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Diabetes mellitus-treatment and psychiatric effects
1. Dr Megha Isac
Junior resident
Dept. of General
Medicine
Diabetes Mellitus
– Management and
psychiatric aspects
2. Criteria for the Diagnosis of Diabetes Mellitus
• Symptoms of diabetes plus random blood glucose concentration
200 mg/dL or
• Fasting plasma glucose ≥126 mg/dL or
• Hemoglobin A1c ≥ 6.5%c or
• 2-h plasma glucose ≥200 mg/dL during an oral glucose tolerance test
(The test should be performed using a glucose load containing the
equivalent of 75 g anhydrous glucose dissolved in water, not
recommended for routine clinical use.)
Source: Adapted from American Diabetes Association: Diabetes Care 37(Suppl
1):S14,2014
3. Essentials of diagnosisEssentials of diagnosis
Type 1 diabetes
Polyuria, polydypsia and weight loss associated with
random plasma glucose >/= 200 mg/dl
Plasma glucose of>/= 126mg/dl after an overnight
fast,documented on more than one occasion.
Ketonemia, ketonuria ,or both.
Islet autoantibodies are frequently present.
4. • Type 2 diabetes
• Most patients are over 40 yrs of age and obese.
• Polyuria and polydypsia ,ketonuria and weight loss
generally are uncommon at the time of diagnosis.
candidial vaginitis in women may be an initial
manifestation. Many patients have few or no symptoms.
• Plasma glucose of >/=126mg/dl after an overnight fast on
more than one occasion.2 hrs after 75 mg oral glucose,
diagnostic values are >/=200 mg/dl
• Hypertension, dyslipidemia and atherosclerosis are
often associated
5. Etiologic Classification of Diabetes
Mellitus
Type 1 diabetes
(beta cell destruction, usually leading to absolute insulin
deficiency)
•A. Immune-mediated
•B. Idiopathic
Type 2 diabetes
(may range from predominantly insulin resistance with
relative insulin deficiency to a predominantly insulin
secretory defect with insulin resistance)
6. Other specific types of diabetes
A.Genetic defects of beta cell development or function
B.Genetic defects in insulin action
C.Diseases of the exocrine pancreas
D.Endocrinopathies
E.Drug- or chemical-induced
glucocorticoids, vacor (a rodenticide), pentamidine,
nicotinic acid, diazoxide, β-adrenergic agonists, thiazides,
calcineurin and mTOR inhibitors, hydantoins,
asparaginase, α-interferon, protease inhibitors,
antipsychotics (atypicals and others), epinephrine
F. Infections
7. G. Uncommon forms of immune-mediated diabetes
-anti-insulin receptor antibodies
H. Other genetic syndromes sometimes associated with
diabetes
Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome,
Huntington’s chorea, myotonic dystrophy
I. Gestational diabetes mellitus (GDM)
Source: Adapted from American Diabetes Association:
Diabetes Care 37(Suppl 1)
8. Worldwide prevalence of diabetes mellitus. Global estimate is 382
million individuals with diabetes. Regional estimates of the number
of individuals with diabetes (20–79 yearsof age) are shown (2013).
IDF Diabetes Atlas, the International Diabetes Federation, 2013.
9. Risk Factors for Type 2 Diabetes Mellitus
Family history of diabetes (i.e., parent or sibling with type 2 diabetes)
Obesity (BMI ≥25 kg/m2 or ethnically relevant definition for overweight)
Physical inactivity
Race/ethnicity (e.g., African American, Latino, Native American, Asian
American, Pacific Islander)
Previously identified with IFG, IGT, or an hemoglobin A1c of 5.7–6.4
History of GDM or delivery of baby >4 kg
Hypertension (blood pressure ≥140/90 mmHg)
HDL cholesterol level <35 mg/dL ) and/or a triglyceride level>250 mg/dL)
Polycystic ovary syndrome or acanthosis nigricans
History of cardiovascular disease
10.
11. The goals of therapy
(1)eliminate symptoms related to hyperglycemia(RBS<200mg/dl)
(2) reduce or eliminate the long-term microvascular and
macrovascular complications of DM
(3) allow the patient to achieve as normal a lifestyle as possible.
