authors describe the results
obtained by treating with pantethine (900-1200 mg daily for 3 to 6
months) a series of 7 children and 65 adults suffering from
hypercholesterolemia alone or associated with hypertriglyceridemia
(types IIa and IIb of Fredrickson's classification). Pantethine
treatment produced significant reduction of the better known risk
factors (total cholesterol, LDL-cholesterol, triglycerides, and apo-B)
and a significant increase of HDL-cholesterol (signally HDL2) and
apolipoprotein A-I. The authors conclude with a discussion of these
results and of the possible role of pantethine in the treatment of
hyperlipoproteinemia, in view of its perfect tolerability and
demonstrated therapeutic effectiveness.

PMID: 3098691 [PubMed - indexed for MEDLINE]
: Atherosclerosis. 1984 Dec;53(3):255-64.     Related Articles, Links

Pantethine reduces plasma cholesterol and the severity of arterial
lesions in experimental hypercholesterolemic rabbits.

Carrara P, Matturri L, Galbussera M, Lovati MR, Franceschini G, Sirtori CR.

Pantethine (P), a coenzyme A precursor, was administered to
cholesterol-fed rabbits (0.5% cholesterol diet + 1% pantethine) for 90
days. At the end of treatment, plasma total cholesterol levels were
reduced 64.7% and the HDL/total cholesterol ratio increased in P-treated
animals; a significant rise of the apo A-I/A-II ratio was detected in
HDL. VLDL lipid and protein levels were, on the other hand, reduced by
P. The cholesterol-ester content of both liver and aortic tissues was
not significantly affected by P. Although the total aortic area with
evident plaques was reduced only 18.2%, the microscopical examination of
sections from the major vessels of P-treated animals, showed a reduction
in the severity of lesions, both in the aorta and in the coronary
arteries. These findings suggest that P, in addition to significantly
lowering plasma cholesterol levels in rabbits on an experimental diet,
may modify lipid deposition in major arteries, possibly by affecting
lipoprotein composition and/or exerting an arterial protective effect.

PMID: 6442152 [PubMed - indexed for MEDLINE]
Clin Ther. 1986;8(5):537-45.     Related Articles, Links

Effectiveness of long-term treatment with pantethine in patients with
dyslipidemia.

Arsenio L, Bodria P, Magnati G, Strata A, Trovato R.

A one-year clinical trial with pantethine was conducted in 24 patients
with established dyslipidemia of Fredrickson's types II A, II B, and IV,
alone or associated with diabetes mellitus. The treatment was well
tolerated by all patients with no subjective complaints or detectable
side effects. Blood lipid assays repeated after 1, 3, 6, 9, and 12
months of treatment revealed consistent and statistically significant
reductions of all atherogenic lipid fractions (total cholesterol,
low-density lipoprotein cholesterol, and apolipoprotein B) with parallel
increases of high-density lipoprotein cholesterol and apolipoprotein A.
The results were equally good in patients with uncomplicated
dyslipidemia and in those with associated diabetes mellitus. The authors
conclude that pantethine (a drug entity related to the natural compound,
pantetheine) represents a valid therapeutic support for patients with
dyslipidemia not amenable to satisfactory correction of blood lipids by
diet alone.

PMID: 3094958 [PubMed - indexed for MEDLINE]
Acta Biomed Ateneo Parmense. 1987;58(5-6):143-52.     Related Articles, Links

[Clinical use of pantethine by parenteral route in the treatment of
hyperlipidemia]

[Article in Italian]

Arsenio L, Bodria P, Bossi S, Lateana M, Strata A.

Servizio di Malattie del Ricambio e Diabetologia, Ospedali Riuniti, Parma.

Recent investigations have confirmed the effectiveness and the excellent
tolerability of pantethine, a derivative of pantetheine, an essential
part of the acetylation coenzyme CoA, administered P.O., in normalizing
the blood lipid concentrations of patients with hyperlipidemias. A group
of 18 patients with hyperlipidemias (9 M, 9 F), with an average age of
52.6 years, was submitted to pantethine parenteral treatment. After a 20
days wash-out, pantethine (400 mg/day; BID) was administered
intramuscularly, for 20 days. Total cholesterol, triglycerides,
HDL-cholesterol, apo A-1 and B lipoprotein, uric acid in serum,
glycemia, CBC, B.U.N., creatininemia, E.S.R., SGOT, SGPT, bilirubinemia,
cardiac frequency, blood pressure and body weight were controlled before
and after treatment. The drug showed to have a therapeutic effectiveness
by a rapid and significant improvement in the blood lipid pattern with
reduction of total cholesterol, triglycerides and apo-B lipoprotein and
increase of HDL-cholesterol and apo A-1 lipoprotein. The tolerability of
pantethine at the stated dosage and mode of administration was
invariably excellent, with non complaints or visible side effects
imputable to the test drug. BUN, creatininemia, glycemia, SGOT, SGPT,
bilirubinemia, E.S.R., CBC, cardiac frequency and blood pressure
readings showed no noteworthy changes throughout the study.

