by Frank Vinicor, MD, MPH, and Jinan Saadine, MD
From the Editor: Because of its length, the following will be carried in two parts. Look for its conclusion in the January 2005 VOICE, Vol. 20, No.1.
Dr. Frank Vinicor is the director of the Division of Diabetes Translation, part of the U.S. Centers for Disease Control and Prevention. He and his colleague, ophthalmologist Dr. Jinan Saadine, addressed the annual meeting of the Diabetes Action Network, held in Atlanta, Georgia, on July 1, 2004, at the annual convention of the National Federation of the Blind. Dr. Saadine began, with a short presentation, and then took questions from the audience.
I am Jinan Saadine, an ophthalmologist for the Center of Disease Control, Division of Diabetes Translation, and I am heading the effort into eye health problems at the CDC. This is my first time to your convention, and I'm happy to have this experience to talk about eye care and vision problems, and what we are doing at the CDC. I'm not a diabetes expert; I'm not going to be able to replace Dr. Vincor because he's the Diabetes expert and he is the head of the Diabetes Division at the Centers for Disease Control and Prevention.
I'm going to give a brief summary of the extra effort that we are doing at the CDC.
I came to CDC about 4 years ago. I was doing research in diabetic retinopathy, and all eye disease among people with diabetes. I realized there is a gap in the public health at the CDC for eye health and vison problems in general -- not just for people with diabetes. So I made an effort, brought an initiative, to the CDC to create a program for public health and ophthalmology. Your interest might be at the other end, mainly rehabilitation, but I'm interested in the whole spectrum: primary prevention, secondary prevention, treatment and rehabilitation; the whole spectrum from preventing the disease from happening, and then looking into more eye disease and vision health, and how it impacts the quality of life and daily activities that we are doing.
I know the clinical definition of visual acuity for blindness is not really the definition we go by. The functional definition is much better is than the "20/20" or "20/40" or "20/200." I realized we at CDC need to deal with the functioning difficulties and the functioning disabilities, more than the just the numbers clinicians use to define blindness and visual acuity or visual impairment.
As you all know, blindness is a big problem in the U.S. We have about 1.1 million blind people, we have about 3.4 million people classed as blind or visually impaired. And this problem is expected to grow in the future, for several reasons. First of all, our population is aging, and we know all these problems get worse in an aging population. The demographic composition of our population also is changing. We have more minority population -- which have more chronic diseases; one of them is diabetes, another is hypertension; and they all relate to eye disease and visual impairment and blindness. So we really want to increase our efforts into working on the CDC mission: to promote health and prevent disease, and to also deal with disabilities and quality of life. So we are trying to put effort into primary prevention, secondary prevention and treatment.
We are also trying to raise awareness. Like the healthy people objective, we have a healthy objective for the whole nation for all health problems. And for the first time we have ten objectives for eye health and vision. And other people, outside the CDC, like the National Eye Institute of Health - a nonprofit organization -- are also working on this problem. We are all partnering to make people more aware of this problem, and to find a solution for it. Our goal is to really look at the impact of eye issues on quality of life, and try to help people to increase their quality of life and visual functioning.
So I'm here to let you know that we are putting some efforts toward that at the CDC. As I said, Dr. Vincor will be talking about diabetes-specific issues and that is what you're probably interested in. I'm here to hear your concern and see if you have any questions I might be able to answer.
Q: I work for the division of blind services. We are the clearinghouse for services for the blind -- but the doctors, the ophthalmologists, aren't calling us. Its as if "blindness" is this evil word. As soon as it is apparent that a loss of vision is happening, they should contact us. But it's just not happening.
A: This is an excellent concern. Our job as doctors is not, should not be, just not diagnosing the disease and treating it. Because even when sight is lost, and you get to blindness, there are so many other things that can be done. So its not the end, it might be the beginning (such as finding yourself, or creating opportunities, or being creative.) So thanks for raising this and I think maybe we need to raise awareness among people that sight loss is not the end of what's happening, but a beginning, and we need to approach it differently. And that is why I am saying although we are an agency that looks at prevention and promoting health -- and we don't do too much in rehabilitation, we can raise awareness. We are going to be looking into the quality of the life -- at the beginning of something new.
