 |
 | Home | Contact Us | FAQ | Search & Site Map | Link to Us |
 | Sign In | Join | Other 45 Sites in Network |
Medical Forum / Diseases and Disorders / Diabetes / December 2005Why not Insulin for everyone?
Hey Still having problems with my bg being too high, especially in the morning. No matter what I do it keeps rising until about 10 am. I have tried low carbs in the morning, high carbs in the morning, no carbs in the morning. high carb snack before bed, low carb snack before bed, no snack before bed. My latest bright idea, that does not work was to get up at 4 am and eat breakfast. Several of you have suggested that I might need to be on insulin. I see my doc on Fri. Actually, I hope she puts me on insulin it sounds better that taking tons for meds and not getting results. So, Is there a reason that docs don't put T2s on insulin instead of meds? I here it is cheaper and sound like it works better. Still just trying to figure this disease out Nirvana 34 year old male 5'8 170 lbs. T2 Metformin (1000mg) dinner Glyburide (10mg) breakfast and dinner Prandin (3mg) breakfast, (1mg) lunch and dinner Hi Nirvana I too had the same problem and converted to Lantus (1 shot on rising) Seems to work ok with me, rising bg 5.5-6.5, 2hr pp back to 6's (don't know what 1hr pp is). My diet is generally lo-GI/lo-carb, breakfast is "English" or linseed (flax seed) "porridge" I had no problems or hang-ups (hangs-up?) with injecting, so good luck if you do "graduate"  SignatureDelboy T2 in reasonable control (Lantus & Metformin) A common mistake that people made when trying to design something completely foolproof was to underestimate the ingenuity of complete fools. Douglas Adams > Hey > [quoted text clipped - 24 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner Forgot to mention; couple of hours gym Mon, Wed & Fri. But then I'm retired so perhaps this is not on for you. SignatureDelboy A common mistake that people made when trying to design something completely foolproof was to underestimate the ingenuity of complete fools. Douglas Adams > Hi Nirvana > [quoted text clipped - 37 lines] > > Glyburide (10mg) breakfast and dinner > > Prandin (3mg) breakfast, (1mg) lunch and dinner > Hey > [quoted text clipped - 24 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner I can't imagine the difficulty T2's must experience juggling a never ending combination of pills. Besides which, some of them aren't too good for your body in the long run. Human Recombinant insulin is as close as you can get to what mother nature has shorted you on. I hope you do better with your DM once you get on insulin. dave >> Hey >> [quoted text clipped - 37 lines] > > dave What Dave said makes a lot of sense. If you look at the side effects of diabetic meds and look at the side effects insulin; insulin wins hands down. Of course, IR lowering drugs are an exception, they lower insulin requirements, natural or injected, and should be a part of T2 treatment. Sarah Type 1 > Of course, IR lowering drugs are an exception, they lower insulin > requirements, natural or injected, and should be a part of T2 treatment. > > Sarah > Type 1 Absolutely, when one is resistant (T2's), drugs are available to help lower the resistance, and hence the amount of insulin needed. The less insulin you can get by with, the less chance you'll get into "roller coaster mode". dave : >> Still just trying to figure this disease out : >> [quoted text clipped - 14 lines] : > : > dave : What Dave said makes a lot of sense. If you look at the side effects of : diabetic meds and look at the side effects insulin; insulin wins hands down. : Of course, IR lowering drugs are an exception, they lower insulin : requirements, natural or injected, and should be a part of T2 treatment. : Sarah : Type 1 I am no expert, but it seems to me tht , if the probellem is not insuling production, but insulin resistance, throwing mre insulin into the blood stream would not be too effective. It would be better to try to reduce the insulin resistance wiht whatever means work, weight loss, exercise adn med, like Metformin or Actos or Avandia. I believe that too much inculin runnign around in the sysem is not the best thing to have hapening. This is searate fro a problem with hypos, which indicate that the resistance is nt precludign the use of the insulin. Wendy Sarah: I'm curious about your comment "natural or injected". Since true T1 diabetics don't have extra benefit if Avandia is added to injected Insulin, maybe injected insulin is reduced in T2s taking avandia only because Avandia improves natural insulin sensitivity hence less injected insulin is needed. My thought is that injected insulin is merely "swamping" the system to help lower BG levels and Avandia isn't involved in that process in any specific way so far as lowering the dose of injected insulin. Maybe Dave and Old Al can add there thoughts. Thanks. Larry > Human Recombinant insulin is as > close as you can get to what mother nature has shorted you on. However, T2s are rarely short on insulin - they generally make plenty. Insulin resistance is their problem. That's why doctors treat the IR rather than giving them more insulin. Later in life, when their beta cells are pooped out, then they become a candidate for insulin. >However, T2s are rarely short on insulin - they generally make plenty. >Insulin resistance is their problem. That's why doctors treat the IR rather >than giving them more insulin. Later in life, when their beta cells are >pooped out, then they become a candidate for insulin. that depends on the level of individual insulin resistance. If the IR is severe enough, even a recently diagnosed type 2(that has not gone undiagnosed for a long time) will need insulin and anti resistance meds. there's simply no one size fits all when it comes to insulin and IR in type 2s. SignatureMâck©® Type 1 