PMID: 2970754 [PubMed - indexed for MEDLINE]

: Acta Biomed Ateneo Parmense. 1987;58(5-6):143-52.    Related Articles, Links

[Clinical use of pantethine by parenteral route in the treatment of
hyperlipidemia]

[Article in Italian]

Arsenio L, Bodria P, Bossi S, Lateana M, Strata A.

Servizio di Malattie del Ricambio e Diabetologia, Ospedali Riuniti, Parma.

Recent investigations have confirmed the effectiveness and the excellent
tolerability of pantethine, a derivative of pantetheine, an essential
part of the acetylation coenzyme CoA, administered P.O., in normalizing
the blood lipid concentrations of patients with hyperlipidemias. A group
of 18 patients with hyperlipidemias (9 M, 9 F), with an average age of
52.6 years, was submitted to pantethine parenteral treatment. After a 20
days wash-out, pantethine (400 mg/day; BID) was administered
intramuscularly, for 20 days. Total cholesterol, triglycerides,
HDL-cholesterol, apo A-1 and B lipoprotein, uric acid in serum,
glycemia, CBC, B.U.N., creatininemia, E.S.R., SGOT, SGPT, bilirubinemia,
cardiac frequency, blood pressure and body weight were controlled before
and after treatment. The drug showed to have a therapeutic effectiveness
by a rapid and significant improvement in the blood lipid pattern with
reduction of total cholesterol, triglycerides and apo-B lipoprotein and
increase of HDL-cholesterol and apo A-1 lipoprotein. The tolerability of
pantethine at the stated dosage and mode of administration was
invariably excellent, with non complaints or visible side effects
imputable to the test drug. BUN, creatininemia, glycemia, SGOT, SGPT,
bilirubinemia, E.S.R., CBC, cardiac frequency and blood pressure
readings showed no noteworthy changes throughout the study.

PMID: 2970754 [PubMed - indexed for MEDLINE]

Atherosclerosis. 1987 Nov;68(1-2):41-9.     Related Articles, Links

    Pantethine lipomodulation: evidence for cysteamine mediation in
vitro and in vivo.

    Wittwer CT, Graves CP, Peterson MA, Jorgensen E, Wilson DE, Thoene
JG, Wyse BW, Windham CT, Hansen RG.

    Department of Pathology, University of Utah Medical School, Salt
Lake City 84132.

    Recent human studies suggest rapid in vivo hydrolysis of the
lipid-lowering drug, pantethine, to the vitamin pantothenic acid and the
small aminothiol compound, cysteamine. To test whether the active agent
is a hydrolysis product, we repeated three experimental models of
pantethine's effect with pantothenate and cysteamine. In vitro
experiments with human fetal fibroblasts showed equivalent modulation of
cholesterol and methyl sterol synthesis by pantethine, cysteamine, or
cystamine (the disulfide of cysteamine), but pantothenate had no effect.
Similarly, in vivo experiments with 0.5% cholesterol-fed rabbits showed
oral pantethine or equimolar cystamine significantly lowered plasma
cholesterol, while pantothenate, cystine, and 2-hydroxyethyl disulfide
did not. Lastly, diabetic male rats (40 mg/kg streptozotocin) fed 0.1%
pantethine and lower plasma free fatty acids after 2 weeks than
controls, an effect not seen with pantothenate and largely duplicated by
cystamine. The efficacy of pantethine has previously been attributed to
altered vitamin metabolism and increased coenzyme A concentration.
Pantethine did increase CoA levels 45% in rat liver homogenates while
equivalent amounts of cystamine or pantothenate did not. However, a
causal relationship between CoA levels and pantethine's action as a
hypolipemic agent has never been shown. At least in 3 independent
experimental models, the lipomodulating effect of pantethine appears
instead to be mediated by the hydrolysis product cysteamine.

    PMID: 3689482 [PubMed - indexed for MEDLINE]

> When I get my weight down to into a desirable range, I'm going to re-
> evaluate the DM medicines I am taking and reduce dosages or eliminate
[quoted text clipped - 9 lines]
> improve as weight loss continues.  I'm not yet down to the recommended
> range for people with DM or CVD though.

