Depression Treatment Page
More than 5.8 million adults in America suffer from depression. The symptoms of depression may include:
- Feeling sad or blue
- Crying spells
- Loss of sleep and appetite
- Significant weight loss/gain
- Trouble concentrating
Once you are being treated for depression at Sponaugle Wellness Institute, you can make lifestyle changes and choices that are forms of self-help through the rough times and may prevent depression from returning.
- Focus on activities that make you feel better. Do not isolate yourself
- Talk with friends and family and consider joining a support group in your city.
- Try to have a positive outlook on life.
- Exercise regularly
- Get enough sleep at night
- Eat healthy foods
At Sponaugle Wellness Institute, we specialize in treating depression. We have successfully treated thousands of patients who were previously labeled as having “refractory depression.” An arbitrary label given by psychiatrists to patients who fail to respond to their treatment regimen, a regimen that often consists of multiple medications.We have found the majority of these “refractory depression” patients failed to get better because their psychiatrist was focused on enhancing the wrong brain chemical or he/she failed to realize the patient’s brain was suffering from excessive toxin load, neurotoxicity.
Depression Research at Sponaugle Wellness Institute
Our sophisticated depression research has correlated the various symptoms experienced by our depression patients with abnormal findings on their brain scans and abnormalities seen in their brain chemistry patterns. In addition, we have correlated their brain scans and brain chemistry patterns with over 500 various biomarkers for the following; gut toxicity, mold toxicity, industrial toxicity, amino acid deficiencies, hormonal deficiencies and brain infections like Lyme disease. No American or European medical center has performed this holistic research in patients suffering from depression. Hence, psychiatrists trained at these medical centers practice with limited knowledge, focusing mostly on the latest antidepressant medications, drugs that fail to treat the underlying cause of depression in most patients.
The brain region most sensitive to neurotoxins is the prefrontal cortex, located behind our forehead. Toxin-induced reduction of electrical activity in the prefrontal cortex is becoming more common each year. Recent PET scan research from Madrid, arguably some of the best in the world, has proven that the glutamatergic receptors in the prefrontal cortex control the release of dopamine in our dopamine driven pleasure center, the nucleus accumbens. Our clinical research in depression patients has proven that neurotoxicity, the excessive accumulation of fatty toxins in the brain, can cause severe depression through down-regulation of electrical activity in the brain’s pleasure center. This is becoming a more common, but rarely diagnosed cause of depression, because each decade we are exposed to more environmental toxins.
Why Depression Treatment Fails
Depression treatment offered by American psychiatrists remains at least 10 years behind the advanced brain research being produced on a daily basis by European and American neuroscientists. When psychiatrists are too complacent to perform research or spend time studying recent PET scan research, they remain ill-knowledgeable regarding multiple, newly known, biochemical and physiological causes of depression, most of which are readily treatable.
Unfortunately, most psychiatrists prefer reading about new psychiatric medications in drug company advertisements. Most of the “new drugs” are actually a new version of an old drug that no longer holds a patent. These drugs normally treat the psychological symptoms but rarely treat the underlying cause of depression. Psychiatrists also demonstrate remarkable tunnel vision when they place their primary focus on using drugs to enhance the serotonin activity in the brain of their depressed patients. This modality of depression treatment was more effective 30 years ago when Americans suffered from less neurotoxicity and less malnutrition.
Patients suffering from melancholic depression suffer experience many other changes in their personality in addition to depression. All of these symptoms are derived from a severely overactive deep limbic system, a walnut sized region located in our midbrain. Patients who unknowingly suffer from an overactive deep limbic system exhibit symptoms of moodiness, irritability and agitation. They constantly fight feelings of hopelessness and excessive guilt which they may hide from family members, family members focus on their moodiness and irritability. These patients also suffer with chronic low self-esteem coupled with low motivation.
