Anxiety disorders are conditions whereby one responds to stress in a disproportionate response. He exhibits maladaptive abilities. The response can be even self–evoked! Remember from a previous Update, we wrote that one area of the brain can start thinking sad thoughts, and set the whole brain afire with it. The same with self–evoked fear.

    Anxiety is fear and/or worry, coupled together, at its worse. Disorders of anxiety are a psychiatric illness that is seen quite frequently by physicians of this discipline. There are six (6) common classifications under this Mood Disorder:

• Generalized Anxiety Disorder that carries a life–time rate of prevalence of 15% to 20%.

• Social Anxiety Disorder that can range from 2% – 14% over one's lifetime.

• Then, we see an extreme fear or worry suddenly come over one. This has a prevalence rate of 2% to 4%. This is the Panic Attack version of anxiety disorder.

• The Post–Traumatic Stress Disorder (PTSD) has a prevalence rate near 8%.

• Specific Phobias acute stress and,

• Obsessive–Compulsive behavior.
  These above clinical presentations are classified under anxiety disorders.

    There's an area of the brain highly concerned with emotions. This is the Limbic System. It involves the cortex and subcortical structures that are framed for emotions. The most prominent is the Cingulate Gyrus, the Hippocampus, and the Amygdala.

    The amygdala is what we are primarily concerned with in this discussion, as this is the area of the brain that is concerned with emotional behavior, sexual behavior, and autonomic behavior. It plays an important role in fear and anxiety (worry).

    The hypothalamus influences the expression of emotion. The amygdala, by its cable connections to the hypothalamus, the stria terminalis, puts the hypothalamus in a very pissy mood when the amygdala is roiling and frontal cortex control of Judgement, Impulse control, and Executive decisions (behavior) are blocked! Many now are presenting with more harder to controlled emotions and hence, we will see more hypothalamic expressions of road rage, postal mode, uncontrollable rage, exhausting fear and worry (anxiety), and even worse.

    The amygdala plays a strong role in Learning To Be Afraid! of new things and in natural fears and phobias.

    And this is Stress's role in this learning to be afraid and anxiety and worry. Stress increases the amygdala's role big time in learning to worry and be afraid. On just a behavioral level, anxiety is increased by stress. And by now, you should know what stress is; recall the chart from Depression–I of this serries. Stress is an excess of glucocorticoid hormones.

    Certain brain areas have receptors—big time—for glucocorticoids in the brain. These areas are the hippocampus (learning new memories), frontal cortex (area concerned with judgement, impulse control, and executive decision), and the third in line is the amygdala. In sustained stress, the amygdala 'drinks' freely of the glucocorticoids. Therefore, with all these hormones in the aggression center of fear and anxiety, it gets better at doing what it does best: Learning to be afraid more and worry more! That's stress for you. But not all stress is bad. We'll discuss this later.

    With all these stress hormones bathing the brain and other areas of the body, the hippocampus shrinks, and forming new memory is harder; recall becomes difficult. Two areas that tend to get bigger under chronic stress is the adrenal glands and, ah yes! The amygdala. Now why do we say the amygdala is learning to be more and more afraid? Because its synapses are becoming more excitable and this brain area can grow new processes which grow bigger and larger and more interconnected. the amygdala is now networking more than ever at learning—teaching you—to become super afraid and more worried than ever. The amygdala is getting bigger and more active metabolically. You now have a possession . . . and the demon (the amygdala; demons from the id) is taking control over you!

    What is happening here is the opposite that is happening in the hippocampus. The unrelenting stress has set you up for an anxiety disorder; one that can take one or more of the forms listed above.

    The medical profession gives antianxiety drugs for this mood disorder. One such drug is benzodiazepine, such as Valium or Librium. Once, they were used constantly for practically everything, and any time a person felt out of sorts and/or had the 'blues.'

    When an organism, due to accidents of nature, or from nature, have lost their two amygdala (one on each side of the brain hemisphere) damage, they could no longer be afraid of anything! This in itself was dangerous. They don't show fear. They strangely trust any circumstance, where angels fear to tread, these blissful individuals rush in.

