Depression Causes Addiction

The number of Americans suffering depression has tripled since 198o. Depression is a common cause of drug addiction and alcoholism. I have successfully treated thousands of patients who became addicted to Oxycontin and alcohol attempting to self-medicate their depression. Most of these patients suffered  depression that did not respond to typical anti-depressant medications. 

Depression

What Is It?

 

The American Psychiatric Association has created a text called the Diagnostic and Statistical Manual of Mental Disorders (DSM IV) in their attempt to define and classify depressive disorders. Many psychiatrists and addiction specialists who specialize in psychological disorders do not agree with all of the definitions or classifications in the DSM IV, however. As stated in the DSM IV, depression is defined as persistent sadness, which lasts two or more weeks and interferes with daily life and normal functioning. Major depressive disorder is the technical term for this type of depression, which is diagnosed by the following specific criteria. 

• Depressed mood (irritable mood in children and adolescents) most of the day, nearly every day, as indicated by either subjective account or observation by others 

• Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day 

• Significant weight loss or weight gain when not dieting, or decrease or increase in appetite nearly every day (in children, consider failure to make expected weight gains) 

• Insomnia or excessive sleep nearly every day 

• Psycho-motor agitation or retardation nearly every day 

• Fatigue or loss of energy nearly every day 

• Feelings of worthlessness or excessive or inappropriate guilt nearly every day 

• Diminished ability to think or concentrate, or indecisiveness, nearly every day 

• Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, a suicide attempt, or a specific plan for committing suicide 

The DSM IV lists two major types of depression– melancholic depression and atypical depression. Recent advances in neuroscience, including the utility of brain imaging, provide a more accurate explanation of the brain physiology involved in specific brain regions that are causative for each of these two types of depression. 

Melancholic Depression

At Florida Detox and Wellness, the symptoms of melancholic depression have been correlated with both SPECT (single photon emission computed tomography) brain imaging and brain chemistry (neurotransmitter) testing. The neurotransmitter testing of patients with melancholic depression consistently reveals the significant deficiencies of two calming brain chemicals – serotonin and taurine. A less frequently found cause of melancholic depression is GABA deficiency (another calming brain chemical) with coexisting glutamate excess (a stimulating brain chemical). 

SPECT brain scans in patients with melancholic depression performed by Dr. Daniel Amen (www.amenclinics.com) for Florida Detox demonstrate the same findings as university PET (positron emission tomography) scans—an overactive deep limbic system, the brain’s emotional center. Looking at the underlying brain chemistry with neurotransmitter testing allows better explanation of what chemical aberration produces the abnormal brain scan seen in these depressed individuals. 

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 the ability of GABA to activate GABA brain receptors. Calming in the brain means decreased electrical stimulation—turning down the voltage. It is important for the GABA nerves in the emotional center to be activated in order to feel emotionally calm and peaceful. With serotonin and taurine deficiency and subsequent decreased GABA activity, the deep limbic system becomes over-electrified and, subsequently, a person commonly experiences symptoms of depression. 

Serotonin also inhibits the activity of two stimulating brain chemicals, dopamine and histamine. Both dopamine and histamine activate the same dopamine receptors in the brain. They turn up the voltage in the brain overall. With substantial serotonin activity, the brain experiences overstimulation. 

With knowledge of brain physiology, it is possible to understand yet another mechanism by which serotonin deficiency can result in an overactive deep limbic system and symptoms of depression. 

Atypical Depression

At Dr. Sponaugle’s clinic, a large number of patients suffering with symptoms of atypical depression have been treated for addiction. After asking many questions of patients addicted to dopamine-enhancing drugs like cocaine and opiate pain medication, Dr. Sponaugle uncovered the real cause of their addiction. 

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 known that their underactive pleasure center is derived from a particular gene—the DRD2 A1 gene. This gene produces a deficiency of dopamine D2 receptors, the so-called “happy receptors” in the brain’s pleasure center. Known as the nucleus accumbens, the brain’s reward center is housed inside the midbrain region called the mesolimbic dopamine system. 

