MODY - It's Not Type 1 and Not Type 2, but Something Else

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MODY - It's Not Type 1 and Not Type 2, but Something Else

Up to 20% of people diagnosed with Type 2 diabetes are not overweight. If you are one of them, it's worth doing some research to make sure that you don't, in fact, have one of the forms of what are often called "Type 1.5" diabetes, forms of diabetes that many doctors do not know about.

There are two major kinds of "Type 1.5." The most common is LADA (Latent Autoimmune Diabetes of Adults) which is a form of slow-developing autoimmune diabetes which has some genetic overlap with both Type 1 and Type 2 diabetes. You can read more about LADA HERE.

The other cause for diabetes in thin people is a selection of genetically-linked forms of diabetes which go under the name MODY, which stands for "Maturity Onset Diabetes of the Young." MODY forms of diabetes are caused by at least nine different genes, some related to each other in function and some not. The commercially available MODY gene test suite only tests for six of these genes.

MODY genes have one major thing in common--they are "monogenic" which means that you only need to inherit one copy of the gene to display the disorder that the gene causes.

MODY forms of diabetes were long believed to affect around 2% of all people diagnosed with both type 1 and type 2 diabetes. However, a study of 586 children diagnosed with Type 1 diabetes found that a full 8% of them were actually carrying one of the three most common MODY genes. It is likely that a similar number of people diagnosed with Type 2 may also have one of these genetic forms of diabetes, too.

Prevalence, Characteristics and Clinical Diagnosis of Maturity Onset Diabetes of the Young Due to Mutations in HNF1A, HNF4A, and Glucokinase: Results From the SEARCH for Diabetes in Youth. Catherine Pihoker et al.J Clin End & Metab October 1, 2013 vol. 98 no. 10 4055-4062.

Recent Research Has Changed Our Understanding of MODY

Until very recently, the MODY form of diabetes were thought to only appear in people under age 25. However, recent genetic studies where the family members of people diagnosed with MODY were given genetic testing turned up the fact that people carrying the MODY genes are often misdiagnosed as having Type 1 or Type 2 diabetes.

It was also learned that MODY can develop into full-fledged diabetes as late as age 50. The Klupa study, referenced below, found that in one kind of MODY diabetes developed in 65% of those who carried the gene by age 25 years and in 100% by age 50 years, so more than 1/3 of all people with this kind of diabetes do not develop it in youth.

Gene testing also revealed that in some forms of MODY, the blood sugar problems may be so mild as to escape diagnosis.

This study explored the insulin secretion of non-diabetic people carrying diagnosed MODY genes.

Altered insulin secretory responses to glucose in diabetic and nondiabetic subjects with mutations in the diabetes susceptibility gene MODY3 on chromosome 12 MM Byrne et. alDiabetes, Vol 45, Issue 11 1503-1510

So while it is usually true that a person must have a parent who carries the MODY gene to develop MODY, the fact that your parents were not diagnosed with MODY does not rule out the possibility that you have it.

This is especially true if you got your MODY gene from your father. If the MODY gene comes from your mother, it is much more likely that she would have developed gestational diabetes during pregnancy and been diagnosed, though even here you can't be sure as testing and treatment of gestational diabetes in people who were not obese was very lax as recently as the 1980s. In addition, being the product of a diabetic pregnancy may change the intensity with which the MODY genes express.

Determinants of the Development of Diabetes (Maturity-Onset Diabetes of the Young-3) in Carriers of HNF-1{alpha} Mutations Evidence for parent-of-origin effect Tomasz Klupa, et. al. Diabetes Care 25:2292-2301, 2002

This next study suggests that specific mutations in the gene causing MODY-1 affect the age at which it becomes severe enough to be diagnosed. Different mutations, different ages of diagnosis.

