| Elevated insulin levels
linked to colon cancer risk
Colorectal cancer and type 2 diabetes share many
risk factors, and insulin resistance appears to be associated with
an increased risk of colorectal cancer. Researchers used the
concentration of plasma C-peptide (an indicator of insulin
production) to determine whether insulin and insulin resistance are
associated with the risk of developing colorectal cancer. Blood
plasma samples were collected between 1982 and 1984 from nearly
15,000 cancer-free men participating in the Physicians' Health
Study. Compared to the 294 matched noncancer control subjects, the
176 men who developed colorectal cancer tended to have higher levels
of C-peptide, indicating higher production of insulin. Men with the
highest C-peptide levels had a 2.7-fold increased risk of colon
cancer compared to those with the lowest levels. The results of this
study indicate that elevated insulin production may help predict the
risk of developing colon cancer, independent of other
insulin-resistance related factors.
The researchers acknowledged that these results
support the argument that avoiding or reducing modifiable risk
factors, such as obesity, inactivity and poor diet, could
effectively decrease the risk of colorectal cancer, type 2 diabetes
and cardiovascular disease.
Jing Ma, Edward Giovannucci, Michael Pollak, Azita
Leavitt, Yuzhen Tao, J.
Michael Gaziano, Meir J. Stampfer. A Prospective
Study of Plasma C-Peptide and
Colorectal Cancer Risk in Men. Journal of the
National Cancer Institute, Vol.
96, No. 7, 546-553, April 7, 2004
Calcium - Not just for bones
It is nearly impossible to open the newspaper or
watch television without hearing about the
growing incidence of childhood obesity. The latest federal
statistics show that the prevalence of being
overweight has increased by 100 percent among
U.S. teens in the last two decades. And almost 14 million children
(24 percent of the population aged 2 to 17) are obese, with an
additional 8.6 million children at risk for obesity.
But the answer to the weight epidemic isn't
restrictive or fad diets. A recent study
conducted by researchers from Harvard examined the eating habits of
nearly 15,000 girls and boys between the ages of 9
-14 for three years and found that kids who
dieted actually gained more weight on average than those who
didn't. The dieters gained an average of two additional pounds per
year compared to the non-dieters. What's
needed are lifestyle changes. Teaching teens
and preteens how to eat nutritiously, increase exercise and cut down
on TV and computer time are much better
avenues to lifelong weight control.
In addition to lifestyle changes, calcium
intake appears to play a specific role in
regulating body fat. Data from six observational studies and three
controlled trials reveal a consistent effect of
higher calcium intakes, expressed as lower
body fat and/or body weight, and reduced
weight gain at midlife. Similarly, studies
relating nutrient intake to body composition report that
reduced body weight at midlife and decreased body fat accumulation
during childhood are associated with greater
intakes of calcium. There is a fairly consistent
effect size, with each 300 mg (one typical dairy serving) increment
in regular calcium intake associated with
approximately 1 kg less body fat in children
and 2.5-3.0 kg lower body weight in adults. Taken together these
data suggest that increasing calcium intake by
the equivalent of two dairy servings per day
could reduce the risk of overweight substantially, perhaps by as
much as 70 percent.
Calcium
is not just for strong bones. When added to a lifestyle of
nutritious eating and increased activity,
calcium intake may be a simple way to assist in reducing
the incidence of childhood and midlife obesity.
Field AE, Austin SB, Taylor CB, Malspeis S, Rosner
B, Rockett HR, Gillman MW,
Colditz GA. Relation between dieting and weight
change among preadolescents and adolescents.
Pediatrics. 2003 Oct;112(4):900-6.
Heaney RP, Davies KM, Barger-Lux MJ. Calcium and
weight: clinical studies. J Am
Coll Nutr. 2002 Apr;21(2):152S-155S.
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