Hello forum; this is my first post. I’m hoping to connect with people with the same circumstances as my son who was diagnosed as a T1D on 9/5/16 at the age of 13. A stranger at a dinner party noticed he was drinking an enormous amount of water and going into the powder room constantly to pee. He said, “I know you don’t know me and I don’t want to alarm you but I’ve noticed your son drinking lots of water and going to the bathroom more often than a kid should. If I were you, I’d check his blood glucose level because my son was doing the same thing at that age and he went into DKA.” He offered to check it with his meter which only goes up to 600. The meter didn’t give a number, it just said “High,” meaning his glucose level was 600+. We took him to the emergency room and they diagnosed him as a T1D within 5 minutes of arrival and sent him by ambulance to Children’s Hospital. His A1C was 12.5 so we learned all about our new normal and went on our way. A few days later, we received his lab results and he had tested negative for all the auto-antibodies in the usual panel of tests normally checked. We had the other two, less common and harder to test auto-antibodies checked, and he tested positive only for the Zinc Transporter 8 antibody (znt8ab). I’m told it’s not uncommon for T1D’s to test positive for that but I understand it’s quite rare to test positive for that only. He started Lantus and Novolog injections and his doctor quickly had to reduce the amount prescribed because he kept going low. We soon transitioned him to the Omnipod and Dexcom G5 CGM. He just turned 14 and he’s extremely active and athletic and stands at 6’4" tall. Since his diagnosis, he’s become a health food and exercise freak. Therefore, we have had to continuously cut back his insulin due to the many extreme lows he was having. It got to the point he felt like he didn’t need insulin. So under his doctor’s supervision, we took what we thought would be a weekend break from insulin that ended up lasting over 6 weeks. His numbers eventually started creeping back up and his doctor wanted him to go back on the pump to get a little insulin so not to stress his pancreas. He now takes no mealtime bolus insulin and only a total of 2.4 units of Humolog per day and he is still getting lows every day. Doctors say it’s probably just his honeymoon period and I’d be on board with that thinking if his C-Peptides had not been in the normal range and he had tested positive for either GADA, IAA, IA-2A, or ICA along with znt8ab. I’ve read where Diabetes may be easier to control in T1Ds who test positive for only znt8ab but I have found little or no additional information on whether or not there may be alternative treatment options available in these cases. I knew very little about Diabetes until it affected our family and I’ve been surprised that it seems most parents have to become their child’s medical researcher and treatment advocate. I incorrectly assumed there would be customized treatment plans based on several factors including why a particular person is classified as a T1D but it appears everyone is treated with the same plan no matter what makes them fall into the T1D category. Had this happened to him a few years ago, he would have been diagnosed a T1D because of the symptoms he presented with but would have been negative for all the tests available at that time since the znt8ab test is fairly new. We are having his genome mapped and are going to search for an expert to see if anything can be gleaned from his DNA to assist in finding other treatment options. If anyone has a similar story and/or advice, I’d love to hear about it. I’d also appreciate comments from anyone who thinks I should not continue to dig deeper in his case. Thanks!
Check back in the next day or so as Melitta will often drop in when her name is mentioned. Good luck with your son. You’re right that a parent’s advocacy is important as a child enters the medical system with a significant diagnosis.
Thanks so much! Terry.
Well, I don’t have any specific advice about that, although I was initially antibody-negative as well. A re-check six months later found low (but significant) levels of GAD and others. Never been tested for the zinc transporter. However, the rest of your story sounds very familiar! I am not on insulin currently, although I have creeping-upwards numbers, and exercise and diet have been fantastically effective in lowering my A1c.
What I can add is that T1 is radically varied in the way it presents. So is T2. So are the MODYs and MIDDs and other rare types of diabetes mellitus. Part of the reason is likely that what we call “Types” are actually aggregations of similar conditions. As a biologist, if someone tests positive for zinc transporters and negative for GAD, I’d assume there are different underlying conditions (possibly based in genetics or possibly based in environmental triggers of autoimmune attack). There is also Type 1b, where autoantibodies are never detected. Also there are now studies showing autoimmune inflammation associated with Type 2 (which likely means hitherto undetected autoantibodies), suggesting there are multiple, unknown genetic and biochemical factors affecting the onset of diabetes.
What all that means, as most of us here have figured out over time, is what people label as Your Diabetes May Vary. What works for one is very likely not going to work perfectly for another. I’m a T1 currently on metformin and no insulin, which would most likely kill the vast majority of T1 diabetics in this forum (by triggering onset of DKA). Regardless of the underlying autoimmune attack, I respond ridiculously positively to exercise. I also like exercise, so it has been very effective in keeping my BG level in the absence of “typical” treatments.