Melancholic depression patients can feel overwhelmed just thinking about their need to approach the tasks and expectations of each day. What would seem like mundane chores to a healthy person, can appear too arduous and too difficult for a patient suffering with melancholic depression. Lack of performance in melancholic depression patients can yet lead to further depression from another brain region. PET brain research has recently proven that when patients continually experience negative outcomes, they can suffer a significant drop out of the dopamine D2 happy receptors in their reward center.
The deep limbic system is saturated with GABA neurons, named for the potent calming brain chemical GABA that activates them. The brain chemicals, serotonin and taurine, are also considered calming because they enhance GABA activity in the brain.
Dr. Sponaugle’s clinical research has proven that the ability of GABA to activate GABA brain receptors is dependent not only on having optimal serotonin levels, but also on having optimal levels of taurine. Optimal GABA activity in the deep limbic system is absolutely necessary if we are to feel happy, emotionally calm and peaceful.
Patients with melancholic depression slowly become more socially isolated. Those who previously enjoyed socializing and were once considered a social butterfly, no longer like to socialize. In severe cases, patients develop such severe social anxiety that they begin to hide from their friends and family. Due to the fact that the social anxiety may progress slowly, many patients believe their lack of desire to socialize is simply a sign that they are becoming more mature. They also become more emotionally sensitive and are more easily offended. They often mistake positive comments made by others as negative or even an outright insult.
Because our research has proven that specific brain chemistry aberrations cause the melancholic depression symptoms, we can normally rid patients of their depression transforming their personality in just two to three weeks.
In the female brain, serotonin receptors do not accept serotonin molecules when estradiol levels fall below 60 to 80 pg/dl. Even when female patients produce optimal levels of serotonin, they will suffer symptoms of melancholic depression if their estradiol levels are suboptimal. Postpartum depression occurs in over 30 percent of females when the ovaries temporarily stop producing strong levels of estradiol. Thus the symptoms of postpartum depression mimic the symptoms of melancholic depression.
Interestingly, 4 to 5 days before menses begins, estradiol production is at the lowest level of the menstrual cycle. Many women have insufficient estradiol during this time period for serotonin to work effectively. This is why premenstrual psychological symptoms mimic many of the symptoms of melancholic depression. Similarly, postmenopausal women often suffer symptoms of an overactive deep limbic system when their ovaries cease to produce estradiol.
Since the end of World War II, we have experienced the widespread use of antibiotics in our poultry feed, cattle feed and in milk cows. Antibiotics are ingested through poultry, milk, beef and increasingly, in our city water. Antibiotic levels recently measured in the water supply of most cities have reached the critical level necessary to destroy our healthy intestinal bacteria.
Destruction of the healthy bacteria in our intestine allows for excessive overgrowth of toxic Candida yeast and toxic bacteria. These pathogenic bugs create toxins that destroy the intestinal lining causing malnutrition and lack of amino acids that are essential for making antidepressant brain chemicals like serotonin and dopamine. Their toxins also migrate from the gut to the brain causing neurotoxin-induced depression as discussed previously. Furthermore, they disable the brain’s pituitary gland shutting down production of healthy hormones that are needed to activate antidepressant brain chemicals.
The majority of these patients suffer from an inherited brain disorder called reward deficiency syndrome (RDS). Since 1990, researchers led by Dr. Kenneth Blum have been gathering data to explain RDS. Today, it is well known that their depression is caused by an underactive reward center and is derived from a particular gene—the DRD2 A1 allele. This gene produces a deficiency of dopamine D2 receptors, the so-called “happy receptors” in the brain’s pleasure center.
The reward circuitry in this brain region controls a person’s ability to experience pleasure, enjoy good things and essentially be happy. When dopamine activates the specific D2 receptor in the brain’s reward center, we experience pleasure.
Patients with Reward Deficiency Syndrome experience less activity in their brain’s pleasure center than normal people, even though they produce normal levels of dopamine. Unknowing psychiatrists frequently misdiagnose these patients and unfortunately prescribe serotonin enhancing medications (SSRIs). These medicines actually exacerbate this type of depression and, sometimes make them suicidal. These patients typically get the label of “refractory depression.”