12. Guidelines for Comprehensive Medical Care for Patients
with Diabetes
• Optimal and individualized glycemic control
• Self-monitoring of blood glucose (individualized frequency)
• HbA1c testing (2–4 times/year)
• Patient education in diabetes management (annual); diabetes-self
management ,education and support
• Medical nutrition therapy and education (annual)
• Eye examination (annual or biannual)
• Foot examination (1–2 times/year by physician; daily by patient)
• Screening for diabetic nephropathy (annual)
• Blood pressure measurement (quarterly)
• Lipid profile and serum creatinine (estimate GFR) (annual)
• Influenza/pneumococcal/hepatitis B immunizations
• Consider antiplatelet therapy
13. Treatment Goals for Adults with
Diabetes
Index Goal
Glycemic control
HbA1c <7.0%c
Preprandial capillary plasma glucose 80–130 mg/dL
Peak postprandial capillary plasma glucose <180 mg/dL
Blood pressure <140/90 mmHg
Lipids
Low-density lipoprotein < 100 mg/dL
High-density lipoprotein >40 mg/dL in men
>50 mg/dL in women
Triglycerides <150 mg/dL
14. Treatment regimenTreatment regimen
• A well balanced nutritious diet remains a fundamental element of therapy
Limiting the carbohydrate intake and substituting some of the calories with
monosaturated fats such as olive oil ,rapeseed (canola) oil can lower TG
and increase HDL.
Weight reduction by caloric restriction is important goal.
High protein intake may cause progression of kidney disease in patients with
diabetic nephropathy; reduction in protein intake to 0.8 kg/day (or about
10% of total calories daily)is recommended.
Limit cholesterol intake to 300 mg /day ,and in individuals with LDL
cholesterol more than 100 mg/day should limit dietary cholesterol to 200
mg daily.
15. Dietary Fiber
ADA recommends food such as oatmeal, cereals and beans
with relatively high soluble fiber content as staple components
of the diet in diabetics.
retards nutrient absorption rates
High soluble fibre content in the diet has favourable effect
on blood cholesterol levels.
16. Artificial and other sweeteners
Aspartame(aspartic acid and phenylalanine) -180 times as sweet as
sucrose, not heat stable
Saccharin,sacralose,acesulfame potassium –used for cooking and baking
Sugar alcohols
eg naturaly occuring in many fruits and vegetables, commercialy made
from sucrose, glucose, starch- sorbitol,xylitol ,mannitol,lactitol, isomalt,
maltitol and hydrogenated starch hydrolysates
used in “sugar free” food products
if consumed in large quantities will raise blood sugars and can cause
bloating and diarrhoea
17. Weight loss and exercise
Multiple positive benefits including
• cardiovascular risk reduction, reduced blood pressure
• maintenance of muscle mass, reduction in body fat, and weight loss.
For individuals with type1 or type 2 DM
•lowers plasma glucose (during and following exercise)
• increasing insulin sensitivity.
Inpatients with diabetes, the ADA recommends 150 min/week
(distributed over at least 3 days) of moderate aerobic physical activity
withno gaps longer than 2 days. The exercise regimen should also
include resistance training.
23. Type 1 Diabetes Mellitus
The goal is to design and implement insulin regimens that
mimic physiologic insulin secretion.
In all regimens
long-acting insulins (NPH, glargine, or detemir) supply
basal insulin
regular, insulin aspart, glulisine, or lispro insulin provides
prandial insulin
24. HOW??HOW MUCH???
Short-acting insulin analogues should be injected just before
(<10 min) or just after a meal; regular insulin is given 30–45 min
prior to a meal. Sometimes short-acting insulin analogues are
injected just after a meal (gastroparesis, unpredictable food
intake).
In general, individuals with type 1 DM require 0.5–1 U/kg per
day of insulin divided into multiple doses, with ~50% of the
insulin given as basal insulin
25. HOW TO ADJUST DOSES????
The insulin dose in such regimens should be adjusted based on SMBG
results with the following general assumptions:
(1) the fasting glucose is primarily determined by the prior evening long-
acting insulin
(2) the pre-lunch glucose is a function of the morning short-acting insulin
(3) the pre-supper glucose is a function of the morning long-acting insulin
(4) the bedtime glucose is a function of the pre-supper, short-acting
insulin.
