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Neuron - Wikipedia, the free encyclopedia
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Neuron

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This article is about cells in the nervous system. For other uses, see Neuron (disambiguation).

“Brain cell” redirects here. For other uses, see Glial cell.

Neuron: neuron (Nerve Cell)
Drawing by Santiago Ramón y Cajal of neurons in the pigeon cerebellum. (A) Denotes Purkinje cells, an example of a multipolar neuron. (B) Denotes granule cells which are also multipolar.
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A neuron (pronounced /ˈnjʊərɒn/ N(Y)OOR-on, also known as a neurone or nerve cell) is an electrically excitable cell that processes and transmits information by electrical and chemical signaling. Chemical signaling occurs via synapses, specialized connections with other cells. Neurons connect to each other to form networks. Neurons are the core components of the nervous system, which includes the brain, spinal cord, and peripheral ganglia. A number of specialized types of neurons exist: sensory neurons respond to touch, sound, light and numerous other stimuli affecting cells of the sensory organs that then send signals to the spinal cord and brain. Motor neurons receive signals from the brain and spinal cord and cause muscle contractions and affect glands. Interneurons connect neurons to other neurons within the same region of the brain or spinal cord.

A typical neuron possesses a cell body (often called the soma), dendrites, and an axon. Dendrites are filaments that arise from the cell body, often extending for hundreds of microns and branching multiple times, giving rise to a complex "dendritic tree". An axon is a special cellular filament that arises from the cell body at a site called the axon hillock and travels for a distance, as far as 1 m in humans or even more in other species. The cell body of a neuron frequently gives rise to multiple dendrites, but never to more than one axon, although the axon may branch hundreds of times before it terminates. At the majority of synapses, signals are sent from the axon of one neuron to a dendrite of another. There are, however, many exceptions to these rules: neurons that lack dendrites, neurons that have no axon, synapses that connect an axon to another axon or a dendrite to another dendrite, etc.

All neurons are electrically excitable, maintaining voltage gradients across their membranes by means of metabolically driven ion pumps, which combine with ion channels embedded in the membrane to generate intracellular-versus-extracellular concentration differences of ions such as sodium, potassium, chloride, and calcium. Changes in the cross-membrane voltage can alter the function of voltage-dependent ion channels. If the voltage changes by a large enough amount, an all-or-none electrochemical pulse called an action potential is generated, which travels rapidly along the cell's axon, and activates synaptic connections with other cells when it arrives.

Neurons of the adult brain do not generally undergo cell division, and usually cannot be replaced after being lost, although there are a few known exceptions. In most cases they are generated by special types of stem cells, although astrocytes (a type of glial cell) have been observed to turn into neurons as they are sometimes pluripotent.

[edit] Overview

**Structure of a typical neuron**
Neuron
Dendrite Soma Axon Nucleus Node of Ranvier Axon terminal Schwann cell Myelin sheath

A neuron is a special type of cell that is found in the bodies of most animals (all members of the group Eumetazoa, to be precise—this excludes only sponges and a few other very simple animals). The features that define a neuron are electrical excitability and the presence of synapses, which are complex membrane junctions used to transmit signals to other cells. The body's neurons, plus the glial cells that give them structural and metabolic support, together constitute the nervous system. In vertebrates, the majority of neurons belong to the central nervous system, but some reside in peripheral ganglia, and many sensory neurons are situated in sensory organs such as the retina and cochlea.

Although neurons are very diverse and there are exceptions to nearly every rule, it is convenient to begin with a schematic description of the structure and function of a "typical" neuron. A typical neuron is divided into three parts: the soma or cell body, dendrites, and axon. The soma is usually compact; the axon and dendrites are filaments that extrude from it. Dendrites typically branch profusely, getting thinner with each branching, and extending their farthest branches a few hundred microns from the soma. The axon leaves the soma at a swelling called the axon hillock, and can extend for great distances, giving rise to hundreds of branches. Unlike dendrites, an axon usually maintains the same diameter as it extends. The soma may give rise to numerous dendrites, but never to more than one axon. Synaptic signals from other neurons are received by the soma and dendrites; signals to other neurons are transmitted by the axon. A typical synapse, then, is a contact between the axon of one neuron and a dendrite or soma of another. Synaptic signals may be excitatory or inhibitory. If the net excitation received by a neuron over a short period of time is large enough, the neuron generates a brief pulse called an action potential, which originates at the soma and propagates rapidly along the axon, activating synapses onto other neurons as it goes.

Many neurons fit the foregoing schema in every respect, but there are also exceptions to most parts of it. There are no neurons that lack a soma, but there are neurons that lack dendrites, and others that lack an axon. Furthermore, in addition to the typical axodendritic and axosomatic synapses, there are axoaxonic (axon-to-axon) and dendrodendritic (dendrite-to-dendrite) synapses.