The Diabetic Phenotype in HNF4A Mutation Carriers Is Moderated By the Expression of HNF4A Isoforms From the P1 Promoter During Fetal Development. Lorna W. Harries, Jonathan M. Locke, Beverley Shields, Neil A. Hanley, Karen Piper Hanley, Anna Steele, P?l R. Nj?lstad, Sian Ellard, and Andrew T. Hattersley. Diabetes 57:1745-1752, 2008

Doctors have discovered that quite a few of the people who were diagnosed with Type 1 diabetes as infants may actually have inherited not one but two copies of a MODY gene. This causes a severe form of diabetes usually misdiagnosed as Type 1 diabetes. But since it is actually a genetically caused failure to secrete insulin, people with this disorder can recover the ability to secrete insulin when treated with sulfonylurea drugs instead of insulin.

Switching from Insulin to Oral Sulfonylureas in Patients with Diabetes Due to Kir6.2 Mutations Ewan R. Pearson, Volume 355:467-477.August 3, 2006, Number 5

People with MODY-3 have been found to have very low Cardiac Specific C-Reactive Protein. (hs-CRP) with the mean of 0.20 mg/l and a range of 0.03 to 1.14 mg/l. This may actually be a cheap and effective screening test for this specific form of MODY as it appears to identify 80% of people with diabetes who actually have MODY. Hs-CRP in people with MODY 2, however, is very close to that of people with regular Type 2 diabetes.

Assessment of High-Sensitivity C-Reactive Protein Levels as Diagnostic Discriminator of Maturity-Onset Diabetes of the Young Due to HNF1A MutationsKatharine R. Owen, et al. Diabetes Care September 2010 vol. 33 no. 9 1919-1924 doi: 10.2337/dc10-0288

Other Useful References for an Overview of MODY:

Clinical Implications of a Molecular Genetic Classification of Monogenic Beta-cell Diabetes. Medscape CME. Rinki Murphy, MBChB; Sian Ellard, PhD, MRCPath; Andrew T. Hattersley, BMBCh, MA, DM, FRCP.

Molecular and Clinical Characterization of Mutations in Transcription Factors.Timothy M. Frayling, Julie C. Evans, Michael P. Bulman, Ewan Pearson, Lisa Allen, Katharine Owen,
Coralie Bingham, Michael Hannemann, Maggie Shepherd, Sian Ellard, and Andrew T. Hattersley.Diabetes.Vol. 50, Sup 1,Feb 2001

Genetic Types of Diabetes Including MODY (UK - Exeter Research & Testing)

Diagnosis and Management of Maturity-Onset Diabetes of the Young.Timsit, Jose; Bellanne-Chantelot, Christine; Dubois-Laforgue, Daniele Velho, Gilberto. Treatments in Endocrinology. 4(1):9-18, 2005.

Mutations at the BLK locus linked to maturity onset diabetes of the young and -cell dysfunction. Maciej Borowie et al. PNAS, Published online before print August 10, 2009, doi: 10.1073/pnas.0906474106

You can read a slightly more informative report on this study here:

Joslin Study Identifies Gene Linked To Rare Form Of Diabetes

How Do You Get Diagnosed with MODY?

Unfortunately, the only way to get a definitive diagnosis it to take a series of up to 6 expensive genetic tests. But these tests may be inconclusive since there are a significant percentage of people with clear-cut MODY symptoms and family histories who don't test positive on these tests.

A study of individuals with clinically labeled type 2 diabetes, found that when HNF1A and HNF4A were sequenced in 80 subjects with diabetes diagnosed <=30 years and/or diabetes diagnosed <=45 years without metabolic syndrome 12 of the subjects were found to have mutations in the HNF1A and HNF4A genes suggestive of MODY. This represents 15% of those 80 subjects.

Most significantly, though, of these 12 subjects, only 47% of MODY subjects identified met current guidelines for diagnostic sequencing. This means that if they took the standard MODY tests their mutation would not have been found.

