Summary/Abstract

Opiate pain medications like Roxycodone and OxyContin, distort brain chemistry, making the brain more sensitive to incoming electrical pain signals.

Content

Dr. Rick Sponaugle recently spoke at the NFL retired players conference. He explained why the players were feeling more pain on OxyContin than they originally felt after their initial football injury. Dr. Sponaugle explained that over time, the opiate pain medications like Roxycodone and OxyContin, distort brain chemistry, making the brain more sensitive to incoming electrical pain signals. Dr. Sponaugle demonstrated clinical research that proves patients who use Vicodin and other opiate medications on a daily basis, develop severe deficiencies of calming brain chemicals like serotonin and taurine - and excessive production of excitatory [electrifying] brain chemicals like histamine and glutamate. The opiate-induced imbalance of brain chemistry produces excessive electrical activity in the brain potentiating or amplifying incoming pain signals. University professors call this phenomenon, hyperslgesia. Dr. Sponaugle prefers the term “Brain Pain” – Why? Because, in addition to increasing the patient's perception of physical pain, the opiate-induced imbalance of brain chemistry also causes anxiety and insomnia. Dr. Sponaugle's clinical research at Florida Detox & Wellness reveals that opiate pain medications also cause severe suppression of the brain's pituitary function. The role of the brain's pituitary gland is to release hormones that “turn on” or stimulate, downstream endocrine glands, including the thyroid, adrenal glands, ovaries and testicles. The opiate-induced suppression of the brain's pituitary gland results in hypothyroidism, adrenal insufficiency [adrenaline deficiency, cortisol deficiency, DHEA deficiency] and deficiencies of the sex hormones, testosterone, estrogen and progesterone. The resultant hormonal deficiencies prevent endorphin production and decrease dopamine receptivity. This causes deactivation of the brain's dopamine-driven pleasure center and subsequent depression. Opiate-induced deficiencies of estradiol and testosterone, disallow serotonin and dopamine, respectully, to activate brain receptors. This causes depression, anxiety and insomnia. In fact, serotonin receptors in the female brain are closed and unavailable for activation by serotonin when estradiol levels fall below 80 pg/ml. The ultimate result of continuous opiate consumption, even at levels prescribed by pain doctors, is a myriad of detrimental biochemical changes that make the brain more sensitive to physical pain and cause the patient to suffer the following symptoms - depression, anxiety, insomnia, memory loss, chronic fatigue, weakness, lethargy, bone loss, muscle loss, weakened immune function, elevated cholesterol, insulin resistance with diabetes, metabolic syndrome and increased risk of heart attack and stroke. Opioid pain medications like Vicodin, Roxycodone and OxyContin ultimately cause a deficiency of the brain chemicals “dopamine” and “serotonin”. These deficiencies disrupt the normal electrical activity in the brain. Specific brain regions such as the brain's pleasure center [nucleus accumbens] and the brain's emotional center [limbic system] influence our brain's sensitivity to incoming pain signals. Dr. Sponaugle explained to the NFL players that the brain's pleasure center resides in the mid-brain and “runs on dopamine.” He explained that some patients inherit a decreased number of Dopamine D2 receptors, the “happy receptors” in the brain's pleasure center. Their pleasure centers are underactive and they normally suffer a mild depression. They don't get as excited as others, and often appear less motivated. They are also more sensitive to physical pain. These patients don't get excited about high school graduation – they can't feel the joy because they can't get the dopamine hit. Patients with this particular brain profile easily succumb to opiate addiction because opiate medications stimulate a temporary “dopamine hit” from brain storage units. The “dopamine hit” makes them “feel more normal.” Long term use of opiate medication depletes the brain dopamine storage units causing a more severe dopamine deficiency. Without proper diagnosis and aggressive treatment at detox, these patients experience a “black hole” after detox. This causes immediate post detox relapse. Dopamine receptivity is compromised in patients with opiate-induced hypothyroidism and testosterone deficiency. The inactive thyroid hormone, T4, cannot convert to the active thyroid hormone, T3, when testosterone is suboptimal. Furthermore, both testosterone and T3 thyroid enhance dopamine receptivity, the ability of dopamine to activate brain receptors. Serotonin deficiency can be severe in patients taking OxyContin and methadone. Opiate-induced serotonin deficiency produces excess electrical activity in two distinct brain regions, the emotional center (deep limbic system) and the anterior cingulate gyrus. An overactive deep limbic system makes the brain more sensitive to incoming pain signals. Patients who suffer from opiate-induced serotonin deficiency, become more sensitive to physical pain and emotional pain. Their personality changes from happy and spontaneous to moody, irritable, stubborn and argumentative. They become more easily offended and lose desire to socialize. You may