Here's a piece of very important information that doctors rarely give people with Type 2 diabetes which can make a huge difference in the success you have controlling your blood sugar.
If you are not injecting insulin or taking a sulfonylurea drug you do NOT have to worry about hypos!
The word "hypo" is short for "hypoglycemia", which in tern is mangled medical-Greek for "low sugar". A true hypo is an emergency when it strikes someone who is injecting insulin or using a sulfonylurea drug because too much insulin, whether injected or provoked by a drug that overstimulates your beta cell, can make your blood sugar drop so low that your brain cannot function.
But if you are not using insulin or insulin stimulating drugs, you are not at risk for dangerous hypos. Neither Metformin, Byetta, Januvia, Precose, Avandia nor Actos provoke hypos nor can you experience a true hypo if you cut way back on your carbs. What you are likely to encounter if you use these drugs or carb restriction to bring your blood sugar down to normal levels, is a "false hypo."
The false hypo is the feeling of being hypo, which, while it is uncomfortable, is not a crisis, and is, in fact, a well-understood phenomenon that can happen if your fasting blood sugar has been more than 20 mg/dl over true normal levels for any period of time.
To understand the difference between a real hypo and a false hypo, you need to understand that a truly normal fasting blood sugar may range from 70 mg/dl (3.9 mmol/L) up to the low 90s (5 mmol/L). In fact, doctors recommend that pregnant women keep their blood sugars between 60 mg/dl (3.3 mmol/) and 90 (5 mmol/L) mg/dl and consider any blood sugar over 95 mg/dl (5.3 mmol/L) dangerous to the baby.
Clearly, then, a blood sugar in the 60-70 range is not a life-threatening emergency!
Hypos do become dangerous when blood sugar starts to drop into the 40s or lower and if your blood sugar drops into the 20s for any extended period of time you can become unconscious. This kind of hypo can be a huge problem for people who inject too much insulin or take too much of an insulin-stimulating drug, but the only time it will happen to anyone else is if they have a very rare kind of tumor that causes uncontrolled insulin secretion.
The reason people not on insulin don't have to fear real hypos is that your body has an exquisitely sensitive feedback system whose job is to push blood sugar back up as soon as it senses that the blood sugar has dropped to more than 20 or 30 mg/dl (1.7-2.2 mmol/L) below your usual fasting blood sugar level. When this happens, this system kicks in with dramatic effect.
It does this by secreting "counter-regulatory hormones" which are your old friends the stress hormones. One good burst of counter-regulatory hormone and your blood sugar will surge back into the safe zone. Unfortunately, the burst of counter-regulatory hormone may also get your pulse pounding, your sweat pouring, and your body feeling as if you'd just narrowly escaped becoming a predator's lunch.
What makes the counter-regulatory response so hard to deal with for Type 2s--and what adds to the confusion about the danger of hypos--is that the body does not have a set, absolute threshold for responding to perceived hypos. It does not say to itself, "Uh-oh, blood sugar approaching 55, time to do Hypo Repair!".
Instead, it uses a relative threshold based on the fasting blood sugar level it is used to. If you've been running a fasting blood sugar of 180 mg/dl (10 mmol/L) for a while, and cut back on your carbs for a few days, when your blood sugar drifts down to 120 mg/dl (6.7 mmol/L), your body may scream, "Blood sugar 60 mg/dl below normal! Hypo! Hypo!" even though your blood sugar is now, for the first time in months, barely approaching a normal level.
When your heart is pounding and you are feeling shaky and faint, it is very tough to do nothing, especially since your body is helpfully suggesting that all would be well if you'd just scarf down some nice, high carb food to "fix" the problem.
It is not unusual to experience the symptoms of a false hypo, rush to your blood sugar meter, test, and discover that your blood sugar is actually higher than your usual fasting level.
The reason this happens is that by the time you feel the impact of those stress hormones, they have already signaled your liver that it needs to dump a load of glucose into your blood stream to raise your blood sugar to correct the false hypo. And when this happens, you may find you are even more insulin resistant than usual for the next couple hours--to say nothing of feeling very jangled!
This response can be a major barrier on the road to achieving normal blood sugars. If you aren't prepared for it, you may end up sabotaging yourself by reacting to the symptoms of a false hypo by gobbling carbs in the belief that you are fighting a life threatening hypo.
The only way to cure his problem is to know that the body resets its glucose "thermostat" over time and that if you don't treat a false hypo as if it were an emergency your body will eventually get used to a new, lower, fasting blood sugar and only give hypo signals when you are truly hypo--which if you are a Type 2 not using insulin or insulin-provoking medications will be never.
It may take a few weeks for this to happen, and it may happen even if your fasting blood sugar was not all that high. I was experiencing overwhelming "hypo" symptoms when I dropped my fasting blood sugar dropped from about the 110 mg/dl it had been permanently set to for many years to 85 mg/dl. The symptoms were so disturbing, I went to see a doctor who instead of explaining that my "hypos" were normal, took me off the drug that was "causing" the hypos!
I have heard from many people who have had similar experiences, including a few who visited nutritionists who warned them that blood sugars under 100 mg/dl (5.6 mg/dl) were "dangerous" and urged them to drink orange juice to bring up that "dangerous" blood sugar level, stat!
If you've been the victim of such advice, it helps to understand that the nutritionist or nurse who gave this poor advice it to you does not understand that the guidelines they were taught apply ONLY to people injecting insulin or overstimulating their beta cells.
A blood sugar of 100 mg/dl is only an "emergency" if you have injected or stimulated far too much insulin and that 100 mg/dl might be an early stop on the way to a blood sugar of 25!
But if you are controlling with diet or safe drugs, when you feel "hypo", grab your blood sugar meter and test your blood sugar. Unless you see a blood sugar level under 70 mg/dl, you need do nothing. If you feel like you need to do something to deal with the unpleasant symptoms you may experience when your blood sugar drops below 80 mg/dl, please visit Treating Mild Hypos without Creating Rebound High Blood Sugar.
Eventually, when your fasting blood sugar arrives at a normal level, you'll find you feel far better than you did in the past when it was high, and the only "problem" you may then encounter is that the very high blood sugar levels you got used to in the past may now start to feel horribly toxic, which is good, because that unpleasant feeling will help motivate you to keep yourself from experiencing those damaging highs.
Thursday, July 26, 2007
Friday, July 20, 2007
Blog helps you keep up with "What They Don't Tell You About Diabetes"
I have had quite a few people ask me to let them know when I update my main site, What They Don't Tell You About Diabetes.
Well, I update it a lot as there is a continual flow of interesting research pertinent to the topics I discuss on the site. So to help you find out what's new, I've put together a new blog, Updates to What they Don't Tell You About Diabetes where I track all significant changes.
In the 9 days since I started this new blog, I've made 6 additions, including a new page. Until I wrote it all down, even I didn't realize how much work I put into this site.
Well, I update it a lot as there is a continual flow of interesting research pertinent to the topics I discuss on the site. So to help you find out what's new, I've put together a new blog, Updates to What they Don't Tell You About Diabetes where I track all significant changes.
In the 9 days since I started this new blog, I've made 6 additions, including a new page. Until I wrote it all down, even I didn't realize how much work I put into this site.
Thursday, July 19, 2007
How Januvia Works
This blog has been getting heavy traffic from people searching for information about Januvia, and I'm also getting a lot of mail on the topic.
Much of it shows that doctors do not understand the way that this new incretin drug works to lower blood sugar and are therefore prescribing it inappropriately. As a result, a lot of people who are taking Januvia report seeing very high blood sugars. Let's look at why this might be and what it tells them about their true medication needs.
