Dear Friends:
    I found a collection of medline abstracts about type 2 diabetes in
children. There was no mention of breastfeeding or lack of breastfeeding as a
factor.  This particular abstract does refer to "abnormal fetal or infantile
nutrition" as a factor. I like this new term for formula feeding = "abnormal
infantile nutrition".

Emerging Epidemic of Type 2 Diabetes in Youth
Rosenbloom AL, Joe JR, Young RS, Winter WE
Diabetes Care. 1999;22(2):345-354
This review considers the epidemiologic evidence of an increasing incidence
of type 2 diabetes in youth, the classification and diagnostic issues related
to diabetes in young populations, pathophysiologic mechanisms relevant to the
increasing incidence, the role of genetics and environment, and the community
challenge for prevention and treatment. Type 2 diabetes in youth has been
recognized to be frequent in populations of native North Americans and to
comprise some 30 percent of new cases of diabetes in the 2nd decade of life,
largely accounted for by minority populations and associated with obesity.
Among Japanese schoolchildren, type 2 diabetes is seven times more common
than type 1, and its incidence has increased more than 30-fold over the past
20 years, concomitant with changing food patterns and increasing obesity
rates. The forms of diabetes seen in children and youth include typical type
1, occurring in all races; type 2, seen predominantly in minority youth;
atypical diabetes, seen as an autosomal dominantly transmitted disorder in
African-American populations; and maturity-onset diabetes of the young
(MODY), seen rarely and only in Caucasians. Of the nonautoimmune forms of
diabetes seen in youth, only type 2 diabetes is increasing in incidence.
Proper classification requires consideration of onset (acute/severe versus
insidious), ethnicity, family history, presence of obesity, and if necessary,
studies of diabetes related autoimmunity. Insulin resistance predicts the
development of diabetes in Pima Indians, in offspring of parents with type 2
diabetes, and in other high-risk populations. African-American children and
youth have greater insulin responses during glucose tolerance testing and
during hyperglycemic clamp study than do whites. There is also evidence of
altered beta-cell function preceding the development of hyperglycemia. Of
particular interest is the evidence that abnormal fetal and infantile
nutrition is associated with the development of type 2 diabetes in adulthood.
The thrifty phenotype hypothesis states that poor nutrition in fetal and
infant life is detrimental to the development and function of the beta-cells
and insulin sensitive tissues, leading to insulin resistance under the stress
of obesity. The thrifty genotype hypothesis proposes that defective insulin
action in utero results in decreased fetal growth as a conservation
mechanism, but at the cost of obesity-induced diabetes in later childhood or
adulthood. The vast majority of type 2 diabetes in adults is polygenic and
associated with obesity. Monogenic forms (MODY, maternally transmitted
mitochondrial mutations) are rare, but are more likely to appear in
childhood. Linkage studies of the common polygenic type 2 diabetes have
emphasized the heterogeneity of the disorder. The prevention and treatment of
type 2 diabetes in children and youth is a daunting challenge because of the
enormous behavioral influence, difficulty in reversing obesity, and typical
nonadherence in this age-group. The emerging epidemic of type 2 diabetes in
the pediatric population, especially among minorities whose proportion in the
U.S. population is increasing, presents a serious public health problem. The
full effect of this epidemic will be felt as these children become adults and
develop the long-term complications of diabetes.

Warmly,
Nikki Lee RN, MSN, Mother of 2, IBCLC, CIMI
craniosacral therapy practitioner
Elkins Park (a suburb of Philadelphia, Pennsylvania; northeastern USA)
supporter of the WHO Code and the Mother Friendly Childbirth Initiative

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