since 1975 http://www.alt-support-diabetes.org http://www.diabetic-talk.org http://www.insulin-pumpers.org "To announce that there must be no criticism of the President, or that we are to stand by the President right or wrong, is not only unpatriotic and servile, but is morally treasonable to the American public." ...Theodore Roosevelt (o o) --ooO-(_)-Ooo-------------------- "I don't know half of you half as well as I should like; and I like less than half of you half as well as you deserve." Jesus never hated anyone. > Hey > [quoted text clipped - 24 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner I'd spread out the Metformin... one before bed. That's what I'm going to try. Maybe 3x500 for me three times a day. I take 2x500 now. One in the morning and one at dinner. I suppose the doc's don't want to go to heavy hammer too soon. You should try to do more about it yourself. Ya know hit the low carb diet all the time, exercise every evening. Stuff like that. You sound like you want to shoot up and then have a huge chocolate cake. Just fooling yourself doing it that way. Anyway your doc would know if you have to be on insulin. Ask him when you see him. -- Dave > So, Is there a reason that docs don't put T2s on insulin instead of meds? > I [quoted text clipped - 6 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner They probably reckon on patient resistance to those nasty needles. There's also the risk of putting on weight. Sounds to me like you could double your metformin - assuming you're insulin resistant? 34 and good BMI isn't exactly classic T2. Nicky. SignatureA1c 10.5/5.6/<6 T2 DX 05/2004 1g Metformin, 100ug Thyroxine 95/74/72Kg > Hey > > Still having problems with my bg being too high, especially in the > morning. No matter what I do it keeps rising until about 10 am. > I have tried low carbs in the morning, high carbs in the morning, no > carbs in the morning. high carb snack before bed, low carb snack > before bed, no snack before bed. My latest bright idea, that does not > work was to get up at 4 am and eat breakfast. > [quoted text clipped - 17 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner You don't say what your fasting bg's actually are. I have heard taking some Metformin at bedtime helps with morning bg's. Also 170 pounds is still chunky for a 5'8". Further weight loss should improve the insulin resistance. What is your overall diet? Are you giving your liver plenty of glucose to use when you are hungry, i.e. overnight? Perhaps your day time carbs are filling up the liver and then nature takes it's course overnight. My best fasting bg's were during the horrid 2 weeks period I tried Atkins induction (<20 gr carb per day). It didn't suit me at all, I felt like crap but it did wonders for fasting bg. I read somewhere it takes about 3 days to get rid of the glucose reserve in the liver. > So, Is there a reason that docs don't put T2s on insulin instead of > meds? I here it is cheaper and sound like it works better. Then what will deal with the insulin resistance? <snip> > So, Is there a reason that docs don't put T2s on insulin instead of meds? I > here it is cheaper and sound like it works better. Yes. Most type 2's already produce plenty of insulin. But we are insulin resistant. Too much insulin causes its own set of problems. That's why it is not our first line of defense. It is usually only used when all other meds have failed. <snip> SignatureSee my webpage: http://mysite.verizon.net/juliebove/index.htm I had the same problem before my Doc added Lantus. Since we got the dose adjusted, my fasting BG averages 90. At the same time, my A1c dropped below 6 and has averaged 5.5 for over a year. Anon > Hey > [quoted text clipped - 27 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner Nirvana wrote in message ... >Hey > [quoted text clipped - 24 lines] >Glyburide (10mg) breakfast and dinner >Prandin (3mg) breakfast, (1mg) lunch and dinner 1. Insulin INSTEAD of meds for T2: If you are T2 then, statistically, your #1 problem is a high risk of Premature Heart Attack due to high Insulin Resistance. Insulin does a fine job of bG control for T2 but not much else**. T2 must address their (statistical high probability of) high Insulin Resistance. Metformin is a fine anti-Insulin Resistance med. Note that the U.S. PDR asserts that the usual maintenance dose is 1500 - 2550 mg/day. http://www.pdrhealth.com/drug_info/rxdrugprofiles/drugs/glu1188.shtml The rest of the anti-Premature Heart Attack equation is: a. Lose fat lb. b. Gain muscle lb. c. Exercise every day d. Eat low carb (Yes, eating low carb helps with bG control but for a high Insulin Resistant T2, it also helps with premature heart attack risk. For many T2, high carb equates to high triglycerides levels. High triglycerides levels equate to high premature heart attack risk. ) If T2 go on insulin-only as their sole therapy, they can achieve superior bG control but are likely to also achieve sky-high triglycerides and thus sky-high risk of premature death. Insulin is a great idea for T2 but anti-Insulin Resistance comes first. Not all T2 have high Insulin Resistance. Check your non-medicated triglycerides/HDL ratio. A ratio of 3 or more means high Insulin Resistance. A HOMA analysis is as good or better. Maybe you can have your doc measure both. See HOMA at: http://www.dtu.ox.ac.uk/index.html?maindoc=/riskengine/ I would be fascinated with your HOMA scores. A recently diagnosed adult-onset diabetic with a BMI of 26 experiencing bG problems despite two beta stimulators and metformin really sounds like adult-onset T1. (**High bG also contribute to premature heart attack risk. Anything which knocks down bG will thus have some sort of anti-Heart attack effect. My interpretation of the medical sites is that high I.R. produces the greater premature heart attack risk ) 2. Insulin AND meds for