The main way that Januvia lowers blood sugar is by raising the level of a substance, GLP-1, which is produced in the gut and has the ability to do several things.
1. GLP-1 stimulates the beta cell to secrete insulin in a manner very similar to that of the sulfonylurea drugs like Amaryl and Glipizide (sulfs). What is different about using Januvia to do this, is that GLP-1 only causes your beta cells to secrete insulin when blood sugar rises to a certain level (for me, it was 120 mg/dl). Thus with GLP-1 stimulation you don't have the problem you have with sulf drugs of insulin being produced all the time, even when there is no glucose coming into the blood stream, and so Januvia does not cause hypos as sulf drugs do.
2. GLP-1 also affects the speed of stomach emptying. This is why larger doses of artificial GLP-1, Byetta, causes vomiting and very slow stomach emptying. The levels of GLP-1 Januvia causes are much lower than those you get with Byetta, so the digestive symptoms are milder, but they are most definitely there.
If you already have digestive problems or slow stomach emptying, Januvia may make them worse. I found the stomach symptoms didn't really kick in until my third month on Januvia, but then it seemed like my whole digestive system pretty much ground to a halt.
3. GLP-1 also affects hunger in the brain. There are GLP-1 receptors in the brain and one of the things they do is down-regulate hunger. So if you end up with a lot of GLP-1 in your system, you may end up with a near-anorexic attitude towards food. Again, I developed this the third month I was on Januvia when I found myself not wanting to eat.
Januvia does NOT create GLP-1. What it does is keep the body from destroying the GLP-1 your body makes on its own by inhibiting an enzyme called DPP-4 whose job, in the gut, is to chop up DPP-4. Januvia will only raise GLP-1 if your body can make GLP-1. Many people with diabetes do not apparently make much of it anymore.
Even more importantly, GLP-1 controls blood sugar by stimulating the beta cells to secrete using a mechanism very similar to Sulf drugs. If you are no longer responding to high doses of a drug like Amaryl or Glipizide it is very unlikely you will have any response to Januvia, because when active, it is doing the same thing these drugs do, but less strongly.
By the same token if Byetta has not given you normal blood sugars, adding Januvia isn't likely to help that much. A shot of Byetta is a very large dose of a GLP-1 analog. If that isn't stimulating insulin production, Januvia isn't likely to help. In theory it would keep that injected GLP-1 active longer, but since Byetta is active for 2 hours already, and you inject it at meal time, if it isn't lowering blood sugar by 2 hours, keeping it around more isn't likely to do much.
I had a very good response to Januvia's stimulation of my beta cells, because I have an oddball form of diabetes that is known to be exquisitely sensitive to stimulation by sulfs. A tiny dose, of Amaryl, caused me to hypo. But most people with Type 2 diabetes are not very sensitive to sulfs. The typical dose they take may be 50 times higher than what I was taking. Even with these much larger doses their blood sugars are much higher than normal. So because they do not respond well to strong beta cell stimulation their response to Januvia will probably be much weaker.
If your beta cells are dead or are no longer secreting insulin in response to Amaryl or Glipizide they will not be able to respond to GLP-1.
I cannot tell you how many people have written to me that their doctors prescribed Januvia along with the sulf drug they were taking even though it had stopped working very well.
Januvia is, not surprisingly, doing nothing for them. This is as you'd expect it to be. If the sulf isn't stimulating insulin secretion, Januvia won't either because GLP-1 stimulates the SAME part of the beta cell.
Paying $6 a pill for a drug that is not going to be able to do anything for you is just plain stupid. Doctors who prescribe Januvia along with Sulfs clearly have not read up on how the drug works.
Doctors are telling many patients, based on claims made by the drug reps and NOT published in any of the legally required documents which receive FDA scrutiny, that they should keep taking Januvia because it will "regenerate" their beta cells.
The lab research this is based on is rodent research where rodents who took various incretin drugs ended up with more beta cell mass--though not anything near normal beta cell mass.
But applying some critical thinking to the few studies that hint at this, it is important to realize that what the research may really show is that when the drug does restore normal blood sugar levels as it does in people with relatively mild diabetes, beta cells stop dying from being poisoned by the very high blood sugars. That this can happen has been proven by a lot of research. Prolonged exposure to blood sugars over 150 mg/dl appear to kill beta cells. So lowering the blood sugar can indeed preserve beta cells from destruction and perhaps help some of them reproduce.
This means, however, that if your blood sugars are over 160 mg/dl all the time while you take Januvia or Beytta, you are still exposing your beta cells to the poisoning effect of high blood sugar and they are not likely to regenerate.
If you are taking Januvia and not seeing the dramatic lowering of blood sugar which some people see, or not seeing any lowering at all, you should not keep taking it in the hope it will rejuvenate your beta cells. The high blood sugars you are maintaining are guaranteed to kill more of them, to say nothing of what those high blood sugars are doing to your retinas, nerves, and kidneys.
Inhibiting DPP-4 affects many other functions this enzyme performs around the body. (Note: In research studies, DPP-4 is also referred to as "CD26")
Among those are:
1. Regulation of the Immune System. DPP-4 inhibition has shown some ability in early studies to turn down autoimmune responses, which would be good news for people with autoimmune diseases like Rheumatoid Arthritis and Multiple Sclerosis, and early research shows it may end up being useful for these conditions.
NOTE: While I had read about DPP-4 inhibitors being used to treat RA and MS, I just stumbled upon a study that found that the LOWER the DPP-4 level the greater the inflammation in Rheumatoid Arthritis in both mouse and human models. Here's the reference:
Circulating CD26 is Negatively Associated with Inflammation in Human and Experimental Arthritis
However, if you do not have an overactive autoimmune system, inhibiting DPP-4 may still lower your immune response. This may not be a good thing if you need to fight infection. Pfizer notes in the required label information that Januvia raises one kind of white blood cell, but comments only that the significance of this is "insignificant." I had my blood tested before and after taking Januvia for 3 months, and sure enough, it had raised just that part of my white blood count.
2. Headache and sinus problems are an early side effect with Januvia that the company also mentions. It is not known what causes them. The increasingly frequent sinus headaches that would not quit all day long were one reason I stopped taking Januvia. It is possible that some inflammatory change in the sinus is at fault.
If you have a non-autoimmune problem with your immune system, be very cautious with Januvia, because it's effect in down-regulating the immune system is not understood and many doctors are blissfully unaware of it, mostly because the articles that discuss this and other effects of incretin drugs, like raising blood pressure, are only available in full to subscribers to the expensive journals that publish them.
3. Mood. Some studies of people undergoing treatment for cancer that raised DPP-4 found that high DPP-4 caused massive depression. Lowering DPP-4 may therefore improve mood.
4. Fighting Cancerous Cells. Raising DPP-4 with radical cutting edge treatments that affect interleukins appear to be effective in several cancers. Suppressing IL-1 to treat rheumatoid arthritis with the drug Anakinra has been shown in one study to raise the incidence of melanoma. I have written at length elsewhere in this blog why I am concerned that inhibiting DPP-4 may be dangerous for people who are melanoma survivors. While not causing melanoma, DPP-4 inhibition may handcuff the mechanism the immune system uses to get rid of metatastic cells once they appear. Prostate cancer is another form of cancer where DPP-4 seems implicated in the body's natural defenses.
The acceptance testing for drugs involves tests that look at whether they cause cancerous changes in cells in the test tube. They also look at whether the drugs cause cancer in rodents, but it's worth remembering rodents live short lives.
What the testing does not look at is whether a drug might cause cancer by crippling the mechanism that the body uses to fight cancer. Since this may be what Januvia does, it has not been looked at.
