Around 500,000 people in the UK have type 1 diabetes – about 10% of the total with diabetes. It can develop at any age, but often in previously very healthy children and young adults. This is the first book in many years that has been published in the UK to support people with type 1 diabetes in managing their condition.
Drawing on his many years working at one of the leading diabetes centres in the UK, Dr David Cavan provides a practical guide to managing all aspects of the condition, including insulin pump therapy and the latest technology available. This cutting-edge book presents invaluable advice that will offer genuine hope to adults with type 1 diabetes and their families.
Dr David Cavan is one of the UK’s leading experts on diabetes self-management. He worked for 17 years as a consultant at the highly-regarded Bournemouth Diabetes and Endocrine Centre and in 2013 moved to Brussels where he worked for three years as the Director of Policy for the International Diabetes Federation. He now lives in the UK, working as an independent consultant supporting the development of diabetes services in the UK and overseas.
Diabetes.co.uk is the world’s largest and fastest-growing community website and forum for people with diabetes. With over 2.2m unique visitors per month and a diabetes support community of over 180,000 members sharing a cumulative 1.5m years of experience, this award-winning website has proven to positively influence health outcomes. Get support at www.diabetes.co.uk/forum
I have worked as a diabetes specialist for over twenty years. Very early on, I came to realise that the vast majority of diabetes management is done by the person with diabetes, and therefore it is essential that everyone with diabetes is given the appropriate training and education that will enable them to manage their diabetes as well as possible. From 1996 until 2013, I worked as a consultant at the Bournemouth Diabetes and Endocrine Centre. During that time I developed my interest in patient education, and in order to ensure people with type 1 diabetes had the appropriate skills to manage their diabetes effectively, in 1999 we launched a self-management programme for people with type 1 diabetes called BERTIE. BERTIE was quickly adopted by many other diabetes centres around the UK and many thousands of people with type 1 diabetes have attended courses based on BERTIE over the past fifteen years. However, aware that many people still did not have access to high quality self-management education, in 2005 we developed an online resource to teach the basics of carbohydrate counting and insulin dose adjustment. This has recently been updated and is available at www.bertieonline.org.uk.
There is a limit to the amount of information that can be provided in an education programme, whether ‘face to face’ or online and so I have written this book with the aim of providing a readily accessible and understandable resource that explains all aspects of the management of type 1 diabetes. My aim is that this book should provide very practical support to self-management. While the book is written for adults with type 1 diabetes, many aspects will be relevant to older teenagers. I am not a children’s diabetes specialist and the book does not cover the management of type 1 diabetes in younger teenagers or children. While some parts of the book may be of interest to the parents of children with type 1 diabetes, I would recommend the following books that specifically address the needs of children and their parents:
Type 1 Diabetes in children, Adolescents and Young Adults, by Dr Ragnar Hanas, a paediatric diabetes specialist from Sweden provides a huge amount of information relevant for the parents of a small baby with type 1 diabetes, right through to the needs of young adults. Help, My Child has Type 1 Diabetes, by Roxana Reynolds, who herself has type 1 diabetes, provides advice, information and real stories for parents and carers of a child with type 1 diabetes.Take Control of Type 1 Diabetes has been written to support people who have just been diagnosed with type 1 diabetes, right through to those that have had the condition for many years. Although there has been a big expansion in availability of patient education in the past fifteen years, it is sadly the case that many people diagnosed before 2000, in the UK at least, received very little education on how to manage their type 1 diabetes. Very often, those who did receive education did so by attending a single course, perhaps many years ago. It is my hope that this book can help all people with type 1 diabetes fill the gaps in their knowledge about the modern management of type 1 diabetes.
The management of type 1 diabetes is entering a very exciting phase, with new insulins and technologies becoming available that have the potential to revolutionise the management of type 1 diabetes. Thus I have aimed to cover the latest developments in insulin pump therapy, continuous glucose monitoring and new insulins that provide great hope for the future. Even with these advances, it is still the case that the person with type 1 diabetes will need to take into account the impact of their lifestyle, physical activity and their food choices on their blood glucose control, and so the book provides extensive details about these aspects.
Since the early years of this century, the focus of much teaching has been to encourage people with type 1 diabetes to eat what they like, in the belief that the modern insulins now available would be able to cope with all types of diet. My experience in the years since then, has led me to the firm belief that this is not always true. Not even the best available insulins and technologies can manage meals with very high sugar or starch content and keep blood glucose within the normal range at all times. In the past several years, therefore, I have encouraged patients with type 1 diabetes to restrict their carbohydrate intake as an important means of achieving good control of their glucose levels, and the rationale for this is discussed in the book.
