News
Voluntary
exercise
does not appear to alleviate anxiety and depression CHICAGO –
Voluntary physical activity does not appear to cause a reduction in anxiety and
depression, but exercise and mood may be associated through a common genetic
factor, according to a report in the August issue of Archives of General
Psychiatry, one of the JAMA/Archives journals. In the general
population, regular exercise is associated with reduced anxious and depressive
symptoms, according to background information in the article. Experiments
involving specific clinical populations have suggested that exercise causes this
reduction in anxiety and depression. However, it is unclear whether this causal
effect also occurs in the larger population or whether there is a third
underlying factor influencing both physical activity and the risk for mood
disorders. Marleen H. M.
De Moor, M.Sc., of VU University Amsterdam, the Netherlands, and colleagues
studied 5,952 twins from the Netherlands Twin Register, along with 1,357
additional siblings and 1,249 parents. Participants, all aged 18 to 50, filled
out surveys about leisure-time exercise and completed four scales measuring
anxious and depressive symptoms. Associations
observed between exercise and anxious and depressive symptoms “were small and
were best explained by common genetic factors with opposite effects on exercise
behavior and symptoms of anxiety and depression,” the authors note. “In
genetically identical twin pairs, the twin who exercised more did not display
fewer anxious and depressive symptoms than the co-twin who exercised less.”
Exercise behavior in one identical twin predicted anxious and depressive
symptoms in the other, meaning that if one twin exercised more, the other tended
to have fewer symptoms. However, the
same was not true of dizygotic (fraternal) twins or other siblings, who share
only part of their genetic material. In addition, analyses over time showed that
individuals who increased their level of exercise did not experience a decrease
in anxious and depressive symptoms. “It is unknown
which genes might be involved in voluntary exercise behavior and in the risk for
anxiety and depression,” the authors write, but genes involved in the brain
pathways that process dopamine, norepinephrine, opioids or serotonin are likely
candidates. The results do
not mean that exercise cannot benefit those with anxiety or depression, the
authors note, only that additional trials would be needed to justify this type
of therapy. “Only voluntary leisure-time exercise is influenced by genetic
factors, whereas the other type of exercise [directed and monitored by someone
else] is environment-driven. The absence of causal effects of voluntary exercise
on symptoms of anxiety and depression does not imply that manipulation of
exercise cannot be used to change such symptoms,” they write. “The
antidepressant effects of exercise may only occur if the exercise is monitored
and part of a therapeutic program.” Arch Gen Psychiatry.
2008;65[8]:897-905. Available on this website, see 'publications', click
'papers'.
Editor’s Note:
This study was supported by grants from the Netherlands Organization for
Scientific Research. Please see the article for additional information,
including other authors, author contributions and affiliations, financial
disclosures, funding and support, etc.
More on this article can be found on these sites:
http://www.medicalnewstoday.com Subtle
differences in DNA of identical twins may help diagnose disease BIRMINGHAM,
Ala. - Identical twins are not completely identical, according to new
research from UAB (University of Alabama at Birmingham), jointly with Leiden
University Medical Center and VU University, The Netherlands; and Uppsala
University and Karolinska Institutet, Sweden. The subtle differences in
twin’s DNA may help researchers learn more about a wide range of hereditary
diseases and provide a quicker diagnosis for genetic disorders. The findings
were
published February 14th 2008 in the American Journal of Human Genetics,
describing results from an international team led by UAB scientists.
The
researchers studied 19 pairs of monozygotic, or identical, twins and found
differences in copy number variation in DNA. Copy number variation (CNV)
occurs when a set of coding letters in DNA are missing, or when extra copies
of segments of DNA are produced. Humans
receive one chromosome from their mother and one from their father,
providing for two copies of the genome. In some cases, bits of DNA are
missing from a chromosome, leaving the offspring with just one copy of that
bit of DNA. In other instances, mutations may produce three, four or more
copies of a particular bit of DNA. In most cases, variation in the number of
copies likely has no impact on health or development. But in others, it may
be one factor in the likelihood of developing a disease. “The
presumption has always been that identical twins are identical down to their
DNA,” said Carl Bruder, Ph.D. and Jan Dumanski, Ph.D., of UAB’s Department
of Genetics and the study’s lead authors. “That’s mostly true, but our
findings suggest that there are small, subtle differences due to CNV. Those
differences may point the way to better understanding of genetic diseases
when we study so-called discordant monozygotic twins….a pair of twins where
one twin has a disorder and the other does not.” Bruder
points out that one twin might develop a particular disease…Parkinson’s, for
example…while the other does not. Previously, it was thought that
environmental factors were the likely culprits, not genetics. Bruder and
Dumanski think their findings indicate that CNV may play a critical role and
this can be efficiently studied in identical twins. “More
importantly, changes in CNV may tell us if a missing gene, or multiple
copies of a gene, are implicated in the onset of disease,” Bruder said. “If
twin A develops Parkinson’s and twin B does not, the region of their genome
where they show differences is a target for further investigation to
discover the basic genetic underpinnings of the disease.” The UAB lab
is one of the few worldwide that can make the full genome BAC (bacterial
artificial chromosome) arrays that are used to find the changed DNA regions.
The
research was funded by support from UAB, the Swedish Cancer Society, the
Swedish Children’s Cancer Foundation, the U.S. Army Research and Material
Command, National Institutes of Health, The Netherlands Genomics Initiative
and the National Institutes of Health.