Melanoma may take much longer to develop than the lifespan of a rodent. My lesion took more than 6 years to become bad enough that a doctor noticed it and demanded a biopsy. It was present 6 years earlier but a skin doctor had dismissed it as normal pigmentation. On biopsy, it was melanoma. Therefore, I know that a 2 year trial is not long enough to show the impact of this drug on melanoma. Because DPP-4 inhibition has been linked with the progress of melanoma this is a very serious issue that has gone unexamined.
And it is worth noting that high levels of Januvia did cause tumors in rodents. The Prescribing Information states: "There was an increased incidence of combined liver adenoma/carcinoma in males and females and of liver carcinoma in females at 500 mg/kg. This dose results in exposures approximately 60 times the human exposure at the maximum recommended daily."
I do not know whether rodents get melanoma. Since they are completely covered with fur they do not get the dose of damaging radiation that we hairless monkeys get.
Even more important, the impact of suppressing DPP-4 on all the many other functions of this enzyme throughout the body and brain are not at all understood and may involve breakdowns of the immune system that could be dangerous. If you are a melanoma survivor, as I am, and may still have melanoma cells in your body, you should not take this drug until its effect on the immune system is better understood. The same may be true for Prostate cancer.
It's up to you if you want to try it. For some people with early Type 2 diabetes it's effects on blood sugar are dramatic, though if you are like me, the side effects may eventually outweigh the benefits of better blood sugar control.
But don't expect it to work well if you are not doing well on Byetta or Sulfonylurea drugs because it is uses a much weaker form of the same mechanism these drugs use.
If your beta cells are dead and your blood sugar does not come down to normal levels with Januvia or Byetta, it is time to move on to the one drug that, dosed correctly, always works. Insulin.
More about Januvia with scholarly citations is on this page on my Main Diabetes Web Site: http://www.phlaunt.com/diabetes/15332388.php Byetta and Januvia.
Much of it shows that doctors do not understand the way that this new incretin drug works to lower blood sugar and are therefore prescribing it inappropriately. As a result, a lot of people who are taking Januvia report seeing very high blood sugars. Let's look at why this might be and what it tells them about their true medication needs.
The main way that Januvia lowers blood sugar is by raising the level of a substance, GLP-1, which is produced in the gut and has the ability to do several things.
1. GLP-1 stimulates the beta cell to secrete insulin in a manner very similar to that of the sulfonylurea drugs like Amaryl and Glipizide (sulfs). What is different about using Januvia to do this, is that GLP-1 only causes your beta cells to secrete insulin when blood sugar rises to a certain level (for me, it was 120 mg/dl). Thus with GLP-1 stimulation you don't have the problem you have with sulf drugs of insulin being produced all the time, even when there is no glucose coming into the blood stream, and so Januvia does not cause hypos as sulf drugs do.
2. GLP-1 also affects the speed of stomach emptying. This is why larger doses of artificial GLP-1, Byetta, causes vomiting and very slow stomach emptying. The levels of GLP-1 Januvia causes are much lower than those you get with Byetta, so the digestive symptoms are milder, but they are most definitely there.
If you already have digestive problems or slow stomach emptying, Januvia may make them worse. I found the stomach symptoms didn't really kick in until my third month on Januvia, but then it seemed like my whole digestive system pretty much ground to a halt.
3. GLP-1 also affects hunger in the brain. There are GLP-1 receptors in the brain and one of the things they do is down-regulate hunger. So if you end up with a lot of GLP-1 in your system, you may end up with a near-anorexic attitude towards food. Again, I developed this the third month I was on Januvia when I found myself not wanting to eat.
Januvia does NOT create GLP-1. What it does is keep the body from destroying the GLP-1 your body makes on its own by inhibiting an enzyme called DPP-4 whose job, in the gut, is to chop up DPP-4. Januvia will only raise GLP-1 if your body can make GLP-1. Many people with diabetes do not apparently make much of it anymore.
Even more importantly, GLP-1 controls blood sugar by stimulating the beta cells to secrete using a mechanism very similar to Sulf drugs. If you are no longer responding to high doses of a drug like Amaryl or Glipizide it is very unlikely you will have any response to Januvia, because when active, it is doing the same thing these drugs do, but less strongly.
By the same token if Byetta has not given you normal blood sugars, adding Januvia isn't likely to help that much. A shot of Byetta is a very large dose of a GLP-1 analog. If that isn't stimulating insulin production, Januvia isn't likely to help. In theory it would keep that injected GLP-1 active longer, but since Byetta is active for 2 hours already, and you inject it at meal time, if it isn't lowering blood sugar by 2 hours, keeping it around more isn't likely to do much.
I had a very good response to Januvia's stimulation of my beta cells, because I have an oddball form of diabetes that is known to be exquisitely sensitive to stimulation by sulfs. A tiny dose, of Amaryl, caused me to hypo. But most people with Type 2 diabetes are not very sensitive to sulfs. The typical dose they take may be 50 times higher than what I was taking. Even with these much larger doses their blood sugars are much higher than normal. So because they do not respond well to strong beta cell stimulation their response to Januvia will probably be much weaker.
If Sulf Drugs Arnen't Normalizing Your Blood Sugar Januvia Won't Either
If your beta cells are dead or are no longer secreting insulin in response to Amaryl or Glipizide they will not be able to respond to GLP-1.
I cannot tell you how many people have written to me that their doctors prescribed Januvia along with the sulf drug they were taking even though it had stopped working very well.
Januvia is, not surprisingly, doing nothing for them. This is as you'd expect it to be. If the sulf isn't stimulating insulin secretion, Januvia won't either because GLP-1 stimulates the SAME part of the beta cell.
Paying $6 a pill for a drug that is not going to be able to do anything for you is just plain stupid. Doctors who prescribe Januvia along with Sulfs clearly have not read up on how the drug works.
The Dream of Beta Cell Regeneration
Doctors are telling many patients, based on claims made by the drug reps and NOT published in any of the legally required documents which receive FDA scrutiny, that they should keep taking Januvia because it will "regenerate" their beta cells.
The lab research this is based on is rodent research where rodents who took various incretin drugs ended up with more beta cell mass--though not anything near normal beta cell mass.
But applying some critical thinking to the few studies that hint at this, it is important to realize that what the research may really show is that when the drug does restore normal blood sugar levels as it does in people with relatively mild diabetes, beta cells stop dying from being poisoned by the very high blood sugars. That this can happen has been proven by a lot of research. Prolonged exposure to blood sugars over 150 mg/dl appear to kill beta cells. So lowering the blood sugar can indeed preserve beta cells from destruction and perhaps help some of them reproduce.
This means, however, that if your blood sugars are over 160 mg/dl all the time while you take Januvia or Beytta, you are still exposing your beta cells to the poisoning effect of high blood sugar and they are not likely to regenerate.
If you are taking Januvia and not seeing the dramatic lowering of blood sugar which some people see, or not seeing any lowering at all, you should not keep taking it in the hope it will rejuvenate your beta cells. The high blood sugars you are maintaining are guaranteed to kill more of them, to say nothing of what those high blood sugars are doing to your retinas, nerves, and kidneys.
Other Known Effects of Januvia
Inhibiting DPP-4 affects many other functions this enzyme performs around the body. (Note: In research studies, DPP-4 is also referred to as "CD26")
Among those are:
1. Regulation of the Immune System. DPP-4 inhibition has shown some ability in early studies to turn down autoimmune responses, which would be good news for people with autoimmune diseases like Rheumatoid Arthritis and Multiple Sclerosis, and early research shows it may end up being useful for these conditions.
