11/16/06njm

**Case Scenario**

A 9 year old girl was brought into the clinic by her family as she had
been having blurry vision and urinating frequently.  As there are
multiple family members with diabetes, including her father and older
sister, they had checked her sugars at home and found them to be well
over 200.  The symptoms started within a few days of her 46 year old
mother's death after a prolonged ICU stay, which capped about 5 years of
serious diabetic complications. 

The 9 year old's mother had been diagnosed with type 2 diabetes for 8
years when she was pregnant with the patient.  Exam was significant for
obesity (\>95^th^ percentile for age and height, BMI of 33), acanthosis
nigricans, and positive serum glucoses confirming the diagnosis of
diabetes.

>  

**Summary of key points:**

Type 2 diabetes is increasingly understood to be multifactorial in
origin.  The International Diabetes Federation convened a conference in
2002 to examine the literature on this issue and identified 4 etiologies
defensible at a level of evidence of either A or B: Genetics, Fetal
Origins, Lifestyle, and Stress (see IDF Consensus Document).  "Fetal
origins" refers to how the prenatal nutritional status of the mother
affects the risk for diabetes in their offspring.  While not discussed
in the IDF Consensus Document, It likely would also include the
increased risk to offspring who are the products of diabetic
pregnancies.  The case study illustrates a child who had all 4 of these
etiological risk factors contributing to her development of diabetes.
 Other risk factors which have been associated with developing obesity
or diabetes, even if not yet proven to be causative, include smoking,
depression, adverse childhood experiences, poverty, prenatal alcohol
and/or smoking exposure, and environmental pollutants.

The tremendous impacts of an individual's life experiences and
environment on health behaviors and outcomes are starting to be realized
and defined.  The prenatal and early life periods are generating
particular attention as health "trajectories" are affected by life
experiences most profoundly while the organism is undergoing
development.  These trajectories, if left unaltered, set a life course
through their physiologic and behavioral effects, including brain
development and synaptic complexity, hypothalamic-pituitary-adrenal
(HPA) axis sensitization, autonomic nervous system reactivity,
sensitivity to hunger/satiety signals, imprinting of parentally modeled
eating behaviors, and others---all of which combine and accumulate to
set a course toward obesity and eventual diabetes.  Given this and that
it has been shown that high fat/high calorie foods turn off the HPA axis
stress response and that carbohydrates modulate brain serotonin levels,
overeating can be seen as an adaptive stress coping mechanism, which
would reframe much of the context for "lifestyle education".  Even the
genetic component of diabetes risk is affected by life experience---as
the emerging field of epigenetics is now revealing, it is not just a
matter of which genes are *inherited*, but also which genes are being
*expressed* in response to environmental stimuli.

Given the limited success seen by many diabetes prevention programs
using the traditional model of lifestyle change education, perhaps it is
time to expand the model to incorporate these newer perspectives.  How
might our diabetes prevention and treatment programs evolve in response
to the science showing the breadth and depth of the multifactorial
nature of type 2 diabetes?

# 

# International Diabetes Federation: Causes of Type 2 Diabetes

Experts reach consensus on causes of Type 2 diabetes

Genetics, foetal origins, lifestyle and stress may all be risk factors
of Type 2 diabetes

PRESS RELEASE, 17 July 2002

<http://www.idf.org/home/index.cfm?node=444>

Consensus on the Aetiology of Type 2 Diabetes Mellitus

International Diabetes Federation

[http://www.idf.org/webdata/docs/Consensus%20Document.doc](http://www.idf.org/webdata/docs/Consensus Document.doc)

**Other Resources: (full text articles available upon request)**

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Rosengren A, Hawken S, Ounpuu S, Sliwa K, Zubaid M, Almahmeed WA,
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