The key to neural function is the synaptic signalling process, which is partly electrical and partly chemical. The electrical aspect depends on properties of the neuron's membrane. Like all animal cells, every neuron is surrounded by a plasma membrane, a bilayer of lipid molecules with many types of protein structures embedded in it. A lipid bilayer is a powerful electrical insulator, but in neurons, many of the protein structures embedded in the membrane are electrically active. These include ion channels that permit electrically charged ions to flow across the membrane, and ion pumps that actively transport ions from one side of the membrane to the other. Most ion channels are permeable only to specific types of ions. Some ion channels are voltage gated, meaning that they can be switched between open and closed states by altering the voltage difference across the membrane. Others are chemically gated, meaning that they can be switched between open and closed states by interactions with chemicals that diffuse through the extracellular fluid. The interactions between ion channels and ion pumps produce a voltage difference across the membrane, typically a bit less than 1/10 of a volt at baseline. This voltage has two functions: first, it provides a power source for an assortment of voltage-dependent protein machinery that is embedded in the membrane; second, it provides a basis for electrical signal transmission between different parts of the membrane.

Neurons communicate by chemical and electrical synapses in a process known as synaptic transmission. The fundamental process that triggers synaptic transmission is the action potential, a propagating electrical signal that is generated by exploiting the electrically excitable membrane of the neuron. This is also known as a wave of depolarization.

[edit] Anatomy and histology

Diagram of a typical myelinated vertebrate motoneuron.

Neurons are highly specialized for the processing and transmission of cellular signals. Given the diversity of functions performed by neurons in different parts of the nervous system, there is, as expected, a wide variety in the shape, size, and electrochemical properties of neurons. For instance, the soma of a neuron can vary from 4 to 100 micrometers in diameter.^[1]

The soma is the central part of the neuron. It contains the nucleus of the cell, and therefore is where most protein synthesis^[2] occurs. The nucleus ranges from 3 to 18 micrometers in diameter.

The dendrites of a neuron are cellular extensions with many branches, and metaphorically this overall shape and structure is referred to as a dendritic tree. This is where the majority of input to the neuron occurs.

The axon is a finer, cable-like projection which can extend tens, hundreds, or even tens of thousands of times the diameter of the soma in length. The axon carries nerve signals away from the soma (and also carries some types of information back to it). Many neurons have only one axon, but this axon may—and usually will—undergo extensive branching, enabling communication with many target cells. The part of the axon where it emerges from the soma is called the axon hillock. Besides being an anatomical structure, the axon hillock is also the part of the neuron that has the greatest density of voltage-dependent sodium channels. This makes it the most easily-excited part of the neuron and the spike initiation zone for the axon: in neurological terms it has the most negative action potential threshold. While the axon and axon hillock are generally involved in information outflow, this region can also receive input from other neurons.

The axon terminal contains synapses, specialized structures where neurotransmitter chemicals are released in order to communicate with target neurons.

Although the canonical view of the neuron attributes dedicated functions to its various anatomical components, dendrites and axons often act in ways contrary to their so-called main function.
Axons and dendrites in the central nervous system are typically only about one micrometer thick, while some in the peripheral nervous system are much thicker. The soma is usually about 10–25 micrometers in diameter and often is not much larger than the cell nucleus it contains. The longest axon of a human motoneuron can be over a meter long, reaching from the base of the spine to the toes. Sensory neurons have axons that run from the toes to the dorsal columns, over 1.5 meters in adults. Giraffes have single axons several meters in length running along the entire length of their necks. Much of what is known about axonal function comes from studying the squid giant axon, an ideal experimental preparation because of its relatively immense size (0.5–1 millimeters thick, several centimeters long).
Fully differentiated neurons are permanently amitotic;^[3] however, recent research shows that additional neurons throughout the brain can originate from neural stem cells found throughout the brain but in particularly high concentrations in the subventricular zone subgranular zone through the process of neurogenesis.^[4] and

[edit] Histology and internal structure

Golgi-stained neurons in human hippocampal tissue.

Nerve cell bodies stained with basophilic dyes show numerous microscopic clumps of Nissl substance (named after German psychiatrist and neuropathologist Franz Nissl, 1860–1919), which consists of rough endoplasmic reticulum and associated ribosomal RNA. The prominence of the Nissl substance can be explained by the fact that nerve cells are metabolically very active, and hence are involved in large amounts of protein synthesis.
The cell body of a neuron is supported by a complex meshwork of structural proteins called neurofilaments, which are assembled into larger neurofibrils. Some neurons also contain pigment granules, such as neuromelanin (a brownish-black pigment, byproduct of synthesis of catecholamines) and lipofuscin (yellowish-brown pigment that accumulates with age).
There are different internal structural characteristics between axons and dendrites. Typical axons almost never contain ribosomes, except some in the initial segment. Dendrites contain granular endoplasmic reticulum or ribosomes, with diminishing amounts with distance from the cell body.