NOTE: While I had read about DPP-4 inhibitors being used to treat RA and MS, I just stumbled upon a study that found that the LOWER the DPP-4 level the greater the inflammation in Rheumatoid Arthritis in both mouse and human models. Here's the reference:
Circulating CD26 is Negatively Associated with Inflammation in Human and Experimental Arthritis
However, if you do not have an overactive autoimmune system, inhibiting DPP-4 may still lower your immune response. This may not be a good thing if you need to fight infection. Pfizer notes in the required label information that Januvia raises one kind of white blood cell, but comments only that the significance of this is "insignificant." I had my blood tested before and after taking Januvia for 3 months, and sure enough, it had raised just that part of my white blood count.
2. Headache and sinus problems are an early side effect with Januvia that the company also mentions. It is not known what causes them. The increasingly frequent sinus headaches that would not quit all day long were one reason I stopped taking Januvia. It is possible that some inflammatory change in the sinus is at fault.
If you have a non-autoimmune problem with your immune system, be very cautious with Januvia, because it's effect in down-regulating the immune system is not understood and many doctors are blissfully unaware of it, mostly because the articles that discuss this and other effects of incretin drugs, like raising blood pressure, are only available in full to subscribers to the expensive journals that publish them.
3. Mood. Some studies of people undergoing treatment for cancer that raised DPP-4 found that high DPP-4 caused massive depression. Lowering DPP-4 may therefore improve mood.
4. Fighting Cancerous Cells. Raising DPP-4 with radical cutting edge treatments that affect interleukins appear to be effective in several cancers. Suppressing IL-1 to treat rheumatoid arthritis with the drug Anakinra has been shown in one study to raise the incidence of melanoma. I have written at length elsewhere in this blog why I am concerned that inhibiting DPP-4 may be dangerous for people who are melanoma survivors. While not causing melanoma, DPP-4 inhibition may handcuff the mechanism the immune system uses to get rid of metatastic cells once they appear. Prostate cancer is another form of cancer where DPP-4 seems implicated in the body's natural defenses.
The acceptance testing for drugs involves tests that look at whether they cause cancerous changes in cells in the test tube. They also look at whether the drugs cause cancer in rodents, but it's worth remembering rodents live short lives.
What the testing does not look at is whether a drug might cause cancer by crippling the mechanism that the body uses to fight cancer. Since this may be what Januvia does, it has not been looked at.
Melanoma may take much longer to develop than the lifespan of a rodent. My lesion took more than 6 years to become bad enough that a doctor noticed it and demanded a biopsy. It was present 6 years earlier but a skin doctor had dismissed it as normal pigmentation. On biopsy, it was melanoma. Therefore, I know that a 2 year trial is not long enough to show the impact of this drug on melanoma. Because DPP-4 inhibition has been linked with the progress of melanoma this is a very serious issue that has gone unexamined.
And it is worth noting that high levels of Januvia did cause tumors in rodents. The Prescribing Information states: "There was an increased incidence of combined liver adenoma/carcinoma in males and females and of liver carcinoma in females at 500 mg/kg. This dose results in exposures approximately 60 times the human exposure at the maximum recommended daily."
I do not know whether rodents get melanoma. Since they are completely covered with fur they do not get the dose of damaging radiation that we hairless monkeys get.
Bottom Line: Januvia works best in people with VERY early diabetes or genetic forms of diabetes that are hyper sensitive to sulfonylurea drugs.
Even more important, the impact of suppressing DPP-4 on all the many other functions of this enzyme throughout the body and brain are not at all understood and may involve breakdowns of the immune system that could be dangerous. If you are a melanoma survivor, as I am, and may still have melanoma cells in your body, you should not take this drug until its effect on the immune system is better understood. The same may be true for Prostate cancer.
It's up to you if you want to try it. For some people with early Type 2 diabetes it's effects on blood sugar are dramatic, though if you are like me, the side effects may eventually outweigh the benefits of better blood sugar control.
But don't expect it to work well if you are not doing well on Byetta or Sulfonylurea drugs because it is uses a much weaker form of the same mechanism these drugs use.
If your Beta Cells ARE Dead
If your beta cells are dead and your blood sugar does not come down to normal levels with Januvia or Byetta, it is time to move on to the one drug that, dosed correctly, always works. Insulin.
More about Januvia with scholarly citations is on this page on my Main Diabetes Web Site: http://www.phlaunt.com/diabetes/15332388.php Byetta and Januvia.
Wednesday, July 18, 2007
Type 1 perceptions of Type 2s -- Type 2s Have it Easy?
An anonymous person posted a comment on the previous entry, explaining that one reason Type 1s have the feelings they do about Type 2s is the perception that they have a much easier time with control and could, if they wanted, control their blood sugars with diet and exercise, but that instead they merely rely on pills which don't work.
This really intrigued me, because the perception of a lot of educated Type 2s is that Type 1s have the advantage in that they get treated by specialists, where most Type 2s are treated by family doctors, and are given a drug that works--insulin, while Type 2s get nasty oral pills that don't.
Type 1s get educated about the impact of carbohydrate on blood sugar. If you are a Type 1 it may come as a shock to you that most Type 2s are NEVER told that carbohydrates raise blood sugar. In fact, quite a few are under the impression that FAT is what raises blood sugar, because the only nutritional message their doctors gave them was that it was important to eat a very low fat diet!
This isn't hearsay. I've heard it from the mouths of otherwise educated Type 2s.
I certainly found I got MUCH better treatment once my family doctor realized I wasn't a Type 2. Until then, he handed my diabetes "education" to a Nurse Ratched who taught me to roll the vial of Lantus (showing she didn't understand that it wasn't NPH), who prescribed a 1 inch needle and turned out not to know that shorter needles were available, and who would have, if I hadn't stopped her, injected me with what turned out to be 3 times the dose of Lantus that was right for me at 2PM when I had a long drive home ahead of me!
Nurse Ratched also did not recognize the symptoms of hypo when I called in with them--waking at 3AM sweating and with pounding pulse--and ended up referring me to a cardiologist for what she was sure was a heart condition!
THAT is the kind of treatment Type 2s get. And my family doctor, I have to say, is considered the be the best in our region and I have found him to be very good at treating every other condition I've shown up with, except diabetes.
The other thing that Type 1s may not understand about Type 2s, is that because of the way Type 2 is diagnosed, many Type 2s--especially women, fasting blood sugar stays near normal long after their post meal blood sugars are in the mid 200s. So they don't get diagnosed until they've had diabetes for a decade.
That is why fully half of Type 2s start treatment with significant neuropathy, and many at diagnosis also have protein in the urine, early retinal changes, and most significantly, 50-80% of their beta cells dead from years of exposure to very high blood sugars. When that many beta cells are gone, the problem is no longer insulin resistance--which can be modified by exercise in many people. It is insulin deficiency, which cannot be reversed by diet or exercise.
But there's more. Another thing Type 1s need to understand about Type 2s is that most of their doctors don't give them any sense of urgency about their care. As a Type 1, you have heard all your life about the bad things that will happen to you if you don't keep your blood sugar under control. You see the doctor every couple months and you are exhorted to get better control.
What a shock, then, to learn that the typical Type 2, treated by a family doctor, may be seen once a year, and is likely to get a pat on the head about their "good control" when they have an A1c of 8%. And no further treatment at all!
In fact, a recent medical journal report found that most family doctors won't even put a Type 2 patient on an oral diabetes drug until they have had an A1c of 8% for over a year.
