WhatYou May Do About It When There Are No Doctors About
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The Thousand Yard Stare
The Look Of Total Stress
The Neurobiology Of |
Mood & Anxiety Disorders
Disorders of Mood and Anxiety are common. They are severe, debilitating, and even
life–threatening diseases/illnesses. It has now become evident that these are illnesses that are apart from just being psychological in origin including only psychological manifestations.
These are diseases of the entire system of a biological organism. It is completely systemic! The by–stander effect of such a disease not only affects the psychological manifestations but also includes multiple systems of the organism. Genetics can play a role in one having this; but, the danger in seeing only this, one misses other functional systems of the body. Depending upon the stressor, different people react differently to similar or different stressors. The stressors ultimately play a huge role in treatment and outcome of such a one afflicted.
The reason such people are often very difficult to treat — and many can't be treated effectively, is because of various underlying biochemical systems and psychological and anatomical measures in one with Mood Disorders. There are neurotransmittor problems; these chemical messengers may be correctly plied by the body or in medication form; however, the cellular signalling may be off, and as such, the patient does not respond. Molecular structures may not be formed correctly; or, slightly different in their modality of operation to the general mass of people.
There are other modalities that affect mood, temperment, and anxiety, such as fuel for the nerves. Glucose may not be utilized quite right and thus, one spirals into a "grand funk!"
More neuroscientists are beginning to think when nothing helps the patient suffering with mood disorders, it may well be a brain nourishment problem. We will discuss this more.
The major mood disorders are comprised of three types of diagnosis:
- Major Depressive Disorder, commonly known as Unipolar Despression
- Dysthymia, A chronic form of depression, but less severe than unipolar depression. This is similar to a mood trait
- Manic–Depressive Disorder, now known as Bipolar Disorders. This form of Mood Dysfunction is characterized with episodic periods of mania (extremely high feelings) and hypomania (extremly low feelings)
There are currently—with all the medications available to the health care teams—oceans of people suffering with depression out there, and they are treatment–resistant. Many such persons have been diagnosed as alcoholics, when in actuality, they suffer with depression, and they have learned that alcohol 'treats' their depression. The same with marijuana, cocaine, and other recreational drugs. There are still a lot of 'somethings' we do not know.
Alcoholism is a disorder that one chronicly relapses into. To help one stay off of alcohol, especially when they have been free of this disorder for years, if they are placed back into a setting of stress similar to what they once were in when inbibing heavily and regularly, they will quite often go back to heavy drinking again. This must be pointed out to one who has gone through a treatment center. However, often, they are not told this aspect of the alcohol problem. It may be their job, or a similar set of circumstances, generating stress, generating depression, causing them to drink—and no one is the wiser for it.
What does the person who drinks learn about why alcohol makes him feel better? Only that "When down, a drink 'bucks' him up!" This is what is occurring. This drug, alcohol, alters the activity of GABAergic transmission of a particular GABA receptor to an effector site or moleculars. Gamma–aminobutyric acid (GABA) is a neurotransmitter. It belongs to an inhibitory class of neurotransmitters in the brain and spinal cord, the same as Glycine, an amino acid.
Alcohol causes the GABA inhibitory circuits in the brain and spinal cord, especially the brain, to be altered in activity. Instead of putting the brakes on a certain action, this circuitry is blocked and thus one demonstrates some drunken behavior aspects when drinking too much because the brakes are put out of commission.
The area of the brain that is highly involved is a region in the midbrain known as Ventral Tegmental Area (VTA) and the Nucleus Accumbens (NA). The point to garner here is that:
The nucleus accumbens and the ventral tegmental area are primary sites where drugs of abuse interact with the processing of neural signals related to emotional reinforcement; they do so by prolonging the action of dopamine [neurotransmitter dealing with reward] in the nucleus accumbens or by potentiating the activation of neurons in the ventral tegmental area and nucleus accumbens.
Under normal conditions (i.e., when illicit drugs are absent), these dopaminergic neurons are only phasically active; when they do fire a barrage of action potentials, however, dopamine is released in the nucleus accumbens and medium spiny neurons are more responsive to coincident excitatory input from telencephalic structures, such as the amygdala [that area of the brain dealing with fear and anxiety] and orbital–medial prefrontal cortex [area dealing with judgement and control of impulses, and executive decisions].— Neuroscience, Fourth Edition. Page 755.
When drinking, the cortex area starts getting 'wiped out' increasingly as more alcohol is imbibed. "The VTA, GABA receptors are predominantly located on GABA neurons." Alcohol reinforces the effects of multiple neuronal systems. It does it this way:
Various opioid systems in ethanol addiction also play an important role. "One locus for opioid effects is in the nucleus accumbens. Opioids influence ethanol reinforcement through both dopamine–dependent and dopamine–independent actions in the nucleus accumbens. Other transmitters (e.g., endocannabinoids and neuropeptide Y) and other brain regions (e.g. the extended amygdala) may also contribute to ethanol action." — Basic Neurochemistry; Molecular, Cellular, and Medical Aspects, page 922.
As you can see, this is a very difficult situation to be under when one goes into the total chaos coming to Planet Earth. It may be helpful, when there are no doctors about, when the earth is roiling with anger and hatred, and you don't know where to turn for help with the immediate above-mentioned problem, we suggest to have on hand, and even start now with Dopa-Tech HGH from ProSource. This puts a little more dopamine into your system and just might help, with alcoholism as well as the depression often associated with this sort of disorder.
