In my opinion the terms strong or weak are not that appropriate for the immune system. Any bacteria with an aggressive rate of growth can outperform the immune system for a while. To prevent this from happening the alertness of the immune system is an important factor to win the race of reproduction. Autoimmunity is a form of higher alertness that comes with a price: to some degree the recognition of friendly tissue is impaired. It is as if the immune system has not been properly trained and some of the T-cells can now show a rogue behaviour towards our own tissue. If this makes us more resistant to illnesses in general is not that clear to me. In my view it can also mean that the immune system is distracted. It can also be argued that high blood glucose is weakening the capabilities of our defence. The rogue behaviour can cause all sorts of autoimmune conditions and most T1 diabetics will face more than one in their lifetime (my own experience). It is the autoimmunity that is inherited from generation to generation - not T1 diabetes. That this autoimmunity will actually cause the development of T1 is very rare. That is why it seems as if T1 is skipping generations. Sometimes all the random events necessary to develop T1 come together at a later stage in life - you can call that LADA or just bad luck. Although it is rare worldwide something important has changed over the last decade: the likelyhood for the development of T1 has risen significantly. In Germany we had an incidence rate of 19,4 per 100000 people per year in 2007. It is projected that this will rise to 37,9 per 100000 people per year in 2026. In Finland they already had 64,2 per 100000 per year in 2005. Obviously some environmental factor is fueling this development.
Denise Faustman has shown that a vaccine can somehow modulate the immune system to clear out the rogue T-cells. The questions is if clearing them out is enough to have long term success. After all the cause for the improper training of the T-cells has not been fixed. At some point in the future it is likely that the immune system will again grow some of the rogue T-cells. But perhaps permanent vaccination can keep that at bay.
Holger, are you saying that like for measles, a vaccination may be able to be given against T1? Is that what Denise Faustman is working towards - amazing!
I took an Immunology course about 10 years ago. The process of your body eliciting an immune response to a pathogen is pretty well understood. I would suggest you look into that and Major Histocompatibility Complexes (MHCs) if you are still interested and have questions.
This is how I remember the process of eliciting an immune response which will likely shed some light on how (many) autoimmune disease may come to be. Your body is presented with a pathogen (virus or bacteria). Your body is able to destroy a few of the bacteria into small pieces (antigen). These antigens are processed by (I think) B and T cells and this will lead to an adaptive immune response. This immune response should be specific to the pathogen and be held in our immune “memory” for a while to fight off the same future infections.
B cells, when activated, will aid in creating an antibody response to bacterial infections (extracellular); while B cells activate mechanisms to destroy intracellular infections (usually viruses) and cells that are improper (cancerous).
Here is where things get very scientific (and fuzy). In order for antibodies to be activated and circulate the body they must pass 2 tests. The first test is to make sure they can be activated and do something (or bind to the pathogen). Sort of like we just built a car now we need to check if it will turn on and move. The second test is to make sure that the antibodys will not bind to things that they should not bind to (like host tissue). It does you no good to create an antibody that will bind to a meningitis bacteria AND it will also bind to cells in your heart. This would lead to the destruction of the infection and damage to your heart and is bad. This would be like, we built a car but the steering wheel gets hot and burns the driver when it is turned on. If an antibody passes these tests, then it is free to circulate the body. When an antibody finds the pathogen, it will bind to it and release signals that attract other immune cells to destroy and remove the infection.
The process to ellicit an immune respone with B cells is quite similar. The main difference is that antibodies are not created, instead leukocytes, T cells, etc. These cells will attack host cells that are problematic (cancerous, infected with a virus, or just plain wrong). They may attack and kill it or simply “flip a switch” telling the cell to die.
The second test is the one that are bodies likely fail at. T1s bodies likely do not throw out the antibodies (or autoantibodies) that attack the infection AND attack our Islet of Langerhans cells in the pancreas. Ufortunately, the immune response is commited to our immunological “memory” and is continually active. If our pancreas was to make further insulin creating cells, then this immune response would kick back up and take them out again.
I have not seen any correlation between autoimmune diseases and a healthier immune system. I would bet that autoimmune disease sufferers get sick very similarly to the general population. I have heard more casual talk that people with autoimmune conditions likely get a few more infections then the general population. The idea here is that their immune system is continually spending a small portion of its time and resources on attacking the host’s tissues.
