I was diagnosed with Lupus in 1992. For the next 15 years, I had been told I was borderline diabetic. I was finally diagnosed as diabetic in 2007. However, it seemed that my blood sugar and blood pressure were mostly out of whack when my lupus had flared up…
I’ve always wondered which was the chicken, which the egg…
Did the lupus cause the diabetes & high blood pressure, or vice versa…
Anti-CD 20 monoclonal antibody, Rituxan, is the $6200 drug I am getting for my life threatening lupus, which United Health care has refused to pay for. Drug has excellent promise for all autoimmune diseases. I asked if it would help my thyroid or pancreas. doctors laughed and said those are already DEAD!
Liz,
I have lupus as well as type 1 and hashimoto’s thyroiditis. I have many serious derangements with my blood and have a rare acquired hemophilia from it. My kidneys are involved as well! I’m getting chemotherapy for it right now. Girl, we need to talk!
Wow, yes we do! Long story short:
As a child, I was sick a lot. Weird assortment of illnesses. Bouts of bronchitis, allergies, joint problems, severe headaches, nose bleeds, extreme fatigue (often mistake for laziness), and collapsing for no apparent reason. Lost a baby in '92, diagnosed with Lupus, later on with degenerative disc disorder, diabetes, high blood pressure, and now wheat and dairy flare up my allergies and asthma. I’m 47, but feel like I’m 74… I’ve often believed it was thyroid related, but no insurance means I can believe all I want, but the most I can hope for is to keep things under control for during flare ups or segments of time when we can afford the doctor visits & meds. (I have boys too! 4 boys: 22, 21, 17 & 15.
Here's a well written article, from BusinessWeek of all places, that goes into more detail about the study and its implications. Unusual for things written in the popular media, it explains the difference between T1 and T2. Unfortunately the drug tested, which decreased insulin resistance, apparently also has significant side effects so don't hold your breath concerning a miracle cure on the horizon. But this study would seem to signal a paradigm shift.The final paragraph is:
“People with type 2 diabetes are often blamed for bringing the disease on, but it’s a combination of genetic and physiological factors exposed to a certain environment. And, this study points out what may be another important biologic factor,”
It may not be the cure, but it certainly seems to be going in the right direction. At the very least, the study points out what many of us have known for a very long time: this isn’t something we did to ourselves! If being overweight was the cause, then every overweight person in the world would be diabetic, and that’s just not the case.
manny:
no offense - like your optimism; and yes science needs to do the research even if it is all over the field and on esoteric items.
But - folks eyes, kidneys, limbs are rotting out still while this research grinds on.
Halting, slowing the rot would be a first great step. What is insulin resistance and what causes it and reseraching it in depth would be great first step.
Type 2 diabetes insulin resistance is not a uniform monolithis disease.
Cure seems to suggest that one will be able to eat anything even in face of following constrints:
Human body relies upon a storage hormone insulin to regulate body BG by routing excess glucose from blood stream to storage resources of liver, fat cells and skeletal muscle cells.
If those cells are filled up based upon constant high levels of calorie/energy input and constantly low levels of exercise - energy burn, its hard to understand how a body can maintain BG levels at safe lower levels.
The old Hunter gatherer gene set/gut/intestine were optimized years ago - for as a friend of mine says - a control engineer to bump along the bottom of food supply and periods of starvation and scrawny food.
As the current human body as best as I can tell was not optimized - organized to thow over the side excess calorie input and instead grabs all calories regardless of how levels of glucose storage are at in the body resulting in the necessity of calorie input management as well as energy burn sufficient to keep energy balance near zero will be part of that final solution.
Like you, I also want a cure. So far as best as I can tell Type 1 lends itself to the cure you are describing. I believe that is 18 to 20 % of all diabetics. The balance are type 2.
Yes, in the end, maybe genes are at fault but without majjor design changes - replumbing of a type 2 Insulin Resistant Diabetics genes, gut/intestine operation; I am unclear how we make progess on the front you describe.