Family doctors often believe that insulin is bad for Type 2s, so they are rarely put on any kind of insulin until their A1c have been way over 10% for a few years. Then they are only given Lantus, which doesn't affect their post-meal blood sugars. Because family doctors are nervous about prescribing meal time insulin and don't have the time to work out dosing with their patients, the typical Type 2 "on insulin" (Lantus or NPH) tests their blood sugar once or twice a week--fasting--and still has an A1c well over 7%. Type 2s rarely, if ever, are sent to Diabetes Educators to learn how to use insulin.
I know one woman who has had Type 2 diabetes for 12 years who is on Lantus who has never been instructed to test her blood sugar after eating and has, in fact, never done so. As long as her fasting blood sugar is around 125, her doctor tells her she is "fine." She likes being fine, so she is very resistant to any suggestion that maybe it would be a good idea to see what that whole wheat bread and pasta with the sugary low fat sauce is doing to her blood sugar.
The most recent NHANES survey, a huge U.S. government funded epidemiological survey which looks at the health of the population every so often, found that the average Type 2 in the U.S. has an A1c of 10% which is far higher than the average was a decade ago.
The reason appears to be that with the heavy promotion of new oral drugs by drug companies, doctors were delaying putting patients on insulin for many more years than they used to. Instead of prescribing insulin to their Type 2s with A1cs as high as 13%, they just keep prescribing oral drugs and the patients' blood sugars keep going up.
So the Type 2s you meet who seem so oblivious may simply be responding to their doctors telling them they are "Fine" when they aren't. The chances are that their doctors tell them that insulin is bad for type 2s and that oral drugs will regenerate their beta cells (which they won't) and that they need to eat a lot of pasta, bananas, and oatmeal to stay healthy.
They may have gone to the gym for a few months and seen no decline in their blood sugars or weight, and concluded that exercise doesn't work--which, if you live on the nutritionist recommended "diet" of bananas, oatmeal and pasta, without any injected insulin to balance them, is quite likely.
In short, none of us has it easy!
This really intrigued me, because the perception of a lot of educated Type 2s is that Type 1s have the advantage in that they get treated by specialists, where most Type 2s are treated by family doctors, and are given a drug that works--insulin, while Type 2s get nasty oral pills that don't.
Type 1s get educated about the impact of carbohydrate on blood sugar. If you are a Type 1 it may come as a shock to you that most Type 2s are NEVER told that carbohydrates raise blood sugar. In fact, quite a few are under the impression that FAT is what raises blood sugar, because the only nutritional message their doctors gave them was that it was important to eat a very low fat diet!
This isn't hearsay. I've heard it from the mouths of otherwise educated Type 2s.
I certainly found I got MUCH better treatment once my family doctor realized I wasn't a Type 2. Until then, he handed my diabetes "education" to a Nurse Ratched who taught me to roll the vial of Lantus (showing she didn't understand that it wasn't NPH), who prescribed a 1 inch needle and turned out not to know that shorter needles were available, and who would have, if I hadn't stopped her, injected me with what turned out to be 3 times the dose of Lantus that was right for me at 2PM when I had a long drive home ahead of me!
Nurse Ratched also did not recognize the symptoms of hypo when I called in with them--waking at 3AM sweating and with pounding pulse--and ended up referring me to a cardiologist for what she was sure was a heart condition!
THAT is the kind of treatment Type 2s get. And my family doctor, I have to say, is considered the be the best in our region and I have found him to be very good at treating every other condition I've shown up with, except diabetes.
The other thing that Type 1s may not understand about Type 2s, is that because of the way Type 2 is diagnosed, many Type 2s--especially women, fasting blood sugar stays near normal long after their post meal blood sugars are in the mid 200s. So they don't get diagnosed until they've had diabetes for a decade.
That is why fully half of Type 2s start treatment with significant neuropathy, and many at diagnosis also have protein in the urine, early retinal changes, and most significantly, 50-80% of their beta cells dead from years of exposure to very high blood sugars. When that many beta cells are gone, the problem is no longer insulin resistance--which can be modified by exercise in many people. It is insulin deficiency, which cannot be reversed by diet or exercise.
But there's more. Another thing Type 1s need to understand about Type 2s is that most of their doctors don't give them any sense of urgency about their care. As a Type 1, you have heard all your life about the bad things that will happen to you if you don't keep your blood sugar under control. You see the doctor every couple months and you are exhorted to get better control.
What a shock, then, to learn that the typical Type 2, treated by a family doctor, may be seen once a year, and is likely to get a pat on the head about their "good control" when they have an A1c of 8%. And no further treatment at all!
In fact, a recent medical journal report found that most family doctors won't even put a Type 2 patient on an oral diabetes drug until they have had an A1c of 8% for over a year.
Family doctors often believe that insulin is bad for Type 2s, so they are rarely put on any kind of insulin until their A1c have been way over 10% for a few years. Then they are only given Lantus, which doesn't affect their post-meal blood sugars. Because family doctors are nervous about prescribing meal time insulin and don't have the time to work out dosing with their patients, the typical Type 2 "on insulin" (Lantus or NPH) tests their blood sugar once or twice a week--fasting--and still has an A1c well over 7%. Type 2s rarely, if ever, are sent to Diabetes Educators to learn how to use insulin.
I know one woman who has had Type 2 diabetes for 12 years who is on Lantus who has never been instructed to test her blood sugar after eating and has, in fact, never done so. As long as her fasting blood sugar is around 125, her doctor tells her she is "fine." She likes being fine, so she is very resistant to any suggestion that maybe it would be a good idea to see what that whole wheat bread and pasta with the sugary low fat sauce is doing to her blood sugar.
The most recent NHANES survey, a huge U.S. government funded epidemiological survey which looks at the health of the population every so often, found that the average Type 2 in the U.S. has an A1c of 10% which is far higher than the average was a decade ago.
The reason appears to be that with the heavy promotion of new oral drugs by drug companies, doctors were delaying putting patients on insulin for many more years than they used to. Instead of prescribing insulin to their Type 2s with A1cs as high as 13%, they just keep prescribing oral drugs and the patients' blood sugars keep going up.
So the Type 2s you meet who seem so oblivious may simply be responding to their doctors telling them they are "Fine" when they aren't. The chances are that their doctors tell them that insulin is bad for type 2s and that oral drugs will regenerate their beta cells (which they won't) and that they need to eat a lot of pasta, bananas, and oatmeal to stay healthy.
They may have gone to the gym for a few months and seen no decline in their blood sugars or weight, and concluded that exercise doesn't work--which, if you live on the nutritionist recommended "diet" of bananas, oatmeal and pasta, without any injected insulin to balance them, is quite likely.
In short, none of us has it easy!
Tuesday, July 17, 2007
Type 1s Hating Type 2s
This post is about one of the dirty little not-so-secrets of the online diabetes community. Type 1s often complain of how much they hate the way that the general public confuses them--innocent victims of an autoimmune attack--with those disgusting, fat, lazy type 2s who caused their own disease.
But despite what you read in the media, the science is very clear on the fact that most Type 2s did not "cause" their diabetes any more than the Type 1s did. Like Type 1s, Type 2s start out with a genetic make up that predisposes them to develop their form of Diabetes. This genetic make up causes them to develop insulin resistance long before they are overweight, and is instrumental in their subsequent weight gain. It may also result in errors in the way that their mitochondria work--the cell's fat burning organelles--so that their bodies deposit fat rather than burning it as a normal person would.
Studies of thin relatives of people with Type 2 show that they show abnormal insulin response decades before they themselves develop either obesity OR diabetes. Twin studies also show that 80% of identical twins of a Type 2 diabetic ALSO become diabetic while fraternal twins do NOT show this concurrence. This is considered very strong proof of a genetic origin for a disease by the scientific community.