The study concludes, "We recommend that all patients diagnosed before age 30 and with presence of C-peptide at 3 years' duration [be] considered for molecular diagnostic analysis." Note that this is not the same as taking Athena Lab's MODY tests but involves looking at the MODY genes for evidence of any significant defect.

Systematic Assessment of Etiology in Adults With a Clinical Diagnosis of Young-Onset Type 2 Diabetes Is a Successful Strategy for Identifying Maturity-Onset Diabetes of the Young. Gaya Thanabalasingham et al. Diabetes Care Diabetes Care June 2012 vol. 35 no. 6 1206-1212

The Joslin Diabetes Center web site states that one third of the families with the symptoms of MODY diabetes that they are following do not have a diabetes that can be diagnosed as one of the six forms of MODY already identified.

Even worse, most health insurers will not pay for these genetic tests. So if you are a thin person with adult-onset diabetes you may have to approach a diagnosis by ruling out autoimmune diabetes (LADA), looking at your family history, your personal history, your weight history, and at indications of how insulin resistant you are.

Here are some issues to consider in deciding whether there is some possibility you have MODY:

  • If you have diabetes through you have always been of a normal or near normal weight or were at a normal weight until shortly before your diabetes diagnosis. (In some forms of MODY the high blood sugars can cause mild insulin resistance which can lead to weight gain.).
  • If your High Sensitivity (cardiac specific) C-Reactive Protein is low, ranging from 0.03 to 1.14 mg/l, but tending towards the lower end of this range.

  • If you have a history of gestational diabetes that occurred when you were at a normal weight and which developed early in the course of the pregnancy. In people without MODY or LADA, gestational diabetes typically develops only in the last trimester.
  • If you have close relatives who had adult onset diabetes who were of normal weight.
  • If taking a drug that improves insulin resistance like Metformin doesn't make a significant change to your A1c.
  • If you have glucose in your urine though your doctor tells you you are not diabetic, especially if there is a history of kidney disease in your family.
  • If you have an very elevated fasting blood sugar--over 125 mg/dl that cannot be lowered with diet, drugs of insulin.

What are the Characteristics of MODY Diabetes?

First of all, it's important to know that MODY comprises a variety of different and unrelated genetic flaws and new ones are being discovered every year. The ADA "Expert's Committee Report on the Criteria for the Diagnosis of Diabetes Mellitus", which was published in 1998 reports there were three such mutations known. Today a web search will turn up the information that there are 6 known genetic flaws that produce MODY. A researcher from the Joslin Diabetes Clinic told me that they are currently doing a study of families with possible MODY to identify new MODY genes and that they expect to find dozens of them.

There are differences between how the different versions of MODY manifest. But here are some of the traits several forms of MODY have in common:

  • People with MODY are usually of normal weight, at least until shortly before their diabetes diagnosis. However, people with MODY do not have the GAD or islet antibodies characteristic of thin people with adult onset diabetes who have LADA.
  • People with one of the forms of MODY that primarily affect the secretion of insulin in response to a meal may have near-normal fasting blood sugar test readings and very high post-meal blood sugars. This can result in an A1c most doctors consider "normal" though the high post-meal blood sugars can cause complications, especially heart disease.
  • The age of onset of diabetes in at least one form of MODY depends on the parent who passed on the mutant allele. It is significantly younger if it was the mother who passed on the gene and if she had diabetes during the pregnancy. That may be because exposure to high blood sugars in the womb affects the expression of the MODY gene in the offspring. If you have been diagnosed with gestational diabetes when not overweight and your child develops pre-diabetes or diabetes by her 20s without obesity, MODY may be a possibility.
  • MODY may develop at any age up to 55. Unfortunately, many documents about MODY repeat the outdated information that MODY only strikes people under 25, and many doctors continue to believe this. More recent research has shown this is not true, especially for people with milder, harder to diagnose, versions of MODY.
  • Women with MODY are often first diagnosed during a first pregnancy. Though not obese, they develop gestational diabetes very quickly.
  • People with MODY often are not insulin resistant. They will respond to very small doses of insulin or drugs that stimulate insulin production. However, this is not always true. In one version of MODY, high blood sugars apparently cause insulin resistance, though the genetic defect is thought to be the primary cause of the diabetes.
  • Some versions of MODY respond very well to drugs that stimulate insulin secretion. In these forms of MODY, the genetic defect causes the beta cell to fail to get the signal telling it to secrete insulin when blood sugar starts to rise. A strong response to a very small dose of a sulfonylurea drug may actually be diagnostic of several forms of MODY.
  • In one common form of MODY, fasting blood sugar is normal, but insulin secretion begins to fail as blood sugars go over 144 mg/dl. This can lead to a difficult to diagnose form of diabetes as fasting blood sugar may remain normal for many years.

