"Stave off complications or halt the progression of diseases already
attacking eyes and kidneys"

Is the above a .. good thing .. ?

That's what happens when you reduce the red blood cell count.

Glorified bloodletting.

DNA tweak no good for diabetics
By Tina Hesman Saey
May 5th, 2008Web edition
Increased protein production could harm eyes, kidneys
A little tweak to a diabetic’s DNA could tip the balance toward
blindness and kidney failure, a new study shows.

Natural variation in just a single base pair — letters of the genetic
alphabet – raises levels of erythropoietin, a protein that stimulates
red blood cell production and the growth of blood vessels. Bumping up
erythropoietin, EPO for short, about doubles the risk that diabetics
will develop diabetic retinopathy and end-stage kidney disease, a
study published online and in the May 13 Proceedings of the National
Academy of Sciences shows.

Controlling erythropoietin levels or blocking its activity could help
diabetics stave off complications or halt the progression of diseases
already attacking eyes and kidneys. The research also sounds a
cautionary note for diabetics who undergo kidney dialysis.
Erythropoietin is often prescribed to dialysis patients to pump up red
blood cell counts, but the new research suggests that EPO should be
used with caution to avoid harming the eyes and kidneys.

Kang Zhang, an ophthalmologist and geneticist at the University of
Utah School of Medicine in Salt Lake City and his colleagues set out
to solve a mystery that doctors who treat diabetics know well.

“We all see patients with their blood sugar completely under control,
but they have complications right and left,” Zhang says. “Then there
are other people whose blood sugar is all out of whack, and yet, they
never get into trouble.”

Diabetic retinopathy results from an excess of blood vessels invading
the retina. The blood vessels can lead to tears in the eye tissue or
detachment of the retina in the most severe form of the disease, known
as proliferative diabetic retinopathy. Nearly every diabetic will
develop some degree of retinopathy over time, but only about half
progress to the severe form.

Still, the eye disease is the leading cause of new cases of blindness
in working adults in the United States and is responsible for about 10
percent of blindness overall.

Eye experts have known for years that a protein called VEGF is
involved in stimulating the unwanted blood vessel growth. Experimental
therapies to block the protein seem promising, but the treatment is
not yet approved for widespread use in the United States.

Zhang and his team chose 10 genes involved in blood vessel growth and
looked for natural variations — called single nucleotide polymorphisms
or SNPs — in the DNA sequence of the genes linked to greater risk of
developing diabetes complications.

The researchers found a change at a particular spot in a stretch of
DNA called a promoter that controls whether the erythropoietin gene is
switched on or off. Some people have the DNA base guanine (G). Others
have thymine (T). The T creates a molecular landing-pad for a protein
called AP1, which is a powerful molecule that turns genes on. AP1
can’t land on promoters that have G instead of T. About half of people
in the general population have the T form.

Non-diabetics who had the T variant in both copies of the
erythropoietin gene (one inherited from their mother, one from the
father) made 7.5 times more erythropoietin in their eyes than non-
diabetics who inherited two copies of the G form.

Diabetics who had two copies of the risky T variant also had double
the risk of developing eye and kidney complications compared with
diabetics with a different form. The result could mean that diabetics
should get genetic testing, called genotyping, to determine which form
they have, Zhang says. People who have the risky variant could then be
given treatments to block EPO in the eye and kidney.

But other eye experts say that controlling blood sugar could make a
bigger difference in avoiding complications from diabetes.

“I don’t think we’re at the point that we’re going to start genotyping
people,” says Emily Chew, deputy director of epidemiology and clinical
research at the National Eye Institute. “If half the people have this,
what’s the point?”

Chew called the study “very exciting,” but she cautioned that
erythropoietin may have complicated interactions with blood sugar and
other proteins.

Zhang agrees that blocking EPO throughout the body is probably not a
good idea.

“EPO is a hugely important factor to maintain our red blood cell
production, so you don’t want to make people anemic,” he says.

Who loves ya.
Tom

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