Eating Disorders and Type 1 DM

Jaco SerfonteinConsultant Psychiatrist

Adult Inpatient Eating Disorder Service,Addenbrooke’s Hospital, Cambridge

AndNorfolk Community Eating Disorder Service,

Norwich

Diabetes mellitus

• Diabetes = “siphon” or “running through”– Large urine volume

• Mellitus = from honey– Glucose in urine

• Uniformly fatal within weeks to months

Patient J.L., December 15, 1922 February 15, 1923

The Miracle of Insulin

Insulin

• First peptide drug• First protein sequenced• First protein structure solved• First hormone measured in blood (RIA)• First hormone gene cloned (at UCSF)• First recombinant and first biotech drug

Insulin Nobel PrizesYear Category Recipient Contribution

1923 Medicine F.G. Banting andJ.J.R. Macleod

Discovery of insulin

1947 Medicine C.F. Cori and G.T.Cori

Discovery of the course of the catalyticconversion of glycogen

1947 Medicine B.A. Houssay Discovery of the role of hormones releasedby the anterior pituitarylobe in the metabolism of sugar

1958 Chemistry F. Sanger Work on the structure of proteins, especiallyinsulin

1971 Medicine E.W. Sutherland Discoveries concerning the mechanisms ofaction of hormones

1977 Medicine R. Yalow Development of radioimmunoassays forpeptide hormones

1992 Medicine E.H. Fischer and E.G.Krebs

Discoveries concerning reversible proteinphosphorylation as a biologicregulatory mechanism

Insulin Stimulates Cellular Glucose Uptake

LiverSkeletal Muscle

Adipocytes

Intestine & Pancreas

InsulinInsulin

Insulin

Type 1 vs. type 2 diabetesLambert P, et al. Medicine 2006; 34(2): 47-51

Nolan JJ. Medicine 2006; 34(2): 52-56

Features of type 2 diabetes• Usually presents in over-30s (but

also seen increasingly in youngerpeople)

• Associated with overweight/obesity• Onset is gradual and diagnosis often

missed (up to 50% of cases)• Not associated with ketoacidosis,

though ketosis can occur• Immune markers in only 10%• Family history is often positive with

almost 100% concordance inidentical twins

Features of type 1 diabetes• Onset in

childhood/adolescence• Lean body habitus• Acute onset of symptoms• Ketosis-prone• Auto-immune illness• Used to be a fatal disease

HBA1C

• Glycosylated haemoglobin• Red blood cells live for 8 to 12 weeks• Gives an indication of glucose control over the

last 8 to 12 weeks• Well-controlled < 7%

Symptoms

• Diabetic Ketoacidosis (DKA)• Polyuria, polydipsia, polyphagia• Weight loss• Fatigue• Infection• Blurred vision

Diabetic ketoacidosis

• ↓ Insulin - ↑ glucagon, glucose released fromliver

• Polyuria - ↓K,Na – polydipsia, thirst• Free fatty acids released and converted to

ketones - ↓pH – hyperventilation• Cerebral oedema

Visual impairment:diabetic retinopathy,

cataract and glaucoma

Kidney disease(diabetic nephropathy)

Sexual dysfunction

Sensory impairment(peripheral neuropathy)

Ulceration

Stroke(cerebrovascular disease)

Heart disease(cardiovascular disease)Bacterial and fungalinfections of the skin

Severe hardening ofthe arteries (atherosclerosis) Autonomic neuropathy

(including slow emptyingof the stomach and diarrhea)

Necrobiosis lipidoica

Gangrene

The major diabetic complications

Poor blood supply to lower limbs(peripheral vascular disease)

Goals of management• Manage symptoms• Prevent acute and late complications• Improve quality of life• Avoid premature diabetes-associated death• An individualised approach

Management

Glycaemiccontrol

BPLipids

Patienteducation

Lifestyle (e.g.diet & exercise)

Foot careEye careMicroalbuminuria

& kidneys

Approximate pharmacokineticprofiles of human insulin and insulin

analoguesHirsch IB. N Engl J Med 2005; 352: 174-83

Which insulin regimens are used?

• Regimen individualised depending on various factors e.g.patient choice and cognitive abilities, age, mealtimes, diet,exercise, shiftwork, target HbA1C, risk or experience ofhypoglycaemia, previous control if already on insulin.