The book has been written primarily for a UK audience; however in order to make it relevant to readers elsewhere, the book includes sections for those for whom the insulins commonly in use in the UK are either not available or affordable. Blood glucose measurements are provided in mmol/l (as used in the UK) as well as in mg/dl (as used in US and many other countries).
Living with type 1 diabetes is not easy. It often develops in children or young people who are very healthy, and then suddenly they have diabetes. It also frequently starts at a time of life where being different is a big deal. It always demands attention be given to food, activity levels and many other day-to-day occurrences that otherwise would not require such consideration. It requires regular injections of insulin and blood glucose checks. It can spring surprises for no obvious reason. It can be physically, emotionally and psychologically draining. It can lead to nasty health problems down the line. It is always there.
These are just some of the truths about living with type 1 diabetes. It is not surprising that all too often, a person with the condition can feel overwhelmed, out of control and worried about their present or future health – or just burnt out. Yet staying healthy demands that a person with type 1 diabetes cannot afford to let such feelings dominate and impact upon their ability to manage their diabetes.
If you or someone close to you has type 1 diabetes, this book has been written for you. My hope and aim is that it will be of support in providing you with the knowledge, skills and tools you need to take control of the diabetes. It is natural to experience concern or worry, but my hope is that in the following chapters you will find practical guidance on how to overcome some of the challenges your diabetes might pose.
I do not have type 1 diabetes, so I cannot claim to have the personal experience of someone that does. However, over more than twenty years I have had direct experience in supporting people with type 1 diabetes, from the time of diagnosis right through to those who have had the condition for decades – including many who remain very healthy. As you will read, I was moved by the problems I saw in those whose diabetes was not well controlled, often through no fault of their own, and determined in my own way to improve the support and education available. This book is my attempt to make that experience available as widely as possible.
The book has been written particularly to support those at the time of diagnosis. The reason for this is that it is well recognised that things that happen around that time – both good and bad – can have a long-lasting effect. So the better you can deal with the diagnosis, the quicker you can take control of your diabetes, and the sooner you can deal with any negative issues surrounding diagnosis – the better the outlook for the future.
If you have recently developed type 1 diabetes, how does this make you feel? Before doing anything else, it is worth pausing to consider this, in order to address any feelings that might get in the way of being able to take control of the condition in the future. People experience a whole range of feelings when they are diagnosed with type 1 diabetes, from relief that they know what was causing troublesome symptoms or anger that it should affect them, to fear for the future, loneliness and a whole host of other feelings and emotions. Such responses are completely natural, and it is good to acknowledge them and if possible to talk about them with someone close to you who is able to listen, even if they don’t have the answers to the many questions you may have.
The reason for discussing this right at the beginning is because if certain emotions are not properly addressed, they can have a massive effect on your physical health, as well as mental health, for years to come. There are a number of helpful and supportive websites, which include discussion forums where you can share your feelings with others who have been through the same experience, which I recommend you look at. Some of these are listed in Appendix 1 (see here).
However, whatever your own situation, I encourage you not to worry. Our understanding of type 1 diabetes, and our ability to control it, has changed beyond all recognition over the past twenty years, and we are learning more all the time. As a result of these advances, the risk of disabling complications has reduced significantly. In addition, there are now education programmes available in many parts of the country and online, where you can learn how to take control of your diabetes and protect your long-term health.
The message of this first chapter is ‘there is always hope’. These were the words of comfort I gratefully received from a caring nurse where my father was admitted on Christmas Eve in 2012. He had been diagnosed with chronic lymphocytic leukaemia. This is a relatively common condition in the elderly and generally does not cause serious health problems. Unfortunately, he had a rare and aggressive form of the condition that did not respond to standard treatment. His specialist explained to us that there was a different treatment that he could have, that it was complex and had significant side-effects but it had a chance of taming his disease. I could tell from the tone of the doctor’s voice that it was serious and that the chances of success were slim. However, I was struck by the focus on the possibility of a positive outcome. And that positivity had a deep and encouraging effect on my father, as well as our family around him.
The day after he was admitted, on Christmas day, I was struck by how ill he looked and I was extremely worried. One of the nurses could see that in my face, and she said to me, very gently and very kindly those four words: ‘There is always hope.’