The reward circuitry in this region of the brain controls a person’s ability to experience pleasure and enjoy good things. When dopamine activates the specific D2 receptor in the brain, pleasure is experienced. Patients with RDS experience less activity in their brain’s pleasure center than normal people, even when they produce normal levels of dopamine. Many of these patients are prescribed serotonin enhancing medications (SSRIs), which actually exacerbate their depression. Unknowing psychiatrists frequently misdiagnose these patients. 

Seasonal Affective Disorder (SAD)

This syndrome is a seasonal variant of depression that is derived from abnormally low dopamine activity in the nucleus accumbens, or pleasure center of the brain. This depression experienced by patients in northern latitudes during the winter months occurs when their exposure to sunshine is markedly decreased. 

What Causes It?

Melancholic Depression 

Gut Imbalance/Candida Overgrowth

Since the widespread use of penicillin began about 65 years ago, antibiotics have been added to poultry and cattle feed. Antibiotics are ingested through poultry, milk, and, increasingly, in city water which is not filtered for antibiotics that enter the waterways. Antibiotic levels found in food and water have reached the critical threshold necessary to slowly destroy the normal flora or healthy bacteria inside the intestine. 

Destruction of the healthy bacteria in the intestine allows excessive overgrowth of toxic Candida yeast and toxic bacteria. These pathogenic bugs create toxins that disable the brain’s pituitary gland6 shutting down production of healthy levels of the natural antidepressant hormones estradiol, testosterone and DHEA. Clinical research at Florida Detox and Wellness reveals that patients presenting with biomarkers of Candida overgrowth frequently suffer a serotonin deficiency that can be ameliorated through supplementation with 5-HTP, suggesting toxic disruption of the initial step of tryptophan conversion in the small intestine. The same intestinal overgrowth of toxic Candida yeast causes deficiency of the brain chemical taurine in people with melancholic depression. 

Inflammation

The innate immune system is involved in the process of inflammation by producing many different molecules called cytokines, some of which are pro-inflammatory and others anti-inflammatory. Pro-inflammatory cytokines induce depression by their impact on three different systems: the 5-HT system, which produces serotonin; the noradrenergic system, which produces epinephrine (adrenaline) and norepinephrine; and the HPA system, which produces cortisol, the stress hormone.7 In the 5-HT system, inflammatory cytokines deplete tryptophan, the primary precursor to serotonin, This means that when inflammation is present, tryptophan is depleted and serotonin is not produced. 

Where does this inflammatory immune response begin? Quite often, in the gut. The gastrointestinal tract is where much immune activation begins. The GI tract encounters far more foreign invaders on a daily basis than the internal (systemic) immune system encounters in an entire lifetime. This is a vital function of the GI tract and plays a role in the gut-brain connection. The body transfers immunological information from the GI tract to the brain via the vagal nerve, a large nerve that extends from the brain to the intestines,9 as well as via the bloodstream. So the health of the gut is essential in regulating immune response and, thus, depression. 

One trigger of these pro-inflammatory cytokines in the gut comes from lipopolysaccharides (bacterial endotoxins) that are produced by pathogenic bacteria. The gut inflammation that ensues creates increased intestinal permeability, or leaky gut, which allows the endotoxins, as well as other dietary and environmental toxins, to pass through the gut wall and into the bloodstream triggering further inflammation that can travel anywhere in the body. In depression, the inflammation manifests in the brain. 

Nutrient Deficiency

Other acquired causes of serotonin deficiency derived from the gut include malabsorption and subsequent deficiency of vitamin D, vitamin B6, vitamin C and magnesium. Magnesium is a necessary cofactor for the chemical conversion of tryptophan to 5-HTP in the small intestine. Vitamins D, C, and B6 are necessary cofactors for the brain conversion of 5-HTP into serotonin. Any of these deficiencies can result in melancholic depression. 

Environmental Toxins

Brain toxicity derived from exposure to industrial solvents like toluene in paint thinners and volatile organic solvents such as benzene in gasoline, diesel fuel, and other industrial chemicals also disable brain serotonin factories, which leads to melancholic depression. 

Prenatal exposure to the toxin bisphenol A (BPA) has been shown to increase depression-like behavior. BPA is found in the lining of food cans and in most hard plastics. It is a known hormone disruptor and should be avoided when possible. 

