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:
Symptoms of acute presentation (diabetic ketoacidosis) include: nausea and vomiting, muscle cramps, abdominal pain, blurred vision, and fever.
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 (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:
Symptoms of complications include:
*It is important to note that people with type 2 diabetes may display no symptoms
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:
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
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:
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
Characteristics suggesting the possibility of a MODY diagnosis in hyperglycemic and diabetic patients:
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:
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
MIDD individuals do not present the following:
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 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
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.
These include trauma, pancreatitis, drug- or chemical-induced, other endocrine and genetic disorders etc.
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Live cell microscopy offers a way to assess a person's nutritional status in terms of vitamin/mineral imbalances, digestive ability and the function of certain organs. By looking at one's internal environment via the blood, one can potentially assess the current health of an individual and work towards health promotion and prevention.
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The first appointment is usually about 1.5 to 2 hrs long, which includes darkfield microscopy, a thorough history intake, a physical examination, and in-house assessments. Subsequent visits range from 30 min to 1 hour, depending on each individual and the treatment plan. Specialized laboratory tests may be suggested.