I’m also not advocating treating LADA (in my case) without insulin. I’d prefer to be on at least mealtime insulin, but haven’t been able to see an endocrinologist, since my low A1c makes the stupid-busy endo offices in my state consistently move me to the bottom of the list. One of the things that has recently come up here is the possibility that some children may have slow-onset Type 1 similar to slow-onset T1 in adults (commonly called Latent Autoimmune Diabetes of Adults). The slow-onset period might be characteristic of some childhood cases, and this might relate to what is sometimes called the “honeymoon” period, where the pancreas still produces significant amounts of insulin. In some people the honeymoon period makes treatment easier (for me, it is making things super-easy), but for some it makes management difficult because of unpredictability of response to exogenous insulin.
With an A1c of 12 and a BG over 600, your son is undoubtedly diabetic, and the autoantibody means Type 1. But…it will just take time, and experimentation, and patience to figure out how to successfully treat your son. The reason why your doctor’s aren’t implementing a specific treatment for your son is because there are no specific treatments for different types of Type 1 not based in n=1 experimentation. Every diabetic case is different, so the standard basal-bolus regime for childhood Type 1 is pretty much where you start. Then it gets modified from there depending on how it works (or doesn’t work). That also happens with adults, although seemingly in the opposite way: I was initially diagnosed as Type 2 based solely on age of diagnosis (40), and that meant Metformin and dietary changes. Almost all adult diabetics are started that way (unless in DKA), and a certain number of us (as many as 20%) turn out to be LADA. Then a series of adjustments in treatment begins: sometimes that is adding more orals, a basal insulin, or more testing; sometimes it is “wait and see.”
There is a lot of experience here with parents helping their kids, and also diabetics that were diagnosed in childhood who have been dealing with changing treatment regimes through time. Also adults with similar issues (including how to deal with insulin treatment and exercise, which is not simple). Asking questions here is a great way to get information and support.
Hi dsanders: @Terry4 and @David49 have given you some excellent advice. Based on diagnostic criteria, your son has Type 1 diabetes. It is also true that the treatment plan for each person must be individualized, and it is also true that we must be our own best advocates within the medical system. Initially, we just want answers! I was able to find one article in Pediatric Diabetes, by Danish researchers, that stated that people with Type 1 who test positive for ZnT8 have higher c-peptide levels, meaning making more of their own insulin. And yes, if a person with Type 1 is making more of his/her own insulin, endogenous insulin, diabetes is easier to control and there are way better health outcomes. In your son’s case, I would say that the trick is to find a level of exogenous insulin, perhaps very very low, that keeps his BGs in control but avoids hypos. I know, easier said than done. I doubt that additional tests (genetic, etc.) will shed more light on his situation–just my opinion. But obviously your son is very fortunate to have a parent such as you who is such a great advocate for him. Kudos to you, and best of luck!
Thanks so much David. That’s a lot to digest for a novice T1D parent but it is very encouraging. I appreciate you sharing your knowledge!
Thank you for the information and kind words, Melitta. I read that same article from the Danish researchers and everything else I could get my hands on, including “Think Like a Pancreas” by Gary Scheiner. I was looking for anything that might tell me his diagnosis could be wrong but I realized it is not. I also read where some people who are initially ZnT8 positive can later be ZnT8 negative on subsequent tests. I thought I was on to something with that but quickly figured out if he tests ZnT8 negative in the future, he will just be a T1D with no documentation which might not be good for insurance purposes. I think we are now in a pretty good place with his treatment, better than most, but I still want all the information I can get. Thanks again!
Hi DSanders: It is really common for parents of Type 1s to want to believe that, during the “honeymoon” period, their child does not have diabetes. Best to avoid denial and face the situation head on, which is what you are doing. Think Like a Pancreas is a great resource–I always recommend that as a “first read.” And most of the autoantibodies go negative eventually; it is the positive test that counts, not a later negative–you have the positive test and that is the documentation. (GAD does seem to persist longer, particularly in those with adult-onset Type 1). And I am providing another of my blogs here that I hope might have parts that are helpful to you–most of my advocacy is around adult-onset Type 1 diabetes and misdiagnosis, so ignore those parts, but I hope you find some of my “top ten tips for the newly diagnosed” useful. Really, your son is so lucky to have you as his advocate.
Given the lows, are you eating low carb? I ask because there is a possibility that if you can reduce the insulin requirement through diet you may be able to reduce insulin doses and avoid lows.
Please check out typeonegrit group. Many parents there using this approach, including me for my daughter.
Just joined and responded to a post and ran across yours. First off, just know that every parent and older children diagnosed go through phases. You have to go through them, it’s something that just is. No one can tell you otherwise. I have to put that knowing that you can be going through this and do not want to come across as anyone with answers.