If you eat low carb, your HDL will likely rise and your TGLs will
plummet.  I doubled my HDL and cut my TGLs from about 300 to 100 within
weeks of switching to a low carb diet.

> I've just started Zetia and will retest lipids after being on that for
> a while.
[quoted text clipped - 4 lines]
> cholesterol reduction using this supplement.  What supplement do you
> find useful for reducing cholesterol counts?

Guy, the only drug I would recommend (even though it wasn't kind to me)
for a type 2 with your issues is metformin, at least 1500 per day, along
with a low carb (throw out all the starches) diet and exercise to the
extent possible.  Pantethine added to that should be a knockout punch.
You sound very focused on drugs, whether natural or pharma, rather than
building your own health.  Preventive methods are always better than
treatments.

Susan
Guy Scharf - 20 Oct 2006 23:09 GMT
>> After seeing what the Zetia does, I plan to try Bio-Lipotrol.
>> This contains Vit B3, Inositol, Guggle Gum extract, Red Yeast
[quoted text clipped - 10 lines]
> whether natural or pharma, rather than building your own health.
> Preventive methods are always better than treatments.

Susan,

On a daily basis, my primary focus is on diet, weight loss and exercise
and I will be continuing that (I just don't have questions about that
right now :-)).  I'm already on a low carb diet.  I'm hoping that after
I get my weight to a more optimal value that I'll be able to reduce the
medications.

The primary medication I rely on for DM is metformin, which I seem to
tolerate well, at 1700 per day.  Without it, my BG is more difficult to
control, as my recent experiment confirmed.

Because of my history of CVD and DM, my doctors want me my LDL below 70
(the new standard for these diseases).  I'm not there yet with diet and
exercise, though I have gotten all cholesterol counts into the normal
range.  I've tried the statins they wanted me to try and rejected them
because of their side effects (although Crestor worked very well for a
year with excellent results in lipid measurements).  I'm willing to try
other supplements if that improves the lipids at least on an interim
basis.  I'm actually cautious about the red yeast rice, since that
itself is what one of the statin drugs was derived from.

For whatever reason, my doctor says that I seem to have more side
effects than would normally be expected for someone keeping BG under as
good control as I have.  Thus the desire to bring all risk factors to
the lowest possible level, even if it takes medications to do that.

Guy
Andrew B. Chung, MD/PhD - 20 Oct 2006 23:26 GMT
Because of its promotion of lipid peroxidation, low-carbing is unwise
especially for folks who already have documented occlusive coronary
atherosclerotic heart disease.

Simply a word to the wise.

May GOD continue to heal your heart, dear neighbor Guy whom I love
unconditionally.

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).

http://groups.google.com/group/sci.med.cardiology/msg/f4dad7fe68478acf?

> >> After seeing what the Zetia does, I plan to try Bio-Lipotrol.
> >> This contains Vit B3, Inositol, Guggle Gum extract, Red Yeast
[quoted text clipped - 39 lines]
>
> Guy
Susan - 21 Oct 2006 01:15 GMT
> Susan,
>
[quoted text clipped - 3 lines]
> I get my weight to a more optimal value that I'll be able to reduce the
> medications.

I'm glad to hear that, Guy.

> The primary medication I rely on for DM is metformin, which I seem to
> tolerate well, at 1700 per day.  Without it, my BG is more difficult to
> control, as my recent experiment confirmed.

Good treatment choice.

> Because of my history of CVD and DM, my doctors want me my LDL below 70
> (the new standard for these diseases).

There is absolutely no evidence to support this target, being foisted on
folks by those selling statins.  None.  In fact, LDL has been clearly
shown to be the least predictive lipid wrt CVD.  TGL and HDL are much
more predictive.

  I'm not there yet with diet and
> exercise, though I have gotten all cholesterol counts into the normal
> range.  I've tried the statins they wanted me to try and rejected them
> because of their side effects (although Crestor worked very well for a
> year with excellent results in lipid measurements).

Crestor may be the worst/most harmful of the bunch.

  I'm willing to try
> other supplements if that improves the lipids at least on an interim
> basis.  I'm actually cautious about the red yeast rice, since that
> itself is what one of the statin drugs was derived from.

It *is* a statin, same as mevacor.

> For whatever reason, my doctor says that I seem to have more side
> effects than would normally be expected for someone keeping BG under as
> good control as I have.  Thus the desire to bring all risk factors to
> the lowest possible level, even if it takes medications to do that.