That focus on the positive, on hope, was a great source of strength. Arguably the hope for a person with type 1 diabetes is so much greater, especially with recent advances in management and technology available, yet often I meet people with type 1 diabetes who seem devoid of hope, as well as some diabetes professionals who focus more on the perceived negatives of having type 1 diabetes than on the positive hope for the future. And so, whether you or someone you love has just been diagnosed with type 1 diabetes, or whether you have had it for many years, my aim is that the information provided in this book will give you a greater sense of hope. There is much about type 1 diabetes that can seem difficult and unfair. Yet, as I have experienced over the past twenty-five years in working with and helping those with type 1 diabetes, there is so much that can be done to make life easier.
So, what are your hopes in respect of your type 1 diabetes? As you read this book, it will be helpful to have set out your goals in doing so. That will help you focus on the areas that are most important to you. I encourage you to think about – and write down – the answers to the following questions. And if you are not really sure just yet, that is fine – I will remind you again later.
What are your reasons for reading this book? What frustrates you most about having diabetes? How do you want things to be different? How will you know when you have achieved this? What is the main thing you would like to change after reading this book?We will look at your answers to these questions in chapter 22.
My hope is that the information in this book will provide reassurance and hope for the future.
The full name of the condition is diabetes mellitus, which literally means ‘passing [perhaps more accurately “pissing”] honey’, as in diabetes the urine contains glucose and so tastes sweet. Diabetes was described in ancient Egypt, in the Papyrus Ebers, which dates from around 1500BC, as a disease where urine is too plentiful. Sushruta of the Hindus wrote in 1000BC that the urine was sweet and that ants and flies were attracted to it. He thought that diabetes was a disease of the urinary tract (kidneys and bladder) and wrote that it could be inherited or develop as a result of dietary excess or obesity (perhaps referring to type 1 and type 2 diabetes). The recommended treatment was exercise. It was not until the seventeenth century that it was discovered that the urine was sweet because it contained sugar and that diabetes was a disease of the pancreas rather than the kidneys. This was established in 1682 by Johann Brunner, who removed the pancreas from dogs and found this led to diabetes. In 1797, John Rollo, the surgeon-general of the Royal Artillery, wrote a book in which he described the case of a Captain Meredith, who took a diet low in carbohydrate and high in fat and protein. His weight fell from 105kg to 73kg (or 230 to 160lb) and the symptoms resolved.1 At that stage diabetes was reported as being relatively rare, and associated with wealth.
It was not until the end of the nineteenth century that the role of insulin became apparent. In 1889 Mehring and Minkowski removed the pancreas from dogs to cause diabetes. This was then reversed by transplantation of small pieces back into the peritoneum (the lining of the abdominal cavity).2 In 1921 Banting and Best isolated an extract of pancreatic islet cells and found this reduced glucose levels in diabetic dogs.3 The following year, this extract (a prototype of insulin) was injected for the first time into a patient with diabetes, a 14-year-old boy called Leonard Thompson.
Piece by piece the puzzle was being completed, such that by the 1920s, it was established that diabetes is characterised by an excess of sugar (glucose) in the blood, causing excess in the urine. The disease was often seen in overweight people, in whom it could be controlled by adopting a low carbohydrate diet. In other patients, insulin, extracted from animal pancreases and given by injection, led to a fall in blood glucose levels.
By the 1970s, it had become clear that there are two distinct types of diabetes:
Since then our understanding has developed further, inasmuch as there are rare forms of diabetes that occur in young people (so called maturity-onset diabetes of the young or MODY). These are inherited conditions, are not associated with weight gain, and there is usually a strong family history of diabetes. Although they usually present in childhood, most cases can be controlled with tablets rather than insulin.
It has also become apparent that the distinction between type 1 and type 2 diabetes is not as clear cut as previously thought, and for those who are diagnosed in the forties and fifties, there may be a period of uncertainty before one can definitely distinguish between the two. For example, some overweight adults present quite acutely with very high glucose levels and require insulin at diagnosis, but can later be switched to tablets. Conversely, there is a type of type 1 diabetes that occurs in older people, sometimes referred to as latent autoimmune diabetes of adulthood (LADA). Like type 1 diabetes, people with this condition are not overweight; however, the onset is more like type 2 diabetes, and they may be treated with tablets for a period. Within a few years, it becomes clear they need insulin, and from that time behave very much like type 1 diabetes.
Gestational diabetes is a condition in which diabetes occurs during pregnancy. It is similar to type 2 diabetes and can be controlled with diet in some cases, otherwise insulin is used, as tablets are generally not advised in pregnancy. It usually reverses once the baby is born, but both the mother and the child are at increased risk of developing type 2 diabetes in later life.