Meanwhile - excessive liver glucose release goes ignored as a major cause of diabetes:
Pitt team identifies key protein causing excess liver production of glucose in diabetes
PITTSBURGH, Sept. 28 – Researchers at the John G. Rangos Sr. Research Center at Children’s Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine have identified a powerful molecular pathway that regulates the liver’s management of insulin and new glucose production, which could lead to new therapies for diabetes. The findings were published online this week in Diabetes, a journal of the American Diabetes Association.
Usually, the liver stores excess blood sugar as glycogen, which it doles out overnight during sleep and other periods of fasting to keep glucose levels within a normal physiological range, explained H. Henry Dong, Ph.D., associate professor of pediatrics, Pitt School of Medicine. But in diabetes, the liver continues to pump out glucose even when insulin is provided as a treatment.
“Scientists have been trying to find the factors that contribute to this liver overproduction of glucose for decades,” Dr. Dong said. “If we can control that pathway, we should be able to help reduce the abnormally high blood sugar levels seen in patients with diabetes.”
He and his team have been studying a family of proteins called Forkhead box or FOX, and for the current project focused on one called FOX06. They found that mice engineered to make too much FOX06 developed signs of metabolic syndrome, the precursor to diabetes, including high blood sugar and high insulin levels during fasting as well as impaired glucose tolerance, while mice that made too little FOX06 had abnormally low blood sugars during fasting.
“In a normal animal, a glucose injection causes blood sugar level to rise initially and then it goes back to normal range within two hours,” Dr. Dong said. “In animals that made too much FOX06, blood sugar after a glucose injection doesn’t normalize within two hours. They have lost the ability to regulate the level while the liver keeps making unneeded glucose.”
Other experiments showed that diabetic mice have abnormally high levels of FOX06 in the liver, he added. Blocking the protein markedly reduced liver production of glucose, although blood sugar did not completely normalize. Within two weeks of treatment, there was significant improvement in blood sugar and glucose metabolism in diabetic mice.
Tests with human liver cells echoed the importance of FOX06’s role in glucose production.
“These findings strongly suggest that FOX06 has potential to be developed as a therapeutic target,” Dr. Dong said. “If we can inhibit its activity, we can possibly slow the liver’s production of glucose in patients with diabetes and better control blood sugar levels.”
Co-authors include lead author Dae Hyun Kim, Ph.D., and other researchers from the University of Pittsburgh’s departments of Pediatrics and of Pathology. The study was funded by the National Institutes of Health.
About the University of Pittsburgh School of Medicine
As one of the nation’s leading academic centers for biomedical research, the University of Pittsburgh School of Medicine integrates advanced technology with basic science across a broad range of disciplines in a continuous quest to harness the power of new knowledge and improve the human condition. Driven mainly by the School of Medicine and its affiliates, Pitt has ranked among the top 10 recipients of funding from the National Institutes of Health since 1997.
Likewise, the School of Medicine is equally committed to advancing the quality and strength of its medical and graduate education programs, for which it is recognized as an innovative leader, and to training highly skilled, compassionate clinicians and creative scientists well-equipped to engage in world-class research. The School of Medicine is the academic partner of UPMC, which has collaborated with the University to raise the standard of medical excellence in Pittsburgh and to position health care as a driving force behind the region’s economy. For more information about the School of Medicine, see www.medschool.pitt.edu.
About Children’s Hospital of Pittsburgh of UPMC
Renowned for its outstanding clinical services, research programs and medical education, Children’s Hospital of Pittsburgh of UPMC has helped establish the standards of excellence in pediatric care. From Ambulatory Care to Transplantation and Cardiac Care, talented and committed pediatric experts care for infants, children and adolescents who make more than 1,000,000 visits to Children’s, its many neighborhood locations, and Children’s Community Pediatrics practices each year.