    Subliminal fear is present in all of us; however, if your amygdala has been damaged, that too is gone. Something could have happened biochemically; or, in your diet such that you are no longer receiving the chemical message(s) and cell signaling you once were receiving and thus, you fall in to an anxiety disorder.

    The stress in your life, could be minimal, but, due to lack of GABA and Glycine inhibitory neurotransmitters, a small, normal amount of" normal" stress sends your chemistry racing headway into a brick wall. We'll work on this too shortly. But, it may not stop there, there may be a problem with dopamine, the pleasure pathway/reward neurotransmitter that has numerous functions in the body. There may be abnormalities with it in people with any form of mood disorders, such as depression or anxiety.

    We need control and predictability in our lives. When we play, we play in a benevolent environment or setting. We have said: "LOoook...we are willing to be stressed as long as it is in a safe context." For instance, just 3 to 5 minutes of a Ferris wheel ride; or, a rollercoaster jaunt. We are willing to accept this stress because we have it under control. We want the stress to generate glucocorticoids to give us an epinephrine high—actually it's a dopamine high, when it stimulates (1) not too long, and (2) is experienced in a safe context. Anything else is out.

    Well...here's the rub: As long as we have Control & Predictability!, we want to play or become the Reality Show. We will be the reality for the "glucocorticoid high' provided it does not get out of control.

    However, we have become conditioned to this, and thus, the fake reality show must be reinforced, as a cocaine addict must take more and more of the stuff to get the same high. We will be the reality when we shout, 'Play time Up!' But it does not end. "Hey, where's the end button? I didn't bargain for this. I have no control nor predictability over reality of my life."

    "I want off . . . I want out!" This is too stressful. But, we just can't get off the Ferris wheel or roller coaster in mid–ride. We have forgotten how to play...or what play is.

    It is going to be a wild ride from now on! Some of the modalities we show you, and have given, may just help...there are no guarantees!

    What is good stress? It is the right kind of stimulation. It is the efficient management of an allostatic response (a response that differs from the normal or usual). The body chemistry is up and running good, such that the response to a stressor that is rather ongoing for a while, the normal response is not enough. Therefore, a slightly different response is plied against the threat and coupled with the normal response, is the efficient management to that stress.

    'Bad Stress' or being 'stressed–out', consists of inefficient or persistent operation of normally adaptive adaptive responses built into the body. One may help in this situation by knowing some of the protocols the body uses in coping with stress. We give a list of certain modalities to consider before the "stress noose" tightens on one.

    Early life events that are stressful, those that involve abuse or neglect, can have a effect upon one for the rest of their lives. The effect is a life–long stress response. Review about Stress–Response Here.

    Basic Neurochemistry: Molecular, Cellular, and Medical Aspects, Seventh Edition, page 857, writes:

Overactivity of the stress hormone axis has been linked to prenatal stress or poor maternal care in rodent models, and this overactivity contributes to increased rates of brain and body aging.

There are gradients of health status across income and education (referred to as 'socioeconomic status' or 'SES') that are not explained by access to health care or other simple explanations. Therefore, it may be of great relevance in the future to understand the role of such factors as a sense of control, helplessness, persistent fear and anxiety, diet, exercise, and the impact of the living and social (e.g. family and work) environments in regulating the allostatic systems; these factors could cause allostatic systems to operate inefficiently and lead to an acceleration of genetic predispositions towards disease.

    As you see, stress is not altogether bad, and some stress is very necessary. Good stress is necessary for stimulation. And without stimulation, the brain deteriorates, the body wastes. You do not want a stress–free life. You want enough controlled stress so you can grow and function correctly.

    Notice in child development and gerontological studies, it is advocated that one have stimulation. And just the right amount of stress does this. Like exercise, it stimulates growth and rids the body of waste products and the 'drosses.' Too much, however, causes glucocorticoids to rise and break down the body, as in stress–generated Rhabdomyolysis, which is the breakdown of muscle fibers resulting in the release of muscle fiber contents (myoglobin) into the bloodstream.

    Under this kind of stress, we secrete the stress hormones as well as more dopamine.