New genes strongly associated with Type 2 diabetes are being identified every year. Most recently, for example, Type 2 diabetes has been strongly associated with defects in PTPN1, found in 20% of white Type 2 diabetics, Calpain-10 in 17% of Mexicans, HNF4-a which raises risk 30% in Finns and is more common in people with Diabetes who are of Ashkenazi Jewish descent, and TCF7L2 which was found to double the risk of developing Type 2 diabetes in an English population.
Another point that gets lost in the simplistic media coverage of Type 2 diabetes, is that while 80% of Type 2s are fat, most obese people do not have diabetes. In fact, two out of three obese people do NOT develop diabetes,
Indeed, here is good reason to believe that many of those people with Type 2 diabetes who are obese are obese because the widely fluctuating blood sugars caused by eating a high carb diet cause intolerable hunger and alterations in the other hormones, besides insulin, that the body uses to maintain weight homeostasis.
The effect that GLP-1 supplementation with Byetta has on the eating patterns some people with diabetes is very telling here, since GLP-1 crosses the blood-brain barrier and impacts on feeding behavior in all kinds of mammals. When we look at intense hunger as a symptom rather than a moral failing, and when we realize that flattening blood sugar swings usually eliminates that hunger, we get a whole new understanding of the relationship of diabetes to weight that has little to do with the "you caused your disease you lazy slob" approach Type 1s buy into when thinking about Type 2s.
Even more relevant to the anger of Type 1s against Type 2s, is the recent research has found that, depending on the study, between 4 and 30% of "Type 2s" in various studies have been found to have GAD antibodies--the same markers of autoimmune attack as Type 1s. The difference appears to be that the autoimmune attack is not as total as that the type 1s experience. This should not be a surprise. Many people with Type 2 also have thyroid disease, which is often due to autoimmune attack.
There's a lot more research along these lines. You can read about some of it, with links to the original research papers at You Did Not Cause Your Diabetes with Reckless Overeating.
Gina Kolata's new book, Rethinking Thin, does a great job of summarizing the research that proves that normal people do not become permanently obese by overeating and that there needs to be an underlying disorder for a person to pack on and retain large amounts of weight.
There's some interesting research floating around that seems to show that the upsurge in autoimmune disorders of all types in children growing up in Western society may be an unintended consequence of our obsession with cleanliness.
This theory argues that children who don't spend hours each day getting filthy outside, where their immune systems meet and conquer a host of microorganisms, are more likely to develop antibodies against their own bodies. A growing immune system that isn't presented with playmates will attack whatever it finds, often the body's own cells or foods--hence the huge growth in food allergies in the young. The growing use of anti-microbial soaps in the home also contributes to this lack of traditional playmates for the developing immune system.
But no one takes this kind of data and uses it to blame the Type 1 or their family for "causing" their disease, because cleanliness is considered a virtue in our society! If it were the other way around, and the kids who were raised in less cleanly homes were more likely to develop Type 1, you would probably see that kind of blame that you see loaded on Type 2s.
The fact is, people love to be able to pin moral blame on those who get a terrible disease, because if we can blame those people for their disease and attribute it to failings we personally don't have, we can feel safe. The alternative is to see innocent people just like us struck down by nasty diseases and feel fear.
But the fact is, the body is an insanely complex mechanism, and we are living in environments that are completely different--biochemically--from those we evolved to fill over many millions of years.
And it is not beyond belief that the many forms of genetic damage that cause Type 2--and the RISE in the incidence of Type 2 Diabetes--may well be a caused by damage to our DNA caused by the chemicals outgassing from the plastics that surround us, from the toxic Teflon that lines our cooking pans, from the petrochemicals we breathe in our air, from the smokestack emissions that contain significant amounts of toxic metals and toxic organic compounds, or even from early life exposure the hormones found in public water supplies, thanks to the huge amount of birth control pills half the population takes, a good amount of which is going down the sewers.
So next time you are tempted to distinguish yourself from those fat slobs with Type 2 diabetes, take a deep breath and use it as a teaching moment. When people with all kinds of diabetes band together, we can make advances for all of us. We can ensure that there is health coverage for all kinds of people with diabetes, no matter where employed, we can get rid of discrimination against people with diabetes, we can do something about the lousy care so many of us receive from doctors who don't keep up with the research, and we can demand that our institutions support the basic research that might free us from the stop gap drugs and devices that are what we have to deal with now.
But despite what you read in the media, the science is very clear on the fact that most Type 2s did not "cause" their diabetes any more than the Type 1s did. Like Type 1s, Type 2s start out with a genetic make up that predisposes them to develop their form of Diabetes. This genetic make up causes them to develop insulin resistance long before they are overweight, and is instrumental in their subsequent weight gain. It may also result in errors in the way that their mitochondria work--the cell's fat burning organelles--so that their bodies deposit fat rather than burning it as a normal person would.
Studies of thin relatives of people with Type 2 show that they show abnormal insulin response decades before they themselves develop either obesity OR diabetes. Twin studies also show that 80% of identical twins of a Type 2 diabetic ALSO become diabetic while fraternal twins do NOT show this concurrence. This is considered very strong proof of a genetic origin for a disease by the scientific community.
New genes strongly associated with Type 2 diabetes are being identified every year. Most recently, for example, Type 2 diabetes has been strongly associated with defects in PTPN1, found in 20% of white Type 2 diabetics, Calpain-10 in 17% of Mexicans, HNF4-a which raises risk 30% in Finns and is more common in people with Diabetes who are of Ashkenazi Jewish descent, and TCF7L2 which was found to double the risk of developing Type 2 diabetes in an English population.
Another point that gets lost in the simplistic media coverage of Type 2 diabetes, is that while 80% of Type 2s are fat, most obese people do not have diabetes. In fact, two out of three obese people do NOT develop diabetes,
Indeed, here is good reason to believe that many of those people with Type 2 diabetes who are obese are obese because the widely fluctuating blood sugars caused by eating a high carb diet cause intolerable hunger and alterations in the other hormones, besides insulin, that the body uses to maintain weight homeostasis.
The effect that GLP-1 supplementation with Byetta has on the eating patterns some people with diabetes is very telling here, since GLP-1 crosses the blood-brain barrier and impacts on feeding behavior in all kinds of mammals. When we look at intense hunger as a symptom rather than a moral failing, and when we realize that flattening blood sugar swings usually eliminates that hunger, we get a whole new understanding of the relationship of diabetes to weight that has little to do with the "you caused your disease you lazy slob" approach Type 1s buy into when thinking about Type 2s.
Even more relevant to the anger of Type 1s against Type 2s, is the recent research has found that, depending on the study, between 4 and 30% of "Type 2s" in various studies have been found to have GAD antibodies--the same markers of autoimmune attack as Type 1s. The difference appears to be that the autoimmune attack is not as total as that the type 1s experience. This should not be a surprise. Many people with Type 2 also have thyroid disease, which is often due to autoimmune attack.
There's a lot more research along these lines. You can read about some of it, with links to the original research papers at You Did Not Cause Your Diabetes with Reckless Overeating.
Gina Kolata's new book, Rethinking Thin, does a great job of summarizing the research that proves that normal people do not become permanently obese by overeating and that there needs to be an underlying disorder for a person to pack on and retain large amounts of weight.
Did Type 1s Cause Their Disease?
There's some interesting research floating around that seems to show that the upsurge in autoimmune disorders of all types in children growing up in Western society may be an unintended consequence of our obsession with cleanliness.