T2: Glyburide and Prandin are beta stimulators which force your dying beta cells to put out more insulin. Many folks think that over-working the beta cells increases their death rate and thus accelerates the arrival of the day on which your betas don't do any good at all. . . ahem. . .like mine. You won't like that. Would you like a detailed explanation based on the PITA I go through every day, or would you please take my word that you won't like that? Of course, using early insulin as a -- supplement -- to protect T2*** beta cells (after doing something to knock down your Insulin Resistance) is much preferable than the down-the-road PITA insulin regime which accompanies mostly dead beta cells. It's sort of "Pay me now or pay me later" with Pay me now being much cheaper. (***Early insulin doesn't do much to protect dying T1 beta cells) IMO, insulin is a better choice than Glyburide and/or Prandin unless you have physical impairments which make the convenience of the pills more important than the risk of accelerated beta cell death. Insulin therapy is much more powerful and much more controllable than the pills. Regards Old Al I downloaded the risk engine. The results are quite depressing. If what they say is true I better get my will in order. Using the numbers from my most recent labs, I have a 10.5% chance of fatal heart attack during the next 10 years. If I plug in my most optimistic improvements, the risk is still 10%. > Nirvana wrote in message ... >>Hey [quoted text clipped - 107 lines] > Regards > Old Al On the other hand you'll have 90% percent chance of survivel... :-) Jan > I downloaded the risk engine. The results are quite depressing. If what they > say is true I better get my will in order. [quoted text clipped - 114 lines] > > Regards > > Old Al Old Al, I had saved a link (previously cited in this group) to http://groups.google.com/group/misc.health.diabetes/msg/b6d01cf3e6c1d7a5?dmode=s ource&hl=en on this topic, a post by Charles Coughran at UCSD, which strongly disputes the theory that sulfonylureas increase the death rate of beta cells in the pancreas. He says that the theory that sulfonylureas cause beta cell burnout made sense when they were the only kind of oral med available, and thus the only kind studied, but that subsequent studies have shown that "It turns out that metformin shows essentially the same rate of secondary failure as sulfonylureas. (This was one outcome of the landmark UKPDS, United Kingdom Prospective Diabetes Study, which is one of the two fundamental studies on which current treatment of diabetes is based.) Treatment with diet and exercise has a similar secondary failure rate. This all leads to the notion that pancreatic beta cell function is lost with time independent of a particular therapy. " Have you previously seen this argument, and if so why have you discounted it? If not, I'd be interested to hear what you think of his overall reasoning when you do read it. As someone who takes a relatively low dosage of Glucotrol, I of course have a very personal reason in trying to evaluate this issue clearly. Thanks in advance for any effort taken in response, Morris As much as I respect Charlie, I don't agree with a lot of his post. First up, the UKPDS dealt with higher A1C's than many are achieving today (from memory the UKPDS trial finished 17 years ago?). Given the fact that glucotoxicity on its own (as well as hyperinsulinemia and lipotoxicity) can cause beta cell destruction or exhaustion, I can't see where a "pat" answer can be given as to whether beta cell burnout is hastened or not hastened by the use of sulfs from results of the UKPDS participants. In other words the UKPDS doesn't show what the results might be in people who keep normal non diabetic numbers. A foregone conclusion cannot be made from test results that are based on higher than non diabetic numbers. Logically, any factor that contributes to beta cell death or exhaustion should be remedied if progression is to be halted or slowed. Beta cell rest (metformin for example) or beta cell stimulation (sulfs). How do we rest the beta cells? That takes us back to Old Al's recommendations. a. Lose fat lb. b. Gain muscle lb. c. Exercise every day d. Eat low carb Why lower carb? It's not just for bg control. The less pressure you put on the beta cells the better? Phase ii insulin response. It's pretty well a given that our phase 1 is shot. It's the loss (or diminishing) of phase 1 that first rears its head in Gestational Diabetes, IGT etc. If you can prevent a rise in bg, then you can rest the beta cells further by not invoking the phase ii response (or too much of it). Lower carb makes it easier to remain euglycemic. morris wrote in message <1135757813.723580.252490@g44g2000cwa.googlegroups.com>... >Old Al, > [quoted text clipped - 26 lines] > >Morris I have found a few references which support the burn-out theory. Unfortunately, there are so many ways for a T2 to kill beta cells that clinical studies tend to be confounded combinations of several factors. In general, the main "beta cell rest" thesis is that: 1. T2 diabetes is marked by a genetic defect in amyloid synthesis. Amyloid, which is co-produced with insulin, precipitates within the beta cells and slowly kills them. Therefore, a. Anything a T2 gene-carrier does to reduce the amount of insulin he/she manufactures will slow the rate of destruction of beta cells. b. Anything a T2 gene-carrier does to increase the amount of insulin he/she must manufacture will increase the rate of destruction of beta cells. 2. There is ample proof that precipitated amyloid kills the beta cells. The main controversies are whether the totally precipitated amyloid polypeptides do the damage or is it the lower molecular weight pre-polymer precursors to the totally precipitated amyloid polypeptides; and of course, is the Amyloid the dominant mechanism and is it death or merely an upset beta cell operating mechanism that causes the problem. 