Q: I have diabetes, thus diabetic retinopathy, but I also have retinitis pigmentosa (RP). I ask my doctor what is the relationship between the two conditions -- and she gives me vague answers, like "depending on diabetes development and how well I take care of myself, and how good my sugars are." I try to keep within my numbers. What is the impact on the retinopathy itself? And the impact of the diabetes on the RP?
A: The impact of your diabetes on your RP, I don't think it is any different than anything else in the prognosis. So having a problem to start with -- you are dealing with two problems now. Diabetics are going to deal with issues of diabetic retinopathy; you have RP as well. So you really need to make an extra effort in controlling your diabetes. If you have a good HbA1c, hemoglobin A1c, and you have a good control of your glucose, blood pressure, cholesterol; if you are physical active, if you are doing the right things, then you will delay all the complications that relate to diabetes. As affecting RP by itself, there isn't literature so far to say that, regardless of controlling your diabetes, your RP will get worse. So the best thing to do in your case is to control your diabetes the best way, as well as your blood pressure, cholesterol, everything that needs to be done for diabetes. You have to delay the diabetes, stop the retinopathy from happening, so you can just deal with the RP.
Q: There are so many devices and gizmos that talk; Is there some way the CDC could recommend/control/push/require to make all meters talk? Then it would cost next to nothing. There is real need. It would help a lot more diabetics take better care of themselves.
A: We, the CDC, don't get involved in service deliveries. That is not our brief, more the FDA's. We just try to educate people.
Q: Does the CDC do research about very rare eye diseases? I have congenital toxoplasmosis. The odds are 1 in 234 million, and there is like half a page in the medical literature on that. I'm the only one in the database at the National Institutes of Health. Is there a way that the CDC can educate about certain diseases and send out pamphlets to ophthalmologists and gynaecologists -- about how it can be prevented?
A: We have another center, that I'm going to be collaborating with, not the Division, but the Center for Birth Defects and Developmental Disabilities. My program is really new; in the last six to eight months we started broadening -- covering more than just diabetes and diabetic retinopathy -- so I'll be collaborating with them, making our program broader. We're trying to get more literature on the web page.
Q: I have diabetes in my family; I've been told that if I get diabetes, I will lose the remainder of my sight.
A: There are many trials, all over the world that prove you can delay or even stop diabetes complications from happening. Proper diet, losing weight, all these things could delay diabetes, even just healthy and exercising, not even strenuous exercising -- you can delay diabetes.
Q: Do you have statistics on how many people lose their sight because of diabetes?
A: We don't have very good incidence data, but the figure that's been roaming around is approximately 12-24,000 individuals a year.
Q: My ophthalmologist was telling me about some new treatment in which a steroid is injected into the eyeball. I have macular degeneration and diabetic retinopathy.
A: There are one or two new studies about injecting cortisone in the back of the eye. They're not completed. Until the trials are over, and until the data are in, and look good, it's not 100% recommended you do that. But there are trials going on, so just wait until they are over. Get the results first.
Q: Is there a relationship between diabetic retinopathy and glaucoma?
A: People with diabetes have a higher risk of getting glaucoma than do people without it. It's not "if you have diabetic retinopathy than your going to have glaucoma." It is just statistically, people with diabetes have a higher risk of getting glaucoma.
Q: Isn't glaucoma a genetic disease?
A: Glaucoma has different definitions/forms. You have congenital glaucoma, open-ended glaucoma, and several others. Yes, there is a congenital glaucoma, but there are other forms, and they are different diseases. If you have the older-onset form of glaucoma, that does not mean your child will get the congenital form -- they are unrelated diseases.
(Editor's Note: At this time Dr. Frank Vinicor, Director of the Division of Diabetes Translation at the CDC, came to the podium.)
I'd like to start by very quickly giving you a sense about what is going on with diabetes. First of all, just how common is it becoming? Where is it becoming common? Things like that. Then I'll talk, a little bit, again very superficially, about our three approaches to this epidemic called diabetes. Those three approaches are: to prevent it, or cure it, or care for it better, and how we seem to be doing at them.