This theory argues that children who don't spend hours each day getting filthy outside, where their immune systems meet and conquer a host of microorganisms, are more likely to develop antibodies against their own bodies. A growing immune system that isn't presented with playmates will attack whatever it finds, often the body's own cells or foods--hence the huge growth in food allergies in the young. The growing use of anti-microbial soaps in the home also contributes to this lack of traditional playmates for the developing immune system.
But no one takes this kind of data and uses it to blame the Type 1 or their family for "causing" their disease, because cleanliness is considered a virtue in our society! If it were the other way around, and the kids who were raised in less cleanly homes were more likely to develop Type 1, you would probably see that kind of blame that you see loaded on Type 2s.
The fact is, people love to be able to pin moral blame on those who get a terrible disease, because if we can blame those people for their disease and attribute it to failings we personally don't have, we can feel safe. The alternative is to see innocent people just like us struck down by nasty diseases and feel fear.
But the fact is, the body is an insanely complex mechanism, and we are living in environments that are completely different--biochemically--from those we evolved to fill over many millions of years.
And it is not beyond belief that the many forms of genetic damage that cause Type 2--and the RISE in the incidence of Type 2 Diabetes--may well be a caused by damage to our DNA caused by the chemicals outgassing from the plastics that surround us, from the toxic Teflon that lines our cooking pans, from the petrochemicals we breathe in our air, from the smokestack emissions that contain significant amounts of toxic metals and toxic organic compounds, or even from early life exposure the hormones found in public water supplies, thanks to the huge amount of birth control pills half the population takes, a good amount of which is going down the sewers.
So next time you are tempted to distinguish yourself from those fat slobs with Type 2 diabetes, take a deep breath and use it as a teaching moment. When people with all kinds of diabetes band together, we can make advances for all of us. We can ensure that there is health coverage for all kinds of people with diabetes, no matter where employed, we can get rid of discrimination against people with diabetes, we can do something about the lousy care so many of us receive from doctors who don't keep up with the research, and we can demand that our institutions support the basic research that might free us from the stop gap drugs and devices that are what we have to deal with now.
Sunday, July 15, 2007
The Wisdom to Know the Difference
Sometimes people ask me why I spend so much time reading, researching, and writing about Diabetes, which is, after all, a disease. I've given this some thought, and come to an interesting realization.
I focus on diabetes because it is the only physical condition I have where it is possible for me to made a difference in my health with what I do.
I was diagnosed with two chronic conditions before diabetes. Both had in common that there was nothing I could do to relieve the symptoms or influence the way that the disorder progressed. I pretty much had to wake up each morning and pray that it was a "good day" instead of a bad one. If it was a bad day, I had to just get through it. If it was a good day, I had to hope the pain and disability would end sooner rather than later. I learned a lot about mental techniques for pain control and about doing what I could with what I have left. But if I wasn't in crisis I did not dwell on these conditions. I did what I could to forget I had them until they worsened again.
So when I finally was diagnosed with diabetes, what a thrill it was to discover that I had finally gotten a diagnosis where I could do something. If my blood sugar was high, I could change what I ate and bring it down. If that didn't work, there were drugs that might help. If they didn't help, there was insulin which, dosed properly, always works.
I did not have to just sit around hoping something bad wouldn't happen. I could keep it from happening!
If you have to have a chronic disorder, what a good one to have!
With my other conditions, if I spent any time reading about them, I'd end up feeling worse. One book even told me that people with one of my conditions frequently committed suicide. When I ventured into online support boards, invariably there would be people posting who were in more pain than I was, or who had had heroic surgeries that didn't work, or who had developed mental illness dealing with intolerable symptoms. I considered joining a support group for one of these other diagnoses years ago but the woman who ran the group scared me so much during our initial phone call when she described how her symptoms had kept her housebound for a decade, that I never went to a meeting.
With diabetes, support groups are full of people who have eliminated symptoms and figured out how to live reasonably normal lives.
With the other conditions, I'd hope some doctor somewhere would come up with some treatment that might work for me. And over the years, I've noticed that the treatments that were prescribed decades ago--including two surgeries I was strongly urged to have, but refused--have been discredited.
With diabetes I learned that doctors were often way behind the patients in understanding what the most recent research was finding about causes and cure. Even better, I learned there that there was even a very powerful treatment--limiting carbs in my diet--that didn't require a doctor's prescription at all.
So over time, I found I was spending a lot of time thinking about diabetes even when it was not dominating my life in other ways. When I do research, instead of finding more cause for dispair, I find more cause for hope. And I love that I can write about something I've experienced or turned up in my research and have perfect strangers write to me that reading what I wrote gave them not only hope, but actual techniques to use that they are finding will work for them.
So far from being a morbid fascination with disease, my time spent on diabetes is time spent on changing one of the very few things that I can. And it definitely takes my mind off the many other things in life I cannot change.
I focus on diabetes because it is the only physical condition I have where it is possible for me to made a difference in my health with what I do.
I was diagnosed with two chronic conditions before diabetes. Both had in common that there was nothing I could do to relieve the symptoms or influence the way that the disorder progressed. I pretty much had to wake up each morning and pray that it was a "good day" instead of a bad one. If it was a bad day, I had to just get through it. If it was a good day, I had to hope the pain and disability would end sooner rather than later. I learned a lot about mental techniques for pain control and about doing what I could with what I have left. But if I wasn't in crisis I did not dwell on these conditions. I did what I could to forget I had them until they worsened again.
So when I finally was diagnosed with diabetes, what a thrill it was to discover that I had finally gotten a diagnosis where I could do something. If my blood sugar was high, I could change what I ate and bring it down. If that didn't work, there were drugs that might help. If they didn't help, there was insulin which, dosed properly, always works.
I did not have to just sit around hoping something bad wouldn't happen. I could keep it from happening!
If you have to have a chronic disorder, what a good one to have!
With my other conditions, if I spent any time reading about them, I'd end up feeling worse. One book even told me that people with one of my conditions frequently committed suicide. When I ventured into online support boards, invariably there would be people posting who were in more pain than I was, or who had had heroic surgeries that didn't work, or who had developed mental illness dealing with intolerable symptoms. I considered joining a support group for one of these other diagnoses years ago but the woman who ran the group scared me so much during our initial phone call when she described how her symptoms had kept her housebound for a decade, that I never went to a meeting.
With diabetes, support groups are full of people who have eliminated symptoms and figured out how to live reasonably normal lives.
With the other conditions, I'd hope some doctor somewhere would come up with some treatment that might work for me. And over the years, I've noticed that the treatments that were prescribed decades ago--including two surgeries I was strongly urged to have, but refused--have been discredited.
With diabetes I learned that doctors were often way behind the patients in understanding what the most recent research was finding about causes and cure. Even better, I learned there that there was even a very powerful treatment--limiting carbs in my diet--that didn't require a doctor's prescription at all.
So over time, I found I was spending a lot of time thinking about diabetes even when it was not dominating my life in other ways. When I do research, instead of finding more cause for dispair, I find more cause for hope. And I love that I can write about something I've experienced or turned up in my research and have perfect strangers write to me that reading what I wrote gave them not only hope, but actual techniques to use that they are finding will work for them.
So far from being a morbid fascination with disease, my time spent on diabetes is time spent on changing one of the very few things that I can. And it definitely takes my mind off the many other things in life I cannot change.
Thursday, July 12, 2007
Taking a Drug Holiday
Every year I go off my metformin for a week or two, usually because my digestive system gets upset enough that it makes sense to cut out a drug notorious for causing stomach issues.
Since I am using insulin at mealtime now, going off metformin does not pose a danger to my health as long as I adjust my insulin dose to match the higher blood sugars I get without metformin in my system.
