Diabulimia is a coined term regarding eating disorders in which insulin is deliberate omitted or manipulated during treatment of type 1 diabetes in order to facilitate weight loss in a similar way to bulimic patients undertaking purgative actions to prevent fat storage in peripheral adipose tissue. Type 1 diabetes mellitus most commonly develops in childhood and adolescence. It has been found that Northern European countries (including the UK) have the highest prevalence of the disease, however the cause of this increased prevalence is largely unknown at this time. It has been shown that adolescent and young female adults with type 1 diabetes are more likely to suffer from an eating disorder such as bulimic disorders such as diabulimia.

Control of Insulin Secretion

The rate of insulin secretion is low, about 25ng/min/kg at normal blood glucose concentration of about 80-100mg/100ml. Both factors are directly related, as insulin secretion increases markedly by 2 stages when blood glucose concentration is elevated 2-3 times normal levels.

1. As a result of preformed insulin in beta cells, there is a sudden increase in plasma insulin levels to almost 10 fold. It then decreases rapidly about halfway back to normal levels in about 5 minutes.

2. Insulin levels then rise steadily to finally reach a plateau beginning from about 15 minutes to 3 hours. This results from additional release of pre-formed insulin coupled with the synthesis of new insulin.

Insulin Switches between Carbohydrate and Glucose Metabolism

Insulin promotes the use of carbohydrates for energy, at the same time suppressing the use of lipid for the same purpose. A lack of insulin therefore promotes the utilization of fats for energy

Pathology of Type 1 Diabetes Mellitus

Type 1 diabetes is an autoimmune disease where the body's own immune system attacks the islet antigens resulting in the destruction of β-cells leading to a decrease in the production of endogenous insulin. The typical symptoms of type 1 diabetes such as hypoglycaemia only become apparent once over 90% of β-cells have been destroyed. This leads us to believe that autoimmune pathogenesis of the disease starts many years before the onset of diabetes.

The main defect of the immune system in type 1 diabetes is a failure of self-tolerance in T-cells. The antigens released by damaged islet cells trigger the first autoreactive T cells. The triggering auto-antigens may include insulin itself. The activated T cells move to the pancreas and start destroying β-cells.

The aetiology of Type 1 diabetes is not fully understood. Current research suggests both genetic and environmental factors. Epidemiological studies comparing concordance rates for Monozygotic and Dizygotic twins suggest a genetic link. Environmental factors such as viral infections are also implicated as a causal factor.

Shortage of insulin leads to hyperglycaemia and diabetic ketoacidosis (DKA)


Insulin is required to remove glucose from the blood and into the muscles and liver where it is converted into glycogen. When there is low or no insulin, as in type 1 diabetes, the glucose is not removed from the blood and thus blood glucose concentration rises. Hyperglycaemia is defined as a blood glucose level of 200 mg/dl (11.1mmol/l) or higher. Chronic hyperglycaemia damages the blood vessels and the organs supplied by them. Among the complications of chronic hyperglycaemia are cardiovascular damage, neurological damage, kidney damage, retinopathies.

If insulin is omitted as in diabulimia, it can lead to acute hyperglycaemia with extremely high levels of glucose which if untreated can result in dehydration and electrolyte imbalance due to osmotic diueresis. Hyperglycaemia can also cause coma, stupor, and cardiac arrhythmias.

Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis is a state of metabolic acidosis which is caused by the excess formation of the ketone bodies by the β-oxidation of fatty acids. This occurs in the absence of insulin as there is increased fat metabolism.

Long Term Effects of Diabulimia

It has been shown that increased levels of HBA1C (an indicator of poor glycemic control, commonly seen in non-adherent type 1 diabetics) in serum are linked to the increased prevalence of microvascular disease, as seen in the opposite graph.

A meta-analysis performed by Nielsen et al showed that type 1 diabetics with bulimic behaviours are at an increased risk of Retinopathy (a diabetic microvascular disease) and other complications associated with poorly controlled blood glucose levels.

Psychology of Diabullimia

The model below can be used to demonstrate the processes involved, and defective thought patterns encountered in Diabulimia. This is based on Leventhal's self regulatory model (1987). The treatment box below includes methods to disrupt the defective thought processes in aim to break the cycle and enable the patient to regain perspective on the body and diabetes treatment.

Stage 1: Interpretation

Increase in BMI/ body fat related to insulin therapy and previous malnutrition. Low BMI due to diabetes.

Symptom perception: weight gain Social messages: Doctor said insulin causes me to store fat Deviation from norm: weight gain is undesirable

Stage 2: coping

Approach coping: insulin= weight gain therefore ceasing insulin = weight loss.

Avoidance coping: related to diabetes, denial of complications/ it wont happen to me'

Stage 3: Appraisal

Weight loss = effective coping strategy

DKA= ineffective strategy: modify dosage instead of insulin omission to narrowly avoid DKA

Stage 3: Appraisal

Weight loss = effective coping strategy

DKA= ineffective strategy: modify dosage instead of insulin omission to narrowly avoid DKA

Simultaneously, treatment interventions such as cognitive behavioural therapy tackles the dysfunctional thoughts generated in stage 1 by rationalisation. It also encourages the patient to make practical decisions that are beneficial and promote positive coping.


Due the complexity of diabulimia, a multi-disciplinary approach is carried out to achieve the management of both medical and psychological issues related to this condition.

Cognitive behavioural therapy (CBT) is commonly used to address the psychological barriers in achieving a good diabetic self-care. It can be carried out by using a goal-oriented and systematic approach through individual or group sessions. The main aims are:

• identify and modify dysfunctional thoughts regarding body weight/image

• promote healthy eating habit and appropriate exercise regimes

• encourage behaviour change regarding insulin omissions

• address poor cognitions concerning long term complications of diabulimia

However, CBT is insufficient alone and further integration of additional patient education, reinforcement by modelling, regular specialist support, adaptation of treatment plan with the addition of antidepressants(whether the patient has clinical depression or not), etc are all essential in combating diabulimia.

Please be aware that the free essay that you were just reading was not written by us. This essay, and all of the others available to view on the website, were provided to us by students in exchange for services that we offer. This relationship helps our students to get an even better deal while also contributing to the biggest free essay resource in the UK!