At least it can be done in mice to some extend. So far the results for the drug BCG point in the same direction for humans. The faustman labs are now preparing for human trials to find the right dosage of BCG. The big question is whether or not humans are capable to regrow their beta cells after decades of autoimmune attacks. It is likely that only some of us will see huge benefits. But even if we do not reach independence of external insulin the small amount of regrown beta cells will help to make our control easier.
But that is the question Capin: Why do we fail the second test? Do we overwhelm the bodies ability because the "attack" of the virus is mounted so heavily our bodies do not have the ability to properly "screen"? This same process (e.g. quick and heavy response) could very likely improve our ability to fight all the bacteria and viruses off.
I have heard more casual talk that people with autoimmune conditions likely get a few more infections then the general population. The idea here is that their immune system is continually spending a small portion of its time and resources on attacking the host's tissues.
I would bet that there are some that get sick MORE than the general population and some less with an average about the same but with a much wider spread. The key here is overall capacity. If the autoimmune comprimised individual has small overall capacity to attack foreign invaders then they would likely be sick more often. On the other hand if the overall capacity is high and you mount heavy responses to foreign invaders it may work out you do not get sick as often.
Of course blood glucose control plays a part. If the person is chronically poorly controlled it will reduce the bodies overall capacity to deal with foreign invaders and thus we get sick.
Most of this is all conjecture on my part but this is why I have the questions. The overall process makes sense but the specifics of an autoimmune process and what this means to the overall immune system are details I am unfamiliar with. I understand WHAT autoimmunity is I just don't understand WHY. I suppose if the questions were easier to answer and readily available we would likely be closer to a cure. Seems to me the "cures" we have been hearing about only deal with the end result of the autoimmune attack not WHY it happened.
I think I got my B and T cells confused earlier, whoops. This secondary test, as I called it, happens with every antibody our bodies create. The test is to exclude autoantibodies and other problem antibodies, but for some reason these autoantibodies are not excluded. I would believe that (besides above) autoimmune inflicted individuals have “normal” activated immune response.
Wow, all sorts of interesting responses popped up while I was sleeping! I'm reading and re-reading the various explanations, because science is not my forte.
If I understand what you are saying correctly, Holger, my own immune system (and perhaps some of the others who've responded), has been especially alert. Then the autoimmunity you describe as a "form of higher alertness" that to some extent misbehaves by targeting our own tissue. So is the antibody response a specific and unique "form" of "high alertness" or is it on a continuum where it is the most intense reaction of alertness which has the price of poor recognition of friendly tissue? That would certainly be the theory I've been wondering about!
In my case, I would say I had the "alert" immune system for a long time in my life. I wasn't diagnosed with Graves hyperthyroid disorder until I was 45 (I might have had it a couple years before). I wasn't diagnosed with Type 1 until I was 58. So the "intense alertness" had been going on for over 40 years before the autoimmune response. My question was more about "hyperalert immune system" as a precursor or causation of autoimmune response. Has that continuum been studied?
So if there is a connection between "hyperalert immune system" and autoimmune response perhaps it's more prevalent in those of us diagnosed older? (and perhaps only one version of how autoimmune response is caused). I think it would be necessary to do research to see if a statistically significant number of Type 1's diagnosed in adulthood or later adulthood had less illness throughout their lives prior to diagnosis. If so, that would be an area to study - how that whole process of a hyper alert immune system can lead to autoimmune response. And if so how to identify those susceptible and intervene in the process (hopefully not with the price of a weakened immune system and more random illness!)
See my response to Holger above, MD. In it I clarified that at least in my case (I realize one person is not statistically significant but it still might provide clues), the "hyperalert immune system" went on for 40 years before the antibody attack. But there's yet another factor (again just for me, which could be meaningless or could be a "good example) I developed antibodies to HepC sometime about 20 years before my first autoimmune attack. I have the antibodies to this day. (but no detectable virus). Since those antibodies were hanging out all those years with no virus to attack could they have "turned on" my own tissue??
Why do I feel like I'm making less sense, not more, as I go on!?
Thanks for posting, Cheryl. Quite a bit technical for me, but perhaps the others will be able to get something from it. It's hard when you have a complex question, but need a simple answer to understand!