Hormonal Imbalance

In the female brain, the serotonin receptors do not effectively receive serotonin when blood estradiol (a form of estrogen) levels fall below 60 to 80 pg/dL. Female patients with normal serotonin levels but low estradiol levels frequently suffer melancholic depression. Postpartum depression occurs in over 30 percent of females when the ovaries temporarily stop producing strong levels of estradiol. This is the reason the symptoms of postpartum depression mimic the symptoms of melancholic depression. 

Interestingly, the premenstrual period, usually 4 to 5 days before menses begins, correlates with the lowest estradiol output in the monthly cycle. Many women have insufficient estradiol during this time period inhibiting the ability of serotonin to work effectively. This is why premenstrual psychological symptoms mimic many of the symptoms of melancholic depression. 

Similarly, postmenopausal women are also found to have decreased serotonin activity as a result of the estradiol depletion that occurs after menopause. 

 

Emotional Experiences

Other non-biochemical causes of melancholic depression include a lack of parental nurturing during childhood, and repeated disappointments or continuous failures and negative experiences in adulthood. The deep limbic system stores the emotional component of memories. When the majority of memories are bad, the limbic system sets a more negative tone that is then reflected in personality. 

Dr. Daniel Amen has performed SPECT brain imaging of the limbic system in patients before and after they were asked to focus on either negative or positive aspects of their life. Directing their focus to positive aspects was recognized on the brain scan as being calming to the deep limbic system—and the patient reported being happier. Directing their focus to the negative aspects clearly revealed over-activity of the deep limbic system—and the patient reported feeling more depressed. This illustrates the power of thought, which can be utilized in treatment protocols. 

Atypical Depression 

Gut Imbalance / Candida Overgrowth

A common cause of atypical depression, which is rarely diagnosed by the average psychiatrist, is the accumulation of microbial toxins—most commonly Klebsiella bacterial toxins, Candida mycotoxins produced from Candida overgrowth, mold toxins derived from water damage inside the home, and toxins produced by the bacteria that causes Lyme disease. These toxins disable the brain’s pituitary gland shutting down the production of natural antidepressant hormones and disrupting normal transmission between brain cells. 

Microbial toxins readily accumulate in the brain, which is approximately 65 percent fat, mostly made up of the beneficial omega-3 and omega-6 fatty acids. The microbial toxins are also fatty acids, and readily displace the good fats from brain tissue. This inhibits the ability of dopamine to attach to its D2 receptor decreasing D2 dopamine activity in the pleasure center. 

Accumulation of toxins in the brain also causes atypical depression because the toxins disable the production of norepinephrine in the A5 nucleus. Depletion of norepinephrine triggers the conversion of dopamine into norepinephrine, thus depleting dopamine with resultant decrease in D2 “happy receptor” activity. If this cycle continues, both dopamine and norepinephrine become depleted. Deficiency of norepinephrine causes lethargy, chronic fatigue and decreased focus, all common symptoms of atypical depression and all associated with gut imbalance and excessive accumulation of brain toxins. 

Hormonal Imbalance

Gut imbalance, with resulting production of microbial toxins, also greatly affects hormonal balance. Many different aspects of hormonal imbalance can lead to atypical depression. Yeast mycotoxins and bacterial endotoxins derived from a dysfunctional gut, contribute to the development of thyroid dysfunction (hypothyroidism) by suppressing the output of thyroid-stimulating hormone from the pituitary gland in the brain. Deficiency of thyroid hormone causes decreased dopamine activity in the pleasure center, because dopamine receptivity is dependent on thyroid for activation. 

Yeast mycotoxins and bacterial endotoxins also suppress the pituitary output of the hormone FSH which stimulates the ovaries to produce estradiol, a form of estrogen. 

In women, estradiol improves dopamine function by both enhancing the conversion of tyrosine into dopamine and also preventing the breakdown of dopamine by inhibiting the enzyme monoamine oxidase (MAO). When estradiol is low, dopamine levels will fall and the pleasure center undergoes decreased activation. 

Gut toxins also suppress the pituitary output of growth hormone and melanocyte stimulating hormone (MSH) deficiencies of which cause depression. These same toxins suppress pituitary output of the hormone ACTH (adrenocorticotropic hormone). Without proper levels of ACTH, the adrenal glands become underactive with resultant deficiency of cortisol, DHEA and epinephrine (pure adrenaline), all factors associated with depression. DHEA and MSH are also necessary for production of endorphins, our natural opiates. Endorphins stimulate the release of dopamine in the brain’s pleasure center. 