This is not an optimal regimen for the patient with type 1 DM, but is
sometimes used for patients with type 2 DM.
26. Amylin
•A 37-amino-acid peptide co-secreted with insulin from pancreatic beta cells,
in normal glucose homeostasis is uncertain.
However, based on the rationale that patients who are insulin deficient are
also amylin deficient, an analogue of amylin (pramlintide) was created and
found to reduce postprandial glycemic excursions in type 1 and type 2
diabetic patients taking insulin.
•Pramlintide injected just before a meal slows gastric emptying and
suppresses glucagon but does not alter insulin levels.
Addition of pramlintide produces a modest reduction in the HbA1c and
seems to dampen meal-related glucose excursions.
In type 1 DM, pramlintide is started as a 15- g SC injection before eachμ
meal and titrated up to a maximum of 30–60 g as tolerated.μ
In type 2 DM, pramlintide is started as a 60- g SC injection before eachμ
meal and may be titrated up to a maximum of 120 g.μ
27. Management of Type 2 Diabetes
Individualized glycemic control
• Diet/lifestyle
• Exercise
• Medication
Treat associated conditions
• Dyslipidemia
• Hypertension
• Obesity
• Coronary heart disease
Screen for/manage complications of diabetes
• Retinopathy
• Cardiovascular disease
• Nephropathy
• Neuropathy
• Other complications
28. Biguanides
Metformin, representative of this class of agents
• reduces hepatic glucose production
• improves peripheral glucose utilization
•Mild increase in insulin sensitivity
Metformin activates AMP-dependent protein kinase and enters cells through
organic cation transporters (polymorphisms of these may influence the
response to metformin).
Recent evidence indicates that metformin’s mechanism for reducing hepatic
glucose production is to antagonize glucagon’s ability to generate cAMP in
hepatocytes.
• reduces fasting plasma glucose (FPG) and insulin
levels
• improves the lipid profile
•Promotes modest weight loss.
29. An extended-release form is available and may have fewer gastrointestinal
side effects (diarrhea, anorexia, nausea, metallic taste).
Because of its relatively slow onset of action and
gastrointestinal symptoms with higher doses, the initial dose
should be low and then escalated every 2–3 weeks based on
SMBG measurements.
Metformin is effective as monotherapy and can be used in combination
with other oral agents or with insulin.
The major toxicity of metformin, lactic acidosis, is very rare and can be
prevented by careful patient selection.
Vitamin B12 levels are ~30% lower during metformin treatment.
30. Metformin should not be used in patients with
1. renal insufficiency (glomerular filtration rate [GFR] <60
mL/min)
2.any form of acidosis
3.unstable congestive heart failure (CHF)
4. liver disease
5.severe hypoxemia.
Metformin should be discontinued in hospitalized patients, in
patients who can take nothing orally, and in those receiving
radiographic contrast material. Insulin should be used until
metformin can be restarted.
31. Insulin secretagogues stimulate insulin secretion by interacting with the
ATP-sensitive potassium channel on the beta cell
These drugs are most effective in individuals with type 2
DM of relatively recent onset (<5 years) who have residual
endogenous insulin
production.
First-generation sulfonylureas (chlorpropamide, tolazamide,
tolbutamide) have a longer half-life, a greater incidence of
hypoglycemia and more frequent drug interactions, and are no longer
used.
Second-generation sulfonylureas have a more rapid onset of action and
better coverage of the postprandial glucose rise, but the shorter half-life
of some agents may require more than once-a-day dosing
32. Sulfonylureas reduce both fasting and postprandial glucose
and should be initiated at low doses and increased at 1- to 2-
week intervals based on SMBG.
In general, sulfonylureas increase insulin acutely and thus
should be taken shortly before a meal; with chronic therapy,
though, the insulin release is more sustained.
Glimepiride and glipizide can be given in a single daily dose
and are preferred over glyburide, especially in the elderly
33. Repaglinide, nateglinide, and mitiglinide are not
sulfonylureas but also interact with the ATP-sensitive
potassium channel.
