Not Just a Man's World

Last week I provided an introduction to diabetes mellitus, the group of metabolic diseases characterised by high blood glucose (sugar) levels.  The most common forms of this are type 1, type 2 and gestational diabetes and over the next few weeks I am going to look in more detail at types 1 and 2, starting this week with some background information about type 1 diabetes.

What is type 1 diabetes?

Type 1 diabetes is defined by the John Hopkins Medical Institutions website as “an inflammatory autoimmune disease of the pancreas, resulting in a lack of insulin” (1).  Without sufficient insulin, the body can’t store the free glucose in the blood, and blood glucose levels can rise unchecked.

Last week, while explaining the process of how our bodies deal with elevated blood glucose levels and what happens when this goes wrong, I made passing mention to beta cells.  These are cells found in the pancreas and are the cells which produce insulin.  In the case of a type 1 diabetic the body does not produce sufficient insulin because it has attacked and killed off most of the beta cells. 

In fact, the John Hopkins site notes that more than 90% of the beta cells will have been destroyed before the clinical symptoms of diabetes develop (1).  In effect, that tells us that by the time someone realises they have diabetes, they have already been developing diabetes for a long time.

How is type 1 diabetes diagnosed?

Classically diagnosis initially comes through a series of glucose tests, establishing how the body responds to the glucose (1).  These tests come in two forms:

• Fasting plasma glucose test, where the glucose levels are measured after 12 hours of fasting.
• Oral glucose tolerance test, where the person is given a glucose fluid test and the glucose levels in the blood are measured at regular intervals to see how well the body does in taking control of the glucose.

There are also various blood tests that medical practitioners are advised to carry out (2). 

Type 1 diabetes can develop quickly (3), although I do question whether this is that the final destruction of the remaining 10% of beta cells happens quickly and that the actually build up of the disease from a fully functioning 100% beta cell position happens over a much longer period of time.

Treatments for type 1 diabetes

Insulin replacement therapy

The standard treatment for type 1 diabetes is insulin replacement therapy.  Insulin has been available since 1921 and this is delivered to the body through either subcutaneous injection or insulin pump.  The aim is to monitor blood glucose levels and use insulin when this gets too high so that blood glucose levels are kept within the 2010 American Diabetes Association Clinical Guidelines of 80-140mg/dl (2).

The risk of this treatment is that it can be easy enough to mismatch the insulin with the food, and physical activity going on at the time so that blood glucose is taken too low and hypoglycaemia occurs.  The list of possible signs and symptoms of hypoglycaemia are too numerous to list here and are frequently contradictory (both feeling hot and feeling cold are on the list as well as rage, irritability, depression and crying).

In the early days of insulin replacement therapy the insulin was extracted from cattle or pigs.  However, extraction of insulin was difficult, erratic and expensive in the early 1920s and until the process was improved there were, for a brief 2 years, attempts to extract insulin from fish instead, which was technically easier though apparently logistically more difficult (4).  Fortunately things have moved on significantly and insulin that is used to treat type 1 diabetics is now produced synthetically.

While the majority of type 1 diabetics use injections as the method to deliver insulin into the system, insulin pumps became available in the 1970s.  According to the ever-helpful Wikipedia, the pump provides continuous infusion of insulin and therefore removes the need for multiple injections throughout the day making it appropriate for intensive insulin therapy.  If you are interested in pumps you can learn more from Diabetes.co.uk.

Other possible treatments

There are a couple of other treatments which are, at the moment, still considered to be experimental.  These include pancreas transplant and islet cell transplant.  Most success with these transplant methods has come with islet cell transplant. 

The islet cells are the beta cells in the pancreas which produce the insulin.  These can either be transplanted from another source or can be “built” using the patient’s stem cells – use of the patient’s own stem cells is more successful as the new cells are less likely to be rejected by the body.  These cells are injected into the liver which takes on the role of the pancreas in the release of insulin.  As far as I can see from the things I’ve read, this use of the liver is partly because the liver is more accessible!

Islet cell transplant is still in the experimental stages but a study carried out in 2005 showed that a year after the transplant 80% of the patients were insulin independent (didn’t need to rely on insulin replacement therapy) (5).  Of course, other things have to be done as well to stop the body just attacking and killing these new, transplanted, cells.

Exercise issues for type 1 diabetes sufferers

When a person exercises, their muscles utilise the glycogen stored within the muscles as energy for those muscles.  As these stores become depleted the liver is triggered to release glucose from its big glucose store into the blood stream.  This elevated free glucose in the blood triggers the insulin to be released by the pancreas and ultimately this free glucose is taken to the muscles to continue providing an energy store and to replenish them for your next muscular challenge.

For a type 1 diabetic the challenge is that the insulin isn’t produced to deal with this and they can rapidly become hyperglycaemic as a result of their workouts.  How significant this increase in blood glucose is will depend on how experienced they are at training and the intensity of their training. 

The following gives an idea of what blood glucose response comes from different exercise levels (6):

• Untrained individuals, high and low intensity: marked increase in blood glucose levels.
• Trained individuals, low/moderate intensity: minimal increase in blood glucose levels.
• Trained individuals, high intensity training: marked increase in blood glucose levels which is even higher once reaching anaerobic levels.

Measurement of personal responses is advisable, but Robb Wolf has taken this information and developed some initial recommendations on how type 1 diabetics should moderate their training approach.  It’s an article well-worth reading.

*****

That’s all I’ve got space for this week so I’m going to save up the piece about a possible cure for diabetes for next week. 

The crux of the problem is that diabetes is believed by most to be neither preventable (7) nor curable, yet there is a growing body of anecdotal evidence and a few tangential studies which together imply that it is being successfully cured in people through nutrition changes.  My belief is that if a disease can be cured then it should be possible, with those same interventions, to prevent it occurring in the first place. 

 

Bibliography

1. Cihakova D: Type 1 Diabetes Mellitus.  John Hopkins Medical Institutions website.
2. American Diabetes Association: Standards of Medical Care in Diabetes – 2010.  Diabetes Care 2010, 33:Supp.1:S11-61 (Executive Summary.  Diabetes Care 2010; 33:Supp.1:S4-10)
3. Cooke D and Plotnick L: Type 1 Diabetes Mellitus in Pediatrics.  Pediatr. Rev. 2008; 29:374-385.
4. Wright J R: From ugly fish to conquer death: J J R Macleod’s fish insulin research, 1922–24.  The Lancet 2002; 359:1238-1242.
5. Bertuzzi F, Marzorati S, Secchi A: Islet Cell Transplantation.  Current Molecular Medicine 2006; 6:369-374.
6. Brooks G, Fahey T, Baldwin K: Exercise Physiology: Human Bioenergetics and its Applications (edition 4).  Macmillan Publishing Company 2004; 193-194
7. World Health Organisation: Diabetes Fact Sheet.  WHO 2011; Fact Sheet 312.