    There are, as mentioned above, 'adrenaline junkies, or more aptly called 'dopamine' junkies. They need this high to get going. The problem here is that they need more and more of their 'fix' in order to keep producing. Why? Because the more fix they get, the more down–regulation they have of their properly involved neurotransmitter receptor sites. Down–regulation is the decrease in number of these very important molecular structures.

    Eventually, these people may run, and often do, up against a brick wall, needing medical help. But, remember, there are oceans of people out there on medications that can't seem to be helped.

    This immediately brings up the idea of stress and addiction. Take cocaine, for instance. It releases dopamine from its nerve endings and one can immediately see why cocaine is so addictive. It has down–regulated the receptors and hence, one needs more regularly because what was good yesterday, will not do the job today; therefore, more is needed to get the same 'buzz' or 'high' feeling that everything is okay. You can see what happens when no more receptors are available to push more dopamine out from. The few remaining revolt and you get, via down–regulation, less and less, so you go for more and more, and thus, an overdose occurs; often resulting in death.

    You saw what happens with alcohol addiction. The patient is often depressed and does not even know it! So he drinks. Eventually it gets to him. The same sub–routine that occurs with cocaine, alcohol, needing stress to produce, occurs with amphetamines. Down–regulation occurs! This sets one up for more and more of the dopamine–related drugs . . . always to no good end! Understand down–regulation now.

    Keep the following in mind When The Hell Breaks in full. By the time you read this, most of you will be experiencing some sort of hell that will only worsen. When 'friend or foe' or you, have 'taken the cure', know well that you are not cured! You may relapse if or when you are placed back in the place or situation where you think you have to take drink or drugs; you go back to your men's club and sink down into a soft leather chair, before you know it, you have had too many drinks—the demon got you back because no one warned you about place and continuing addiction. Wherever you are, and it is your place of 'bucking' up, the demon in you will pull you back down to the depths of hell once more.

    Remember your frontal cortex, where you do the thinking that involves judgement, impulse control, and making executive decisions (behaviors). If you have an addictive personality and secrete more stress hormones (glucocorticoids) than other personalities, after a stressor has ceased, you will tend to still be secreting highly. Now, a problem comes up and revolves around the pleasure or reward pathway of dopamine. Your brain starts generating an 'anticipation of reward' in subliminal language. This language is brought before the supreme judge, the frontal cortex. This area has to do the hard thing! Say no! And no again...and again....

    You must be very careful around holidays and situations that generate a lot of stress, such as with what is coming our way. You can become very, very sad and melancholic, or extremely anxious to the point of aggressiveness. Follow the modalities given in this particular document and others for such a condition, if it should strike you. You need to tell somebody about your situation. You can become so helpless, you cannot even take the modalities given to help yourself. Somebody will have to help you with it. You could become so violent, no one could get near you to give you what you need. Mention all this to your trusted person before this happens, so when they see it coming on, they can start plying you with the modalities given. But if you are already on it, you may just breeze through the situation, with no more than a little bump in the road.

    We recommend one consider DopaTech–HGH. This helps form dopamine after several enzymatic steps in the brain. It just may help one keep from relapsing. We further suggest the herb, Valerian Root, as this is akin to Benzodiazepine!

    The problem is: Most people do not take enough of the natural remedies to create a pharmocodynamic (drug–like) effect in the body. We know one old lady who says, "I never take more than one of anything." You nurses out there know the kind. You see this attitude often.

    In the next issue, Depression: Part V, we will give more modalities to consider. But for now, study the following, if you have any one of these addictions, consider what you have just read, in the light of the other documents in this series:

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Alcohol

Alcohol passes directly from the digestive tract into the blood vessels. In minutes, the blood transports the alcohol to all parts of the body, including the brain.

Alcohol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate.

Click on the labels in the diagram to the right to see an animation about how alcohol affects a GABA synapse. GABA’s effect is to reduce neural activity by allowing chloride ions to enter the post-synaptic neuron. These ions have a negative electrical charge, which helps to make the neuron less excitable. This physiological effect is amplified when alcohol binds to the GABA receptor, probably because it enables the ion channel to stay open longer and thus let more Cl- ions into the cell.

The neuron’s activity would thus be further diminished, thus explaining the sedative effect of alcohol. This effect is accentuated because alcohol also reduces glutamate’s excitatory effect on NMDA receptors.