Diabetes can also arise as a result of other diseases affecting hormones (e.g. acromegaly, caused by too much growth hormone, or Cushing’s disease, caused by too much cortisol). These cases generally reverse once the underlying condition has been treated. Cortisol is the body’s natural steroid, and people who have been treated with steroids for long periods of time for conditions such as asthma may develop diabetes. Diabetes also occurs if the pancreas is affected by other diseases, or if the pancreas has been wholly or partly removed.
The typical symptoms of diabetes include excessive urination, excessive thirst, tiredness, blurred vision, weight loss and infections such as thrush. These arise because in diabetes, glucose cannot enter the body’s cells and so it accumulates in the blood stream. As glucose is not getting into the body’s cells, these are starved of energy leading to weight loss and tiredness. As the blood glucose rises, the kidneys try and excrete the excess glucose in the urine. This explains why glucose can be detected in the urine, causing infections such as urine infections and thrush. In order to excrete glucose, the kidneys need to emit a larger volume of water (otherwise you would pee out sugar lumps), and this leads to dehydration. In turn this prompts excessive thirst, and high glucose levels in the eyes lead to blurred vision.
In many cases of type 1 diabetes, especially in children or young adults, the onset of symptoms is quite rapid and diagnosis can easily be made by measuring the blood glucose level. The symptoms of type 1 diabetes can deteriorate rapidly, leading to a condition known as diabetic ketoacidosis due to lack of insulin. This can lead to coma and even death if insulin treatment is not started, and is discussed in more detail in chapter 5.
Type 1 diabetes can also be mistaken for other conditions, especially in parts of the world where it is quite rare, and in some countries medical staff may make a mistaken diagnosis of malaria, TB or even HIV in young children with diabetes. Even in countries such as the UK, where type 1 diabetes is relatively common (although still much less common than type 2 diabetes), early symptoms may be missed, leading to uncontrolled high glucose levels and the development of ketoacidosis. Especially in those diagnosed in their thirties or above, type 1 diabetes is often of slower onset and with much milder symptoms causing an initial diagnosis of type 2 diabetes as described above.
Diabetes is diagnosed by blood tests. This means that if you have symptoms which you think may be due to diabetes but the blood tests are normal, you do not have diabetes. On the other hand, if your blood tests are diagnostic of diabetes, then you have diabetes even if you do not have any symptoms. The tests that are used to diagnose diabetes are either a measurement of random blood glucose, a fasting blood glucose test, a glucose tolerance test or by a glycated haemoglobin test.
With type 1 diabetes, the rapid onset usually means that the random glucose level is high enough to make a diagnosis of diabetes, and it is rarely necessary to use one of the other diagnostic tests.
This is often the first test that will be done. It is taken at any time of the day after breakfast. The results are expressed as the amount of glucose molecules per litre of blood (mmol/l) in the UK or as the weight of glucose per decilitre of blood (mg/dl) as used in the US, Germany and many other countries. They are interpreted as follows:
| Random blood glucose level | Interpretation |
| Up to 7.7mmol/l (139mg/dl) | Normal |
| 7.8 to 11.1mmol/l (140–200mg/dl) | Impaired glucose tolerance |
| Above 11.1mmol/l (200mg/dl) | Diabetes |
If the random glucose is normal it is unlikely that the person has diabetes; however, if it is within the impaired glucose tolerance range, then a fasting glucose or a glucose tolerance test will usually be performed, as described below. Impaired glucose tolerance and impaired fasting hyperglycaemia (see below) describe an intermediate state, sometimes known as ‘pre-diabetes’, that identifies people at risk of developing type 2 diabetes. It is rarely relevant in the diagnosis of type 1 diabetes.
This is a blood test taken after a fast of 12 hours, during which time only water can be taken by mouth. It is generally taken first thing in the morning. The results are expressed as the amount of glucose molecules per litre of blood and interpreted as follows:
| Fasting blood glucose level | Interpretation |
| Up to 6.0mmol/l (109mg/dl) | Normal |
| 6.1 to 7.0mmol/l (110 to 126mg/dl) | Impaired fasting hyperglycaemia |
| Above 7.0mmol/l (126mg/dl) | Diabetes |
If both the fasting and random glucose levels are normal, then the diagnosis is not diabetes.
This is a standardised test where a fasting glucose level is measured, and then the patient is asked to drink a liquid that contains 75 grams of glucose. A further blood test is taken two hours after the drink to see how high the glucose level has risen. The results are interpreted in the same way as the fasting and random tests above. If either the fasting OR the two-hour values are diagnostic, then the patient has diabetes. Both have to be normal to exclude the diagnosis.