First of all, where are we are with diabetes? Diabetes is a bad problem, bad throughout the United States, especially over the last decade or so, and it is going to get worse before it gets better. That is the reality of diabetes.
The U.S. Centers for Disease Control, along with other agencies, collects a lot of information about diabetes, about how many people have it, and about what kind of problems they get into. Here are some statistics for you, based on a nominal 24-hour period. So between when you woke up this morning, and when you wake up tomorrow morning, this is what is happening in the United States: There are going to be 3,400 people diagnosed with diabetes by tomorrow morning, and approximately 500 people (this is an underestimate) will die from diabetes between this morning and tomorrow morning. There are going to be about 200 amputations from diabetes between this morning and tomorrow morning, and about 125 people will enter End Stage Renal Disease (ESRD) kidney programs (go on dialysis or have kidney transplants) in that 24 hour period, and, unfortunately, about 75 people will lose their vision. This is going to happen every day of the week; its going to happen on Sunday, and its going to happen on the fourth of July. That is the average of what happens in the United States, every 24 hours. That is a lot. A lot of hurt, a lot of loss of personal independence, a lot of cost and the like.
The situation is not unique to the United States. It is happening throughout the world. For example, right now there are approximately 175 million people with diabetes in the world -- but the most recent study (that just came out about a month ago) said that by 2030 (roughly 25 years from now), there are going to be 380 million people with the condition. Diabetes is increasing throughout the world.
Just to give you a flavor of where it is taking place, if you had to think to the year 2030, and identify the top five countries in the world in terms of the number of people with diabetes (now we're not talking about "prevalence," or percentage of the population, but total number of people with diabetes), what countries do you think would be in the top five?
India is first, China is second, the United States is third, Indonesia fourth, and Pakistan is fifth. Those are the top five countries. Japan is up there, Mexico is up there, and though no one country in Africa is that high, the continent is getting up there. India has only a billion people, and is very westernized, in a sense. They aren't fat in the same way we see in America. They have what is called "gut obesity" vs. "butt obesity." Gut obesity is the kind of the bad obesity, I have that kind myself.
One of the reasons why China is only #2 is because large parts of China are still very rural. People there are still very active physically, so they're not as heavy.
The other reason is that, in China, people are going to soon be dying of cigarette-related diseases, so they won't be living long enough to develop diabetes.
So to sum it up, diabetes is getting more common, particularly type 2 diabetes, what we use to call adult onset, or maturity onset or NIDDM, but we now call type 2. That is Arabic 2, not Roman numeral II. When we went out to talk to people, they thought there was type 1 diabetes and type 11 diabetes. They thought we were hiding nine types of diabetes. So, for clarity, they actually changed from Roman to the Arabic 1 and Arabic 2.
But most of this is type 2 diabetes; though certainly not all of it, and, as you can tell by the top five countries on the list, the majority of growth of diabetes in future will come from countries that really are struggling in ways we don't struggle; people like India, China, Indonesia, and Pakistan. They have what is known as the "double epidemic." They still have the infectious disease problems, but they also are developing the chronic disease problems -- where in general we just have the chronic disease problems.
So how big a problem is diabetes? It's big, it's now everywhere in the world, and at times it may seem overwhelming. But we aren't paralyzed. We're not without our own responses and our own weapons. Let's talk about what we could do, and about what science says will or won't work.
As I mentioned, we really have only three choices. We could prevent it, and that's good. If you don't have diabetes, you don't have to worry about diabetic eye disease or kidney disease. We could cure it. So you get it, but it goes away through some treatment. Or, we could provide good care. Those are the three choices, and we could do all three. Let me talk about where we are with each of those. It's helpful to talk a little bit about type 1 and type 2 separately.
When we talk about type 1 diabetes, we're talking about a disease in which, for whatever reason, the body decides to destroy its own insulin-producing cells. This is autoimmunity. Ultimately, when you destroy enough of the 1 million insulin producing cells (the Beta cells), diabetes develops. We used to say, for type 1 diabetes, "you're healthy on Tuesday and sick as can be on Wednesday." It was assumed to be an acute disease, sudden in its onset.