Now, onto some useful info you might find informative/helpful. To be clear, there is no known cure sadly. Every single diabetic wishes there was and there are potential answers every other week. However, in learning a lot in the last year doing some “current” research, the beta cells in the pancreas are the most commonly attacked with T1D. These beta cells produce several hormones which include insulin, GAD and amylin among them.
GAD is used by the body to convert Glutamate into GABA. GABA is also a supplement that many anxious people take in hopes of becoming calmer. GABA is produced both in the brain and in the pancreas, hence some find results when taking GABA to slow/calm the mind (a ton of controversy over the blood/brain barrier and how oral supplements can’t make it to the brain, yadda, yadda, yadda).
Oddly enough, just like cortisol, one of GABAs roles is to control/slow down the immune system whereas Glutamate excites it so the body someway/somehow determines how much of each to use to control the immune system. There is a clinical trial in the pipeline and research, just like every other possible “cure” to diabetes, to use GABA (think mainly through injections vs oral) to try and calm the immune system to either 1) extend the honeymoon period or 2) by the grace of God tell the immune system to knock it off and behave in it’s early stages of going crazy.
IF you try anything, my best advice is to hope for the best but expect the worst to avoid any emotional roller coaster rides. Might work with doctor to check current Vitamin D and Vitamin B12/folate levels in addition to any GABA supplement as these are also immunomodulators and been researched at one point or another to affect the immune system. These are the easiest and relatively cheaper and non-scamming solutions you can try to extend the honeymoon period (I pray to still be in my honeymoon period to try these things – I was diagnosed at ~5 years old and none of this was known yet – they discovered the GAD antibodies after my diagnosis).
Good luck and please share anything you try. I’ve had discussions with my endo and the look on his face when I can out talk him and understand/connect the dotts amazes him. Also self-diagnosed “addison’s disease” 5 years prior to 3 endo’s – PCP recalls me pushing for it to be checked byendo’s, and fighting with them they never did the tests until I went to ER with dangerously elevated levels of potassium. (Addison’s can be another autoimmune syndrome where it attacks the adrenal glands which produce many other hormones that include the balance of sodium/potassium). Gotta keep them on their toes!!!
Additional/non-relevant information. The Omentum (the tummy “fat layer”) has been discovered to (possibly) play a role in the immune system. It’s believed it might be the source of the t-cells of the immune system. When an active t-cell comes into contact with it, it dies whereas inactive t-cells do not. There is another study going on to see if the omentum has equal or better results of islet cell transplants since it’s in the same circulatory system as the liver where they’re done today, also the same circulatory system as the pancreas, and the initial end-goal is to see if the islets survive just as long or longer islet cell tranplants than the liver and if so, then investigate the potential of survival without immunosuppressive drugs (years away at this point since the current process can already last 5+ years.)
Hi Eric - Can you explain more about GAD and GABA or point me in a direction to read? Would type 1’s with GAD auto antibodies then be more prone to anxiety? And are you suggesting that some studies point to GABA supplementation as a possible response to both anxiety and the autoimmune response. This is fascinating!
More info here for diabetes (1st link is the key study): https://www.google.com/search?q=site%3Anih.gov+gaba+diabettes&oq=site%3Anih.gov+gaba+diabettes&aqs=chrome..69i57j69i58.6930j0j7&sourceid=chrome&ie=UTF-8&safe=active&ssui=on#q=site:nih.gov+gaba+diabetes+rats+human+islet&safe=active&ssui=on
More info here on GABA and anxiety: https://www.google.com/search?q=site%3Anih.gov+gaba+diabettes&oq=site%3Anih.gov+gaba+diabettes&aqs=chrome..69i57j69i58.6930j0j7&sourceid=chrome&ie=UTF-8&safe=active&ssui=on#safe=active&q=site:nih.gov+gad+gaba+anxiety
GABA produced by the pancreas AND in the brain and anxiety is of great controversy but yes, the GABA produced in the brain is believed to help with anxiety. Whether the oral kind makes it to the brain is the debate. Many say it helps with anxiety when taken orally, but certainly not everyone. The debate is that 99% of anything consumed rarely makes it to the brain.
The pituitary separates the brain “compartment” and the “body” compartment (hence the blood/brain barrier). Pituitary is what interfaces the two compartments – receives commands form the hypothalamus and sends commands to the adrenal glands via the blood stream because the hypothalamus resides only in the “brain” compartment. (My opinion is just like all the different types of diabetes, there are many causes of anxiety too).
What exactly do you mean by the current process can last 5 plus years? I’ve spoken to Dr. Rocordi who is the doctor who does the transplants. There is so much hope in this and so much information that I can’t even begin to discuss in the begging stages at this point.