Another inherited gene that may increase the likelihood of depression involves an over-active COMT enzyme, the enzyme responsible for breaking down dopamine at the nerve synapse (the space between two neurons in the brain). When this enzyme is overactive, dopamine is broken down before it can activate Dopamine D2 receptors in the pleasure center. Less common is the genetics for excessive production of the MAO enzyme which metabolizes dopamine into an inactive chemical, Dopac.
Acquired Causes of Atypical Depression
Another common cause of atypical depression, which is rarely diagnosed by psychiatrists, is the accumulation of microbial toxins, most commonly Candida, Klebsiella and Enterobacteraciae toxins that disable the brain’s pituitary gland shutting down the production of antidepressant hormones and disrupting normal transmission between brain cells.
Microbial toxins readily accumulate in the brain, which is approximately 65 percent fat, consisting mostly of the beneficial omega-3 and omega-6 fatty acids. Microbial toxins are “fatty in nature.” Therefore, they readily displace good fats from our brain tissue. They inhibit the ability of dopamine to attach to the D2 happy receptor in our brain’s reward/pleasure center. Accumulation of toxins in the brain also suppresses the production of norepinephrine in the brain’s A5 nucleus. Depletion of norepinephrine triggers the conversion of dopamine into norepinephrine, thus depleting dopamine levels with resultant reduction of D2 receptor activity. Deficiency of norepinephrine causes lethargy, chronic fatigue and decreased focus, all common symptoms in patients with atypical depression.
Testosterone levels must be optimal in both genders, for dopamine receptivity, the ability of dopamine to activate brain receptors. In women, Estradiol plays a primary role in enhancing dopamine activity in the brain. Estradiol improves dopamine function by enhancing the conversion of tyrosine into dopamine and by preventing the breakdown of dopamine through inhibition of monoamine oxidase (MAO). Estradiol deficiency therefore reduces dopamine activity in the brain causing depression and brain fog. DHEA and MSH are both necessary for production of endorphins, our natural opiates. Endorphins stimulate the release of dopamine in the brain’s pleasure center.
Nutrient deficiency, can lead to the development of both melancholic and atypical depression. Decreased thyroid function, as previously discussed, can lead to decreased dopamine activity in our reward center. The majority of thyroid hormone must be from the inactive T4 hormone into the active T3 hormone. The process of T4 conversion into T3 is dependent on many different nutrients and minerals including vitamin D, vitamin B6, magnesium, iron and selenium. When these nutrients are deficient, T4 to T3 conversion fails to take place. In addition, deficiencies of vitamin D, B6 and iron result in decreased dopamine production as they are necessary for activation of Tyrosine Hydroxylase, the enzyme that converts Tyrosine into Dopamine. Vitamin D is also necessary for the production of our natural opiates, endorphins. Endorphins stimulate the release of dopamine in the brain’s pleasure center.
Heavy Metal Toxicity
Heavy metal exposure may contribute to the development of atypical depression. The heavy metals arsenic and mercury also indirectly decrease dopamine D2 activity because they interfere with the normal function of selenium, a necessary nutrient for conversion of inactive T4 to active T3 thyroid hormone.
Gluten sensitivity is another factor that should be considered when treating patients with depression. Gluteomorphins or gliadorphins, are opiate-like peptides produced from the improper digestion of gluten. They enter the blood stream (through a leaky gut) and travel to the brain disrupting normal endorphin function. Depression and anxiety are common in patients with celiac disease.
Vitamin D Deficiency
Seasonal affective disorder experienced by patients in northern latitudes during the winter months occurs when their exposure to sunshine is markedly decreased. Natural sunshine converts cholesterol in our skin into Vitamin D, which enhances the conversion of tyrosine into dopamine. Therefore, dopamine production is reduced when there is less sun shine. Dr Sponaugle determined by 2005 that those patients who are susceptible to SAD are those who are already genetically predisposed to reduced Dopamine D2 activity in their reward center.
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