We now know that is not the case. We now know that for years people have been undergoing this self-destruction process, this autoimmune attack, and the body has been destroying five of its own insulin-producing cells today, and ten tomorrow and ten the day after, and the process has been going on for years. Now it's true that you may develop what we call "clinical" diabetes over one or two days, but the destructive process has been going on for years and years. So that is what we call type 1.
Now for type 2. We use to think of it as over, under, over: Over 40, under active, over weight. There appears to be a problem, initially, with insulin resistance with our muscle cells and fat cells not responding to the body's own insulin, and eventually the insulin-producing cells peter out, they give out, they get exhausted -- and that is when diabetes comes up. That is what we mean by type 2 diabetes.
It is not accurate anymore to say type 1 diabetes occurs only in the young, and if type 2 diabetes occurs only in people over 40. It's not that simple. We are seeing kids who have type 2 diabetes and adults who have new type 1 diabetes. But, for discussion, lets just think we live in a nice clean world and there is only type 1 in the young and type 2 in the adults. Just for the heck of it. So it would be nice if we could prevent them.
Right now, studies are underway on preventing type 1 diabetes, trying to see if this autoimmune destruction process can be stopped. You can find people who, because of their genetics, or because of what is in their bloodstream, have these antibodies that can destroy the islet cells. You can get very good at predicting who might develop type 1 diabetes, before they develop it.
There have been large studies to see whether or not, if the process of autoimmune cell destruction was stopped, the patient wouldn't develop type 1 diabetes. The sad news is that the studies didn't prove successful. Any effort has not yet worked. It doesn't mean that people are giving up. They are trying to find better ways to stop the immune destruction. But the studies to date have not worked. So, in terms of prevention of type 1 diabetes, we are still very much in the scientific/experimental phase.
With type 2 diabetes, there is a completely different picture. There now been five studies, published in the last two or three years, showing that if you have a situation in which you are at high risk for developing type 2 diabetes, particularly if you have this thing called pre-diabetes, where your blood sugars aren't normal, but they're also not high enough for you to be told you have diabetes. They are in a grey area, but we know there is a high likelihood you will go on to develop regular garden variety type 2 diabetes.
There have been now five studies that show that, particularly with some of what are called "behavioral interventions," such as losing 8 pounds, lets say, walking 150 minutes a week, that's like 30 minutes five days a week -- if you do that, and you are in this high risk category, you can reduce the likelihood of developing type 2 diabetes by over 50 percent. And it worked, whether if you were black, Hispanic, Asian Pacific islander, native American, white...It worked whether you were 20 or were 70. It worked regardless of how much you weighed. So, for the first time, we now have a lot of evidence, scientific evidence, that you can, at a minium, delay the onset of type 2 diabetes by years, if not prevent it outright.
And the challenge for us is to find a way to take these results and make them part of what we all do everyday, and that is not an easy task. But we now know you can prevent a lot of type 2 diabetes.
I have said we have three approaches: Prevention, Cure, Care. Prevention works for type 2 diabetes, but we are still in the experimental studies for type 1 diabetes.
Lets go on to cure. Ok, you didn't prevent my diabetes, can you do something to cure it? So we want to cure diabetes. It's just the opposite of what we know about prevention. We actually have now learned that for type 2 diabetes, it's probably unlikely that we're really ever going to cure it. When you first develop type 2 diabetes, if you lose some weight and get active, you can kind of push it back a little bit, for a few months or maybe even a year or two. But it turns out, from other studies, particularly done in the United Kingdom, in England, it looks like there is a continuing loss of insulin producing Beta cells. We don't know how to stop that loss, so we don't know how to cure type 2 diabetes. But it's different for type 1.