Optimizing hormonal function, as well as gut function, is important when treating patients with depression. 

Nutrient Deficiency

Nutrient deficiency, which may develop from poor diet and many different digestive issues, can lead to the development of depression. One way in which his occurs is by affecting thyroid hormone function, which, as described previously, can lead to decreased dopamine activity and, thus, atypical depression. 

The majority of thyroid hormone in the body is converted from the inactive T4 form to the active T3 form. It has recently been determined that T3 makes the D2 dopamine receptor more sensitive to dopamine. The process of T3 conversion to T4 is dependent on many different nutrients, most notably vitamin D, vitamin B6, magnesium, iron and selenium. If these nutrients are deficient, this important conversion cannot take place, thus, dopamine activity in the pleasure center will be compromised. 

In addition, deficiencies in vitamin D, B6 and iron result in decreased dopamine production because they are needed for the conversion of the amino acid tyrosine (derived from protein in the diet) into dopamine. Vitamin D is also necessary for the production of estradiol, the importance of which was previously mentioned. Additionally, vitamin D is necessary for the production of natural opiates called endorphins. Endorphins stimulate the release of dopamine in the pleasure center. 

Heavy Metal Toxins

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

Gluten sensitivity is another factor that should be considered with depression. Gluteomorphins or gliadorphins, opiate-like peptides, produced from the improper digestion of wheat gluten in the gut, enter the blood stream (through a leaky gut) and travel throughout the body ultimately reaching the brain. Neurological disorders or findings have been found in up to 51 percent of patients with celiac disease, the most severe form of gluten sensitivity. Depression and anxiety were both found to be common features among those with celiac disease. Additionally, adherence to a gluten-free diet was found to improve depressive symptoms in celiac patients. This is yet another example of the gut-brain connection. 

Genetic Predispositon

As previously discussed, some people inherit the DRD2 A1 gene that produces a decreased number of D2 receptors in the pleasure center as compared to normal individuals. These people experience atypical depression. Another inherited gene that may increase the likelihood that a person develops atypical depression involves the production of 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 the dopamine D2 receptor in the pleasure center. Other inherited genes involved cause excessive production of the MAO enzyme. MAO breaks down dopamine inside brain cells; excessive MAO causes dopamine deficiency. 

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 the skin to vitamin D, which enhances the conversion of tyrosine into dopamine, and, therefore, dopamine production is reduced when there is less sunshine-induced vitamin D production. 

What Are the Signs and Symptoms?

Melancholic Depression 

Symptoms of melancholic depression are described in the psychiatric community as: 

• Lost reactivity to events
• Dread about the future
• Decrease in appetite
• Anxiety
• Insomnia
• Weight loss
• Excessive guilt
• Worsening of depression in the morning

 

Patients with melancholic depression at Florida Detox and Wellness clearly describe an inability to enjoy recreational or other activities that once brought them pleasure. Patients also develop moodiness. They become more irritable and more easily agitated. They constantly fight feelings of hopelessness and excessive guilt. They suffer from chronic low self-esteem coupled with low motivation which leaves them feeling overwhelmed as they approach the tasks and expectations of each day. 

Patients with melancholic depression slowly become more isolated. Patients who previously enjoyed socializing and were considered social butterflies develop an adversity to social situations. They become more awkward as their overactive emotional center (deep limbic region of the brain) makes them more sensitive and more easily offended by things other people say. They often mistake positive comments made by others as negative or even an outright insult. 

In the most severe cases, patients develop social anxiety resulting in lifestyle changes. They begin choosing quiet weekends at home instead of socializing with their friends and families. Due to the fact that this change is insidious, they initially assume they are simply becoming more mature. However, as the depression worsens, they have difficulty making it through their workday which requires them to interact with the other employees. They fake a smile at work, only to come home and hide out in their bedroom. 

