Medical Forum / General / Cardiology / October 2006
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
 Signature S Jersey USA Zone 5 Shade Beware Of THINK LIKE THIS 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 - 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
 Signature S Jersey USA Zone 5 Shade Beware Of THINK LIKE THIS 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 - 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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