When the level of blood glucose is higher than normal, the excess glucose attaches to a number of different molecules in the body. (So, for example, glucose attaching to the lens in the eye can lead to cataracts developing, or attaching to soft tissue in the shoulder can lead to frozen shoulder.) This is termed glycation. Red blood cells contain haemoglobin. This is the substance that carries oxygen in the blood cells, to take to the different tissues around the body (and which gives blood its red colour). A small amount of haemoglobin is glycated, and how much depends on the amount of glucose in the bloodstream. Red blood cells last for about 4 months before they are ‘recycled’, and the amount of glycated haemoglobin in any one cell gradually increases over this time. Blood glucose levels change constantly according to food intake and activity levels, and so a single measurement is of little use in monitoring diabetic control. Glycated haemoglobin (abbreviated as HbA1c), on the other hand, is used to assess glucose levels over a longer period of time, and for many years has been the gold standard means of assessing diabetic control. In 2009 it was also introduced as a means of diagnosing diabetes.
Historically, HbA1c was expressed as the percentage of haemoglobin that was glycated. In 2011, a new system of units was introduced, which expresses the glycated component as a concentration of the total haemoglobin (mmol/mol). It was intended that this system should be adopted globally, however, old habits die hard, and many countries, and much international literature, still use the old system. I will therefore present both units in this book. In people without diabetes, glycated haemoglobin is generally below 40mmol/mol (5.8 per cent). A measurement of 48mmol/mol (6.5 per cent) or above is considered diagnostic of diabetes. However, it is important to be aware that a level below this does not rule out diabetes, and if there is any doubt then a glucose tolerance test should be performed.
In order to understand why glucose levels rise in people with diabetes, it is important to understand how insulin controls glucose levels when everything is working normally.
Glucose is a type of sugar which is used by nearly all cells in the body for energy. It is essential that all parts of the body have a steady supply of glucose. This glucose is obtained from the food we eat: all carbohydrates (sugars and starch) that we eat are broken down into glucose, which is then absorbed from the gut into the bloodstream, so that it can be carried to all tissues and used as energy. Any spare glucose is taken up into the muscles and liver where it is stored in the form of glycogen. Glycogen in the muscles is then available for later use if the muscles need extra energy (for example, during intensive exercise). Once the glycogen stores are full, excess glucose is converted to fat and stored in the liver.
While glucose only enters the body when we eat or drink, the body’s cells require a constant supply of glucose to function properly. This is provided by the liver, which releases some of its stored glucose into the bloodstream to ensure that just the right amount is available during periods when we are not eating – for example, overnight. In a person without diabetes, the amount of glucose in the bloodstream is kept at around 4–6mmol per litre (70–110mg/dl).
The level of glucose in the bloodstream is controlled by insulin, a hormone produced by the pancreas. The pancreas is an organ which sits just below the rib cage, behind the stomach. Like many of the body’s organs, the pancreas does lots of different things. However, it has two main functions. One is to produce enzymes, which are released directly into the small intestine to break down food so it can be absorbed into the bloodstream. These enzymes include amylase, which breaks down starch into glucose; lipase, which breaks down fat; and protease, which breaks down proteins.
The other main function of the pancreas is to produce hormones. These are chemicals which are released into the bloodstream and have effects all around the body. Insulin is one of the hormones produced by the pancreas, and its job is to regulate the amount of glucose in the bloodstream to ensure that cells get the right amount of glucose at all times. Insulin is produced by specialised cells, known as beta cells, which are found located in clumps of cells scattered throughout the pancreas and known as the Islets of Langerhans, or islets for short. Insulin acts in the following ways:
In type 1 diabetes, the body stops producing insulin as a result of the body’s immune system destroying the insulin-producing beta cells in the pancreas. This means there is no insulin to turn off the tap releasing glucose stored in the liver into the bloodstream, or to open the doors to allow glucose to enter body cells after a meal. As a result, glucose accumulates in the blood and rapidly rises to high levels. In type 1 diabetes, treatment with insulin rapidly restores glucose levels to normal.
This is in contrast to the situation in type 2 diabetes, where the body produces insulin but it doesn’t work very well. It seems that the problem starts in the liver, which becomes ‘immune’ or resistant to the effect of insulin, so that even if insulin is present, the liver just keeps releasing glucose into the blood stream. This is called ‘insulin resistance’ and to try and get around this, the pancreas produces more and more insulin in an attempt to control the release of glucose from the liver. Therefore, treatment with insulin is rarely as effective as with type 1 diabetes. For a while this may work in keeping the blood glucose level under control, but eventually the liver becomes resistant to even these high levels of insulin, and the level of glucose in the blood rises high enough to make the diagnosis of diabetes.