3. As Ozgirl explains, T2 beta cells are thought to be damaged/killed by a variety of mechanisms: a. Precipitated amylin (amyloid polypeptides) b. Free Fatty Acids (FFA) c. High blood sugar d. High insulin levels e. High blood pressure f. High triglycerides levels "a" is active all during life. "b" and "d" are active in folks with high Insulin Resistance and high carb intake. "e" is active in the later stages of the T2 damage progression when b.p. rises. "c" is active in full-blown diabetics who exhibit POOR SUGAR CONTROL. The fact that poorly-controlled diabetics in the UKPDS suffered continued beta cell death despite the use of metformin merely helps set some limits to the destruction process. Any T2 can defeat any therapy by overeating if they so desire. I also object to the "loss of beta cells as a constant rate" implication. There are just too many death mechanisms to expect all of them to cooperate by generating a constant loss rate. In contrast, the success in delaying the onset of full-blown T2 in the DPT-2 using anti-Insulin Resistance techniques (daily exercise, fat loss, metformin) supports the amyloid theory. It also supports the FFA/triglycerides theories though IMO less strongly than the amyloid. I favor the amyloid theory because it very neatly explains 15-year old, full blown T2 and it offers an explanation for the fact that some folks can exhibit high Insulin Resistance but don't end up as T2. IMO, if the latter don't have the defective amyloid mechanism, the high Insulin Resistance mechanisms (triglycerides, FFA, high b.p., high insulin levels) don't kill enough beta cells to produce T2. (BTW, a corollary is that the non-diabetic but high Insulin Resistance folks have a fatal syndrome but haven't a clue. T2 at least know that there is a problem, know what ought to be done about it, and the docs will prescribe anti-Insulin Resistance meds to help them) My best Amyloid URL is dead http://www.amyloiddiabetes.com/ However, Prof. Melvin Hayden of the Univ. of Missouri Medical School asserts that: http://www.joplink.net/prev/200107/200107_02.pdf ". . . .Also, employ newer medications that lower glucose and HbA1c values without elevating endogenous insulin or amylin. By lowering the amyloidogenic substrate amylin (in addition to the other substrates of the A-FLIGHT toxicities) we may be able to slow or prevent the progressive ADIA deposition within the islet and preserve beta cell function . .." ". . .Lower glucose without elevating endogenous insulin. . ." means knock down bG without forcing the beta cells to manufacture more insulin. Insulin injections fit that definition as does reducing Insulin Resistance. However, injections can reduce self-manufactured (endogenous) insulin more dramatically than anti-Insulin Resistance meds. Consider that high Insulin Resistance folks must attack their Insulin Resistance independently of any effects on bG. Insulin injections are an added feature thought to protect beta cells. Adding insulin to anti-Insulin Resistance meds is sort of a belt and suspenders approach which more endos are favoring. See page 129 of the above URL for the Amyloid theory explained in serious doctor-ese. AFAIK, nobody has run the direct clinical trial with precautionary insulin to delay T2. However, some moderately clear evidence comes from Dr Reaven's work which I cannot find directly cited on the Internet. Indirect cite at: http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=2867 ". . .Dr. Gerald Reaven put 32 Type 2 diabetes patients, one at a time on the Biostator (artificial pancreas) for 2 weeks. He clamped their blood glucose at 90mg/dl. The starting average A1c was about 9.3% and after just 2 weeks the average A1c went to 7.9%. The patients then went home and went back to doing what they did before they went into the hospital. . . .It took almost 2 years for their A1c’s to go back to where they were before.. . ." In essence, the only therapy they had was "beta cell rest" therapy via insulin injection (no metformin back then) which ended up pushing down their A1c for 2 years. The inference is that the beta cell rest allowed any still-functioning T2 beta cell replacement processes to somewhat replenish their supplies. I became more aggressive on this topic after watching one of our local endos, on Community -TV assert that insulin protects beta cells. Unfortunately, he didn't cite any references. The docs have noted similar effects with intensive therapy with the TZD's. Rezulin, Actos and Avandia clinical trials have produced an increase in the patients' abilities to produce self-generated insulin. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Ab stract&list_uids=15610048 Lister CA et al. Diabetologia 1999;42(suppl 1):A150 (abstr 556) The HOPE trial produced evidence that Avandia produces regeneration. The DREAM trial is a more intensive follow up http://www.bermancenter.org/studiestrials/diabetes/dream.html Much more yet much less than you wanted to hear. Regards Old Al <lots of good stuff snipped> > The docs have noted similar effects with intensive therapy with the TZD's. > Rezulin, Actos and Avandia clinical trials have produced an increase in the [quoted text clipped - 6 lines] > > The HOPE trial produced evidence that Avandia produces regeneration. No! The HOPE trial showed that Ramipril appeared to decrease heart disease and decreased progression to diabetes. No glitazone was tested. The follow-up study adds Avandia to Ramipril. You are probably thinking of the TRIPOD study which looked at Rezulin in a population of Hispanic women with gestational diabetes considered at high risk for developing full blown diabetes. Buchanan TA, Xiang AH, Peters RK, et al. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk Hispanic women. Diabetes, Sep 2002, 51(9) p2796-803 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=12196473&query_hl=2&itool=pubmed_docsum That study found that for one clearly defined sub group, which the researchers called "responders" taking Rezulin very quickly led to improved blood sugars which persisted long after the study was over. However, outside of the group of "responders" there was a much less dramatic effect. Unfortunately, this study was done with a relatively small group, and one that has what is probably a specific genetic form of diabetes (since they were all Hispanic), and worst of all, the study was terminated early since Rezulin was taken off the market. It's worth also remembering that Rezulin, when it didn't kill people, seems to have given patients much better control than Avandia and Actos without the enormous problem of edema. That's what doctors have told me, anyway. So the evidence that Avandia and/or Actos really provide beta cell rest is far from proven and may only be true for an unidentified sub-population with some specific genetic flaw. At the same time, evidence is accumulating that these drugs heighten the incidence of macular edema which leads to blindness. Jenny wrote in message ... . . .(snip). . >> >> The HOPE trial produced evidence that Avandia produces regeneration. > >No! The HOPE trial showed that Ramipril appeared to decrease heart >disease and decreased progression to diabetes. No glitazone was tested. >The follow-up study adds Avandia to Ramipril. You're right. The Professors at McMasters Univ. were discussing the HOPE results, a third study with TZD and the DREAM Avandia + Ramipril plans in the same press release and I combined HOPE and the third study. Regards Old Al Hi Al, Thanks for taking the time to respond. Being a medical non-professional with no college chemistry or biology, I won't pretend to understand all of it, but I get the gist I think. My situation is that almost 3 years ago I started avandia and metformin upon diagnosis with an HbA1c of 11.4. At first 1000 mg/day metformin, then 1500, then 2000. 3 months after diagnosis I started taking glucotrol (5 mg/2X daily) as well. The difference was dramatic. The week before I had averaged 141 fbg, the week after I broke 100 for the first time. That week I also hit the max of 2550 metformin. A month later I averaged 82 fbg for a week and reduced to 1700 metformin My blood sugar decreased slightly again and over the next fewo months gradually cut out the metformin entirely, about a year after diagnosis. Basically the glucotrol coincided well with getting good control, and cutting back on the metformin had no effect. Over the last two years, my fasting and pre-meal bg have averaged in the 80s, and my HbA1c has averaged 5.1, with my most recent at 4.9. Almost a year ago, afer a couple of low experiinces I reduced the Glucotrol by 25% to 5/2.5 mg daily. I have seen at least one study that suggest that sulfonylureas at this level do not shorten the life of beta cells. Using the PI/I ratio as an indiction of beta cell function, a Japanese study, summarized at http://finance.messages.yahoo.com/bbs?.mm=FN&action=m&board=7076553&tid=amln&sid =7076553&mid=108770 concluded that "The use of high-dose sulfonylureas increased the ratio, whereas low-dose sulfonylureas and use of drugs other than sulfonylureas did not increase this ratio. Duration of diabetes was also associated with progressive reduction in insulin secretion. The investigators concluded that the use of high-dose sulfonylureas promotes premature exhaustion of the beta cell." I also have found another study that Avandia seems to promote beta cell function. From the abstract at http://jcem.endojournals.org/cgi/content/abstract/89/12/6048 I read that "Treatment with rosiglitazone for 26 wk (study 1) produced significant dose-dependent decreases in both plasma PI concentrations (18-29%) and the PI:IRI ratio compared with baseline (7-14%) and placebo (19-29%) (P < 0.001). A significant increase in the PI:IRI ratio in placebo-treated patients occurred (P < 0.001). In study 2, rosiglitazone also significantly reduced both plasma PI and the PI:IRI ratio compared with baseline (P < 0.001)." I had previously found a study of people taking both Avandia and sulfonylureas, which I can no longer find the URL for, which concludes that, apparently, the avandia makes up for any negative effects of the glucotrol: "the addition of RSG (avandia) to SU (glucotrol) had a durable effect on reducing insulin and improving pancreatic beta-cell function compared with SU alone, which had deleterious effects on beta-cell function. Thus, it appears that the addition of RSG to SU, even in older subjects with compromised beta-cell function, is capable of improving that function and, in so doing, seems to abrogate the progressive decline in beta-cell function characteristic of the disease." And this was at my dosage, 4mg, 2x/day,. of avandia, and a maximum dose of glucotrol of 40 mg/day. Since I am taking 7.5 mg/day of glucotrol, I found that rather reassuring, even if, as I suspect, there must be more studies out there. My recent c-peptide reading of 3.6 indicates to my doctor that my insulin production is relatively strong; when I asked, he opined that the 2.5 mg of glucotrol taken over the previous 24 hours probably only elevated the reading slightly. But when I skip the glucotrol, my numbers go up dramatically (for me)--abpout 10-15 points on average. I had enough experience with neuropathy before diagnosis, and discovered retinopathy afterwards, and although I have been quite fortunate in reversing the neuropathy about 90% and treating and stabilizing the retinopathy, I have little desire for any cutback in medication that might risk the re-emergence of these complications. The glucotrol seems to work, and even if, as I suspect, my