Faustman refers to them as rogue T-cells. As far as I have understood these rogue cells are just a small fraction of the T-cells. Maybe there is just one stem cell that has inherited the genes for autoimmunity. The T-cells being born from this stem cell will inherit the genes. At some point the T-cells turn into active rogue cells. Somehow the vaccine BCG creates a response in these rogue T-cells and this will normalize their activity. Behave, look closer, this is your tissue you morons, LOL!
I find this area fascinating. I have 2 autoimmune disorders myself, hashimotos and Type 1. I am not sure what provoked either disorder, but I developed symptoms of diabetes right around my diagnosis for hashimoto's. I actually incorrectly thought that my hypothyroidism/synthroid were causing them at first.
I've also read that thyroid disorders and type 1 diabetes have a genetic connection with certain psychiatric disorders, including schizophrenia. If only medicine could keep the body from attacking itself! So many people could benefit!
I've seen a high correlation between thyroid disorders and some forms of mental illness, but more the mood disorders such as Depression and some Anxiety Disorders, not particularly Schizophrenia. In the past, people were commonly diagnosed with one of those illnesses and it was later found to resolve once the thyroid was dealt with. Thyroid affects many many things including mood (more likely anxiety if you are hyperthyroid and depression if you are hypo). Now, it's common to suggest people reporting those symptoms have their thyroid tested.Since coming on this board, I've noticed a higher degree of people self-reporting as suffering from Bipolar, Depression and Anxiety disorders but I think Depression, in general is twice as common in the Diabetic community due, not so much to biology as to the difficulty of managing this disease.
I meant more like people with schizophrenia are more likely than someone from the general population to have a first degree relative with thyroid disease/diabetes, suggesting that they are from similar genes. just for some reason or another, one family member's brain was targeted and the other's endocrine glands were.
But I do agree, depression and diabetes are so intertwined that it is unclear as to which came first or if diabetes leads to depression. The important thing here is that health care providers know to ask the tough questions to screen everyone with diabetes for depression so they can get help!
I'm not aware of any genetic link between schizophrenia and thyroid or diabetes, though the genetic aspects of mental illness is not my area of expertise!
I do agree with you very much that the psychological aspects of D are really not paid much attention! I don't have a lot of hope that endos let alone PCP's are qualified or have the time to assess for depression. But they can certainly ask a few key questions and make a referral for further assessment!
Fascinating! Did you happen to see the part about olmesartan oxi(whatever) towards the end. Why have I never hear of this? This guy was claiming he was reversing Type 1 DM (amongst other autoimmune diseases) on his slide at the end of his presentation with this drug.
I would like to add that T1 diabetics should watch for these additional autoimmune conditions:
-thyroid: hashimoto, graves disease - can lead to slower or faster metabolism and can cause problems in glucose control -digestion: coeliac disease - can lead to malnutrition in amino acids and vitamins. Can cause depression, nerve damages and problems in glucose control
-adrenal gland: addison's disease - can lead to weakness
-skin: lichen sclerosus, lichen ruber, vitiligo - psychic side effects
-brain: myasthenia gravis - can lead to muscle weakness
-...
Holger,This is exactly why I travel to The Massachusetts General Hospital in Boston, at my own expense, once yearly; in order to donate my Type One blood for Dr.Faustman's research. Her efforts point to a "cure" or at least significant reduction of insulin needed to maintain good control and consequently, better health for type one diabetics. You explained autoimmunity and diabetes VERY well. Thanks.
Also thanks to you Zoe, for posting this thread. I ,too, rarely get sick from viruses, infections and the like. I thought it was because I worked 30+ years in a school system, and had been exposed and rendered immune by the drippy nosed hugs, coughs/sneezes in my face, and wet touches I received from my little students (lol).
The healthy body can produce around 20 units of insulin per hour. Just image this BCG treatment could restore 10% of this capacity. That are 2 units of insulin. For me this would result in having the capacity to reduce the blood glucose by more than 70 mg/dl. Just imagine how easier the control must be. Furthermore we would have some residual c-Peptide and even a small fraction of Amylin. All said to play an important role in the long term development of complications. The potential is there and your travels are really worth the effords.