Type 2 diabetes is increasing rapidly across the world, and is associated with modern day lifestyles characterised by unhealthy diets (especially of processed foods high in sugar, salt and unhealthy fats), lack of physical activity and increased body weight. People with type 2 diabetes are often perceived as being in some way to blame for their condition; while there is undoubtedly an element of choice in what we eat and what we do, the big rise in type 2 diabetes has resulted from significant changes to our food, and our physical and work environments, that are often not in the control of any one individual. Such stigmatisation is thus inappropriate.
It is even more unfortunate that many members of the general public (and even some health professionals) fail to distinguish between type 1 and type 2 diabetes and apply the same stigma to people with type 1 diabetes. It is thus easy to understand why some with type 1 diabetes would prefer it had a different name to avoid this confusion.
Earlier in this chapter we learnt that the distinction between type 1 and type 2 diabetes is not as clear-cut as was once thought, and several different ‘types’ of type 2 diabetes have now been identified. The diagnosis of type 1 or type 2 diabetes is usually done clinically, that is according to the symptoms and signs present at the time of diagnosis rather than by any formal testing. The reason for this is that there is no readily available test that will say for definite whether a person has type 1 or type 2 diabetes. The nearest we have are tests to check the levels of different antibodies to the islet cells that are present in many, but not all, people with type 1 diabetes. If these antibodies are present in the bloodstream it is very likely the person has type 1 diabetes. However, if they are not found, the individual may still have type 1 diabetes.
The other test that can be performed is to check the level of c-peptide in the blood. C-peptide is a by-product of the production of insulin, and for every molecule of insulin produced in the pancreas, one molecule of c-peptide is also produced. It is uncertain whether c-peptide has any biological effect, but it is very useful as a marker of insulin production. So, if it is found in the blood, it means that insulin is definitely being produced and the person is therefore likely to have type 2 diabetes. This information has to be used with caution as many people with type 1 diabetes continue to produce insulin for up to two years (during the honeymoon period as explained starting here), and there is now evidence that some insulin production may last for up to five years.)
There is also the matter of ketones: ketones are substances found in the blood that result from the breakdown of fat. When the body cannot produce the insulin required to enable glucose to be used by the body’s cells for energy, then fat is broken down for the necessary energy instead, and this in turn produces ketones. At high levels ketones can cause the blood to become acidic, and this is the basis of the condition known as diabetic ketoacidosis (DKA). Ketones can be tested for in the blood using a special meter and test strips, similar to those used to test blood glucose. Alternatively, a urine test (using a ketone test strip) can be performed to check for evidence of ketone production. A small amount of ketones will be present in the urine of someone who has not eaten for several hours, but higher levels of ketones in someone with diabetes generally mean that they are deficient in insulin, and need insulin treatment.
It was generally thought that if a person had ketones in their urine (or blood) at the time they were diagnosed with diabetes it meant they had type 1 diabetes. They would then be started on insulin and told they would need insulin treatment for life. Over recent years, however, it has become apparent that some people labelled, in all good faith, as having type 1 diabetes, do not actually have it. When tested they have c-peptide in their blood, demonstrating that they are producing insulin, and, in some cases it has been possible for them to stop insulin treatment altogether.
While some parts of this book may be helpful to people with other types of diabetes, it is intended specifically to help people with type 1 diabetes learn how to manage their condition. The rest of this book refers solely to type 1 diabetes.
The relatively easy part of the answer to this question is that type 1 diabetes results from the destruction of the beta cells in the pancreas.
To recap, the pancreas is a very interesting organ that sits just behind the stomach. It has two distinct functions. The first is to produce enzymes that are released into the gut to digest food. The second function is to produce hormones. These are chemicals that are released into the bloodstream and exert their action on cells in different parts of the body, as with the example of insulin.
The hormone-producing cells are found in small clumps of cells called the Islets of Langerhans, which are dispersed through the pancreas. The insulin-producing cells are called beta cells. However, the islets contain a number of different cells that produce other hormones. The main one relevant to people with diabetes is glucagon, which is produced by the alpha cells. Glucagon has effects that are the opposite to insulin, including raising blood glucose levels if they fall too low. It is available as an emergency treatment to treat hypoglycaemia, or dangerously low blood glucose levels. Other types of islet cell include delta cells that produce somatostatin (a hormone involved in the regulation of the production of insulin and glucagon) and gamma cells that produce pancreatic polypeptide (which regulates the production of stomach and pancreatic enzymes that digest food).
