Types of Diabetes


Type 1 diabetes

Type 1 diabetes (old name Insulin-dependent diabetes mellitus) occurs when pancreatic beta-cells are destroyed by the immune system and no longer produce insulin. According to conventional views, there is no known way to prevent type 1 diabetes.  However, naturopathic medicine, depending on the individual, believes that it may potentially be preventable.  Type 1 is diagnosed before 30 years of age, but most often in childhood or adolescence.  About 5-10% of people with diabetes have type 1.  People with type 1 require insulin replacement and can be managed quite well with a balanced lifestyle and diet.

Contributory or risk factors for type 1:

  • A positive family history in 10% of patients
  • Genetic susceptibility – histocompatibility (HLA) alleles DR3 and DR4
  • Exposure to virus
  • Presence of autoantibodies
  • Early introduction to dairy, wheat
  • Early cessation of breast-feeding has also been linked to increased risk of developing type 1 diabetes, but the association is unproven and controversial
  • Low essential fatty acids (EFAs) and Vitamin D


  • Polydipsia (excessive thirst)
  • Polyuria (excessive urination)
  • Polyphagia (excessive eating, classic symptom but uncommon)
  • Weight loss
  • Increased fatigue
  • Muscle cramps
  • Mood swings
  • Recurrent minor infections
  • Malaise

Symptoms of acute presentation (diabetic ketoacidosis) include:  nausea and vomiting, muscle cramps, abdominal pain, blurred vision, and fever.


  • Normal physical exam (often)
  • Ketotic breath
  • Dehydration – dry mucous membranes, sunken eyes
  • Loose skin folds from rapid weight loss
  • Skin infections

 Signs of acute presentation (diabetic ketoacidosis) include: dehydration and electrolyte imbalance, fruity smelling breath, Kussmaul breathing (rapid deep respirations), hypovolemia (leading to shock), altered consciousness/coma, and signs of precipitating illness.


Type 2 diabetes

Type 2 diabetes (old name Non-Insulin dependent diabetes mellitus) occurs when the body does not produce enough insulin and/or does not respond well to the insulin it makes (insulin resistance).  Type 2 typically affects people after the age of 40, although it is now also being seen in children and adolescents.  About 90-95% of people with diabetes have type 2.  This type of diabetes is associated with obesity and is preventable.  Treatment is usually dietary and lifestyle modifications, with the option of medication (oral hypoglycemics and/or injectable therapy (insulin)).

Contributory or risk factors for type 2:

  • Sedentary lifestyle and physical inactivity
  • Obesity, especially abdominal (centripetal) obesity (in 85% of patients diagnosed)
  • Diet – excessive eating habits, increased consumption of refined carbohydrates and fats
  • Age – risk increases with age
  • Presence of coexisting hypertension and dyslipidemia
  • Family history of diabetes increases risk; especially if one or more parents or siblings have type 2 diabetes
  • Past history of gestational diabetes
  • Certain ethnic groups are predisposed to type 2 diabetes
  • Intrauterine factors may play a role in the development of type 2 diabetes
  • Rare causes include genetic defects associated with beta islet cell dysfunction (MODY and LADA) and insulin resistance (i.e. Polycystic ovary syndrome); acquired insulin resistance syndromes, drug-induced diabetes, and associated endocrine disorders (i.e. Cushing’s syndrome, acromegaly, phechromocytoma and hyperthyroidism)


  • Polydipsia (excessive thirst)
  • Polyuria (frequent urination)
  • Malaise
  • Lethargy
  • Blurred vision
  • Muscle cramps
  • Poor wound healing
  • Frequent infections

Symptoms of complications include:

  • Angina
  • Neuropathy – numbness/paresthesias (skin sensation, such as burning, prickling, itching, or tingling, with no apparent physical cause)
  • Visual deterioration and blurred vision
  • Intermittent claudication
  • Impotence


  • Obesity – BMI >26kg/m2, especially centripetal obesity
  • Eyes – cataracts, microaneurysms, haemorrhages, macular degeneration etc.
  • Cardiac – previous myocardial infarction (heart attack), congestive heart failure
  • Associated hypertension and high cholesterol
  • Foot – decreases peripheral pulses and sensation, absent ankle-jerk reflex, and ulcers
  • Neuropathy
  • Impaired immune system, thus poor wound healing