Children’s also consistently has been named to several elite lists of pediatric health care facilities, including U.S. News & World Report’s Honor Roll of America’s “Best Children’s Hsopitals” and the Leapfrog Group. Also, Pediatric research programs at Children’s Hospital and the University of Pittsburgh School of Medicine ranked eighth in number of grants from the NIH for fiscal year 2010.
Here is excellent summary and text dealing with Insulin Resistance and T2 and work done doing studies on skeletal muscle cells and mag resonance spectography looking at glycon storage levels.
Very interesting.
4518-DiabetesMellitus_paper_williams_wilkins.doc (607 KB)
Old thread, but if you're interested, here is a link that talks more about it:
http://med.stanford.edu/ism/2011/april/engleman.html
Or you can Google Stanford University Type 2 Diabetes Autoimmunity, and get a whole raft of articles.
To those of you who are concerned about other issues, like what about the folks who aren't overweight or obese, I'd like to remind you that T2 is a GARBAGE CAN diagnosis -- anyone who doesn't have the classic T1 antibodies is, by definition, T2, but that doesn't mean they all have the same disease. Those who ARE obese, and have metabolic syndrome and are demonstrably insulin-resistant, fit what I call "classic T2" (NO blame intended!), but there are a significant number, although a minority, of people who are called T2 but who DON'T have the classic disease. No one has actually described what these people have (excluding those who actually have LADA or MODY), so I have called it Type Weird for many years.
The term "Thin T2" is a bad one, because it points doctors' thinking in the wrong direction -- right straight towards insulin resistance and weight loss, when that might not be the problem at all. But the fact is that NO ONE knows what the problem is. If you want to talk about an orphan disease, you guys are IT. That's why I like Type Weird -- at least I'M acknowledging that you're NOT classic T1, nor classic T2, nor MODY nor LADA if you've been tested for them. Wish I was a scientist and wish I had the funds to research it!
Aeon:
You are asking most difficult question. As I am not doctor/medical person; the issues you raise really require some expertise.
Having used said instrument and struggling with my own condition, the present available tool I used was the Dexcom. My Doctor and I actually caught the actual liver mis-behaviour using caveman machine and 30 strips a day before cgms. The cgms with its data logging confirmed the suspicions as well as providing greater glues to digestive process and timing. One cannot get trend direction on a single caveman strip but requires a number of the caveman strips in a row.
At the present costs of strips, sensors and the cgms; costs are a key concern.
Can you afford that? on a daily basis.
Bloggers I have watched and read seem in my mind struggling with its high cost versus benefit especially on a long term basis.
If money no issue - get one - otherwise you will want to tread carefully.
Whether it can help your specific case; many suggestions I have heard and would seem to be helpful is to get the temporary short range cost limited test review and see if you can get sufficient data to help you sufficiently so you can go back to caveman machine knowing the trends of your body. The only problem with that is the up to speed experience and training to get climatized to the CGMS and its pecularities - a couple of weeks.
More advanced test gear can always surface more detailed data that might assist in your particular case looking at trends, real time fast issues, eating, liver activity so your Doctor/endo can better isolate cure steps, diet, meds that may provide the best hope for stabalizing your issues.
If there was a unit for $ 200, sensors lasted a year - cost of sensor for year was $ 80- and price of test strips was under 20 cents a strip. You bet get one. I prefer having a live gas meter data logger watching me every 5 minutes 24/7 so I can quickly see what my body is doing alomg with the real time gronks and police body tighter allowing me to predict early and prempt problems by a early warning trend system
As to whether you are missing anything, more advanced tools and data logging will always provide more data than one can get on single prick caveman machines - but at what cost impact and value of extra data. This is issue that can only be wrung out with doctors and other specialists. A1c readings will be a gating item as to quality/capability of present diabetes control.
Best wishes. My goal and hope is that we can get costs of the cgms and sensors down to more reasonable high volume PC style of manufacture so they become more available to more people wishing to have better visibilty of glucose trends and body control of their diabetes.