In type 1 diabetes, the beta cells are destroyed as a result of attack by the body’s immune system. Interestingly, the other islet cells continue to function normally, although over time alpha cell function can become impaired, leading to reduced secretion of glucagon. Quite why the immune system singles out the beta cells for attack remains much of a mystery, despite years of research to try and find the answer. What is known is that type 1 diabetes results from a combination of having the right (or wrong) types of genes that prime the immune system to attack the beta cells, and exposure to something in the environment that acts as the trigger to launch the attack.
I am often asked whether type 1 diabetes is hereditary, and the answer is not entirely straightforward. From the above, it is clear that our genes play a role and as these are inherited from our parents, then this part of the risk of developing type 1 diabetes is indeed hereditary. However, diabetes only develops after the immune attack has been triggered, and the trigger is almost certainly something in the environment, such as a virus for example. Thus type 1 diabetes is not a true hereditary disease such as cystic fibrosis, which is always present in a child who inherits the affected gene from both parents. However, a child of a mother who has type 1 diabetes has a 3 per cent risk of developing it; this compares to a 5 per cent risk in a child whose father has type 1 diabetes and an 8 per cent risk in a child whose brother or sister has it.4 This is much greater than the 0.1 per cent risk in a child who has no immediate family members affected and shows the influence of genes in increasing the risk of developing type 1 diabetes. However, it is still a relatively low risk, underlining that while genes play a role, there is something else that triggers the onset of type 1 diabetes.
For many years, it has been known that certain genes are associated with an increased risk of developing type 1 diabetes. The strongest associations are with so-called HLA genes that regulate the immune system. Many years ago, in the early 1990s, I spent three years working in a laboratory as part of a team that was trying to pinpoint which of these genes were most closely linked to type 1 diabetes and why. I learnt many things in that time. I learnt that there were many different genes associated with type 1 diabetes, and that these associations were different in different races. I also learnt that laboratory scientists have to work extremely precisely for their experiments to be successful; and as a result of many unsuccessful experiments, I realised I was not really suited to a life working in a laboratory. Twenty-five years later, automated machines now undertake many of the procedures that relied on my (lack of) precision and our understanding of the detail of these genetic influences has increased exponentially. But we are still far from knowing all the answers about how and why certain genes increase the risk of type 1 diabetes. So, what do we now know?
Perhaps the strongest associations are with the HLA genes known as DR3 and DR4; individuals who have one of these two genes are at increased risk of type 1 diabetes; those that possess both are at an even greater risk. On the other hand, the gene DR2 appears to protect from type 1 diabetes (although it is associated with other autoimmune conditions such as multiple sclerosis).
Earlier in this chapter I mentioned that certain antibodies are present in many people with type 1 diabetes, especially before or around the time of diagnosis. The commonest antibodies are to insulin itself, known as insulin antibodies, and antibodies to the enzyme called glutamic acid decarboxylase (GAD). GAD is an enzyme involved in the production of GABA, a chemical used to transmit signals between nerve cells in the brain (a neurotransmitter). It appears that GAD is also produced in the islet cells, which provides a possible link with type 1 diabetes. It is now recognised that people with different HLA genes tend to have different antibodies: those with HLA DR3 tend to produce GAD antibodies, initially at least, whereas individuals with DR4 tend to produce insulin antibodies first.
Antibodies are molecules produced by the immune system to react with or bind other molecules and facilitate their destruction by specialised immune cells. These associations suggest that the genes related to type 1 diabetes are therefore in some way associated with the immune attack that eventually leads to beta cell destruction. However, the situation is much more complex than just the few genes we have discussed so far as over 50 distinct genes have been identified that influence the risk of developing type 1 diabetes.
The first part of the puzzle of what causes type 1 diabetes is the genetic make-up, which increases the likelihood of the immune system attacking the islet cells. The second part of the puzzle is the trigger that sets off the immune attack. The fact that the numbers of new cases of type 1 diabetes are increasing in many parts of the world suggests that something within the environment has changed to trigger these new cases (as our genetic makeup will not have changed that much to cause the increase).