However, chronic consumption of alcohol gradually makes the NMDA receptors hypersensitive to glutamate while desensitizing the GABAergic receptors. It is this sort of adaptation that would cause the state of excitation characteristic of alcohol withdrawal.

Alcohol also helps to increase the release of dopamine, by a process that is still poorly understood but that appears to involve curtailing the activity of the enzyme that breaks dopamine down. — Alcohol

    If one suffers with alcoholism, especially the hangover stage and the depression that often follows, it has been recommended that one take DMAE. DMAE shortens the hangover stage and depression. However, if one suffers from Bipolar disorder, it is not recommended.

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Opiates (heroin, morphine, etc.)

The human body naturally produces its own opiate-like substances and uses them as neurotransmitters. These substances include endorphins, enkephalins, and dynorphin, often collectively known as endogenous opioids. Endogenous opioids modulate our reactions to painful stimuli. They also regulate vital functions such as hunger and thirst and are involved in mood control, immune response, and other processes.

The reason that opiates such as heroin and morphine affect us so powerfully is that these exogenous substances bind to the same receptors as our endogenous opioids. There are three kinds of receptors widely distributed throughout the brain: mu, delta, and kappa receptors.

These receptors, through second messengers, influence the likelihood that ion channels will open, which in certain cases reduces the excitability of neurons. This reduced excitability is the likely source of the euphoric effect of opiates and appears to be mediated by the mu and delta receptors.

This euphoric effect also appears to involve another mechanism in which the GABA-inhibitory interneurons of the ventral tegmental area come into play. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released (see animation). Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt.

Chronic consumption of opiates inhibits the production of cAMP, but this inhibition is offset in the long run by other cAMP production mechanisms. When no opiates are available, this increased cAMP production capacity comes to the fore and results in neural hyperactivity and the sensation of craving the drug. — Opiates (heroin, morphine, etc.)

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Cocaine

Cocaine acts by blocking the reuptake of certain neurotransmitters such as dopamine, norepinephrine, and serotonin. By binding to the transporters that normally remove the excess of these neurotransmitters from the synaptic gap, cocaine prevents them from being reabsorbed by the neurons that released them and thus increases their concentration in the synapses (see animation). As a result, the natural effect of dopamine on the post-synaptic neurons is amplified. The group of neurons thus modified produces much more dependency (from dopamine), feelings of confidence (from serotonin), and energy (from norepinephrine) typically experienced by people who take cocaine.

In addition, because the norepinephrine neurons in the locus coeruleus project their axons into all the main structures of the forebrain, the powerful overall effect of cocaine can be readily understood.

In chronic cocaine consumers, the brain comes to rely on this exogenous drug to maintain the high degree of pleasure associated with the artificially elevated levels of some neurotransmitters in its reward circuits. The postsynaptic membrane can even adapt so much to these high dopamine levels that it actually manufactures new receptors. The resulting increased sensitivity produces depression and cravings if cocaine consumption ceases and dopamine levels return to normal.

Dependency on cocaine is thus closely related to its effect on the neurons of the reward circuit. Cocaine

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Nicotine in Tobacco

Nicotine imitates the action of a natural neurotransmitter called acetylcholine and binds to a particular type of acetylcholine receptor, known as the nicotinic receptor.

Whether it is acetylcholine or nicotine that binds to this receptor, it responds in the same way: it changes its conformation, which causes its associated ion channel to open for a few milliseconds. This channel then allows sodium ions to enter the neuron, depolarizing the membrane and exciting the cell. Then the channel closes again, and the nicotinic receptor becomes temporarily unresponsive to any neurotransmitters. It is this state of desensitization that is artificially prolonged by continual exposure to nicotine.

Tobacco dependency, which then develops very quickly, arises because nicotinic receptors are present on the neurons of the ventral tegmental area which project their terminations into the nucleus accumbens. In smokers, repeated nicotine stimulation thus increases the amount of dopamine released in the nucleus accumbens. Between cigarettes, however, chronic smokers maintain a high enough concentration of nicotine to deactivate the receptors and slow down their recovery. This is why smokers develop a tolerance to nicotine and experience reduced pleasure from it.