Atypical Depression 

While it is difficult to work within the arbitrary constraints of the DSM IV manual, the symptoms as described for atypical depression are as follows: 

• Fatigue
• Lethargy
• Excessive sleep
• Disconnectedness
• Emotional response to events
• Social avoidance
• Sensitivity to rejection
• Increase in appetite
• Weight gain
• Worsening of depression at night

These symptoms are, for the most part, caused by an underactive reward or pleasure center. These individuals are unable to feel the so called “dopamine hit” in their pleasure center that most people experience when they hug a five-month old baby or a wriggly puppy. They often admit, behind closed doors, that when growing up, they just didn’t get as excited as their sisters or brothers when they got a new bicycle. 

They will remember how excited classmates became at their high school graduation. They wanted to feel it too, but they just couldn’t. They threw their cap with the others, pretending to be just as excited as their friends. These patients will sometimes work diligently to hide their underlying sadness. Their depression does not have the symptoms of melancholic depression which are derived from an overactive limbic system, unless they also suffer serotonin deficiency. 

These patients may appear to be “just a quart low” on happiness and not outwardly depressed. They frequently lack motivation because motivation is somewhat dependent on dopamine activity in the reward center. 

They often appear lethargic and fatigued. They frequently have great difficulty getting out of bed in the morning. Their mothers will remember waking them three or four times in the morning, and that getting them to school on time was a struggle. 

How Is It Diagnosed?

Depression is traditionally diagnosed according to the DSM IV criteria as described in the “What is It?” section. Further breakdown of the type of depression is determined according to the more specific symptoms as described in the previous section. 

Progressive doctors, like Dr. Sponaugle, use further diagnostic tests which look at what is actually going on biochemically in the body. Since what happens in the mind often reflects what is occurring in the body, these tests can provide insight into what may be triggering or worsening depressive episodes. Some tests that may be used include: 

• Adrenal stress test
• Neurotransmitter metabolite test
• Amino acid profile
• High sensitivity C-reactive protein (hs-CRP)
• Celiac profile
• Hormonal testing
• Comprehensive stool analysis (CSA)
• Essential fatty acid red blood count (EFA RBC)
• SPECT scan

Dr. Sponaugle prefers to diagnose brain disorders based on which brain regions are underactive and overactive, and what brain chemical imbalance is causing the symptom. Dr. Sponaugle feels the DSM IV places too much emphasis on symptom-based arbitrary labels. 

SPECT (single photon-emission computed tomography) scans or PET (positron-emission tomography) scans may be used to determine the activity levels of different regions of the brain. In depression, SPECT scans show an increase in activity in the deep limbic area of the brain. The deep limbic system can be seen as the filter through which one views life. When this brain region becomes overactive, its filter shades events as negative. The deep limbic system also affects motivation and drive, bonding, and social connectedness, all symptoms of melancholic depression. Deep limbic activation is also seen during times of hormonal change in women, which correlates to times when depression is more likely. All these factors support the use of SPECT scans in the diagnosis of depression. Functional MRI and PET scans more readily measure pleasure center D2 dopamine activity than SPECT scans. 

 

Depression in Children and Adolescents

In children, major depressive disorder is common. Of children aged 6 to 12, one to two percent are depressed. In adolescents aged 13 to 18, up to 25 percent experience at least one episode of major depression. Until they reach puberty, both boys and girls experience depression equally. After puberty, however, girls experience depression twice as often as boys. As in adults, depression usually lasts several months and recurs in most patients. Adolescents who experience depression are likely to become adults who experience depression. Signs and symptoms of depression in children include: 

• Irritability or anger
• Continuous feelings of sadness, hopelessness
• Social withdrawal
• Increased sensitivity to rejection
• Changes in appetite
• Changes in sleep
• Vocal outbursts or crying

What Is the Standard Medical Treatment?

In traditional medicine, the first line treatment for major depression is antidepressant medication, but only about half of those with moderate to severe depression will improve with this standard drug treatment. The most popular of the antidepressant drugs are the selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac), citalopram (Celexa), paroxetine (Paxil), and sertraline (Zoloft). SSRIs increase the availability of serotonin in the brain. Worldwide, sales of SSRIs are over $10 billion per year. Norepinephrinere uptake inhibitors are another medication that increase the available norepinephrine in the brain. Dual-action antidepressants are another form of medication that target more than one neurotransmitter, like serotonin and norepinephrine. Other medications that may be used for depression include MAO inhibitors and tricyclic antidepressants, both of which are more likely to produce adverse side effects. MAO inhibitors tend to be more effective for atypical depression, while tricyclic antidepressants are not. Additional drugs, depending on the patient, may be added. Mood stabilizers and antipsychotic agents are the most common of these adjunctive drugs. 