natural insulin resistance is now low, the Avandia may be helping preserve beta cell function and reducing the risk of cardiovascular complications, so it is hard to argue with that. I usually try to avoid long, self-centered posts, so if anyone has made it this far, please accept my apology. I do wonder if I am somenhow misreading the studies I have seen, being that medical-ese is not my specialty, and would be grateful for any futher observations. Hi Morris: The study I am siting below yours does reinforce the point you were making. > I had previously found a study of people taking both Avandia and > sulfonylureas, which I can no longer find the URL for, which concludes [quoted text clipped - 10 lines] > of glucotrol, I found that rather reassuring, even if, as I suspect, > there must be more studies out there. "β-cell preservation: a potential role for thiazolidinediones to improve clinical care in Type 2 diabetes - L. A. Leiter Type 2 diabetes is caused by progressively increasing insulin resistance coupled with deteriorating β-cell function, and there is a growing body of evidence to suggest that both of these defects precede hyperglycaemia by many years. Several studies have demonstrated the importance of maintaining β-cell function in patients with Type 2 diabetes. This review explores parameters used to indicate β-cell dysfunction, in Type 2 diabetes and in individuals with a predisposition to the disease. A genetic element undoubtedly underlies β-cell dysfunction; however, a number of modifiable components are also associated with β-cell deterioration, such as chronic hyperglycaemia and elevated free fatty acids. There is also evidence for a link between pro-inflammatory cytokines and impairment of insulin-signalling pathways in the β-cell, and the potential role of islet amyloid deposition in β-cell deterioration continues to be a subject for debate. The thiazolidinediones are a class of agents that have demonstrated clinical improvements in indices of β-cell dysfunction and have the potential to improve β-cell function. Data are accumulating to show that this therapeutic group offers a number of advantages over traditionally employed oral agents, and these data demonstrate the growing importance of thiazolidinediones in Type 2 diabetes management. Diabet. Med. 22, 963–972 (2005)" http://www.blackwell-synergy.com/doi/abs/10.1111/j.1464-5491.2005.01605.x The following gives some explanation why insulin injections are often needed as the progression of beta-cell function decreases. Deteriorating beta-cell function in type 2 diabetes: a long-term model http://qjmed.oxfordjournals.org/cgi/content/full/96/4/281 Frank > "β-cell preservation: a potential role for thiazolidinediones to improve > clinical care in Type 2 diabetes - L. A. Leiter <snip> Several studies have demonstrated the importance of > maintaining β-cell function in patients with Type 2 diabetes. This > review explores parameters used to indicate β-cell dysfunction, in Type > 2 diabetes and in individuals with a predisposition to the disease. <snip> The > thiazolidinediones are a class of agents that have demonstrated clinical > improvements in indices of β-cell dysfunction and have the potential to [quoted text clipped - 5 lines] > Diabet. Med. 22, 963–972 (2005)" > http://www.blackwell-synergy.com/doi/abs/10.1111/j.1464-5491.2005.01605.x Just note that there is no actual research here, it's a review-- a summary of what a nutritionist read elsewhere. In fact, I have NOT been able to find any conclusive study in humans showing that Thiazolidinediones (the -glitazone drugs) actually improve beta cell function. And there is growing concern about the side effects. Once again you have to be very careful to screen out drug company puffery from fact. That doesn't mean that I'm saying these drugs are useless, only that their real effects and long term side effects are not known because they haven't been on the market long enough for us to know. One good thing about Metformin is that it has been in use for more than 20 years (in Europe) so its long term effects are much better understood. Generic metformin is quite cheap and that all these glitazones are extremely expensive, with no generics available. So there is a lot of incentive for the manufacturers to try to make them sound a lot better than existing therapies. A couple major issues to remember. 1. Metformin causes weight loss, Avandia and Actos causes the birth of new fat cells and weight gain. 2. Metformin improves lipids especially triglycerides. Actos raises "bad" LDL. 3. Metformin does not worsen any existing diabetic condition. Avandia and Actos can exacerbate congestive heart failure and cause retinal damage. Remember that the drug companies are spending millions selling these new drugs to doctors to replace cheaper generic metformin and make informed decisions. And that, to date, there is NO conclusive evidence from humans that these drugs reinvigorate beta cells. > The following gives some explanation why insulin injections are often > needed as the progression of beta-cell function decreases. [quoted text clipped - 3 lines] > > Frank I quite understand that drug companies are in it for the buck and that a major component of that is buying favorable research and pushing its findings on medical professionals and patients alike. But I also have to temper my skepticism with my personal experience. to wit "A couple major issues to remember. 