After a brief period without smoking (a night’s sleep, for example), the baseline concentration of nicotine drops again, and some of the receptors regain their sensitivity. When all these receptors become functional again, cholinergic neurotransmission is raised to an abnormally high level that affects all the cholinergic pathways in the brain. Smokers then experience the agitation and discomfort that leads them to smoke another cigarette.

Another substance in tobacco smoke, not yet clearly identified, inhibits monoamine oxydase B (MAO B), an enzyme that breaks down dopamine after its reuptake. The result is a higher concentration of dopamine in the reward circuit, which also contributes to the smoker’s dependency. Nicotine

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Caffeine

The stimulant effect of coffee comes largely from the way it acts on the adenosine receptors in the neural membrane. Adenosine is a central nervous system neuromodulator that has specific receptors. When adenosine binds to its receptors, neural activity slows down, and you feel sleepy. Adenosine thus facilitates sleep and dilates the blood vessels, probably to ensure good oxygenation during sleep.

Caffeine acts as an adenosine-receptor antagonist. This means that it binds to these same receptors, but without reducing neural activity. Fewer receptors are thus available to the natural “braking” action of adenosine, and neural activity therefore speeds up (see animation).

The activation of numerous neural circuits by caffeine also causes the pituitary gland to secrete hormones that in turn cause the adrenal glands to produce more adrenalin. Adrenalin is the “fight or flight” hormone, so it increases your attention level and gives your entire system an extra burst of energy. This is exactly the effect that many coffee drinkers are looking for.

In general, you get some stimulating effect from every cup of coffee you drink, and any tolerance you build up is minimal. On the other hand, caffeine can create a physical dependency. The symptoms of withdrawal from caffeine begin within one or two days after you stop consuming it. They consist mainly of headaches, nausea and sleepiness and affect about one out of every two individuals.

Lastly, like most drugs, caffeine increases the production of dopamine in the brain’s pleasure circuits, thus helping to maintain the dependency on this drug, which is consumed daily by 90% of all adults in the U.S. Caffeine

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Amphetamines

Amphetamines are drugs used to combat fatigue. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. As the animation to the right shows, once inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse.

Amphetamines also seem to act by several other mechanisms. For example, they seem to reduce the reuptake of dopamine and, in high concentrations, to inhibit monoamine oxydase A (MAO-A).

Amphetamines may also excite dopaminergic neurons via glutamate neurons. Amphetamines would thus remove an inhibiting effect due to metabotropic glutamate receptors. By thus releasing this natural brake, amphetamines would make the dopaminergic neurons more readily excitable. Amphetamines

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Cannabis

The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body’s natural morphines.

Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.

THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain’s neural networks is thus reduced as well.

However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.

In chronic consumers of cannabis, the loss of CB1 receptors in the brain’s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability. Cannabis

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Ecstasy

Ecstasy (MDMA) is a synthetic drug. It acts simultaneously as a stimulant and a hallucinogen because of its molecular structure, which is similar to that of both amphetamines and LSD. Like amphetamines and cocaine, ecstasy blocks the reuptake pumps for certain neurotransmitters, thus increasing their levels in the synaptic gap and their effect on the post-synaptic neurons’ receptors.

While ecstasy also potentiates the effects of norepinephrine and dopamine, it is distinguished from other psychostimulants by its strong affinity for serotonin transporters. The initial effect of ecstasy is thus an increased release of serotonin by the serotonergic neurons. The individual may then experience increased energy, euphoria, and the suppression of certain inhibitions in relating to other people.

A few hours later, there is a decrease in serotonin levels, amplified by the reduced activity of tryptophane hydroxylase, the enzyme responsible for synthesizing serotonin. This decrease can last much longer than the initial increase. Once again, an artificial increase in the level of a neurotransmitter exercises negative feedback on the enzyme that manufactures it. As a result, when intake of the drug ceases, the excess turns into a shortage.

Like all psychoactive drugs that produce a sensation of pleasure, ecstasy also increases the release of dopamine into the reward circuit. In addition, the extra serotonin produced by ecstasy leads indirectly to excitement of the dopaminergic neurons by the serotonergic neurons that connect to them.

