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Screening for type 2 diabetes
Tim Kenealey and colleagues’ excellent article on
screening for type 2 diabetes gives good guidance to general practitioners and
wisely leaves options open to initiate an early therapeutic
opportunity1.
As advocated for more than twenty years an excellent chance
to estimate residual beta cell reserve function is when the patient turns fifty
years of age. They can then be advised to have a really very large three course
mid day birthday dinner (possibly with other older brothers and sisters?). They
present at the laboratory exactly two hours after the meal has been finished.
This time suits most people and laboratories. Values returned over 7.0mmol/L
will suggest beta cell reserves less than 30% rather than the more likely 50%
expected in the average New Zealander.
An oral glucose tolerance test giving 2 hour values 7.8
– 11mmol/L will allow a diagnosis of impaired glucose tolerance, always a
forerunner of diabetes and low levels of beta cell residual capacity. Two hour
values over 11.0mmol/L on the OGTT make an “official” diagnosis of
type 2 diabetes.1 In the United Kingdom there
is usually a period of twelve years from onset to diagnosis.
Such two hour values relate much better to functioning
residual beta cell mass, to future cardiovascular disease and to all cause
mortality than do fasting blood glucose values alone – a late diagnostic
feature.2-5
Diabetes NZ Inc, the Federation of thirty seven voluntary
societies representing the 105 000 people with diabetes strongly supports
earliest possible diagnosis set out in the Pricewaterhouse Coopers report of
2001.
Two other key issues emerge in respect to the widespread
loss by midlife or earlier of non renewable beta cell function in so many people
in New Zealand. It is now accepted that the earliest diagnosis is cost
effective.6 Evidence for this has been
reviewed.7 It is also now
accepted8-10 that 150 minutes of active
exercise weekly and four visits yearly for dietetic advice on weight management
and reduction of saturated fat intake prevents diabetes. Our high New Zealand
weight and animal fat levels were not designed for the beta cells or liver
enzymes of our huntergather ancestors.
Five fold increases in animal fat ingestion increases
insulin demand and often body mass index and, unless modified, accelerate B cell
destruction.
This 50% prevention of progression to diabetes with the
above lifestyle changes is exciting but a less well known finding of the last
five years.
Let us all now initiate action and do something modern about
diabetes in our country.
Sue Benny,
Diabetes Health Promoter. Professor D W Beaven,
Prof Emeritus, Diabetes Life Education and Patron Diabetes NZ, Christchurch.
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