  • People with another common form of MODY, where the defect is in the production of Glucokinase, have elevated fasting blood sugars (125-140 mg/dl) which cannot be lowered, however this form of diabetes rarely progresses and can be controlled with diet. It is usually described as rarely causing the severe complications of other forms, though I have received anecdotal reports from people whose families carry this gene that fatal heart attacks in the 50s are common--a very significant diabetic complication!.

  • In several forms of MODY people may spill glucose into their urine at very low blood sugar levels--140 mg/dl(7.8 mmol/L) or less. People with some forms of MODY often have subtle or more obvious congenital kidney defects and may even have signs of kidney disease before they are diagnosed with diabetes.

Here's a journal article that describes a family where a father is misdiagnosed as having type 2 and his daughter as having type 1. After genetic testing, both turned out to have MODY-1.(HNF4-a Gene)

Identification of MODY:The implications for Holly. Journal of Diabetes Nursing, Jan, 2004 by Jo Dalton, Maggie Shepherd

Indications You Do NOT Have MODY

Because I have been getting a lot of email from site visitors who are wondering if they have MODY, I want to cite some symptoms that make it unlikely you would have a form of MODY.
  • Low fasting insulin or c-peptide level. People with several of the more common forms of MODY usually have normal or near normal fasting insulin levels. The genetic defects they have primarily affect post-meal insulin secretion. A low fasting insulin or C-peptide is much more likely to point to LADA. Read about LADA HERE. LADA is much more common than MODY and the most frequent cause for abnormal blood sugars in thin people misdiagnosed with Type 2 diabetes.

  • GAD or Islet Antibodies or Diagnosis of Other Autoimmune Disease These characteristics make it much more likely that you have a form of autoimmune Diabetes, either Type 1 or LADA.

  • Sudden onset of abnormal blood sugars that deteriorate swiftly. People with MODY are born with MODY and will have, at a minimum, slightly abnormal post-meal blood sugars or, in MODY-2 a mildly elevated fasting blood sugar, all their lives. Blood sugars may become worse with increasing age but in general the progress is gradual. The sudden onset of abnormal blood sugar or a blood sugar that deteriorates dramatically over a brief period is more likely to point to LADA.

  • Use of normal Type 1 insulin doses. If you are using a typical Type 1 dose of insulin, you aren't likely to have MODY. People with MODY typically use the very small insulin doses used during the Type 1 "honeymoon" period all their lives. A typical Total Daily Dose for a person with MODY may be 10 to 20 units depending on body size. In addition, because there is often intact basal insulin secretion, a person with MODY may need much more meal-time insulin than basal insulin.

  • Use of normal Type 2 insulin doses People with MODY are insulin sensitive--often highly insulin sensitive. If you are using over 10 units a day of basal insulin or injecting more than 10 units at meal time you are unlikely to have MODY.

  • Normal Responses to Type 2 Drugs People with MODY rarely see any significant effect from drugs that lower insulin resistance. At the same time, they have a dramatic response to very low doses of drugs that stimulate insulin secretion like sulfonylurea drugs (glipizide, glimipiride, glyburide etc.) or repaglinide (Prandin).