Because of their short half-life, these agents are given with
each meal or immediately before to reduce meal-related
glucose excursions.
34. Insulin secretagogues, especially the longer acting ones, have the
potential to cause hypoglycemia, especially in elderly individuals.
Most sulfonylureas are metabolized in the liver to compounds (some
of which are active) that are cleared by the kidney.
Thus, their use in individuals with significant hepatic or renal
dysfunction is not advisable.
Weight gain, a common side effect of sulfonylurea therapy, results
from the increased insulin levels and improvement in glycemic
control.
Some sulfonylureas have significant drug interactions with alcohol and
some medications including warfarin, aspirin, ketoconazole, α-
glucosidase inhibitors, and fluconazole
35. DPP-IV inhibitors inhibit degradation of native GLP-1 and thus
enhance the incretin effect. Incretins” amplify glucose-stimulated
insulin secretion.
DPP-IV, which is widely expressed on the cell surface of
endothelial cells and some lymphocytes, degrades a wide range of
peptides (not GLP-1 specific).
Exenatide is an analogue of GLP-1. Unlike native GLP-1, which
has a half-life of >5 min, differences in the exenatide amino acid
sequence render it resistant to the enzyme that degrades GLP-1
(dipeptidyl peptidase IV [DPP-IV]).
Thus, exenatide has prolonged GLP-1-like action and binds to
GLP-1 receptors found in islets, the gastrointestinal tract, and the
brain.
GLP-1 receptor agonists increase glucose-stimulated
insulin secretion, suppress glucagon, and slow gastric
emptying
36. DPP-IV inhibitors promote insulin secretion in the absence of
hypoglycemia (unless there is concomitant use of an agent that can lead to
hypoglycemia—sulfonylureas, etc.) or weight gain and appear to have a
preferential effect on postprandial blood glucose.
The levels of GLP-1 action in the patient are greater with the GLP-1
receptor agonists than with DPP-IV inhibitors.
Reduced doses should be given to patients with renal insufficiency
.
Initial concerns about the pancreatic side effects of GLP-1 receptor
agonists and DPP-IV inhibitors (pancreatitis, possible premalignant lesions)
appear to be unfounded.
37. These agents do not promote weight gain; in fact, most
patients experience modest weight loss and appetite
suppression.
Treatment with these agents should start at a low dose to minimize
initial side effects (nausea being the limiting one). The major side
effects are nausea, vomiting, and diarrhea
Some patients taking insulin secretagogues may require a
reduction in those agents to prevent hypoglycemia.
38. α-Glucosidase inhibitor
• reduce postprandial hyperglycemia by delaying glucose
absorption
Postprandial hyperglycemia, secondary to impaired hepatic and
peripheral glucose disposal, contributes significantly to the hyperglycemic
state in type 2 DM.
These drugs, taken just before each meal, reduce glucose absorption by
inhibiting the enzyme that cleaves oligosaccharides into simple sugars in
the intestinal lumen.
The major side effects (diarrhea, flatulence, abdominal distention) are
related to increased delivery of oligosaccharides to he large bowel and can
be reduced somewhat by gradual upward dose titration
39. Simultaneous treatment with bile acid resins and antacids should be
avoided.
These agents should not be used in individuals with
• inflammatory bowel disease
• gastroparesis
•serum creatinine >2 mg/dL
This class of agents is not as potent as other oral agents in lowering the
HbA1c but is unique because it reduces the postprandial glucose rise
even in individuals with type 1 DM
40. Thiazolidinediones
reduce insulin resistance by binding to the PPAR- (peroxisomeγ
proliferator–activated receptor ) nuclear receptor (which forms aγ
heterodimer with the retinoid X receptor).
Agonists of this receptor regulate a large number of genes
•promote adipocyte differentiation
•reduce hepatic fat accumulation
• promote fatty acid storage.
• redistribution of fat from central to peripheral locations.
•Circulating insulin levels decrease indicating a reduction in insulin
resistance.
41. Thiazolidinediones are associated with:
• weight gain (2–3 kg)
•small reduction in the hematocrit
•a mild increase in plasma volume
• Peripheral edema and CHF are more common in individuals treated
with these agents.