 *It is important to note that people with type 2 diabetes may display no symptoms

 Gestational diabetes

This type of diabetes develops in women during pregnancy and disappears after delivery. Gestational diabetes affects about 4% of all pregnant women and increases the risk of both the mother and the child to developing type 2 diabetes.  The common causes of gestational diabetes include:  carbohydrate intolerance with onset during pregnancy (90%); pre-existing diabetes complicating pregnancy (10%); and insulin resistance, possibly due to hormones like progesterone and placental lactogen, which is common in the third trimester.  A rare cause would be the onset of undiagnosed Type 1 diabetes.  As a screening tool, a glucose tolerance test is performed in all pregnant women at 24 to 28 weeks of gestation.  However, prior to this, an indication of gestational diabetes can simply be the presence of glucose in the urine or an abnormally high glucose reading from a random glucose test.  Conventional treatments include dietary and lifestyle changes and possibly insulin for those with poor blood sugar control.

Contributory or risk factors for gestational diabetes:

  • Age over 25 years
  • Body mass index >25 kg/m2
  • Marked weight gain during pregnancy
  • History of glucose intolerance
  • History of large-for-gestational-age infants
  • History of gestational diabetes during previous pregnancies
  • Family history of Type 2 diabetes in first-degree relative(s)
  • History of polycystic ovary syndrome
  • History of type 1 diabetes or type 2 diabetes
  • Ethnicity – African-American, South or East Asian, Hispanic, or Native American
  • Elevated fasting or random blood glucose levels during pregnancy



  • No specific symptoms in most pregnant women:
  • Polyuria, polydipsia, and polyphagia may be non-specific during late pregnancy
  • Fatigue and abdominal discomfort (vague)
  • Weight loss
  • Women who are already diabetes may have symptoms related to diabetes complications – i.e. neuropathy or retinopathy


  • Elevated serum glucose levels: overtly elevated blood glucose level on random glucose testing precludes the need for screening
  • Glucosuria (glucose found in urine) is of uncertain significance during pregnancy
  • Ketonuria (acetone bodies in urine)
  • Elevated glycosylated hemoglobin
  • Weight loss
  • There may be a history of previous pregnancies complicated by macrosomia or poor outcomes
  • Ultrasound may provide clues, such as greater than normal fetal abdominal circumference


LADA is short for Latent Autoimmune Diabetes in Adults or Slowly Progressive Diabetes (SPIDDM).  It is sometimes referred to as Type 1.5 or slow onset type 1.  LADA is a genetically-linked, hereditary autoimmune disorder that causes the pancreatic beta islet cells to be attacked and destroyed.  It is usually diagnosed in people 35 years or older (usually 35-55 years of age).


Typical presentation of a LADA patient is one who is slender (although some are heavy weighted), with little insulin resistance (not as much as in type 2), and no rapid weight loss and ketoacidosis as normally found in type 1 diabetics.  It is typically misdiagnosed and treated as type 2, but patients will eventually require insulin.  About 20% of people diagnosed with non-obesity-related type 2 diabetes may actually have LADA.


LADA can be properly diagnosed with conventional laboratory tests:

C-peptide (also known as insulin C-peptide, connecting peptide) – this test measures residual beta cell function by determining the level of insulin secretion.  LADA individuals typically have low, sometimes moderate, levels of C-peptide.  Higher levels are typically found in type 2 diabetes due to an over production of insulin.


Diabetes mellitus autoantibody panel


Glutamic acid decarboxylase (GAD) – commonly found in type 1 diabetes and positive in LADA

Radioimmunoassay (RIA)

Insulin antibodies (IAA) tests – positive in LADA, rarely positive in type 2 diabetics

Islet Cell Antibodies (ICA) tests – helps to differentiate between LADA and type 2 diabetes LADA is often positive for ICA, whereas it is only seldom positive in type 2 diabetics


Other determining factors for LADA include:

  • Often, but not always, has a lack of family history for type 2 diabetes
  • Human leukocyte antigen (HLA) genes associated with type 1 are seen in LADA, but not in type 2 diabetes.
  • LADA patients require insulin injections around 3 to 12 years after being diagnoses as type 2.  Type 2 diabetes does not normally require insulin.


