states are merely homeostatic resting states, and that
the very concept of meditation (which imputes
simulus-response or S-R causes of relaxation) be abandoned?
Yes, and here is a simple explanation why.
The question is not to dispute whether relaxation as
the core element of ‘meditation’ is a response, but
rather if a ‘relaxation response’ is homeostatic in
nature, or in other words, is a taxonomy for automatic
self regulation mechanisms that represent a state of
equilibrium. Like sleep, respiration, or other self
regulatory mechanisms, rest has been shown to require
no stimulus event for its induction, and no contingent
event for its reinforcement. Given this fact, then
inductive procedures for rest do not mediate or cause
resting, but rather eliminate behavioral events (e.g.
thoughts, distractions) that interfere with resting
and move the body from a steady state or set point
which is rest. In other words, such procedures
indirectly rather than directly mediate rest. It
follows that states of rest occur when such behavioral
events are eliminated. This may be achieved through
any procedure which performs this function, whether it
be focused attention (TM, Benson’s Relaxation
Response) (Benson, 1974), deprivation of stimuli
through flotation rest (Jacobs et al. 1984, Fine &
Turner, 1982), or avoidance of thoughtful rumination
and distraction (Davidson et al., 2003 ) (resting,
mindfulness meditation). This results in the
prediction that the dependent measures of rest across
procedures should be the same, a prediction generally
confirmed by a recent comparison of the dependent
neurological measures of different meditative
protocols (Newberg & Iverson, 2003).
Although the question that rest is a taxonomy for a
collection of homeostatic mechanisms has never been
addressed directly in the experimental literature,
separate findings do point to this conclusion. For
example, resting reflects involuntary responses that
have a behavioral representation in increased levels
of endogenous opiods and decreased levels of
epinephrine, norepinephrine, and cortisol (Turner and
Fine, 1983), and unique neural activation
patterns(Raichle et al., 2001, Greicius et al., 2003).
These correlate in turn with subjective
representations of pleasure, resistance to pain
(Turner and Fine, 1985), and enhanced self
awareness(Wicker et al., 2003). It may be argued that
these events parallel the objective and subjective
measure of meditation in all its forms.
If resting is indeed a homeostatic response set, then
its metaphorical representation as meditation or the
relaxation response must be abandoned, because the
stimulus-response or S-R mechanisms imputed
by these concepts (attention-relaxation link) could
Finally, this argument corresponds with Holmes
(1984,1988) original meta analysis comparing and
equating resting and meditative induction procedures
with dependent variables as measured by biochemical,
neurological, and other somatic indices. Although
Holmes addressed the issue of correlation, he did not
define rest nor address the equally important issue of
causation, thus leaving open the question whether
relaxation was a function of S-R mechanisms
(attention-relaxation link), or was a state of
homeostasis. Indeed, if relaxation is homeostatic in
nature, it indirectly confirms Holmes original
conclusion that meditative states are equivalent with
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