•Changes in lipid profile
•(Rosiglitazone raises low-density lipoprotein (LDL), high-density
lipoprotein (HDL), and triglycerides slightly. Pioglitazone raises HDL
to a greater degree and LDL a lesser degree but lowers triglycerides.)
•worsening of diabetic macular edema.
•increased risk of fractures has been noted in women
•induce ovulation in premenopausal women with polycystic ovary
syndrome.
These agents are contraindicated in patients with liver disease or CHF
(class III or IV).
42. Concerns about increased cardiovascular risk associated with
rosiglitazone led to considerable restrictions on its use and to the FDA
issuing a “black box” warning in 2007. However, based on new
information, the FDA has revised its guidelines and categorizes
rosiglitazone similar to other drugs for type 2 DM. Because of a
possible increased risk of bladder cancer, pioglitazone is part of an
ongoing FDA safety review.
43. Sodium-Glucose Co-Transporter 2 Inhibitors (SLGT2)
These agents lower the blood glucose by selectively inhibiting this
co- transporter, which is expressed almost exclusively in them
proximal, convoluted tubule in the kidney
. This inhibits glucose reabsorption, lowers the renal threshold for
glucose, and leads to increased urinary glucose excretion.
Thus, the glucose-lowering effect is insulin independent and not
related to changes in insulin sensitivity or secretion.
Adverse effects
•urinary or vaginal infections are more common
•the diuretic effect can lead to reduced intravascular volume.
• increased incidence of hyperkalemia
44. Insulin therapy in type 2 DM.
As the initial therapy in type 2 DM
•in lean individuals or those with severe weight loss
• in individuals with underlying renal or hepatic disease
•in individuals who are hospitalized or acutely ill.
Insulin therapy is ultimately required by a substantial number of
individuals with type 2 DM because of the progressive nature of the
disorder and the relative insulin deficiency that develops in patients
with long-standing diabetes.
Both physician and patient reluctance often delay the initiation of
insulin therapy, but glucose control and patient well-being are
improved by insulin therapy in patients who have not reached the
glycemic target.
45. Choice of initial glucose-lowering agent :
The level of hyperglycemia and the patient’s individualized goal should
influence the initial choice of therapy.
Assuming that maximal benefit of MNT and increased physical activity has
been realized, patients with mild to moderate hyperglycemia (FPG 200–
250 mg/dL) often respond well to a single, oral glucose-lowering agent.
Patients with more severe hyperglycemia (FPG >250 mg/dL) may respond
partially but are unlikely to achieve normoglycemia with oral monotherapy.
46. A stepwise approach that starts with a single agent and adds a second
agent to achieve the glycemic target can be used
Insulin can be used as initial therapy in individuals with severe
hyperglycemia (FPG < [250–300 mg/dL]) or in those who are
symptomatic from the hyperglycemia.
This approach is based on the rationale that more rapid glycemic control
will reduce “glucose toxicity” to the islet cells, improve endogenous
insulin secretion, and possibly allow oral glucose-lowering agents to be
more effective. If this occurs, the insulin may be discontinued
47. Patient with type 2 diabetes
Individualized glycemic goal
Medical nutrition therapy,
increased physical activity,
weight loss
+
metformin
Reassess HbA1c
Combination therapy
-metformin + second agent
Reassess HbA1c
Combination therapy
-metformin + two
other agents
Insulin + metforminReassess HbA1c
48. Metformin’s advantages are that it
• promotes mild weight loss
• lowers insulin levels
•improves the lipid profile slightly
Based on SMBG results and the HbA1c, the dose of metformin
should be increased until the glycemic target is achieved or maximum
dose is reached.
If metformin is not tolerated, then initial therapy with an insulin
secretagogue or DPP-IV inhibitor is reasonable.
49.
50. In clinical practice it is clear that a diabetic who is poorly
endowed or emotionally unstable can pose a considerable
therapeautic problem-
Cooperation in treatment is essential
There is indications that psychological stresses can be
important in aggravating the disorder or precipitating
episodes of loss of control, and even suggestions that
emotional factors may sometimes bring the disorder in to
being.