Conventional treatment for LADA includes dietary and lifestyle changes with progression towards insulin dependency (since may not be required at time of diagnosis).  If LADA patients are diagnosed early and put on insulin at time of diagnosis, some of their beta islet cells might be preserved for longer.   Some LADA patients may initially respond to oral hypoglycemic medications, however, due to the continual destruction of beta islet cells, insulin will eventually be required.



MODY stands for Mature Onset Diabetes of the Young (Also called Monogenic Diabetes.)  It characterizes any of several hereditary forms of diabetes caused by mutations in an autosomal dominant gene affecting insulin secretion.  It can be inherited from either parent and occurs at any age.  If you are positive for MODY, your children will have 50% chance of inheriting the condition.  Classic MODY occurs predominantly in Caucasians and before age 25, is non-ketotic, and is usually non-insulin dependent.  Less than 5% of cases of childhood diabetes in Caucasians are caused by MODY.

Mutations in five genes can cause MODY.  MODY 2 and MODY3 are the most common forms.  The following are the classifications of MODY:

MODY 1 – Mutation in the hepatocyte nuclear factor-4 alpha (HNF-4 alpha) gene

MODY 2 – Mutation in glucokinase gene

MODY 3 – Mutation in the hepatocyte nuclear factor-1 alpha (HNF-1 alpha) gene

MODY 4 – Mutation in the insulin promoter factor-1 (IPF-1) gene

MODY 5 – Mutation in the hepatocyte nuclear factor-1 beta (HNF-1 beta) gene

MODY 6 – Mutation in the transcription factor neurogenic differentiation 1 gene

 MODY commonly acts like a very mild version of type 1 diabetes, but does not usually require long-term insulin for survival, as patients still have continued partial insulin production and normal insulin sensitivity.

Signs and Symptoms

  • There are two general types of clinical presentation:
  • Significant hyperglycemia with typical signs and symptoms of diabetes (i.e. increased thirst and urination)
  • No signs or symptoms.  MODY is diagnosed either by accident (in testing for other reasons) or by screening of relatives of a diabetic individual.  However, it is particularly  characteristic for MODY when a pregnant individual is found to have mildly high blood glucose during a routine glucose tolerance test.


Characteristics suggesting the possibility of a MODY diagnosis in hyperglycemic and diabetic patients:

  • Mild to moderate hyperglycemia (typically 130-250 mg/dl, or 7-14 mmol/L) discovered before 30 years of age. However, anyone under 50 can develop MODY.
  • A first degree relative with a similar degree of diabetes.
  • Absence of positive antibodies or other autoimmunity (e.g., thyroiditis) in patient and family.
  • Persistence of a low insulin requirement (e.g., less than 0.5 u/kg/day) past the usual "honeymoon" period.
  • Absence of obesity (although overweight or obese people can get MODY), or other problems associated with type 2 diabetes or metabolic syndrome (e.g. hypertension, hyperlipidemia, polycystic ovary syndrome).
  • Insulin resistance very rarely happens.
  • Cystic kidney disease in patient or close relatives.
  • Non-transient neonatal diabetes, or apparent type 1 diabetes with onset before 6 months of age.


Diagnosis of MODY

The definitive diagnosis of MODY is genetic testing for MODY mutations, but it is expensive and only performed at a select number of laboratories.  The diagnosis can also be made through a careful evaluation of the patient’s clinical course, family history and the severity of hyperglycemia.


In a non-obese patient of any age or in an obese patient less than 50 years old:

  • Test for higher than normal blood glucose
  • No ketones in urine
  • Test for diabetic antibodies is negative
  • A Monogenic Diabetes (MODY) Evaluation test is done
  • Positive test is MODY (if negative, you are type 2 diabetic)

Treatment of MODY is similar to other types of diabetes.  Insulin may or may not be necessary, and oral hypoglycemic medications can be used.  Certain MODY types are also associated with other health conditions or complications (i.e. MODY Type 1 also affects fatty acid synthesis in the liver) and thus may require additional treatments.  Genetic counselling is also an option for genetically susceptible families.  In any case, it is important to diagnose the type of MODY correctly in order to treat it properly and effectively.





MIDD is known as Maternally Inherited Diabetes and Deafness.  MIDD is due to mitochondrial DNA mutations and is only inherited via the mother.  It is a very rare form of Type 2 diabetes and accounts for only 1% of diabetics.