We further suggest that one Strongly consider also,
- "Alcohol enhances GABA–A receptor transmission in VTA, ethanol inhibits these GABA neurons, thus disinhibiting the dopamine neurons." In other words, GABA–A receptor plus alcohol generates an inhibition of GABA and this inhibition causes an increase in dopamine release circuits and the pleasure reward pathway is enhanced and not inhibited somewhat as when GABA–A receptors are allowed to inhibit too much dopaminergic pathway activity!
- "Ethanol also directly excites dopamine neurons by decreasing a potassium conductance. After chronic ethanol exposure, adaptations develop in the mesolimbic (emotional brain area) dopamine to offset excitatory effects of ethanol,
- "Such that withdrawal from chronic ethanol leads to decreased dopamine cell activity and extracellular dopamine levels in the nucleus accumbens. This leads to dysphoria."
We have used these modalities in our private practice with great success on patients who were refractory to the usual treatments. However, we offer no guarantees. There is the possibility, as with medications, your situation could get worse because of the way your receptor molecules are and your cell-signaling pathways have developed; or, some other modality not yet considered in science. It is a wonder that science does help as many as it does with this dysfunction—depression. Yet, there are many more not helped.
We strongly advise, if you are bipolar, to avoid lecithin or foods such as egg yolks that are high in lecithin. It would further be advisable to avoid any type of measure that would increase choline in your diet.
The reason for these precautions is because in some cases lecithin will reduce mania, but induce depression, and lecithin is an acetylcholine precursor. Be warned of the cholinergic properties of certain foods.
If you are bipolar, and an alcoholic, just simply eating a high-salt meal or any ingestion of a nutraceutical or vitamin compound high in a metal with a +1 valance charge, can throw your lithium balance into the netherlands—if you're on lithium, and you find yourself in a living hell once more.
We do not advise one to take L-Tryptophan(e); nor its metabolite, 5–HTP (5–hydroxytryptophan). There can be problems with it that we will investigate in a later issue of this series of ChemBio Update. For now, if you do take 5–HTP, we recommend one take with the prescription drug, Carbodopa, to allow 5–HTP to metabolize in the brain, where it should, and not in the bloodstream. In a small few, no way to ascertain who, it can cause strokes, when the metabolism occurs in the bloodstream.
Remington: The Science and Practice of Pharmacy, 21st Edition, writes on page 1419:
- GABA Plus by Twinlabs, or GABA Complex by Good 'N Natural.
However, if one drinks because of depression, and this drinking makes the patient feel better; avoid GABA. We suggest to try Dopa-Tech HGH from ProSource.
- Additionally, one should consider Glycine capsules.
- Also, Copper capsules or tablets, which usually come in 2 or 3 mg strengths,
- Vitamin C, L-phenylalanine, and L-tyrosine.
- If you don't have bipolar disorder, and a drinking problem as well, then taking SAMe may also help with the depression if this is causing your drinking problem. SAMe makes mania worse or may bring it on.
- A high dose B-complex, along with P-5-P (pyridoxal 5' phosphate from Kal vitamins and Vitamin Research Products), a converted form of Vitamin B-6, will also be helpful.
- For Seasonal Affective Disorder (SAD), we recommend throughout the year 5,000 IUs daily of Vitamin D3. It affects the methylation inside our bodies. Taken with SAMe or Tri–Methyl Glycine, TMG (methylators) help keep the 'trigger' down that causes SAD.
It is essential that levodopa and 5–hydroxytryptophan be decarboxylated in the brain to their respective biogenic amine products, dopamine and serotonin (5–hydroxytryptamine), which are the active agents. But in the periphery it is not desirable that these amino acids be decarboxylated.
Below are two charts, which show you why some of the above recommendations are given.
We Now Reccommend One Review:
The Psychology Of Depression
The Depressive Spirit Now Cometh
It will be like Atlanta, burn and slash! Total chaos just around the corner!
... To Be Continued ...
Basic Medical Biochemistry: A Clinical Approach, Marks, D.B., Marks, A.D., Smith, C. M., Lippincott Williams & Wilkins, Pennsylvania, 1996.
Basic Neurochemistry: Molecular, Cellular, and Medical Aspects: Seventh Edition, Editors: Siegel, Albers, Brady, Price, Elsevier Academic Press, 2006.
Biochemistry and Molecular Biology: Third Edition, Elliott, W.H., Elliott, D.C., Oxford University Press. NY; 2005.
Cell And Molecular Biology: Concepts And Experiments. Fourth Edition Karp, Gerald. John Wiley & Sons, 2005.
Instant Notes in Biochemistry, Hames, B.D., Hooper, N.M., & Houghton, J. D., Bios Scientific Publishers, NY, Reprinted 1999.
NeuroScience: Fourth Edition, Editors: Purves, Augustine, Fitzpatrick, et. al., Sinauer Associates, Inc. Sunderland, Massachusetts, U.S.A 2008.
Remington: The Science and Practice of Pharmacy, 21 Edition, Lippincott Williams & Wilkins, 2006.
Stress and Your Body, Transcript Book. Professor Robert Sapolsky, Stanford University. The Great Courses®, Science & Mathematics by The Teaching Company. DVD; 2010.
Peat, Ray, Ph.D., Serotonin, Depression, And Aggression: The Problem of Brain Energy. RayPeat.com, 2009.
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