proteins in the very chain reaction by
which cholesterol and isoprenoids are
produced. Prives and Freed-Pastor
showed in cell-based experiments that
adding a statin substantially impedes this
disaster, limiting the ability of mutant
p53 to switch on these genes. When the
researchers treated breast cancer cells
with Zocor in a lab, the cells died or
showed slower growth.
There are other biological arguments
in the case for statins against cancer. By
thwarting isoprenoid production, Lipkin
says, statins also disable a process that
triggers activation of a proliferation molecule called Ras, which has been implicated in several cancers. Other evidence
suggests that starving a tumor cell of cholesterol might slow runaway cell growth
because cells use cholesterol as a building
block for their fatty membranes.
Several studies have linked high cholesterol with prostate cancer risk, and
there is molecular evidence that bottling
up HMGCR thwarts this cancer. A 2008
study showed that prostate cancer cell
lines exposed to statins are more apt to
undergo stalled growth or programmed
cell suicide than unexposed cells. “The
prostate cancer data actually look pretty
strong,” Lipkin says.
Men who underwent prostate removal
for cancer were less likely to have a recurrence if they were on statins beforehand than men not getting the drugs,
Johns Hopkins University researchers
reported last year. While this population
finding doesn’t prove cause and effect,
“what we’re seeing does make sense
in the biological data. It’s nice that it
hangs together,” says Alison Mondul, an
epidemiologist at the National Cancer
Institute who coauthored the study
while at Johns Hopkins.
Some say it ain’t so
Inflammation and cancer aren’t the only
conditions beyond the heart that statins
might address. Recent studies suggest
that statins might counteract dementia,
cataracts, multiple sclerosis, Parkinson’s
and depression. A National Institutes
of Health website lists hundreds of clinical trials — finished, ongoing or still
25
Cancer blow a recent study shows that
statins induced programmed cell death in three
prostate cancer cell lines in the lab, suggesting
a mechanism underlying the cancer-fighting
effect seen in population studies.
Statins versus prostate cancer
100
Percent programmed cell death
control
75
Lovastatin
simvastatin
50
0
PC3 Du145
Cancer cell line
source: a. hoque ET AL/CANCER EPIDEMIOL. BIOMARKERS
PREV. 2008
LnCap
recruiting participants — that focus on
statins’ impact outside of heart disease
or stroke. But some scientists remain
unconvinced that statins hold more
wonder drug potential.
Beatrice Golomb, a physician and
neurobiologist at the University of
California, San Diego, notes that studies
have found some pretty bad side effects
associated with statins, including muscle
pain and liver damage, as well as perhaps
memory loss and diabetes. Such side
effects, combined with the widespread
prescribing of such drugs, have led to a
backlash against statins among some
scientists.
Golomb says population studies aren’t
nearly adequate to outweigh these
doubts. “This is a class of studies that
should not be used for causal inferences
of a drug and its outcomes,” she says, citing the “healthy-user effect.” People who
obtain statins might have better insurance, more education and better access
to health care than people who don’t get
the drugs, skewing the outcomes.
But physician and epidemiologist
Reimar Thomsen of Aarhus University
in Denmark says that while the United
States does have wide disparities in
health coverage, Denmark doesn’t. His
population study of statins and pneumonia included people covered by the same
health system. “Everyone goes to the hospital for free — funded by taxes,” he says.
Factors such as the variation in
statins’ ability to permeate cell mem-
branes might explain some of the mixed
results seen in recent studies. What’s
more, some patients might be hardwired
to benefit more from statins than others,
Lipkin says. He cites a 2005 population
study that found that colorectal cancer
appears to be vulnerable to statins in
some people but not all.
Explore more
s c. Mihos and o. santana. “pleiotropic
effects of the hMg-coa reductase
inhibitors.” International Journal of
General Medicine. april 2011.