The toxicity of ecstasy for humans has not been clearly established, but animal studies have shown that chronic high doses of MDMA lead to selective destruction of the terminal buttons of the serotonergic neurons. Ecstasy

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Benzodiazepines

Benzodiazepines, such as diazepam (Valium) and clonazepam (Rivotril) are anxiolytics that can also have hypnotic or amnesia-inducing effects. Like alcohol, these drugs increase the efficiency of synaptic transmission of the neurotransmitter GABA by acting on its receptors.

A GABA receptor is actually a macromolecular complex that, in addition to containing sites for binding GABA, also contains sites for binding other molecules such as benzodiazepines that modulate GABA’s activity.

When benzodiazepines bind to a specific site on a GABA receptor, they do not stimulate it directly. Instead, they make it more efficient by increasing the frequency with which the chlorine channel opens when GABA binds to its own site on this receptor (see animation). The resulting increase in the concentration of Cl- ions in the post-synaptic neuron immediately hyperpolarizes this neuron, thus making it less excitable.

Barbiturates bind to another site on the GABA receptor, with similar effects. But the advantage of benzodiazepines is that, unlike barbiturates, they do not open the Cl- channels directly, but instead act more subtly by potentiating the effect of GABA. Mixing benzodiazepines with alcohol is still very dangerous, however, because their respective effects on the Cl- channels can be additive.

We now know that benzodiazepines can cause a drug dependency even in what are considered therapeutic doses, and even in a short course of treatment. Benzodiazepines

    Below are two charts, which show you why some of the above recommendations are given. For tryptophan to go to melatonin, you need TMG (tri–methyl glycine); or SAMe, or eat plenty of red beets until you have continuously red stool.

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To form dopamine, we suggest in addition to DopaTech–HGH, take L–phenylalanine, L–Tyrosine, P–5'–P (pyridoxal five prime phosphate), copper supplement three two to three times per week, Vitamin C, 500 to 2,000 mg per day and S–Adenosylomethionine (SAMe).

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    We suggest one review the highlights of modalities suggested. We now offer more.

    For anxiety, it just may be that God's simplest measures may do the thing for one and make him feel whole again. Read the following from Basic Neurochemistry, page 905:

Inositol, the building block of the phosphoinisitide intracellular signaling pathway, has been examined as a potential anxiolytic. In clinical trials, inositol has reported to be effective in both panic disorder and depression, and animal data are also favorable. Because of inositol's status as a dietary supplement, there is little financial backing for studies of its ifficacy and safety. The mechanism of action of inositol is not entirely clear, but it is believed to facilitate phosphoinositide–signaling–coupled neurotransmission.

    Therefore, we have had good success in patients that were refractory from their medical teams. We recommend high doses of inositol, GABA, Glycine, Taurine, MCTs (medium–chain triglycerides)—as you will learn in the following issue, much mood disorder appears now to involve energy metabolism in the brain. As we said in the first issue of this series, it is now appearing more and more that glucose is not being used, or being used effectively, in the brain, leading to mood disorders and memory dysfunction, including that found in Alzheimer's disease.

    We suggest also one take valerian root—it stinks like hell, you know it must work! Remember, it is akin to benzodiazepine. We have had great success when patients follow directions. Basic Neurochemistry says, "Traditionally, the neurochemical systems targeted in the treatment of anxiety disorders have been GABA, serotonin, and norepinephrine." This is another reason why we recommended L–phenylalanine and L–tyrosine, along with Copper and Vitamin C, after the dopamine has been formed in the brain, to then form norepinephrine. Give Mother Nature a chance, if nothing else has worked!

    We highly recommend, as before, get off the damned PUFAs! You get enough of that by incident. Those are your unsaturated fatty acids and are extremely toxic to enzyme systems in the body.

    Get these suggested natural remedies at your local natural foods store. Be aware that the cheapest price does not necessarily equate to the best supplement for your money. All too often, there is a reason why one brand is cheap. It may have "China" written all over it!

... To Be Continued ...

Sources

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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.

In An UpComing Issue:
Depression: Part V—What You Can Do About It When No Doctor Is About!

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