Three basic regimens NICE. Type 1 diabetes Clinical Guideline 15, 2004

• One, two or three insulin injections/day• Multiple daily injection• Continuous subcutaneous insulin infusion

OR

DAFNE

• Dose Adjustment For Normal Eating• Structured 5 day course• Delivered in group format• Estimating carbohydrate content in meals and

adjusting insulin dose accordingly• Living as normal a life as possible

Prevalence

• AN – 0.3%• BN – 1%• ED-NOS – 2%• T1DM – 2.4X increased rates of ED• 25% of females with T1DM develop clinically

important disturbances of eating habits andattitudes in their lives

Medical Risks

• Insulin purging women>>men• Comorbid DM + ED – ↑risk of DM

complica ons, ↑risk of ED complica ons• DM mortality 2.2 per 1000 persons per year• DM + AN mortality 34.6 per 1000 persons per

year (Nielsen et al., 2002)

• Mean age of death 45y (58y T1DM) (Goebel-Fabbri,2008)

• Increased psychiatric comorbidity

• To explore the thoughts, feelings and experiencesof patients with type 1 diabetes and EatingDisorders or disordered eating/weight concernsin order to inform the development of:– effective strategies to prevent the development of

eating disorders in patients with type 1 diabetes– early identification of patients at risk of and with

emerging eating disorders/disordered eating.– appropriate treatment approaches for patients with

established co-morbid Type 1 Diabetes and eatingdisorders

Rigidity

Perfectionism

Family difficulties

Weight loss

Diagnosis of DM

Weight gain

Focus on importanceof weight, food,healthy living

Body dissatisfaction

Impact ofdiagnosis

Loss of control

Low mood

Fear ofhypoglycaemia/injecting

GuiltExcessiverestriction

Binge eating

Purging/insulinomission

Poorglycaemiccontrol

Anorexia nervosa Bulimia nervosa BED

Perfectionism surroundingsugars and excessivetesting

↑HbA1c Considerable weight gain

Recurrent hypoglycaemiarequiring third-partyassistance

Recurrent hospitalisations/DKA

High insulin requirements

Unusual patterns ofexercise

Reluctance to inject I frontof others

High levels ofdistress/depressionsurrounding food intake

Insulin omission to preventhunger

Concurrentpsychopathology

Low mood

Possible medical concernsregarding purging

Treasure and Ridge, 2012

‘A’ ‘B’ ‘C’

AN 0 1 49

BN 1 7 9

BED 2 5 2

EDNOS 0 0 1

NICE (2004)• 1.1.6.3 Young people with type 1

diabetes and poor treatmentadherence should be screened andassessed for the presence of an eatingdisorder.

• 1.1.4.2 Treatment of both subthresholdand clinical cases of an eating disorderin people with diabetes is essentialbecause of the greatly increasedphysical risk in this group.

• 1.1.4.3 People with type 1 diabetes andan eating disorder should haveintensive regular physical monitoringbecause they are at high risk ofretinopathy and other complications.

Screening – The SCOFF questionnaire

• Do you make yourself Sick because you feel uncomfortably full?• Do you worry you have lost Control over how much you eat?• Have you recently lost more than One stone in a 3 month period?• Do you believe yourself to be Fat when others say you are too thin?• Would you say that Food dominates your life?

• 2 or more out of 5 predicts an ED with 100% sensitivity and 87.5%specificity Morgan et al (1999)

• Do you sometimes take less insulin than you should to manage yourweight?

Screening

• Diabetes Eating Problem Survey (DEPS-R)– Self-report, <10 min, Cronbach’s α = 0.86 (Markowitz et

al, 2010)

Treatment• Might be pre-contemplative• ED egosyntotic• Motivational interviewing• Avoid setting difficult/unattainable goals• Focusing excessively on glycaemic control may be

counterproductive, be flexible• Do not prescribe a strict or rigid meal plan• Initial focus could be as small as completing basal

insulin doses to prevent DKA (Goebbel-Fabbri, 2009)• Relax the rules around blood glucose targets

temporarily – patient safety is the main goal

Treatment

• Psychoeduction – mixed results, someimprovement in ED pathology, but does notimprove metabolic control, treatmentadherence or decrease the frequency ofinsulin omission.

• Motivational Interviewing strategies• Individual or Group therapy (CBT)• Inpatient treatment

The Role of the Family

• Treatment mostly onoutpatient basis

• Families should not be seenas problem, but as part ofthe solution

• Family therapy inadolescents

• Maudsley model ofcollaborative care

In summary

• Weak evidence base• Complex, high risk, difficult to treat patients• Requiring joint working and direct

communication between different disciplines