-Wilkinson D.G.(1981) Psychiatric aspects of diabetes mellitus
.British Journal of psychiatry 138,1-9.
-Tattersall R.B (1981) Psychiatric aspects of diabetes – a physician ‘s
view.British Journal of Psychiatry 139,485-493.
51. Emotional influences on the course of
diabetes
Emotionally stressful experiences can produce
fluctuations in levels of blood glucose and ketone
bodies,both in diabetic and non diabetic persons.
-Hinkle L.E and Wolf S. (1952b)A summary of experimental
evidence relating life stress to Diabetes Mellitus.Journal of the
Mount Sinai Hospital 19,537-570.
It has proved difficult,however to define the extent to
which such factors may be operative in the actual
disease.
52. Diabetes is a disorder of adaptation and that persons showing
it have reacted to various life stresses with a physiological
response that is appropriate to starvation.The pathway for
such emotional origin would be via hypothalamic autonomic
or pituitary endocrine relationships.
-Treuting. T.F (1962) The role of emotional factors in the etiology and
course of diabetes mellitus:a review of the recent literature.American
journal of medical sciences 244,93-109
However no increase in incidence among battle casualities
from 1st
and 2nd
world war.
Stress may sometimes change a latent case of diabetes into an
active one.
53. In long term studies by Hinkle & Wolf (1952)
extending over several years, periods of exacerbation
and remission were correlated with events in the life
situation. Events which were consciously or
unconsciously interpreted by the patients as threatening
to their security appeared to be particularly liable to
lead to loss of control.
?extend of direct metabolic consequences
?effect of abandoning dietary regimes or medicines
?effect of alcohol
?deliberately induced coma to secure attention
54. Insulin dependent Diabetes
– ”the manipulators delight”
Tattersall R.B (1981) Psychiatric aspects of diabetes – a
physician ‘s view.British Journal of Psychiatry 139,485-493.
55. Baker and Barcai(1970) – a small number of juvenile
diabetics in whom the emotional arousal led directly to
ketoacidosis mediated by an increased ketone response to
endogenous catecholamines.
-Baker L. & Barcai A.(1970)Psychosomatic aspects of Diabetes
Mellitus.Ch 7. in Modern trends of psychosomatic medicine.Vol 2,ed
Hill.O.W. Butterworths:London
-Treuting. T.F (1962) The role of emotional factors in the etiology and
course of diabetes mellitus:a review of the recent literature.American
journal of medical sciences 244,93-10
56. Psychological problems in Diabetes
Juvenile Diabetics:
Neurotic developments or disturbed family relationships,and
hypochondriacal attitudes may be established
Eating disorders including bulimia, anorexia nervosa more
common.
Difficulty in adhering to treatment especialy during loneliness,
depression or tension. Explosive rebellion and wilful neglect of
treatment.
The anxiety of mother may be transferred to the child or a
perfectionist mother may gain control over the illness at the cost of
behaviour difficulties
Child may utilise illness to manipulate home environment
57. • Minor abnormalities in measures of
dependence/independence, self perception, manifest and
latent anxiety and sexual identification.
-Sterky G.(1963) Diabetic school children .Acta Pediatrica
Scandinavica ,Suppl.144,1-39.
-Swift C.R .,Seidman F & Stein h.(1967)Adjustment problems in
juvenile diabetics .Psychosomatic Medicine 29, .555-571.
58. In adult life
Employment or marriage prospects affected.
Pruritis and decreased sexual interest, impotence and
amenorrhoea,ocular problems may contribute to
emotional complications and family life.
Delayed psychosexual development when diabetes sets
in an early age.
-Surridge et al(1984) psychiatric aspects of Diabetes Mellitus.
British journal of psychiatry 145,269-276.
.
59. Increased frequency of impotence in men and anorgasmia in
women.
-Kolodny R.C 1971 .Sexual dysfunctions in diabetic females.Diabetes
20,557-559
Disturbances in ejaculation.
-Fairburn et al(1982) The clinical features of diabetic impotence : A
preliminary study .British journal of Psychiatry 140,447-452
60. Hypoglycemia
Fear of attack
May cause lassitude, depression, undue difficulty in
waking, early morning headaches ,nocturnal fits.
