Hey y’all! I’m a mom of a 7 year old struggling to find answers. In June of this year my 7 year old starting peeing the bed, had lost 8 lbs, drinking a lot, eating a lot, and we started checking blood sugars her A1C came back 5.6. Her randoms are anywhere from 140-216 her morning fasting averages at 130. We have been diet controlling. We have since seen an endocrinologist for labs and she said possibly very on set early type 1. So far her labs have came back pretty normal Her c peptide was 1.38 fasting (0.90-7.10 normal) immunoglobulin A 44.9 (41-345 normal) her glutamic acid decarboxylase antibody <5.0 (0-5.0 normal) insulin antibody <.4 (0-.4 normal) IA-2 <5.4 (0-7.4 normal) zinc transporter 8 ab <10. (0-15.0 normal). Her urine WBC was high but it was cultured last month and it didn’t grow anything. Her urine osmolality was slightly low and her total bilirubin was low. Her endocrinologist should be calling us back with what she recommends next which might be 2 hour glucose tolerance test. I’m just curious if anyone else has experienced any of this. Most stories I read there kids are in DKA and blood sugars 200+. I’m just concerned and need help.


There is another possibility other than type 1 DM. I’m just throwing this out without any expertise, It could be what is called, Pediatric Mature Onset Diabetes of the Young (MODY). This is caused by a single gene mutation causes problems with the development of insulin producing Beta cells. It is not type 1 or 2. It normally presents in adolescence and your child is only 8, but all these tests being normal makes MODI something to consider. While it is a single gene, if I understand correctly, MODI can be caused by one of 30 genes.

I know you are worried, I would be too, if one of my children had these symptoms, especially the weight loss. Good luck to you and yours, Mom.

The following is from

Monogenic forms of diabetes account for approximately 1–2% of diabetes in children and adolescents, and its incidence has increased in recent years due to greater awareness and wider availability of genetic testing. Monogenic diabetes is due to single gene defects that primarily affect beta cell function with more than 30 different genes reported. Children with antibody-negative, C-peptide-positive diabetes should be evaluated and genetically tested for monogenic diabetes. Accurate genetic diagnosis impacts treatment in the most common types of monogenic diabetes, including the use of sulfonylureas in place of insulin or other glucose-lowering agents or discontinuing pharmacologic treatment altogether.

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These are same symptoms I had at age 5 (55+ years ago!!). My kindergarten teacher wondered why I started using BR every day (1/2 day), and my Mom noticed similar frequent trips overnight, along with huge appetite and taking naps after school. I think your child may be in earlier stage or slower attack on pancreas.

My bilirubin has always been low (first known as adult), but no treatment or knowledge that it is related to diabetes.

Fortunately my Mom got me to doctor who immediately sent me to hospital, where I was diagnosed and started insulin injections (and given IV fluids the first few days). The pediatrician smelled my breath and knew immediately due to ketones (fruity smell). Today they would check urine ketones.

The progression of loss of beta cells can vary, and there is often a honeymoon period for children where pancreas may increase/decrease ability to produce insulin.

Are you doing regular bg checks? Fasting and after carby meals would help identify how much insulin she is producing. Lower carb will reduce demand for insulin.

I think most folks see the signs, but don’t think it’s serious, until they get to DKA, so great that you knew something was off, like my mom did.


This was me at age 15. We did the glucose fasting test, and I passed with no issues. The doctor said, look, there is nothing we can do here. Go live his life, and it will be resolved to diabetes or not. It did in 17 months. It was miserable, and I am not saying that anyone should use 1973 technology or thinking today. Heck, half those tests were not around in 1973. I wish your daughter the very best. I know it is tough.



Sounds like typical DM symptoms. The numbers don’t look too concerning yet, but I’m sure that the kid isn’t feeling very well. 8 lbs is a LOT of weight for a 7 year old. The endo will know what to do.

Hang in there. Your walking through the right process. If you feel a bit panicky and like you need to do some research, you could start googling things like, “Dexcom continuous glucose monitor.” That will start acquainting you with medical devices that people like us use. Dexcom’s are very helpful and it might put you at ease to know that they exist.

Dr Richard Bernstein has lots of videos to learn about diabetes. “Sugar surfing,” is a good book. Joslin Diabetes Center, American Diabetes Association, and JDRF (Juvenile Diabetes Research Foundation), and International Diabetes Federation will have resources to learn from.