This past week, off the metformin, has been very interesting. As expected, my digestive system got a lot happier very quickly. No heartburn or weird feelings in the heart region that turn out to be signals from the esophagus or top of the stomach. (If you take Metformin, you probably know what I'm talking about.)
But after stopping, I was surprised at how much more energy I got. I'd been very sleepy in the evenings the last couple months but now, after almost a week without met, I'm bright and alert at 10 PM. My mind feels clearer during the day, too. Interesting!
My insulin needs have gone up, though my carb/insulin ratio is still that of a non-insulin resistant person--1 unit to 11 or 12 grams rather than 1 unit to 15. It took me a few days to adjust my dosage up, very carefully, a half unit at a time. Now I'm using 4.5 or 5 units, instead of 2.5 or 3 per 40-50 gram meal.
I do find it easier to go low with the higher amount of insulin, hence the higher carb intake. I'm not eating those 50 grams all at once, but instead eating a some at 2 or 3 hours to prevent lows. I'm using R, which hits hardest between 2-3 hours. Novolog would require a different approach, but I haven't had the time to work it out.
I'm also hungrier--which is one reason I started taking metformin, because without it I can be hungry and that pushes up my intake and weight. I consider hunger a symptom, not a moral failing, and for years metformin has been helpful in giving me normal hunger patterns. That's one reason I might go back to taking it.
Metformin also lowers my triglycerides dramatically, and since they are one of the more predictive elements in the lipid profile, I see that as good reason to take it. I'm sure my triglycerides are nastier now as I'm eating a bit more carb than usual, reworking the insulin dosing.
Finally, for some reason, taking metformin also lowers my blood pressure enough that when I take a blood pressure pill along with metformin, I can have serious problems with BP going very low. Now that I'm off the Met, I'm taking my blood pressure pills more frequently. I can't take the Diovan every day, never could. For years one Diovan would last me 2 days, and when I'm on Metformin it often controls my blood pressure very well for four! Any more Diovan and I'm likely to find myself flat on my back in the garden seeing stars if I bend over to pick a weed.
But I'm wondering, now that I feel so much more alert and awake without metformin, what this tells me about potential side effects. Is it subtly poisoning me in ways I didn't know about? We know it acts on the liver, and, well, I'm fond of my liver and would really like to keep it around for years to come. Metformin has been used for decades, so it has a pretty good safety record, but even so, the old "listen to your body" thing is telling me that maybe a little less Metformin might be in order.
I'm going to stay off the Metformin for a while longer and then go back on it and see if the sleepiness comes back. This kind of "challenge test" is what my endo instructed me to do years ago when I expressed other concerns about metformin side effects.
All in all, I think it probably is a very good idea to go off any drug we are taking day in and day out after we've taken it for years, to see if 1) it is still actually doing anything--many drugs don't after a while and 2) whether the drug has been causing side effects we haven't connected with it.
Obviously, if you stop a drug you need to closely monitor the area it impacts. You don't stop a blood pressure medicine without testing your blood pressure several times a day. Ditto blood sugar meds and blood sugar.
A Word of CAUTION
For many meds you can't stop cold turkey, because, although doctors often fail to mention this, the drugs are physiologically addictive and you'll have very nasty rebound symptoms or even, in the case of beta blocker blood pressure meds, a heightened risk of heart attack. If you feel a drug vacation is in order discuss your particular drug with your doctor before you stop taking it.
But it is well worth reviewing the rationale behind any drug you've been taking for a few years or more. Your condition changes, other drugs you have added since starting a drug may be duplicating the effect of that older drug, or the drug you have been taking may have become ineffective over time. A good doctor will take these concerns seriously and help you understand how to audit what you are taking and decide if it's time for you to try a drug holiday.
Since I am using insulin at mealtime now, going off metformin does not pose a danger to my health as long as I adjust my insulin dose to match the higher blood sugars I get without metformin in my system.
This past week, off the metformin, has been very interesting. As expected, my digestive system got a lot happier very quickly. No heartburn or weird feelings in the heart region that turn out to be signals from the esophagus or top of the stomach. (If you take Metformin, you probably know what I'm talking about.)
But after stopping, I was surprised at how much more energy I got. I'd been very sleepy in the evenings the last couple months but now, after almost a week without met, I'm bright and alert at 10 PM. My mind feels clearer during the day, too. Interesting!
My insulin needs have gone up, though my carb/insulin ratio is still that of a non-insulin resistant person--1 unit to 11 or 12 grams rather than 1 unit to 15. It took me a few days to adjust my dosage up, very carefully, a half unit at a time. Now I'm using 4.5 or 5 units, instead of 2.5 or 3 per 40-50 gram meal.
I do find it easier to go low with the higher amount of insulin, hence the higher carb intake. I'm not eating those 50 grams all at once, but instead eating a some at 2 or 3 hours to prevent lows. I'm using R, which hits hardest between 2-3 hours. Novolog would require a different approach, but I haven't had the time to work it out.
I'm also hungrier--which is one reason I started taking metformin, because without it I can be hungry and that pushes up my intake and weight. I consider hunger a symptom, not a moral failing, and for years metformin has been helpful in giving me normal hunger patterns. That's one reason I might go back to taking it.
Metformin also lowers my triglycerides dramatically, and since they are one of the more predictive elements in the lipid profile, I see that as good reason to take it. I'm sure my triglycerides are nastier now as I'm eating a bit more carb than usual, reworking the insulin dosing.
Finally, for some reason, taking metformin also lowers my blood pressure enough that when I take a blood pressure pill along with metformin, I can have serious problems with BP going very low. Now that I'm off the Met, I'm taking my blood pressure pills more frequently. I can't take the Diovan every day, never could. For years one Diovan would last me 2 days, and when I'm on Metformin it often controls my blood pressure very well for four! Any more Diovan and I'm likely to find myself flat on my back in the garden seeing stars if I bend over to pick a weed.
But I'm wondering, now that I feel so much more alert and awake without metformin, what this tells me about potential side effects. Is it subtly poisoning me in ways I didn't know about? We know it acts on the liver, and, well, I'm fond of my liver and would really like to keep it around for years to come. Metformin has been used for decades, so it has a pretty good safety record, but even so, the old "listen to your body" thing is telling me that maybe a little less Metformin might be in order.
I'm going to stay off the Metformin for a while longer and then go back on it and see if the sleepiness comes back. This kind of "challenge test" is what my endo instructed me to do years ago when I expressed other concerns about metformin side effects.
All in all, I think it probably is a very good idea to go off any drug we are taking day in and day out after we've taken it for years, to see if 1) it is still actually doing anything--many drugs don't after a while and 2) whether the drug has been causing side effects we haven't connected with it.
Obviously, if you stop a drug you need to closely monitor the area it impacts. You don't stop a blood pressure medicine without testing your blood pressure several times a day. Ditto blood sugar meds and blood sugar.
A Word of CAUTION
For many meds you can't stop cold turkey, because, although doctors often fail to mention this, the drugs are physiologically addictive and you'll have very nasty rebound symptoms or even, in the case of beta blocker blood pressure meds, a heightened risk of heart attack. If you feel a drug vacation is in order discuss your particular drug with your doctor before you stop taking it.
But it is well worth reviewing the rationale behind any drug you've been taking for a few years or more. Your condition changes, other drugs you have added since starting a drug may be duplicating the effect of that older drug, or the drug you have been taking may have become ineffective over time. A good doctor will take these concerns seriously and help you understand how to audit what you are taking and decide if it's time for you to try a drug holiday.
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