What if You Have MODY?

  • MODY is very like Type 2 diabetes in its effect on your body. Elevated blood sugars injure you slowly over many years, causing neuropathy, retinopathy, heart disease and the other ugly complications of diabetes.
  • The recommended treatment for MODY depends on the severity of the diabetes. Some people with MODY can maintain normal blood sugar levels by restricting carbohydrates. The Glucokinase version of MODY is the one most amenable to dietary control.

    Others, however, may be treated with very low doses of drugs that stimulate insulin secretion. Dr. Andrew Hattersley, the MODY expert who has published the most about MODY, recommends very low doses of Gliclazide (Diamicron), a mild sulfonylurea that is not available in the United States.

    The related sulfonylurea drugs that are available in the U.S. are Amaryl and Glipizide though some people with MODY report these drugs are too powerful. Alternatives are the newer "glinide" drugs, Prandin or Starlix. Others use injected insulin. Doctors assume you'd prefer a pill to shots, so they often suggest the oral drugs that stimulate insulin secretion rather than insulin. But the side effects of the sulfonylurea drugs, can be a problem. They may cause relentless hunger and weight gain and they may possibly raise the risk of heart attack. Sulfonylurea drugs also tend to cause hypos at doses high enough to give near-normal blood sugars.

    The "glinide" drugs, Prandin and Starlix, may be too weak or may lose their effectiveness with daily use.

    There has been concern that using all these drugs over time causes the pancreas beta cells to become exhausted and burn out. A recent study may have found the mechanism by which the sulfonylurea drugs appear to cause beta cell burn out if used too consistently. This study suggests that stopping and starting these drugs rather than taking them consistently will restore beta cell function.

    Mechanism For Sulfonylurea Treatment Failure In Type 2?s
  • Many people with MODY diabetes report that insulin gives them better control and is less likely to cause hypos at doses that give tight blood sugar control. Used in the tiny doses characteristic of MODY insulin won't usually cause weight gain. However, there is another school of thought that believes it is better to stimulate insulin secretion in the beta cell, if possible, rather than inject synthetic forms of insulin because insulin produced by our own beta cells is produced along with a substance called C-peptide.

    C-peptide was long believed to be inert, but much recent research has found that, in fact, C-peptide plays an important part in preventing vascular complications. Injecting insulin may shut down native insulin production, so a person with MODY who injects insulin might therefore end up with much less C-peptide, which might make them more prone to develop microvascular complications.

    This may be the reason that the MODY expert Dr. Hattersley recommends the use of sulfonylureas rather than insulin for people with MODY-1 and MODY-3.

    Fasting Plasma C-Peptide and Micro- and Macrovascular Complications in a Large Clinic-Based Cohort of Type 1 Diabetic Patients
    Francesco Panero et al, Diabetes Care February 2009 vol. 32 no. 2 301-305

    Insights into the Beta-cell from patients with monogenic diabetes. Andrew Hattersley. EASD lecture, Sept 15, 2015.

    Unfortunately, the specific sulfonylurea drug he recommends, Gliclazide (Diamicron) is not available in the U.S..

    If you can get good control with an oral drug it might be worth pursuing, but if you cannot get normal blood sugar readings any advantage you get from manufacturing C-peptide might be outweighed by the damage done by high blood sugars.

    The newer incretin drugs, Byetta and Januvia also produces normal or near normal blood sugars for some people with forms of MODY that respond to beta cell stimulation. But Januvia's potential to promote cancer should rule it out as a treatment. Byetta is a much safer drug if you wish to stimulate insulin secretion in a more physiological manner. If the dose of Byetta dispensed by the lowest dose pen is too strong, it is possible to use a syringe to administer a lower dose. A good endocrinologist can tell you how.