But for type 1 diabetes, since it's a problem with losing insulin-producing cells, and since we know how to transplant kidneys, eyes, and hearts, why we can't we correct it, cure it, by transplanting the insulin-producing cells? Thus the islet cell transplantation study. And our friends in Canada have provided a real boost. It used to be that if you transplanted islet cells, it didn't seem to work; you had to take immune rejection drugs that were so dangerous and powerful that they themselves could cause difficulty or even cause worsening of diabetes -- and the transplanted cells didn't last. Then Dr. Shapiro and colleagues in Edmonton, Canada, developed what's called the Edmonton Protocol. They had an article published about 3 to 4 years ago in which 7 or 8 people with diabetes, really very brittle diabetes, received transplanted islets.
The researchers developed a system of more easily and effectively collecting insulin-producing cells from cadavers (people who perhaps had died in an automobile accident or something similar). They transplanted them, not through major surgery, but by a little catheter, through the abdomen, into the liver vessels -- and they injected just the insulin-producing cells, which would set up housekeeping in the liver, where they would start making insulin. Most of the patients, again a small study initially, actually were able to get off insulin, and all of them, even those who had to stay on it, could reduce their insulin dose.
To prevent the body from rejecting these foreign cells, because they were someone else's islets, the Edmonton researchers used a new combination of anti-rejection drugs, one that didn't cause as many problems. It was very exciting.
Those studies have now been expanded to about 10 centers throughout the world, mostly in the United States, to gain more experience. The studies have just been released, at this year's American Diabetes Association meeting.
There are right now around 60 to 70 people who have had these islet cell transplantations, and there is a learning curve. You have to learn how to safely collect these insulin-producing islet cells; learn how to put the catheter, safely, into the liver -- so there is a learning curve. But for those centers who have learned and done well, they are having equal success. A lot of these studies are sponsored by the National Institute of Health, and there is now a movement to expand it beyond these 10 centers -- to start moving into larger number of people who might be eligible for this study.
So again, I don't want to imply that it is here for everyone today, but it's not ten years down the line either. It will be here soon. There continue to be two major issues. The biggest one is finding enough islet cells, beta cells, insulin-producing cells (same thing) to transplant. When you are born, you have about a million insulin-producing cells in your body. And you probably need 300-400,000 to make it go, to become insulin-independent, if you get a transplant. You probably can get maybe 200,000 viable islets from a cadaver pancreas. To do so, you have to take that pancreas, put it in some kind of safe Waring Blendor, chop it up, get rid of all the other stuff, and only get the insulin producing cells--and you inevitably destroy some of those in the process.
Most of the people in the Edmonton protocol didn't have one injection of cadaveric islet cells; they had two and three and four. Again, its not that likely that there are going to be two, three, or four cadavers, who come in from automobile accidents, who happen to have your particular genetic makeup. So getting the number of islet cells you need is a real challenge. And that is why they are looking at other ways to go to find these islet cells. And that always gets you into politics and such things. But there are several things to think of. Maybe I can get fetal islets and allow them to grow and then those would be a source of beta cells. The whole idea of stem cell research - that is, finding very early cells and training them to be beta cells instead of muscle cells, is another way.
Yet another way might be to create an artificial pancreas -- that is, a machine that does the same thing as a pancreas. It would have a reservoir of insulin, a pump that pumps out the right amount of insulin, and some kind of glucose sensor that says "my blood sugar is going up; you just had some ice cream." Then it would squeeze out some insulin.
A fourth or fifth way; I can't remember how many I've mentioned, is that every cell in your body has the genetic structure and instructions to make insulin -- its just that somehow my bone cells have been turned off; instructed not to make insulin, but to be strong, but they got the message somehow, because we all come from one cell, at conception.
They are trying to find someway to take, for example, fat cells (and I could be the donor source), take a safe virus (to which has been attached an insulin gene) and insert it into the fat cell, which becomes then an insulin-producing cell. They can do that. The problem is they just don't know if they can control the way that new fat cell/insulin-producing cell releases its insulin. The worst thing you'd want, if you didn't eat, is these new cells releasing insulin willy nilly. Finding sources of beta cells is the major challenge. But they are moving there.
And the other big issue, of course, is anti-rejection drugs. I mentioned that they are better now; they're a lot safer, but they are not weak drugs. Will they cause you to be prone for cancers? Will they cause you to be prone for infections, because you're stopping the body's responses? So those are the two main challenges but, for type 1 diabetes, we're getting there. And I'd say within two to three years we'll see more evidence.
