“I got diabetes after my car accident”, “I got diabetes after a loved one passed away suddenly”, “When I became a teenager I got diabetes”; I hear these statements and many alike in my practice daily. This leads to the question: Does stress cause diabetes? To answer this, we have to consider the pathophysiology of the disease separately.
Type 1 diabetes is an autoimmune disease that starts when the immune system gets turned on. Antibodies are formed and attack the body. In the case of Type 1 diabetes, the organ that is attacked is the pancreas. Every human being is born with a normal amount of beta cells. After birth, the attack from antibodies start due to a genetic, environmental or immunological factors.
The susceptibility to develop Type 1 diabetes involves multiple genes; the major susceptible gene is located on chromosome 6. The region on this gene which is involved with diabetes is also associated with the immune response. There are also genes that protect against the development of diabetes.
The risk of developing Type 1 is relatively low; it is 3-4% if a parent has Type 1, and 5-15% in a sibling. Hence most patients with Type 1 diabetes do not have a first degree relative with this disorder1.
The immune process is in the pancreas, but only directed against the beta cells, even though the alpha cells, delta cells and pancreatic polypeptide producing (PP) cells are all embryonically and functionally similar to the beta cells – the reason for this is unclear. One theory is that the inflammation, called insulinites, spreads from beta cell to beta cell, destroying the beta cells only in this way.
Do markers exist to diagnose this process?
The markers available to make sure of the diagnosis of autoimmune disease are called islet cell antibodies (ICA). The one that is commercially available is GAD. This marker is very useful and is positive in 85% of individuals with Type 1 diabetes and in 5-10% of patients with Type 2 diabetes.
ICA is positive in 3-4% of first degree relatives of individuals with diabetes. Should these people also have an impaired glucose tolerance testing, it predicts a greater than 50% increased risk that this person will develop diabetes within the next five years. This is currently only a research tool since nothing much can be done in the non-diabetic population to prevent the destruction of the beta cell.
Numerous environmental factors have been proposed as a trigger for the onset of the immune response in genetically susceptible individuals.
Theses factors are:
- Viruses – Coxsackie, rubella (German measles) and enterovirus
- Bovine milk proteins
- Nitrosoureas – a group of cancer drugs called alkylating agents because they act by the process of alkylation to inhibit DNA repair.
This immune process can last for years before a person becomes symptomatic. The slope from normal beta cells to 20% beta cell reserve varies between individuals. This can be very abrupt or a slow progressive decline. Usually when there is about 70-80% of pancreatic beta cells destroyed, the body start to show symptoms during stress situations such as our examples.
Why does the body only show symptoms then?
During stressful situations, the body produces cortisol – a steroid – to help the body with its stressful requirements. Cortisol is produced in normal amounts by the adrenal gland that is situated just above the kidney. During emergency situations, such as physical or emotional stress, the adrenal gland has the ability to produce large amounts of cortisol as an emergency response.
Cortisol and the other stress hormones – glucagon and adrenaline – elevate the blood sugar. Because of this more insulin is needed to get back to a normal blood glucose level; the pancreas is at a reserve state and can not handle the extra requirement and this causes blood sugars to then raise ‘suddenly’.
In most cases, after the stressful period is over, the person with the newly diagnosed diabetes reverts back to normal glucose for a period – this is known as the honeymoon period and can last up to one to two years. This period should be handled with caution to make sure the blood glucose levels stay normal two hours after meals. Low dosage basal insulin is usually only needed, but in rare situations no insulin is required.
Unfortunately, the autoimmune attack continues progressively until there is no beta cell reserve and the patient will then require more insulin, usually in basal-bolus format or insulin pump therapy.
To answer the question ‘Does stress cause diabetes?’ The answer is no – stress only serves as a flashlight to illuminate an already decreased beta cell function. This can help to preserve the endogenous beta cells still present by using small amounts of insulin and by following a diabetic diet.
Many trials are ongoing to try and stop the attack of the beta cell with different chemotherapeutic medicines, but up to date there is no successful drug available to stop this autoimmune process.
Interesting trials that are currently ongoing to try and prevent Type 1 diabetes are:
- GAD vaccine
- Anti-CD3 monoclonal antibodies
- Anti –B –lymphocyte monoclonal antibodies
The preliminary data shows a reduction in beta cell decline. This is an active area of investigation.
Until we can stop the disease, the best answer is the ‘artificial pancreas’, also referred to as the closed-loop system.