Just because you can not walk up to God and say "Did you create the universe Monday morning and rest on Sunday?" and have him say "Yes" it does not pull away validity from the fact that prayer works. Science has tested it and even for those who do not believe in it Prayer definitely works.

What are the physiological responses that occur during prayer? How are they measured?
Tell me what you know about autonomic response. How about the neuroendocrine system? What do you know of its regulation and connection to disease states?

Functional and structural neuroimaging has gained tremendous popularity to localize brain-areas related to neuropsychiatry disorders, their metabolic status, drug-receptor docking etc. to evaluate the underlying emotional and cognitive processing and also to set relevant treatment plan in the concerned illnesses. PET, SPECT and fMRI are popular methods, practiced in psychiatric research either alone or in combination.

PET studies are important in chemical and physiological brain imaging as it can detect in-vivo brain metabolism, disturbances in cerebral blood flow and glucose metabolism (McClure et al, 1998). Selective PET studies of recent past have shown that alike normal subjects in schizophrenics, orbitofrontal cortex, amygdala, right temporal pole are activated during processing sadness but no activation of amygdala while viewing angry faces (Blair et al, 1999), fear is processed in the central gray matter of midbrain, bilaterally in the hypothalamus, thalamus, left striatum, right and left anterior cingulated and right prefrontal cortex (Fischer et al, 2000), pleasant emotion is processed in the ventral striatum, midbrain, amygdala, orbitofrontal cortex, and ventral prefrontal cortex (Blood et al, 2001).

Functional Magnetic Resonance Imaging (fMRI) is another useful technique to analyze the cerebral areas at the cellular level, their interconnectivities, blood-oxygen level dissociation, drug paradigms, and intermediate phenotypes in search of genes involved in the underlying mental illnesses (Callicott and Weinberger, 1999). Studies using fMRI has found that auditory emotions (e.g. threat word listening) in the right handed subjects involve the left posterior cingulated gyrus (Maddock et al, 1997), facial recognition memory for known faces are processed in the right middle temporal gyrus and left prefrontal cortex, for unknown faces right middle occipital cortex, for happy faces limbic structure as a whole are activated and no activation for sad face viewing (Philips et al, 1998).

Combined studies using PET and fMRI have found that during emotional processing, medial prefrontal cortex is principally activated in the schizophrenic brain alike normal subjects (Phan et al., 2002).

PET, SPECT and fMRI combined study by Kucharska et al, (2001) have observed that posterior temporal cortex, orbitalfrontal cortex, amygdaloid nucleus and insula are the chief areas of emotional processing in the schizophrenic as well as normal brain.

Where prayer is concerned, the value of prayer can be tested and hypothesized upon, and correlations shown. If a correlation is shown, the question "why" is likely to remain for some time.

They'd just rather do anything than go on a diet and exercise.

For the record, I'm all for speeding up this process, but I think it needs to be handled by organizations that in no way represent companies.

Effect of dimethyl sulphoxide on oxidative stress, activation of mitogen activated protein kinase (MAPK) and necrosis caused by thioacetamide in the rat liver. Eur J Pharmacol. 2007 Mar 12; [Epub ahead of print]

Thioacetamide (400 mg/kg body weight, i.p.) was administered to rats. After 12 h the activity of plasma glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) was significantly higher than that of the control group, and after 24 h plasma GOT and GPT activities strongly increased. These results indicated that the necrotic process was initiated at about 12 h and developed thereafter. By co-administration of dimethyl sulphoxide (DMSO, 18 and 1 h before, and 8 h after administration of thioacetamide: each time, 2.5 ml/kg body weight, p.o.), plasma GOT and GPT were significantly decreased and were even comparable to the control group, showing that DMSO totally prevented the necrotic action of thioacetamide. After 12 and 24 h of thioacetamide administration, the hepatic level of vitamin C, the most sensitive chemical indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 12 h after thioacetamide intoxication and thereafter. DMSO totally restored the liver vitamin C level, demonstrating that DMSO effectively ameliorated the oxidative stress caused by thioacetamide, resulting in the prevention of necrosis of the liver. Phosphorylated c-Jun NH(2)-terminal kinase (JNK) significantly increased transiently 12 h after treatment with thioacetamide. These results indicated that oxidative stress and the activation of JNK took place almost simultaneously. Phosphorylated extracellular signal-related kinase (ERK) 2 was significantly increased 6-12 h after thioacetamide injection. Phosphorylated p38 MAPK (mitogen activated protein kinase) was significantly decreased 24 h after administration of thioacetamide. DMSO treatment inhibited the change of these MAPKs by thioacetamide, corresponding with the prevention of the liver necrosis as well as the attenuation of oxidative stress.

Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Marks PA and R Breslow. Memorial Sloan-Kettering Cancer Center, New York. Nat Biotechnol. 2007 Jan;25(1):84-90.

In our quest to understand why dimethyl sulfoxide (DMSO) can cause growth arrest and terminal differentiation of transformed cells, we followed a path that led us to discover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolinza)), which is a histone deacetylase inhibitor. SAHA reacts with and blocks the catalytic site of these enzymes. Extensive structure-activity studies were done along the path from DMSO to SAHA. SAHA can cause growth arrest and death of a broad variety of transformed cells both in vitro and in tumor-bearing animals at concentrations not toxic to normal cells. SAHA has many protein targets whose structure and function are altered by acetylation, including chromatin-associated histones, nonhistone gene transcription factors and proteins involved in regulation of cell proliferation, migration and death. In clinical trials, SAHA has shown significant anticancer activity against both hematologic and solid tumors at doses well tolerated by patients. A new drug application was approved by the US Food and Drug Administration for vorinostat for treatment of cutaneous T-cell lymphoma. More potent analogs of SAHA have shown unacceptable toxicity.

DMSO is an interesting topic to bring up. When I was ski racing years ago, this came up as common treatment for nerve damage, including such things as spinal injuries. I saw the FDA mentioned, but I don't think the FDA is directly relevant here. DMSO is medically available in the USA [ie, FDA-approved], but only veterinary-approved in Canada [ie, not CFDA-approved]. Professional athletes go south for treatment, with DMSO reputably reducing scar tissue formation as well as allowing nerves to heal which wouldn't normally.