But, for pediatric, I recommend the Juicebox podcast as a starting point. He’s gonna talk about Looping in more recent podcasts - that’s not for you. Start with older podcast episodes, like this one.

Reach out to us with any questions or concerns. There is someone always here to talk. There is a special parents section of this forum if you need it. It can be accessed by selecting “Type 1 and LADA” from the dropdown menu on the forum page. Then, select “Parents of Children with Type 1 Diabetes.”


Thank you! I’ll research just wanting to know what’s going on and kinda driving myself crazy. Luckily we are usually on the lower side on 100 ive only seen below 100 2 times and only over 200 2 times so far but we aren’t checking that often just usually am fasting and 1 time throughout the day.

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Believe it or not your child’s doctor may not be aware of MODI. We tend to know a lot about a very specific thing where doctors have to have such a wide spread knowledge, so, it is possible for them to miss stuff.

Usually if your kid is thin and losing weight, you are likely looking at type 1 .
If your kid is obese, then Mody is possibly, but it’s pretty rare in a 7 year old.

Sometimes type 1 has a slow burn and takes a while of ups and downs.

Really though a blood test can determine this.

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She is by no means obese. She has always been thicker/more filled out. She is a lot taller than most kids her age. Her BMI I think is 18?

We have tested her for all of the following
Poct glucose, hemoglobin A1C, ketone, comprehensive metabolic panel, c-peptide, free T4, Glutamic Acid Decarboxylase Antibody, Immunoglobulin A, insulin antibody, islet antigen-2 (IA-2) autoantibody, lipid profile + ldl, thyroid antibodies, TSH, tissue transglutaminase IGA, zinc transporter 8 Ab, urinalysis, urine osmolality. and apparently they’ve ordered more testing because we called today because everything initially ordered came back and were hoping we’d get results but they said they were waiting on a few more things to come back

Good you got some comprehensive tests.
The real answers will be the c peptide and the antibody tests.

If her c peptide is high and her antibodies are negative, she’s type 2.

If she positive for antibodies she’s type 1

If she’s negative for antibodies but has a low c peptide, they you are back where you started.

Some type 1 don’t have the antibodies.

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Consider calling Joslin Diabetes in Boston for an appointment. 617-309-2440. You could ask your Doc to refer you to the Pediatric Clinic: 617-732-2603. They have seen it all and could be your best chance of getting a correct diagnosis. Best of luck.

FBG 130 with lower c-pep. It looks like T1. either way, a good thing it’s being diagnosed early. There won’t be a DKA with a week in hospital, like some poor kids.

I don’t know if anyone has already mentioned this, but you ought to reach out to Dr. Raghu G. Mirmira in Indianapolis if your daughter is in early onset stages. He is working on reversing type 1 diabetes. I saw him at the 2020 T1D Summit and his work is cutting edge. https://medicine.iu.edu/faculty/5094/mirmira-raghu

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Thank you I will try to look into this. I’m just not getting anywhere she is set up for fasting GGT on the 9th of September and her endo said sometime it is caught early and take more steps to diagnose

Hi Razorbacks1113,
My name is Ken and I am a MODY-type (aka monogenic-type) diabetic. There are three so-called Hepatic Nuclear Factor types/genes within known MODY forms of diabetes overall. These are:
a. HNF1-alpha (this is the gene with mutations underexpressing insulin that I inherited)
b. HNF4-alpha (this is another one – quite similar phenotypically/genotypically to HNF1-alpha in terms of the diabetes manifestation and hyperglycemic properties)
c. HNF1-beta (this is the third one, and it is in the longer term the most serious because it affects kidneys and can cause earlier death (e.g. in middle age) due to kidney failure that is independent of the diabetic hyperglycemia (if poorly controlled or managed with or without insulin).
I am very well studied on the biology of all forms of diabetes, and not just the monogenic forms. Most monogenic forms are underpinned by single (hence, “mono” genetic) genes that are autosomal-dominant from the (Mendelian) inheritance point of view. That means that if one parent has the gene mutation, there is a 50%/50% chance of inheritance.
You should be aware of some important factors:

  1. Some of the more common (including HNF types) monogenic forms of diabetes are unlikely to be diagnosed by any MD, including any endocrinologist. It would be very unusual for any diabetologist or endocrinologist to be significantly familiar with these forms of diabetes, and all of the conventional guidelines and testing methods are WRONG and/or inappropriate for these forms of diabetes, and incorrect conclusions will most likely be derived, if any.
  2. If, after much more diagnostic work and effort and so forth, you are able to identify a monogenic form of diabetes (which CAN be done, but you are unlikely to be able to find competent MD assistance for this – I can help you if you would like), I would strongly advise NOT to use any form of insulin secretagogue as treatment, but rather to use insulin. I use human insulin (Insulin Regular and Insulin NPH) exclusively, and this is more than adequate for tight BG management/control for me, and would be for an early T1D as well.
  3. Your child would be exhibiting polyuria and polydipsia at an unusually early age for most or all of the more common forms of MODY, but there are many, many less common (more rare) forms, and some of these are more likely to result in <20% of normal beta-cell function at childhood/younger ages.
  4. Regardless of form of diabetes, once ~80% of normal (non-diabetic) beta-cell FUNCTION is lost, all of a sudden one or both of the two symptoms you report for your child suddenly appear. So you can count on the fact that, for whatever reason, your child has lost roughly 80% of normal beta-cell function already. This is VERY serious – you have a true childhood-onset diabetic daughter.
  5. The CAUSE of the clinically-recognized symptoms of (4) is abrupt LOSS of insulin granulation in the remaining beta cells. Insulin granules are the STORAGE form of insulin within the beta cells. The remaining beta cell population and total/aggregate function are too overtaxed to be able to build up / manufacture the stored form of insulin anymore.
  6. Once granulation is lost, the ACUTE insulin response (to meals, and presence of amino acids and glucose in portal vein as they are delivered from small intestine to liver from that meal) is LOST. This is why, all of a sudden, there is abrupt loss of BG regulation during the prandial nutrient-absorption interval which will typically last many hours, and up to twelve or more for a meal with substantial protein content.
    It would be my informed guess that your child is more likely to be a childhood-onset T1D than a monogenic type, but both are definitely possible and need to be thoroughly investigated ASAP using well-informed methods. I can help you with all of these, and for any form of diabetes.
    In any case, I would recommend insulin therapy to be initiated IMMEDIATELY. YOU will have to manage this for reasons explained above. And to do so you must self-educate. And I can help you. If you want to pursue this path, we should establish private comm’s (by email and/or phone) independent of this forum. There is far too much biology and information (e.g. testing methods) involved for any other channel of regular comm’s.
    If your child indeed has incompletely-matured T1DM it is even more critical, for preservation of remaining beta cells (which could make an enormous difference to the remainder of her life) to IMMEDIATELY get her started on a strict, animal-foods only diet with absolutely NO significant carb content whatsoever, in addition to a very discriplined form of insulin therapy. This can DEFINITELY save/salvage her remaining beta cells, and you likely still have a year or more of time before which your child would become “insulin-dependent” without proper therapies – that is, lose virtually all remaining beta cells.
    For the autoimmune form of diabetes (T1DM) you MUST absolutely minimize the antigenic stimulation of antibodies, and this is in direct proportion to portal AAs (amino acids) and glucose. NO homo sapien needs ANY carbohydrate content in diet. NONE – believe me. And it is anti-evolutionary to include these in our diet(s) as well. And glucose is ~4x more powerful an insulin secretagogue than AAs. And your child (and all of us homo sapiens, for life) NEED AAs in the form of animal proteins – these are vital for growth and health, and ESPECIALLY in youth for certain developmental needs, and in older/elderly age for good smooth/skeletal muscle health and avoidance of sarcopenia.
    You should get your daughter tested for all three of the most common forms of antibodies (each associated with a specific molecular antigen secreted by beta cells in response to AAs and glucose in islet blood via portal vein). IMMEDIATELY. REGARDLESS of what any MD tells you. Find one who will order the tests for you, or order them yourself via the LabCorp or Quest Diagnostics front-end online “storefront” services. I think, and can check online to be sure, that you likely can get at least one of these (the most common one, which is for an enzyme antigen) by ordering online.
    This is how to test for T1DM – it is straightforward and definitive. If, and only if, your daughter were to test negative (maybe two times for redundancy and reliability) for all three pairings of antigen/antibody (it is the antibodies that will be tested for in serum sample(s)), then I can help you to analyze and test for one of the many forms of monogenic diabetes – this is a longer and more complex diagnostic process but also less urgent – far less urgent.
    Let me know, by replying, if you want to pursue the avenues described above. You will not find any MD in the world, I believe, who knows as much broadly about the biology of diabetes as I do. I have read ALL of the basic research literature and biological research literature and genetic research literature and clinical research literature relating to non-diabetic and diabetic blood glucose regulation – EVERYTHING. Noone else in the world, as far as I am aware, has done anything even close to this. There are narrowly focused specialties for the most basic biological research fields. I have absorbed all of the knowledge from all of the many focused areas of research, and hence have a full understanding of the BIOLOGY. Without understanding the biology, one cannot understand how to diagnose and optimize therapies/management for the clinical condition(s).
    Anyway, enough said for now. Just let me know if you want my help. I have three different rare genetic conditions, by the way, and the most serious one is CVID (a primary/polygenic immunodeficiency – in my case I have essentially NO B-cell (not to be confused with beta cell(s)) function at all). The third condition, genetically related to the HNF1a-mutations, is a congenital malformation of both kidneys – quite severely so. HNF1a is a homeobox gene, and this gene is very critically expressed in liver, intestine, kidneys, and endocrine pancreas (aka islets of Langerhans, where the beta and alpha and delta cells are located). So these conditions, the CVID and diabetes having required self-diagnosis, are part of the reason for my very unusually broad and deep reading of the literature for between one and two decades now. Lest you think I am simply engaging in hyperbolic braggadocio. I have helped a lot of people with a variety of life-threatening and serious medical conditions over the years. But it takes a very committed individual on the other side, which would be you in this case and more usually has been an adult patient. If you prefer to rely solely upon the medical community, alternatively, I sincerely wish good luck to you.