MIDD is caused by the mutation of the MTTL1 gene, located on the mitochondrial DNA.  Since the mitochondria is responsible for generating energy (ATP) and that ATP is critical in the production and release of insulin, it appears that the lowered amount of ATP in MIDD is responsible for the change in function of the pancreatic beta islet cells.

 Signs and Symptoms

  • Usually develops around ages 25-35 years or later
  • Generally non-obese; tend to have low BMI
  • Many have impaired hearing and cannot perceive high-frequency tones; however, this seldom leads to total deafness
  • High incidence of kidney disease
  • Tends to become insulin-dependent faster and at an earlier age than other Type 2 diabetics
  • Commonly have macular pattern dystrophy
  • Reduced insulin secretion
  • Has both cardiomyopathy and neurological symptoms
  • Increased lactate production with physical activity

MIDD individuals do not present the following:

  • No insulin resistance
  • No beta cell destruction in spite of reduced insulin secretion
  • No islet antibodies (no autoantibodies)
  • No visceral obesity

Genetic testing for MIDD is mainly for research purposes only.  Since merely a tiny part of the population is affected, it is probably not financially feasible to make it part of a general screening tool.


There is currently no cure for MIDD.  We can try to slow down the symptoms, or, if fortunate, reverse them.  It is always important to maintain a healthy lifestyle and diet (but not increased physical exercise as it can lead to excess lactic acid).  Medication, like Sulphonylureas, can be used as long as insulin is still being secreted.  Insulin therapy may be necessary.  Please note that Metformin is contraindicated in MIDD patients as it can induce lactic acidosis.


Neonatal Diabetes Mellitus (NDM)

Neonatal diabetes is diagnosed in the first few months of an infant’s life and occurs in approximately 1 in every 400,000 births.  There are two types:  Permanent Neonatal Diabetes Mellitus (PNDM) and Transient Neonatal Diabetes Mellitus (TNDM).  These are very rare non-autoimmune diseases, and not much is known about them.

Signs and Symptoms

  • Dehydration
  • Lethargy
  • Difficulty breathing
  • High glucose in blood and urine
  • Infants may have low birth weight

Genetic testing can be used to differentiate the two types, although the transient type will eventually disappear.


Permanent Neonatal Diabetes Mellitus

PNDM can develop within days to months of delivery and remains for life.  If the diabetes remains after the first year, it is PNDM.  PNDM is caused by a gene mutation, but not always the same gene.  About half of the cases have a mutation in the KCNJ11 gene, which tends to develop later than other forms and can lead to complications like delayed motor development or epilepsy.  These infants have non-existent c-petide levels.  PNDM does respond to sulfonylurea drugs (still some pancreatic activity remains), but if the mutated gene is a transcription factor (IPF-1 or GCK), there may be no beta-cell activity and insulin is required.


Transient Neonatal Diabetes Mellitus

TNDM is not permanent.  It develops within days and disappears in weeks or months.  Insulin is usually given for the first 3 months of life and Type 2 diabetes may reoccur in adolescence.  The cause is unknown.



This is also known as borderline diabetes, chemical diabetes, sugar dysregulation, or potential diabetes.  It is a term given to people where the blood glucose levels are elevated, but not high enough to be termed diabetic.  The two tests used to diagnose pre-diabetes are the Fasting Plasma Glucose test (FPG) and the Oral Glucose Tolerance test (OGTT).  Pre-diabetics have a fasting plasma glucose (FPG) reading between 6.1 – 6.9 mmol/L and an oral glucose tolerance between 7.8 to 11mmol/L after a 2-hour oral glucose tolerance test.  It is estimated that 4 million Canadians between the ages 40 and 74 have impaired fasting glucose and 1.8 million Canadians have impaired glucose tolerance. 


Pre-diabetes is a risk factor for type 2 diabetes, with a greater risk of stroke or heart attack.  The risks of developing pre-diabetes are basically the same as those for Type 2 diabetes (see Type 2 Diabetes).  By maintaining a healthy lifestyle and diet, it is possible delay and even prevent the progression of pre-diabetes to type 2 diabetes. 


Other types

These include trauma, pancreatitis, drug- or chemical-induced, other endocrine and genetic disorders etc.