Let me quickly conclude with care. If you have diabetes, if you have to have it, its better to have it in 2004 than it was in 1994 or 1984, etc. There are so many more medicines and insulins to mix and match, so many more tablets to take, so many more, and better, blood pressure drugs, so many more, better, cholesterol-lowering drugs. We have so many more and better ways to test blood sugar and blood pressure. We know that aspirin is important now to prevent heart attacks. We basically know that if we can work together, and get the body's metabolism under control: blood pressure, blood cholesterol, blood sugar, that your chances of developing all these complications of diabetes can be reduced by 30 to 50 to 60% by good care. Again, that is for both type 1 and type 2.
So the challenge for care is not, necessarily, brand new breakthrough discoveries (though that's always great), but the real challenge for care is to be sure that everybody can get access to the care we know, that works. That is the challenge.
Even though the problems are getting bigger, in the sense that more people are developing it, we are not paralyzed. We can do things together. And we know now that we can prevent type 2 diabetes to a great degree, but we have a way to go for type 1. We are beginning to learn that we can probably soon cure type 1, but we're not sure about type 2. And for both of them, we must work together to be sure we get the best care we can -- and it'll make a huge difference in people's lives so they can be as healthy as they want to be and not have to worry about these complications.
Editor's Note: At this point Dr. Vinicor took questions from the audience.
Q: I'm a type 2; what should I do? Is it helpful to lose weight? What steps should I take? Lower the blood sugar? Lower the blood pressure? If I lost weight, would my blood sugar levels go down?
A: In general, anytime any of us gain weight, and, lets say, we already have diabetes, we are more likely to have our blood pressure, cholesterol, and sugar to go up. So the heavier we are, the more the body responds with higher blood pressure, sugar, and cholesterol. Getting the weight down, and doing it in a way in which you're physically active (I'm not talking about running a marathon; just regularly walking) -- the more we can do that, the easier it is to control blood sugar, blood pressure and blood lipids. It doesn't mean you won't need medicine -- but the amounts of medicines you'll have to take will be less, and the blood sugar fluctuations will be less. As a general rule, the better we can control our weight, the easier it is to control our diabetes.
Q: Is there an ideal weight for a person of a given size?
A: The more you lose, the better -- but we don't want to make people be like Twiggy -- but in general getting down to reasonable weight is good. There are people who can help you. Again, I want to emphasize that we know clinically, from this important diabetes prevention study, that if you weigh, say 220 pounds, you don't have to get down to 140 pounds to see the benefit. You will see benefit if you get down to 210 pounds. And the more you get down, the more benefit you will see. You don't have to become a skinny mini,--a lean, mean fighting machine,-- to see the benefits.
Q: What is the role of autoimmunity in the development of diabetes? If someone had measles at age two and got diabetes at six, is that an example?
A: It's helpful to think about it this way: Let's say you have identical twins. f one of the twins happens to develop type 2, it is highly likely, 90 to 95 percent of the time, the other twin will also develop type 2 diabetes. What if there are identical twins, and one twin has type 1 diabetes? It turns out that only in 30 to 40 percent of the time will other twin ever develop type 1 diabetes. This says that since they both have the same genetic structure, there must be something outside of the body, perhaps an environmental risk factor, that in one twin triggers this autoimmune process -- and the other twin didn't get exposed to it -- since they've got the same genes. The nature of such process, what it is, is not clear. Whether it's a virus, or something we ate, whether its stress, we don't know what the environmental trigger is that sets up the immune destruction process. A large study is going on now -- it's called the Teddy study, like "Teddy-bear," and I honestly can't remember what it stands for, but it is trying to identify what it is, outside our bodies, that would trigger this autoimmune destruction. I don't know what it is -- jillions of kids develop measles, but only a few go on to develop diabetes. So it's gotta be more than just measles. We still don't know what the trigger is.
Q: Dr. Shapiro from Canada had stated there was a problem with encapsulation of the islet cells. Was that the same study you're talking about?