Affected appeared pale, apathetic, torpid and
demoralised, others complained of lethargy, depression
and difficulty in concentration
-Gale E.A.M and Tattersall R.B. (1979) unrecognised nocturnal
hypoglycemia in insulin treated diabetes. Lancet I,1049-1052
61. Diabetics chronically overtreated with insulin; their
symptoms included excessive appetite , polydipsia,
vertigo, mood swings ,irritability and chronic fatigue.
-Schwandt P.,Richter W &Wilkening J.(1979) Chronic insulin
overtreatment,Lancet 2,261-262
In management of manic depressive illness in diabetics it
may sometimes be necessary to consider the possibility
that insulin requirements increase during markedly
depressive phases:
-Crammer and Gillies(1981)
-Kronfol et al. (1981)Psychiatric aspects of Diabetes
Mellitus:diabetes and depression .British Journal of Psychiatry
139,172-173
62. The causal roles are unclear, although impaired central
nervous system glucose metabolism, sedentary lifestyle,
diet and smoking may all contribute.
A recent study has shown that leptin, originally studied in
relation to adipose tissue, has receptors in the limbic
system and could have a potential role in emotional
processes. Increasing the leptin signals in brain may be a
new approach to treat depressive disorders.
-Haupt D, Newcomer J. Depression is associated with hyperglycemia
and other metabolic abnormalities. Diabetes Spectr 2004; 17 : 154-5.
- Lu XY, Kim CS, Frazer A, Zhang W. Leptin: a potential novel
antidepressant. Proc Natl Acad Sci USA 2006; 103 : 1593-8.
63. Persons with diabetes were twice as likely to have
depression compared to those without diabetes.
The odds of depression occurring in women were
higher than in men
64. Brain damage in diabetics
Episodes of hypoglycemia or diabetic coma may have
contributed to brain damage, or associated
atherosclerosis may be responsible.
Study reflected some degree of brain damage or merely
the psychological impact of a chronic disease at young
age(<5yrs)
-Act et al(1961) Intelligence in children with diabetes
mellitus.Pediatrics 28,764-770
65. Ives(1963) surveyed 380 adult diabetics in the general
hospital and found that 45 were mentally abnormal.
18- organic brain syndromes
9- personality disorders
4- psychotic
-cerebral atherosclerosis was probably the responsible
factor
Similar studies by Bale(1973)
It is possible that the association between
impaired cognitive capacity and hypoglycemic
episodes may merely reflect the fact that
patients with poor endowement manage their
diabetes less well
66. Incidence of brain parenchymal changes secondary to
vascular changes are more in diabetics
-Dandona et al(1978), Reske Neilsen and Lundback(1963),Grunnet
(1963), Alex et al (1962).
67. Co-existence of diabetes and psychiatric
illness
Diabetes is difficult to manage as such, but patients with mental
health disorders receive even less intensive medical care for
diabetes
- Desai MM, Rosenheck RA, Druss B, Perlin JB. Mental disorders and
quality of diabetes care in the Veterans Health Administration. Am J
Psychiatry 2002; 159 : 1584-90.
- Frayne SM, Halanych JH, Miller DR, Wang F, Lin H, Pogach L, et al.
Disparities in diabetes care: impact of mental illness. Arch Intern Med
2005; 165 : 2631-8.
Self care behaviour in diabetes was adversely affected by the
occurrence of natural calamities
-Ramachandran A. Experiences of the WHO Collaborating Centre for
Diabetes in India in managing tsunami victims with diabetes. Pract
Diabetes Int 2005; 22 : 98-9.
68. Lesser degree of psychological distress not amounting to
psychiatric morbidity is more common.
Sridhar GR, Madhu K. Psychosocial and cultural issues in diabetes
mellitus. Curr Sci 2002; 83 : 1556-64
There is recent intriguing evidence that maternal pre- and
peri-natal depression can adversely impact the health of their
infants, leading to poorer growth.
Rahman A, Iqbal Z, Bunn J, Lovel H, Harrington R. Impact of maternal
depression on infant nutritional status and illness: a cohort study. Arch
Gen Psychiatry 2004; 61 : 946-52.