1. Metformin causes weight loss, Avandia and Actos causes the birth of new fat cells and weight gain. ---These things that these drugs "cause" are often cited, particularly by patients who are gaining weight. It must be the insulin or the Avandia or the Actos . I would not wsay that it does not happen to some people, but my experience is that in 3 years of taking Avandia, and with over a year of taking metformin, my weight has changed 5 pounds (downwards). I think we have to be careful to state that these are potential side-effects that happen to some poeple, rahter than saying these drugs cause those things as a blanket statement. "2. Metformin improves lipids especially triglycerides. Actos raises "bad" LDL." --can't really comment on that one since I don;t take Actos. Metformin and dietary changes at the same time showed only a modest improvement in my lipids. It took lipitor to make a substantial change. "3. Metformin does not worsen any existing diabetic condition. Avandia and Actos can exacerbate congestive heart failure and cause retinal damage." --for me, Avandia has not caused retinal damage--I had that before i started taking Avandia and it has improved since I started taking it. Of course I wouldn;t say it has improved because of the Avandia. It has improved because of good blood sugar control. As for causing congestive heart failure, the research seems to indicate it helps prevent cardiovasuclar disease. It seems to me that we have to be careful not to fall into the same boat of saying that research, which may be contradictory or inconclusive, proves our pre-decided point of view, while at the same time saying that research that indicates something else is inconclusive. Morris Morris, It's great that these drugs work for you. It's just important to stay balanced when we are exposed to the drug company hype and for patients to get the whole story on a drug before trusting their lives to it, because, sadly, we can no longer trust that our doctors will be independent enough to research new drugs for us and protect us from drug company hype. All too often, they are the loudest cheerleaders for the least understood (and most expensive) new treatments. > ---These things that these drugs "cause" are often cited, particularly > by patients who are gaining weight. The effects I mentioned aren't anecdotal. They come from the drugs' prescribing information or journal articles published in mainstream journals. There is one study, funded by the maker of Avandia, where they went in and biopsied people's body fat and did a lot of intensive measurements because they were expecting to find that Avandia decreased visceral fat (the bad kind that is associated with cardiac problems.) Instead, what they found was that these drugs did not diminish visceral fat but packed new fat on to the arms and legs. And this fat was in the form of new cells, not just more fat going into existing cells, which means that after the drug is discontinued, the person is still stuck with more fat. So these side effects are real. If you are lucky enough not to have suffered them, that doesn't mean that they aren't happening to other people and that some of them can ruin lives. So caution is required. > As for causing congestive > heart failure, the research seems to indicate it helps prevent > cardiovasuclar disease. The "research" is often press releases written by the drug companies who pay doctors to put their names on the papers. Take a look at this article to see how journal articles supposedly written by doctors turn out to have been written by writers in the employ of the drug company whose drug was being discussed. This information, I am told, also appeared in the Wall Street Journal recently. (Subscription, only or I'd cite it.) http://preventdisease.com/news/articles/121405_writing_scientific_studies.shtm >Morris, > [quoted text clipped - 41 lines] > >http://preventdisease.com/news/articles/121405_writing_scientific_studies.shtm Also remember that while 1 person may have suffered from a side effect, hundreds of others may not have. Don't assume that because 1 person had problems, that you will too. That said, an informed user is the safest user. Be aware of, and in watch for side effects. Sleepy "I used to think I was poor. Then they told me I wasn't poor, I was needy. Then they told me it was self-defeating to think of myself as needy, I was deprived. Then they told me deprived was a bad image, I was underprivileged. Then they told me underprivileged was overused, I was disadvantaged. I still don't have a dime, but I sure have a great vocabulary." -Unknown I did not mean to imply that the side effects of these drugs do not occur just because I did not experience them. My quibble is with stating it without qualifiers: x drug causes y, which makes y sound like the inevitable consequesnce of taking x. In many if not most case the studies will show that, for example, 53% of patients (amazingly high compared to most 'side'-effects) will experience diarrhea with Glucophage, but only 8% will experience diarrhea with Glucorhage XL (or is that XR?). So for 47% or 92% of the people taking those drugs, diarrhea will not be a consequence. When we say that a drug causes something, it influences a lot of people who have been told they should take something into avoiding effective therapy because they don't want to gain weight or have the trots or whatever. I just think that the credibiility of our reasoning demands that we not overstate the facts on things we are discussing. > I did not mean to imply that the side effects of these drugs do not > occur just because I did not experience them. My quibble is with [quoted text clipped - 11 lines] > whatever. I just think that the credibiility of our reasoning demands > that we not overstate the facts on things we are discussing. Morris, I do understand where you are coming from, but I live, daily, with a drug-induced "side effect" permanent ringing in my ears, which really erodes my pleasure in life. The doctors was very remiss in not taking me off the drug when the symptom first emerged (and when it was reversible) assuring me it was nothing to worry about and could be controlled by lowering the dose. She was wrong, it became permanent after one more "lower" dose, and 9 years later, I'm still paying the price. So now I take a very paranoid approach to drugs carefully weighing the potential benefits against possible damage, getting whatever testing is recommended to make sure a drug is safe for me, and avoiding those where the potential downside is something permanent. I find Googling very helpful in this regard, because for many drugs you will see posting after posting mentioning terrible permanent side effects, while for others, you see only transient ones. This means that, for example, I would not take a floxin for a urinary tract infection, because there are other, much safer drugs available for that condition and floxins occasionally cause permanent brain damage. I would take it for Anthrax because that is a life and death situation and brain damage is better than death. >I did not mean to imply that the side effects of these drugs do not >occur just because I did not experience them. My quibble is with [quoted text clipped - 11 lines] >whatever. I just think that the credibiility of our reasoning demands >that we not overstate the facts on things we are discussing. After a bit you will notice it is the same few who constantly try to spread fear of meds in this ng. You will often notice that the same people are huge supporters and pushers of unregulated supplements. Not always the same people, but often enough to establish a pattern. Not saying there are no bad meds, because history shows us there are. When taken as a whole however, the number of meds that were misrepresented as safe and efficacious when they were not, is miniscule compared to the number of meds out there. It is up to each of us to check with our docs, pharmacists, and online, in order to make an educated decision as to whether to use a med or not. Though some may disbelieve me, I use a few supplements myself. That said the unregulated supplement industry is a national disgrace. As many supps are manufactured in Utah, and Orrin Hatch is an extremely influential and senior repug Senator, the industry is free to put anything into a bottle, call it anything they want, and then made absurd unsubstantiated claims about what it does. As long as they call it a dietary supplement they can do as they please. Like many other things, the US is one of the only "civilized" societies that allows this to happen. Enough for today! Sleepy "I used to think I was poor. Then they told me I wasn't poor, I was needy. Then they told me it was self-defeating to think of myself as needy, I was deprived. Then they told me deprived was a bad image, I was underprivileged. Then they told me underprivileged was overused, I was disadvantaged. I still don't have a dime, but I sure have a great vocabulary." -Unknown >>I did not mean to imply that the side effects of these drugs do not >>occur just because I did not experience them. My quibble is with [quoted text clipped - 22 lines] > docs, pharmacists, and online, in order to make an educated decision > as to whether to use a med or not. Whether these persons try to spread fear or not is another issue, but some people have an anti-agenda that is about like a one note Samba. ;) Frank > After a bit you will notice it is the same few who constantly try to > spread fear of meds in this ng. You will often notice that the same > people are huge supporters and pushers of unregulated supplements. Since I am the person who posted the drug warning being discussed here, I'd like to make it crystal clear that I have never promoted any supplements here and have, in fact, posted quite a few messages challenging whatever the latest "Vitamin X or Food Product Y prevents Z" fad might be. I had high morning numbers for years. Insulin worked better than anything. If your doctor is reading current research, she may must welcome your suggestion of insulin. The barrier to insulin usually resides within the mind of the diabetic--needle fears--feelings of failure. > Hey > [quoted text clipped - 24 lines] > Glyburide (10mg) breakfast and dinner > Prandin (3mg) breakfast, (1mg) lunch and dinner >Hey > [quoted text clipped - 13 lines] >So, Is there a reason that docs don't put T2s on insulin instead of meds? I >here it is cheaper and sound like it works better. You are correct in that novolog is cheaper than oral meds for us T2's. Eventually, the vast majority of us T2s will be on insulin anyway. If you have to pay for it yourself, get it for $39 from http://www.getcanadiandrugs.com/search.php?PHPSESSID=3387599e5946d98036e2f51d563 d09ee&Search=novolog&x=0&y=0. The only problem with insulin and T2s is the presence of IR. I have great difficulty in determining the right amount of novolog for a given meal condition. Excess insulin can make you fat. Be careful to monitor your weight closely when using insulin - long term or short term. _____________________________________________ http://www.healthdiabeticsoftware.com/ Free > Hey > [quoted text clipped - 13 lines] > So, Is there a reason that docs don't put T2s on insulin instead of meds? I > here it is cheaper and sound like it works better. That decision is based on individual circumstances. Taking insulin requires a commitment and change in lifestyle that is rather drastic for those who do not need it, such as me. I respond quite well to 500MG of Metformin each morning and other 500MG at night. I am no expert, but taking insulin shots seems to me to be a step that should be taken only if other steps do not help to bring your blood glucose levels into control. |
Reply to this Message |
 Sign In
 Join
 My Latest Posts My Monitored Threads My Blog My Photo Gallery My Profile My Homepage Start New Thread Enable EMail Alerts Rate this Thread
|
©2009 Advenet LLC Privacy Policy - Terms of Use
This website includes both content owned or controlled by Advenet as well as content owned or controlled by third parties.