Hi! Welcome to the club none of us have ever wanted to join. I want to echo another poster- @mohe0001 look up the Juicebox podcast. juiceboxpodcast.com Seriously, Scott is the best and so encouraging. There is also a facebook page and the people on there are some of the most level headed, kind, informed diabetes people out there. Tons of parents going through what you’ve gone through. Diabetes is completely overwhelming at first so go slowly, listen to your endocrinologist, and give yourself lots of grace and breathing room. Again, I’m sorry your here, but there are so many knowledgeable people here. You’re in the right place…

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P.S. I had meant to include one more consideration with respect to potential MODY. That would involve the father. Further points:

  1. While my paternal grandfather was diagnosed with diabetes in his mid/late 40s, my own father was never diagnosed. HNF1-alpha was not ID’d as the underlying homeobox gene for MODY-3 familial inheritance until the early/mid 90s. About half of HNF1-alpha diabetics, if they become “overt” by accruing a loss (usually by combination of genetic underexpression of insulin – the deficit at birth, and often further additional diet-induced or secretagogue drug-induced loss of beta-cell function on top) are misdiagnosed as T2Ds and the other half as T1Ds. I have 40% beta-cell function – rock-solid stable and this will remain for life. This is VERY serious in terms of diabetic complications that will accrue without recognition and ensuing insulin management, but this takes years and years of hyper-normal necrosis/apoptosis of neural and vascular tissues due to the acute/transient hyperglycemic response to EVERY meal without exogenously/subcutaneously-administered insulin. If treated with sulfonylurea(s), further progressive beta-cell loss will be induced by the drug-secretagogue – that is guaranteed regardless of what any clinician might claim otherwise. Similarly, as in pre-T2DM and overt T2DM (after loss of 80% or more of non-diabetic/normal beta-cell function), exceeding carb tolerance in diet WILL induce further beta cell loss as well.
  2. My father had very ugly-looking feet, which I now recognize as those that come with diabetic complications. But he was never even diagnosed, because he, unlike his father, never lost an additional 20% of beta-cell function (due to modern, urban diet) as did his father, and hence never developed the polydipsia or polyuria symptoms that are almost ALWAYS required for diagnosis by an MD of any form of diabetes whatsoever. Your daughter has already manifested these symptoms. And so you can also rule out MODY-2 – this is due to underexpressed glucokinase (a form of hexokinase expressed only in liver and endocrine pancreas), and does not induce ANY complications and should NEVER be treated medically at all. Clinical polyuria/polydipsia are absolutely never seen with MODY-2.
  3. You should know your own HbA1C, at a minimum. It is possible, although less likely than maybe for the father of your daughter, that if your daughter has inherited a MODY-type gene with mutations you could be the parent with the source of inherited allele. Or it could be the father. Same goes for him – investigate HbA1c at a minimum if possible.
  4. But as I wrote earlier, there is much more time for investigating potential MODY, and it is also more likely in my opinion that your daughter has developed T1DM but has still ~20% of beta-cell function remaining. And for T1DM specifically, that is equivalent to 20% of her beta-cell population remaining. Because in T1DM, unlike T2DM, either the beta cells have been destroyed by autoimmune response, and so are not there in the islets anymore, or else they have full and normal uncompromised function.
  5. So once again, to reiterate, it is urgently and vitally important to get ALL of the clinically available antibody testing for T1DM done ASAP. The three recognized forms of ICAs (islet-cell antibodies/antigens) are:
    a. glutamic acid decarboxylase (aka GAA or GAD) enzyme(s) – most common in T1Ds of the three
    b. insulin (the hormone itself), aka IAA (insulin autoantibodies/autoantigen)
    c. protein tyrosine phosphatase (aka IA2 or ICA512), another enzyme associated with acute pulsatile insulin response/secretion by beta cells