A: Dr. Shapiro, who heads the Edmonton team, may have been speaking about encapsulation, but no, they don't encapsulate the islet cells in the Edmonton protocol. They just blast them into the liver. Any time someone puts someone else's tissue into your body, your body says: "I don't want it." It tries to reject it. You therefore have to try to protect whatever it was they put in your body -- could be a lens, could be a heart, a kidney, or islet cells. There are different ways to try to protect it. One is to give medicines that shut off your anti-rejection response. Then your body just doesn't have the gumption, the ability, to kick out the foreign tissue.
Another is to put into your body cells that have for whatever reason, lost their "identity" as foreign. I mentioned fetal islet cells. They're generally pretty neutral. They don't have as many foreign components on the outside of the cell. They're not viewed by the body as being "foreign." They're much less likely to be destroyed.
Another way would be to take the islet cells and protect them. For example, put them in a little seaweed-like structure about the size of a small straw, and that little straw, made of seaweed, would have holes in it, of a certain size, that they will allow sugar to come in and insulin to go out....but the holes are too small to allow these big, destructive proteins or white blood cells to get in. That's encapsulation. But the body is so darn smart, when it can't get in and destroy the foreign islet cells, it will start scarring over the encapsulated straw -- just covering it up. These are challenges because your body is so smart -- it knows how to get rid of foreign tissue. So far, encapsulation hasn't worked, and that's probably what Dr. Shapiro was saying. His way doesn't use it.
Q: Regarding non-fetal stem cells, what of the possibility of donating your own? Could such cells be used the same way?
A: Both fetal and stem cell research are very controversial, very political, and people have strong feelings about them. Very few people are neutral. In general, I've been told, stem cells from fetuses are easier to work with, and better to direct one way or another than are adult stem cells.
We all have stem cells in our body. Right now, in my bone marrow, hopefully, there are stem cells there, making decisions to go on to develop red blood cells, platelets, or white blood cells, -- they all come from stem cells. So you can get stem cells from adults, but they're much harder to get, and harder to manipulate. In general, there are political issues here; they relate to abortion issues, and principles and all the like, and it's a very controversial area.
Q: I have pituitary failure, and I was diagnosed with diabetes when I had congestive heart failure. I was struggling with autoimmune deficiency at time. Weren't sure if type 1 or type 2 diabetes at the time. How might they have played on the development of diabetes?
A: It's not as easy as it was earlier to tell who has type 1 or type 2 diabetes. We are trying, and there are many cases in which you know someone has the one or the other, but its just not as easy. So, with your question about which one you have, you join a larger crowd who aren't sure. Is it important to know which one you have? Maybe, in some circumstances. Type 1 diabetes, because it is a autoimmune disease, is some cases associated with other endocrine gland failures (such as your pituitary gland failure, which is unusual, but not unheard of); some people with type 1 diabetes develop thyroid failure, or adrenal gland failure, or skin failure (vitaligo), where they develop white patches. Those are manifestations of a more generalized autoimmune process. It is not common, but no longer do you hear "What's going on here?" Now we know it can happen. So it is possible in your situation you have a more generalized autoimmune process underway.
Q: I have been having neuropathy problems in my hands and feet. Is there anything I can do about that? It is irritating and itchy.
A: Neuropathy is a very common problem for people with diabetes. It is generally viewed as the most common complication, and it can be severe. For some people, if the bedsheet touches their feet, it just sends them through the wall. There are a lot of treatments and medicines, which tells you we really don't know what to do about it. If you go in the bookstore, and go up to the nutrition/diet section, and you see there are 375 books on nutrition and diet control, that should tell you at least one thing: "we don't know how to do it." If you go up there, and you see maybe one or two, and they all say the same thing, that means we've learned something. It's like that with treatment of neuropathy. There is a list of 5, 6, maybe 7 different medicines available. It's trial and error. Try one; see if it works; if it doesn't, then try another. One of them is an anti-seizure medicine; one is a medicine for anxiety. There are different kinds; try them. Usually you can find one that works, for you. But it is not easy, and it is not quick.
To be continued...