The Alan Sondheim Mail Archive

November 9, 2009

My strange music

What distinguishes it from other musician's work: I always play at my
limits; I don't play what I know, but nearby areas, what I might extend
myself into, where I might fail. So it's not a question of comfort with
improvisation or instrument, but pushing past that to discomfort; at
times, everything falls apart. The limits of my ability are the limits of
my world. The limits are the limits of my body in its functioning, of
muscle memory, musical kludging. I played electric oud last night at the
benefit; I hadn't played it before the previous night (in fact I hadn't
played oud before the previous night). The instrument is fretless, of
course, with a fingerboard over two feet long that goes almost up to the
bridge. The pickup is piezo. So it was a gamble; I kludge on fretless,
look for fifths and consonance and proceed from them. It's harder with
chords. So playing it involves a problematic - what can be done with
limited recourse and recourses - what happens near the boundaries of
failure - how can one tunnel through them - how can one survive on the
other side? This is different than knowing what one's doing. Myk knows
what he's doing (I think!), has amazing sureness and grace on the lap
steel. Azure works with songs that are relatively fixed: there's constant
structure. I'm broken, playing broken, assembling, bricolage; instead of
lost in music, I'm lost in a thumb muscle that's not responding the way I
want it to. What to do? Skip the thumb, let other fingers take over, slow
things down. Go back after a while; try the thumb again. If it works, use
it sparingly. If not, try the fourth finger, for example. That partially-
flattened second is giving another problem; hit the octave (for example,
e' on d' octaved with the e two strings down: e/a/d'(e')), and work
backwards to the flattened second (i.e. between major and minor), which
might be checked by the minor third. Once that's down, construct a riff
that might help me remember the position later on (repeated complex
flurries of notes bury the problem, create rhythm and backup for Myk and
Azure). Argh! The thumb's fine, slight cramp in the right index finger;
try the third finger as replacement. For this reason, most of the time I
don't think of myself as a musician, but as a fraud; my music is fraud
music, in a neurotic world of its own. On the other hand, there are times
I feel I'm playing well, and I lose myself in the playing - only to smile,
and watch (as if from a distance), the smile break through everything, and
self-conscious- ness rules again. - this is a different recording
(line out, in the club) that may be clearer beauty shredding; the piece
sounds other than the first (there are no perfect recordings) (there is no
perfect music) (there are no musicians, in the sense that there are no
authors) (of course we're dreaming in the wrong direction) (rewind) (rewind)

Azure, voice; Myk, lap steel; Alan, electric saz, electric oud.

---------- Forwarded message ----------
Date: Mon, 09 Nov 2009 23:37:43 -0000
From: rk_stonjek <>
Subject: [evol-psych] News: Early stress alters epigenome

Early stress alters  epigenome Posted by Jef Akst [Entry posted at 8th
November 2009 06:00 PM GMT]       Scientists have figured out how stress
experienced early in  life can cause long-lasting changes in physiology
and behavior -- via  epigenetics.

     Image: Max-Planck Institute of
Psychiatry,  MunichSpecifically, early stress  appears to induce
epigenetic changes in a specific regulatory region of the  genome,
affecting the expression of a hormone important in controlling mood and
cognition into adulthood, according to a study published online today
(November  8) in Nature Neuroscience.

This is the first study to depict a  molecular mechanism by which
"stress early in life can cause effects that remain  later in life,"
said epigeneticist Moshe Szyf of McGill University in Montreal.  "This
can explain a lot of things that happen to us as humans and our behavior
later in life."

Stress endured early in life can influence the quality  of physical and
mental health in adulthood, such as by causing hormonal  alterations
associated with mood and cognitive disorders. But until now,  scientists
did not understand the mechanism by which early life experiences can
produce such long-lasting effects.

According to a common hypothesis, the  environment affects mental health
by causing alterations to the physical  properties of the genome that
influence gene expression -- the epigenome.  Indeed, research suggests
that DNA methylation, one of the most intensely  studied forms of
epigenetics, may explain why maternal care has a long-term  influence on
behavior and hormones in rats.

To explore whether DNA  methylation is behind the changes associated
with stress experienced early in  life, molecular biologists Chris
Murgatroyd and Dietmar Spengler of the Max  Planck Institute of
Psychiatry in Germany and colleagues examined the  methylation patterns
of mice that were separated from their mothers for three  hours a day
for the first ten days of their lives. Specifically, the researchers
looked for differences in the gene that encodes arginine vasopressin
(AVP), a  hormone associated with mood and cognitive behaviors. The AVP
receptor is also a  promising therapeutic target for stress-related

From 6 weeks  of age all the way up to 1 year, mice that experienced
early stress -- and  showed the predicted behavioral and hormonal
differences -- also displayed  significantly lower levels of methylation
in the regulatory region of the  Avp gene in the brain. This
hypomethylation was specific to a subset of  neurons in the hypothalamic
paraventricular nucleus -- a brain area involved in  regulating hormones
linked to stress. These mice also had higher levels of  Avp mRNA,
suggesting that lower methylation levels do indeed affect  hormone

"Essentially the genome memorizes that [early life]  stress," said Szyf,
who was not involved in the study. "Stress changes  methylation, and
that stays the whole life."

The researchers further  determined that the decreases in methylation in
stressed mice result from the  inactivation of a protein known as MeCP2,
which is involved in the initial  recruitment of proteins that methylate
the DNA.

The concept that social  states in early life can affect health in later
life is "a completely  revolutionary idea," Szyf said. This paper
provides a "detailed" molecular  mechanism by which this can occur, and
"gives substance" to this theory.

Understanding the molecular details underlying this phenomenon is
essential to developing potential therapies for mental disorders that
stem from  early adverse experiences, Murgatroyd added. "This has given
us new insight in  how to possibly develop drugs for [these illnesses]."

Treatments for  reversing the effects of early life stress should begin
as early as possible,  Spengler said. Reversing the inactivation of
MeCP2 might be possible, but "once  [methylation] is laid down, you
cannot erase [it]," he said. "This is a mark  that is very stable."
Treatments given later in life, then, must find ways to  ameliorate the
phenotype, such as by blocking AVP receptors in animals with  higher AVP
levels, he added.

Related stories:    * Epigenetic suicide  note
[August 2009]
     * An epigenetic  inheritance
[19th January 2009]
     * Epigenetics:  Genome, Meet Your Environment
[5th July  2004]
    Source: TheScientist
<>    Posted by
Robert Karl Stonjek

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