69. At the next step, a variety of psychological distress can
occur when diabetes mellitus is first diagnosed:
denial, anger, guilt, reactive depression and finally
acceptance.
Physicians must be aware of these reactions which are
anticipated with chronic conditions. They must be
trained to manage these, which may take months to
resolve
70. In clinical practice, identification of depression in diabetes is
often overlooked for a variety of reasons:
•societal disapproval of depression
•complicity between physicians and patients not to discuss
depressive symptoms
• wrongly considering depression as a ‘normal consequence
of difficult medical illness’
The potential benefits of treatment are thereby missed.
Lustman PJ, Clouse RE. Practical considerations in the management of
depression in diabetes. Diabetes Spectr 2004; 17 : 160-6.
71. Use of antidepressant medications can disturb
glycaemic control:
•tricyclic antidepressants stimulate appetite
•selective serotonin reuptake inhibitors suppress appetite,
enhance insulin sensitivity and lead to hypoglycaemia if
diet is not regulated.
Besides, once depression is treated eating habits exercise
and drug compliance may change, leading to unstable
metabolic control.
In the presence of autonomic neuropathy tricyclic
antidepressants may worsen orthostatic hypotension,
induce constipation and urinary retention
Sridhar GR, Madhu K. Depression and psychosocial stress in diabetes
mellitus. In: Kapur A, Joshi JK, editors. Novo nordisk diabetes update
proc. Mumbai: Business Networ Inc; 2002 p. 87-92.
72. Psychotic disorders, obesity, metabolic syndrome
and type 2 diabetes mellitus
Schizophrenia was believed to be a predisposing factor to
diabetes
Patients with severe mental illness had higher prevalence of
metabolic syndrome
Outpatients with bipolar disorder had greater severity of illness
with increasing number of co-morbid conditions including
diabetes mellitus.
There is evidence for type 2 diabetes and Alzheimer’s to occur
together, because of common underlying pathogenetic
mechanisms.
73. Atypical antipsychotic drugs have a propensity to induce
weight gain in the following order:
clozapine > olanzapine > thioridazine > quetiapine >
chlorpromazine > risperidone > haloperidol > fluphenazine >
ziprasidone
The average short-term weight gain varies from a mean of
0.43 to 4.45 kg, with its attendant effects on carbohydrate and
lipid metabolism.
Clozapine and olanzapine, with a greater propensity to
induce weight gain seem to be frequently associated with type
2 diabetes mellitus
Consensus development conference on antipsychotic drugs and obesity
and diabetes. Diabetes Care 2004; 27 : 596-601.
.
74. A similar hierarchy exists for hyperlipidaemia: high for
clozapine and olanzapine; low for risperidone.
However a recent study from India which compared
the use of olanzapine and haloperidol/trifluoperazine
for 12 wk did not find a change in glycaemic status,
weight or body mass index among the three drugs
Guha P, Roy K, Sanyal D, Dasgupta T, Bhattacharya K.
Olanzapine-induced obesity and diabetes in Indian patients: a
prospective trial comparing olanzapine with typical antipsychotics.
J Indian Med Assoc 2005; 103 : 660-4.
75. Mechanism
-direct stimulation of appetite via feeding areas of the brain
Indirectly by endocrine effects such as hyperprolactinaemia,
decreased gonadal levels and hypercortisolism
Environmental factors also contribute
Even though definite conclusions cannot yet be drawn leptin and
ghrelin levels are also being evaluated. Drug-induced insulin
resistance, either directly or via stimulation of cytokine production,
and interference with glucose transport across membranes.
Tighe S, Dinan T. An overview of the central control of weight
regulation and the effect of antipsychotic medication. J
Psychopharmacology 2005; 19 (Suppl) : 36-46.
76. Conclusions
Atypical Antipsychotic drugs Diabetes mellitus
Cooperation in treatment is essential
There is indications that psychological stresses can be
important in aggravating the disorder or precipitating
episodes of loss of control, and even suggestions that
emotional factors may sometimes bring the disorder in to
being.
Increased incidence of DM with psychiatric illness