Nonpharmacologic therapies used for depression are often used in conjunction or even in place of medication. These therapies include psychotherapy and electroconvulsive therapy (ECT). Psychotherapy techniques, such as cognitive behavioral therapy, interpersonal therapy and problem-solving therapies, are effective for acute episodes of depression as well as to postpone relapse during treatment of mild to moderate depression. Electroshock therapy is a controversial treatment that involves inducing a seizure via electric shock. It is used for patients who fail to respond to other treatments, who have psychotic features or psychomotor retardation. ECT usually consists of six to 12 treatments two or three times a week. Confusion and loss of memory are common side effects of this severe treatment. 

The brain’s pleasure center runs on dopamine. Any drug that releases dopamine from brain storage units stimulates the pleasure center, thus, it will temporarily ameliorate the patient’s depression. Drugs that patients commonly use to stimulate a “dopamine hit”  in their pleasure center include; Oxycontin like pain medications, heroin, alcohol, marijuana, cocaine, methamphetamine and nicotine. Nicotine is actually stronger than cocaine and heroin in it’s dopamine stimulating effect. 

I also treat many non-addicted patients who have suffered life long depression because they never responded to typical antidepressant therapy. Many of these women have been labeled “refractory depression” by their psychiatrists because they did not respond to treating the wrong brain chemical! These women from throughout the United States and Canada are continuously misdiagnosed and placed on the wrong treatment regimen. 

They typically give a history of failing to respond to various combination of anti-depressants prescribed by multiple psychiatrists. The  treatment regimens they have failed normally consist of different combinations of SSRI [serotonin boosting] anti-depressants. They have had trials of many different drugs, but, the different drugs all work on the same brain chemical, serotonin! 

Where is the common sense in medicine, not in American psychiatry? Why do psychiatrists create cocktails of multiple SSRI, serotonin boosting, anti-depressant medications when the first one doesn’t work? Why do they have such embarrassing tunnel vision that they don’t get it, that they are treating the wrong brain chemical? 

After depressed patients continuously fail to respond to a doctors various antidepressant drug regimens, regimens that all treat the wrong brain chemical, the ill-knowledgeable psychiatrist labels them as having  “refractory depression.” Then, he/she offers the patient shock therapy which kills brain neurons and causes early onset of Alzheimer’s disease. 

These patients are refractory to treatment for serotonin deficiency, why, because serotonin deficiency is not the cause of their depression. Serotonin deficiency is a common cause of depression in Americans, however, it is not the cause of depression in 50 percent of my depressed patients. Many patients suffering depression have inherited an underactive pleasure center. The brain’s pleasure center is called the nucleus accumbens, it resides in the midbrain. 

We learned in 2000 that our brain’s pleasure center runs on dopamine, yet, ten years later, physicians in America practice brain medicine with tunnel vision, especially when they treat patients suffering with depression. Physicians automatically assume that their patient’s depression is derived from serotonin deficiency –  and they attempt to treat all depressed patients with SSRI medications. Misdiagnosis in patients suffering depression from dopamine deficiency is frequently a cause of suicide. 

Fifty percent of depressed patients suffer depression because of an underactive pleasure center, this can be caused by a dopamine deficiency or by Reward Deficiency Syndrome, RDS.  Reward Deficiency Syndrome is genetic, patients inherit the D2DR gene which causes an abnormal reduction of  ”happy receptors” in their pleasure center, thus patients feel depressed. 

It is disheartening to see patients who fight suicidal thoughts on a daily basis because, they have been dangerously misdiagnosed by psychiatrists. These patients have usually suffered depression for years. Their depression was worsened when their doctor prescribed a serotonin enhancing medication like Paxil or Lexapro. 

These patients suffer from an underactive pleasure center, they have Reward Deficiency Syndrome. PET scan research has proven that some of these patients have inherited up to half the normal level of Dopamine D2 “happy” receptors in their pleasure center. They cannot get excited when good things happen and they cannot feel joy like normal people. 