  • If you suspect you have MODY and your doctor wants you to start insulin, a sulfonylurea drug, or a drug like Prandin, be sure to start at a very low dose. The starting dose of either a sulfonylurea drug or insulin that is appropriate for a person who is an insulin resistant Type 2 may be anywhere from two to ten times higher than the dose that works well for a person with MODY. So a typical type 2 dose may cause dramatic hypos.

    The recommended starting dose for Amaryl for someone with MODY, for example, was .25 mg, but since this doesn't adjust for body size, if you are small, even this dose may be way too much. With insulin, start with 1 unit and work up to the dose that gives you good control for a given number of grams of carbohydrate. Many people with MODY may do well with as little as 2-5 units a meal.
  • If you suspect you have MODY diabetes and are of childbearing age, and if there is diabetes in your spouse's family, consider genetic testing. Though it is very rare to have two copies of the same MODY gene, a child who inherits two copies of the same MODY gene will be born with a severe form of diabetes.

The Complications Seen With MODY Vary But Tight Blood Sugar Control is Still Essential

High blood sugars damage your organs no matter what kind of diabetes you have. So you will still want to strive for Healthy Blood Sugar Targets. The more normal your blood sugars, the less likely you are to develop complications.

Even in families that carry "Mild" versions of MODY genes, while there is often no history of retinopathy or kidney failure, there may be a family history of a much higher incidence of fatal heart attacks in people in their fifties. This is because heart attack risk rises with even modestly elevated post-meal blood sugars and people with "mild" forms of MODY have these elevated post-meal blood sugars all their lives. You can learn more about this connection here: A1c and Elevated Post-Meal Blood Sugars Predict Heart Attack. If your doctor is not willing to work with you to help you achieve safe blood sugar levels, look for a doctor who will be more supportive.

The gene defects that cause MODY-3 and MODY-5 also may cause congenital kidney problems that are not the same as the kidney problems caused by high blood sugars. If you are diagnosed with either of these kinds of MODY, you must insist on seeing a highly qualified kidney specialist who can help you learn the best preventative treatments for the specific kidney malformation you might have.

Do You Need MODY Testing?

Right now, MODY testing is extremely expensive and may not be covered by your insurance. Each gene tested for may cost up to $500, but experts on MODY say there are probably dozens more MODY genes we don't yet know about so you may have all the symptoms of a form of MODY diabetes but still have your tests come up negative.

It is also possible that there are non-monogenic forms of diabetes that have the same symptoms as MODY diabetes that are caused by recessive genes that damage the same genes involved in MODY. These genes may not show up in standard MODY testing.

If you are considering getting this testing and must pay for it yourself, ask yourself, "What changes would a positive test make in my treatment plan?" For many of us, the answer is, "none." If this is the case for you, there is no immediate reason to pursue testing.

The Glucokinase version of diabetes does not require any treatment beyond carb restriction. The main thing testing will tell you if you have this form of diabetes is that the "thermostat" that governs how high your blood sugar stays when fasting is broken. If that is the case, you should not obsess if you can't get your fasting blood sugar to a normal level, because in this form of MODY fasting blood sugar will not drop. If you have it, keep an eye on your post-meal blood sugars, as they may promote heart disease. The low carb diet is recommended for this form of MODY (MODY-2). But since the incidence of classic diabetic complications--retinopathy and kidney damage--is very low with MODY-2, keeping post meal blood sugars as close to normal as possible should avoid problems.

With MODY-3 and MODY-1 it has been found that sulfonylurea drugs and the "glinide" drugs like Prandin may be effective in controlling blood sugars. This means you if you are currently on insulin but are diagnosed with one of these MODYs, you could take these pills instead of shots.