have noticed that an OxyContin-addicted family member has become more defensive and over-sensitive to things you say - remarks that normally would not have offended them before they started taking pain medicine. They may not share their inner most feelings with you, but they begin to feel more hopeless and suffer excessive guilt. They lose interest in things they used to consider fun. Opiate-induced serotonin deficiency also causes excessive electrical activity in the anterior cingulate gyrus. A calm cingulate serves as the brain's 'gear shifter' - it says forgive, forget, move on, today is a new day. An overactive cingulate prevents patients from “shifting gears” and they become overfocused on all the negative aspects of their life, especially their chronic pain. Patients who suffer from an overactive anterior cingulate become stubborn, they develop an attitude of “my way or the highway.” They become more argumentative and easily disgruntled if someone “moves their cheese” or “messes with their stuff.” They also develop an obsessive worry syndrome. As patients develop an overactive deep limbic system, they lose their desire to socialize. They can even begin experiencing social anxiety. After a few years of using OxyContin or methadone, the patient who once enjoyed socializing on weekends, prefers the security of their home. Addiction doctors who lack this intricate knowledge of brain physiology, including many university professors, suggest these patients are hiding from their friends because they don't want them to know they are addicted. The truth is, these patients no longer enjoy socializing. Serotonin inhibits the release of norepinephrine from the A5 nucleus, a factory in the brain that manufactures 90 percent of our noradrenaline or norepinephrine. When chronic opiate consumption causes serotonin deficiency, the A5 nucleus releases an excessive level of circulating norepinephrine. Norepinephrine metabolites stimulate increased electrical current throughout the brain and body. This amplifies the electric pain signals from injured nerves in the body. Elevated norepinephrine levels caused by opiate-induced serotonin deficiency, cause vasoconstriction increasing blood pressure, norepinephrine is a powerful vasoconstrictor. When I optimize the brain chemistry of my addicted patients, they can often stop taking blood pressure medication. Excessive noradrenaline levels derived from opiate-induced serotonin deficiency, stimulate excessive electrical current in the brain. This produces anxiety and insomnia disorders – in severe cases fibromyalgia disorders. When we treat these patients with our comprehensive biochemcial makeover, they no longer suffer anxiety, insomnia, or fibromyalgia. Fibromyalgia is derived from excessive electrical current running throughout the nerves in the body. Unknowing physicians treat it with opiate pain medication, they are unaware that fibromyalgia pain is ultimately worsened by the opiate induced changes in brain chemistry and hormonal levels. Opiate-induced serotonin deficiency yields excess norepinephrine release from the brain's central factory, the A5 nucleus. Subsequently, the excessive circulating norepinephrine produces increased electrical firing of neuron circuits throughout the brain and body. The over electrified nerves in the body send an intensified electrical pain signal to the brain, then, the overelectrified brain amplifies the incoming pain signal. Women develop fibromyalgia more often than men when taking opiate pain medication. OxyContin, Actiq and methadone shut down pituitary output of both, LH and FSH - the hormones that stimulate ovarian production of progesterone and estradiol, respectively. Both female hormones are powerful modulators of the brain's electrical circuitry. Opiate induced Estradiol deficiency decreases the activity of the calming brain chemical serotonin, thus, increasing electrical firing in nerves. Opiate induced progesterone deficiency causes decreased GABA activity. Progesterone decreases electrical current in the brain and body by activating the same receptor as Xanax, the GABA receptor. GABA is the primary calming neurotransmitter in the brain and body. I presented an alarming study at the 2009 American Academy of Anti-aging Medicine conference which demonstrated that 100 percent (30 of 30) twenty-something females who were prescribed methadone (80 mg per day) suffered complete shut down of their ovarian production, the young twenty something women had post menopausal ovarian production like their grandmothers! These young women no longer produced any estradiol, progesterone or testosterone because methadone had suppressed their pituitary production of the hormones LH and FSH, hormones that stimulate the ovaries to produce sex hormones.Opiate-induced pituitary suppression is a triple whammy for female patients with chronic pain. They suffer opiate-induced estradiol deficiency, opiate-induced progesterone deficiency and opiate-induced testosterone deficiency. Dr. Sponaugle emphasized to the NFL players that, “When we detox the opiate dependent pain patient, we immediately begin the restoration of more than 60 biochemicals, this optimizes brain function in our patients and prevents any amplification of incoming electrical pain signals. Most of our patients report an 80 to 90 percent reduction of their physical pain in the immediate post detox period.”