We have discussed how the appearance of antibodies provides evidence of the immune attack against the beta cells. These antibodies generally appear in early childhood, in toddlers between the ages of one and two, although type 1 diabetes may not actually occur until some years later. By studying children known to have these antibodies, researchers have identified a number of possible triggers that set off the immune attack. These possible triggers, or environmental risk factors, include viral infections, particular foods in the diet and toxins. The strongest link with viruses is with enteroviruses. These are viruses found in the gut – one of the most well-known is the polio virus, others cause symptoms of the common cold or can lead to meningitis. One theory is that an enterovirus infection during pregnancy is associated with a later immune attack in the child to cause type 1 diabetes. Some studies have suggested that frequent respiratory infections in the first six months of life could also be associated with an increased risk of type 1 diabetes.5
Some studies showed that breastfeeding protects from type 1 diabetes and it has been suggested that early intake of cow’s milk could increase the risk of type 1 diabetes in children. A small study showed that babies who received cow’s milk had double the risk of developing islet cell antibodies later in childhood compared to babies who did not. However, it has not been shown conclusively that this led to increased development of type 1 diabetes.6
Type 1 diabetes is more common in areas that are further from the equator. Therefore, rates are higher in Scandinavia and Australia than, for example, in Africa.7 One explanation for this finding is that low levels of vitamin D increase the risk of developing type 1 diabetes. Vitamin D has many important functions, relating to bone strength and also in regulating the immune system. The body can make vitamin D, but adequate exposure to sunlight is necessary to produce sufficient amounts. As sunlight decreases with increasing distance from the equator, then populations living in colder climates have lower vitamin D levels – and higher rates of type 1 diabetes. Paradoxically, in the far north of Norway, there is less type 1 diabetes than further south, despite there being very little sunlight to make vitamin D during winter. However, in these areas, there is a high intake of fish in the diet, and fish oil is a rich source of vitamin D. A number of studies have shown that providing vitamin D supplements in childhood does protect against the development of type 1 diabetes.8
The final possible type of trigger is so-called beta cell stress. It has been suggested that a number of factors that increase the need for insulin to be secreted could place too heavy a demand on the beta cells that then become stressed. Such factors include being overweight, puberty, infections and trauma. Major life events (such as a death in the family) and other psychological traumas lead to increased stress hormones such as cortisol, that also cause beta cell stress. Regardless of the cause, it has been suggested that excessive demands on the beta cells can prompt a reaction of events within the cells triggering the autoimmune process that leads to type 1 diabetes.
So how do we put all this together? It is evident that there are still a number of possible theories about what causes type 1 diabetes, and it is likely that the precise cause is different in different people. We can say with some degree of certainty that certain people are at increased risk of developing type 1 diabetes because of their genes. However, having these genes in itself is not sufficient – there also needs to be the right combination of environmental factors in early life. Two of the most likely culprits are early exposure to cow’s milk and low vitamin D levels. (This is remarkably similar to the situation in multiple sclerosis, another autoimmune disease that affects the nervous system.) Finally, in those with the right genes and the right environmental factors, there is often an acute event, such as an infection, that leads to the disease showing itself. From this, it will be clear that type 1 diabetes is not primarily determined by any specific behaviours by the person who develops type 1 diabetes.
Having read the previous chapter, you will hopefully have a reasonable understanding about the metabolic abnormalities that are present in type 1 diabetes. The following chapters will provide greater detail about the complexities of managing type 1 diabetes (and as I said right at the beginning, the successful management of type 1 diabetes is not easy, and it can be very complex). The aim of this chapter is to provide a broad overview of the principles of treatment. These principles will underpin the approach recommended in the rest of the book.
In the last chapter, we discussed how type 1 diabetes results from an immune attack on the beta cells that produce insulin. Although some insulin production can continue for a few of years after diagnosis (the so-called ‘honeymoon period’), at the end of the day, the impact of type 1 diabetes is a complete lack of the hormone insulin. And so the main focus of the treatment of type 1 diabetes is to replace insulin as closely as possible to how the pancreas secretes insulin naturally. Indeed, one of the best-known books that promotes this principle is called Think Like a Pancreas.9 And ‘thinking like a pancreas’ is a good place to start. Unlike type 2 diabetes, type 1 diabetes is not a condition related to unhealthy lifestyles, obesity or excess liver fat causing problems with insulin resistance. A person just diagnosed with type 1 diabetes is usually young, fit and healthy, but with a pancreas that no longer produces insulin. So, the principle is to replace the lacking hormone, just as those whose thyroid gland no longer works have to take tablets to replace the missing thyroid hormone, or those whose adrenal glands no longer work take tablets to replace the missing cortisol.