In a recent ABC NEWS interview, I explained that ill-knowledgeable psychiatrists frequently cause a worsening of their patient’s depression, even to the point of suicidality, when they prescribe serotonin enhancing medications [SSRI drugs like Paxil and Lexapro] to patients with Reward Deficiency Syndrome. Because serotonin activity prevents the release of dopamine from brain storage units, prescribing serotonergic medication to RDS patients further decreases activity in their dopamine driven pleasure center. 

When we differentiate whether the patient’s depression is derived from serotonin deficiency, dopamine deficiency or both, we can optimize their brain chemistry and their life long depression disappears within days. Dr. Sponaugle has successfully treated more than 1000 depressed patients, mostly women, who failed to respond to depression treatment from multiple medical centers. Treating brain disorders requires extensive and in depth knowledge of brain chemistry, knowledge that is not taught in the DSM4 psychiatric manual. 

Many addicted patients who present to Florida Detox and Wellness are simply using drugs like Vicodin, Percocet, Oxycontin, cocaine, marijuana and alcohol to self-medicate their depression. All of the drugs listed here produce a temporary dopamine surge or “dopamine hit” in the brain’s dopamine driven pleasure center. Patients with RDS and depression “feel normal” when they use dopaminergic drugs. These patients don’t use drugs to get high, they use them to get higher, to normal! 

Before coming to Florida Detox and Wellness, the majority of the addicted patients with RDS, those who suffer a genetic deficiency of  “Dopamine D2 Receptors” in their nucleus accumbens [pleasure center], have been through multiple, some more than ten, previous rehab programs - expensive rehabs where they had spent hundreds of thousands of dollars to be repeatedly misdiagnosed and labeled a drug addict or alcoholic. 

The nicest counselors at other addiction treatment centers had attempted to talk these patients out of their addiction, group therapy didn’t work because it can’t change a biochemical problem. With advanced knowledge of brain science, it is easier to see why America’s addiction centers have a ninety percent relapse rate. You can’t talk patients out of their biochemical craving, craving they experience for the biochemical effect of a drug that made them “feel normal” for the first time in their life. 

There are multiple biochemical causes of depression. Reward Deficiency Syndrome is the most common inherited cause of depression. We will now begin to discuss the most common acquired causes of depression which are serotonin deficiency and hormonal deficiencies in men and women. 

In women, hormonal deficiencies are often the cause of a new onset depression. The prevalence of depression in females doubles after puberty. Hormonal imbalance can drastically change a woman’s brain chemistry. This can cause major depression as well as anxiety and insomnia. All of these disorders can ultimately lead to addiction. 

Unfortunately, most doctors in America are unaware that serotonin activity is greatly compromised in a woman’s brain when her estradiol levels fall below 80 pg/dl. Even with normal serotonin levels, she can suffer symptoms of a low serotonin brain when estradiol is suboptimal. Estrogen dropout, postpartum and in midlife, can create tremendous depression and anxiety disorders in females. The initial evaluation of new onset depression in a female should always begin with measurement of estradiol and testosterone. See Hormones and Addiction, an article written by Dr. Sponaugle for the American Academy of Anti-aging Medicine. 

Most doctors in America assume that all depression is caused by serotonin deficiency. We have known since 2001 that our brain’s pleasure center [nucleus accumbens] actually runs on dopamine. Dopamine deficiency is much more common in causation of depression than American physicians realize. Because they do not study new concepts in neuroscience or practice with tunnel vision, their knee jerk reflex is usually to treat all depressed patients with an SSRI mediation. 

A classic depression patient presents to Florida Detox addicted to Vicodin after she has failed treatment for depression from her local physician. She has received multiple serotonin antidepressants all of which caused worsening of her depression symptoms. The only drug that effectively treated her depression is the Vicodin her friend gave her for menstrual cramps. Opioid pain pills cause a temporary release of dopamine from brain storage units. This is an effective but dangerous treatment that many frustrated, repeatedly misdiagnosed dopamine deficient patients will use. 

Raising serotonin activity inhibits dopamine release to the pleasure center, and causes more depression in a patient whose depression is not from serotonin deficiency, but rather, a dopamine deficient pleasure center. When we accurately diagnose and treat these patients with dopamine enhancing medication, their depression subsides as does their craving for dopaminergic drugs and alcohol.