I think that you can order (a), at least, online. This will probably ID 9 out of 10 (very roughly, as I recall – might be a bit off in that stat) T1Ds. For (b) and (c) you might need order from MD. I can help you with this too. Not uncommonly more than one of the antibody types will be tested for with positive/non-zero results. Concentration in serum of each antibody is also indicative of rate of progression, or this is the conventional clinical thinking anyway. I think that your daughter, if indeed a T1D, has a slower-than-typical rate of progression for a childhood-onset T1D. That is good news, if so, for early T1DM at any age. You will be more likely to prevent clinical insulin-dependence (loss of all beta cells) for the rest of her lifetime as a result. And likely, if so, regeneration back toward 100%. Probably NOT anywhere near 100%, but likely >> 20% after many years. Beta-cell regeneration after age five is very slow in our species. But they WILL regenerate if the autoimmune response is suppressed, albeit slowly. And they DO in ALL T1Ds, but they are killed off just as fast normally/usually in fully-mature T1DM. Your daughter, if indeed T1D, can avoid this with the proper discipline of diet (most/more importantly) and highly-disciplined insulin therapy.

P.S. My comment on potential T2DM is that this is virtually ruled out by your case description. Highly unlikely – nothing is impossible, but T2DM for your daughter comes awfully close. I would completely put that out of mind for now. T1DM most likely, by far, and potentially/secondarily one of the monogenic forms. There is much time with little short-term consequence to test for and diagnose monogenic diabetes. Concentrate on the T1DM. That is more urgent to diagnose ASAP and then to intervene to prevent insulin dependence, which is the clinical term/phrase for susceptibility to DKA (ketoacidosis) without continuous exogenously supplied/administered insulin. And that is only one of many lifelong consequences that can be avoided, with proper intervention, for your daughter if she is a T1D as I would most likely think. You may likely have a year or more still to rescue her from fully mature T1DM and insulin dependence for the remainder of her lifetime, based upon your reports of the case.

P.S. Razorbacks1114, I very infrequently visit this forum. I happened to read your post. I will try to remember to check at least once daily for the next few days, to look for a reply from you. Thereafter I might not visit the forum again for months.
My sole purpose in ever visiting this forum, at least at this stage, is to potentially spot a case report for which I might be able to help. I have little to nothing further to learn about diabetes of any form from, really, anyone in the world.
Your daughter is a rare case of not-yet fully mature T1DM. I doubt that any of the T1Ds who participate in this forum are not fully mature. They are knowledgeable – T1Ds typically are much more knowledgeable than T2Ds. That is, in terms of clinical methods and BG management and so forth.
But your daughter is a special case, if indeed she is a relatively early T1D. It probably took >> 1 year for her to lose 80% of her beta cells from inception of the autoimmune response. But this pre-clinical loss is only detectable by means of the most discerning use of HbA1c, for the most part. It is rare for any MD or individual to detect pre-clinical diabetes in any form this way (as I myself did, eventually at age 51). Anyway, your child is no longer pre-clinical. She has overt diabetes now. Probably of autoimmune type/form.
I hope you will respond within the next few days while I log in to check for this. I am tempted to publish my cell phone # herein, but will hold off for now or maybe indefinitely. I don’t know of a more secure means of letting you know what my direct contact info is via this forum.
If any others know of such means, please advise in response, and thanks.
My landline phone # is in the public white pages. You can leave a voice message that I will receive within a day normally. This phone # is:
978 453-7426
I have little problem divulging this # – it is already public.