The adverse reactions to statins are worst in those who may have a
certain genetic profile, I've read.  I wouldn't take a statin on a dare.
Nor would I ever try to get my LDL to 70 because the ratios of lipids
and LDL particle size may matter, but the LDL does not.

I'm a type 2 DM, very content (as is my doc) with my LDL at 126, but
very low VLDL, TGL and high HDL.  My HDL had been 24 for about 10 years
til I low carbed.  Now it's 70.

Good luck.

Susan
Guy Scharf - 22 Oct 2006 22:08 GMT
>> Do you know if there is a relationship between atenelol and
>> sleep?  I've found that since stopping the atenelol that I have
[quoted text clipped - 5 lines]
> even if I'm exhausted.  If atenolol works by blocking your adrenal
> response, that could play a part in the sleep issue, I suppose.

fwiw, I've determined that the sleep pattern changes were caused by the
Zetia, not by the Atenelol.  Another medication bites the dust, which
is fine with me (although I'd prefer not to have so many negative
reactions in case I someday really, really need a medication).!  

Guy
Susan - 22 Oct 2006 22:32 GMT
> fwiw, I've determined that the sleep pattern changes were caused by the
> Zetia, not by the Atenelol.  Another medication bites the dust, which
> is fine with me (although I'd prefer not to have so many negative
> reactions in case I someday really, really need a medication).!  

Guy, I've found that the fewer meds I take, including ones I thought I
needed, the healthier I am.

I have a lot of weird, adverse reactions, too.  I think that's a message
not to screw with meds unless my life depends upon it.

Susan
William Wagner - 22 Oct 2006 23:03 GMT
> I have a lot of weird, adverse reactions, too.  I think that's a message
> not to screw with meds unless my life depends upon it.
>
> Susan

I agree.  But how does one know ?

A few side effects got my attention but the dam data says it i t
reduces risk in my case after cabg.  #49   Muscle pain/loss  is an
attention getter so I said enough after awhile.   Subtle  changes go
unnoticed.  

Unknowable
Saw a branch break  today
No reason just broke.

http://www.ti.ubc.ca/pages/letter49.htm

Bill

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Susan - 23 Oct 2006 01:00 GMT
> I agree.  But how does one know ?

In my case, a lot of trial, a lot of error.  And a LOT of Medline cruising.

>  A few side effects got my attention but the dam data says it i t
> reduces risk in my case after cabg.

atory properties that matter, there are lots of those that won't harm

>  #49   Muscle pain/loss  is an
> attention getter so I said enough after awhile.   Subtle  changes go
> unnoticed.  

Not unknowable, you have to listen to your body.  And do a LOT of research.

For me, diet and a few good supplements are going to have to do.  I'm
spending a lot of time trying to recover from medical treatment fallout.

Susan
William Wagner - 23 Oct 2006 12:01 GMT
> atory

Susan do you mean to write

atopy
    n : an allergic reaction that becomes apparent in a sensitized
        person only minutes after contact [syn: {immediate
        allergy}, {atopic allergy}, {type I allergic reaction}]

New word for me.

Thank You!

Bill

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Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.

Susan - 23 Oct 2006 14:21 GMT
>>atory
>
[quoted text clipped - 10 lines]
>
> Bill

Nope, I meant to cut and paste better.

I had written that there are supplements with anti inflammatory
properties, and this property is now alleged to be the defining one
statins have.

Susan
Andrew B. Chung, MD/PhD - 20 Oct 2006 18:29 GMT
> > To my surprise, I've also found that weight loss -- on the same diet --
> > has resumed at its previous rate after stopping the Atenelol.
[quoted text clipped - 6 lines]
>
> Atenolol promotes weight gain:

It does not for those using the 2PD-OMER Approach:

http://HeartMDPhD.com/wtloss.asp

The reason it does for others is because of an increase in their
healthy appetite.

Folks using the 2PD-OMER Approach do not eat more despite being
hungrier for any reason.

May GOD continue to keep your heart beating, dear neighbor Susan whom I
love unconditionally.

Prayerfully in Christ's amazing love,

Andrew <><
--
Andrew B. Chung
Cardiologist, Atlanta, Georgia, USA
http://HeartMDPhD.com/HolySpirit

As for knowing who are the very elect, these you will know by the
unconditional love they have for everyone including their enemies
(Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17).

http://groups.google.com/group/sci.med.cardiology/msg/f4dad7fe68478acf?

> (Hypertension. 2001;37:250.)
> © 2001 American Heart Association, Inc.
[quoted text clipped - 39 lines]
>
> Susan
 
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