Doctors often think this is what patients would like, but my own experience and that of several other people with MODY-1 and MODY-3 who have contacted me is that these sulfonylurea drugs, while very effective at lowering blood sugar at very low dosages, produce constant, gnawing hunger, which makes them unpleasant to take. Small doses of insulin, in contrast, control blood sugars equally well without the hunger side effect. In addition, insulin can be matched to incoming food, while the pills cause an unregulated release of insulin which forces you to eat to keep up with the insulin. I personally have found that Prandin works for me for certain meals, and I alternate between injecting insulin and using Prandin.

If you are already controlling your diabetes on small doses of insulin, and don't want to change, then testing might not be all that useful for you right now. If you would like to try the pills and meet the other criteria for diagnosing MODY-1 or MODY-3, you might ask your doctor for a brief, supervised trial of Amaryl or Prandin using the dosing data published by the Royal Devon and Exeter hospital pm this page:
Guidance for transferring HNF1a or HNF4a patients from insulin to sulfonylureas

There is contact information on The Royal Devon and Exeter Hospital web site which will allow your doctor to discuss this with professionals who have published extensively on this subject. This site also provides genetic testing. It is not-for-profit, unlike the other sites offering MODY testing, and I have heard reports of good experiences with their service.

The other reason you might want a MODY diagnosis is if you are normal weight with an A1c your doctor considers good (high 5% to 6.5%) but find it impossible to keep your post-meal blood sugars near normal. Because MODY-1 and MODY-3 mainly effect post-meal blood sugars people with milder forms of these MODYs may have trouble getting the treatment they need, which may be small dose insulin after meals.

More severe forms of MODY-1, MODY-3 and MODY-5 may be indistinguishable from Type 1 and people with them may do very well on insulin pumps.

Finally, if you and a child are diagnosed with diabetes and the rest of your family history is suggestive of MODY you should ask for testing because it might allow for more flexibility in treatment for your child, plus a positive test result will give an informed doctor a better understanding of what are otherwise confusing responses to insulin.

The Renal Threshold Test for MODY-3

There is one useful home test you can do on your own that can help you determine if you may have MODY-3, the most common form of MODY, which affects the HNF1-a transcription factor.

People with MODY-3 usually have an abnormally low renal threshold for glucose. This means that they will spill glucose into urine at abnormally low levels. A normal renal threshold is usually found when blood sugar reaches around 180 mg/dl. However, people with MODY-3 may find glucose in their urine when blood sugar is at 140 mg/dl.

You can test your own renal threshold using glucose urine test strips which you can buy at any pharmacy for about US$10. Test 2 or 3 hours after eating. If you see glucose in your urine when your blood sugar is no higher than 150 mg/dl, in conjunction with the other symptoms of MODY discussed above, the likelihood is higher that you do, in fact, have MODY-3.

People with MODY-3 are more likely to develop kidney disease, so if you find a low renal threshold, you will want to pursue extremely tight blood sugar control--keeping blood sugars below your renal thresholds as much as possible, and should demand that your doctor does the microalbumin test every year.

Insulin Sensitive Type 2 Diabetes

There is another possibility to consider if you have many of the symptoms described above. There are other not yet identified genetic defects besides the ones that are defined as MODY which cause insulin sensitive forms of Type 2 diabetes. Though the genetic determinant may be different from those causing MODY, the clinical manifestations may be the same: high blood sugars along with a lack of obesity, the development of gestational diabetes at a normal weight, and normal or high sensitivity to injected insulin. The treatment options for these kinds of Type 2 diabetes are similar to the treatment options for MODY. Low dose insulin after meals, sulfonylurea drugs at low doses, and the incretin hormone drug, Byetta, which may turn out, after more years of testing reveals their true side effect profile, to be especially useful to people who fall into this category.

If You Think You Have MODY - Join Our Data Collection Effort

The mail that I've been getting from readers of this page suggests there are many more people with MODY out there than doctors realize, probably because so many of us get misdiagnosed.

If you'd like to join the effort to collect and share more information about people with diagnosed or suspected MODY please EMAIL us with information about your own experience with MODY diabetes.

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