[edit] Classes

Image of pyramidal neurons in mouse cerebral cortex expressing green fluorescent protein. The red staining indicates GABAergic interneurons. Source PLoS Biology [1]

SMI32-stained pyramidal neurons in cerebral cortex.

Neurons exist in a number of different shapes and sizes and can be classified by their morphology and function. The anatomist Camillo Golgi grouped neurons into two types; type I with long axons used to move signals over long distances and type II with short axons, which can often be confused with dendrites. Type I cells can be further divided by where the cell body or soma is located. The basic morphology of type I neurons, represented by spinal motor neurons, consists of a cell body called the soma and a long thin axon which is covered by the myelin sheath. Around the cell body is a branching dendritic tree that receives signals from other neurons. The end of the axon has branching terminals (axon terminal) that release neurotransmitters into a gap called the synaptic cleft between the terminals and the dendrites of the next neuron.

[edit] Structural classification

[edit] Polarity

Most neurons can be anatomically characterized as:

Unipolar or pseudounipolar: dendrite and axon emerging from same process.
Bipolar: axon and single dendrite on opposite ends of the soma.
Multipolar: more than two dendrites:
- Golgi I: neurons with long-projecting axonal processes; examples are pyramidal cells, Purkinje cells, and anterior horn cells.
- Golgi II: neurons whose axonal process projects locally; the best example is the granule cell.

[edit] Other

Furthermore, some unique neuronal types can be identified according to their location in the nervous system and distinct shape. Some examples are:

Basket cells, interneurons that form a dense plexus of terminals around the soma of target cells, found in the cortex and cerebellum.
Betz cells, large motor neurons.
Medium spiny neurons, most neurons in the corpus striatum.
Purkinje cells, huge neurons in the cerebellum, a type of Golgi I multipolar neuron.
Pyramidal cells, neurons with triangular soma, a type of Golgi I.
Renshaw cells, neurons with both ends linked to alpha motor neurons.
Granule cells, a type of Golgi II neuron.
anterior horn cells, motoneurons located in the spinal cord.

[edit] Functional classification

[edit] Direction

Afferent neurons convey information from tissues and organs into the central nervous system and are sometimes also called sensory neurons.
Efferent neurons transmit signals from the central nervous system to the effector cells and are sometimes called motor neurons.
Interneurons connect neurons within specific regions of the central nervous system.

Afferent and efferent can also refer generally to neurons which, respectively, bring information to or send information from the brain region.

[edit] Action on other neurons

A neuron affects other neurons by releasing a neurotransmitter that binds to chemical receptors. The effect upon the target neuron is determined not by the source neuron or by the neurotransmitter, but by the type of receptor that is activated. A neurotransmitter can be thought of as a key, and a receptor as a lock: the same type of key can here be used to open many different types of locks. Receptors can be classified broadly as excitatory (causing an increase in firing rate), inhibitory (causing a decrease in firing rate), or modulatory (causing long-lasting effects not directly related to firing rate).

In fact, however, the two most common neurotransmitters in the brain, glutamate and GABA, have actions that are largely consistent. Glutamate acts on several different types of receptors, but most of them have effects that are excitatory. Similarly GABA acts on several different types of receptors, but all of them have effects (in adult animals, at least) that are inhibitory. Because of this consistency, it is common for neuroscientists to simplify the terminology by referring to cells that release glutamate as "excitatory neurons," and cells that release GABA as "inhibitory neurons." Since well over 90% of the neurons in the brain release either glutamate or GABA, these labels encompass the great majority of neurons. There are also other types of neurons that have consistent effects on their targets, for example "excitatory" motor neurons in the spinal cord that release acetylcholine, and "inhibitory" spinal neurons that release glycine.

The distinction between excitatory and inhibitory neurotransmitters is not absolute, however. Rather, it depends on the class of chemical receptors present on the target neuron. In principle, a single neuron, releasing a single neurotransmitter, can have excitatory effects on some targets, inhibitory effects on others, and modulatory effects on others still. For example, photoreceptors in the retina constantly release the neurotransmitter glutamate in the absence of light. So-called OFF bipolar cells are, like most neurons, excited by the released glutamate. However, neighboring target neurons called ON bipolar cells are instead inhibited by glutamate, because they lack the typical ionotropic glutamate receptors and instead express a class of inhibitory metabotropic glutamate receptors.^[5] When light is present, the photoreceptors cease releasing glutamate, which relieves the ON bipolar cells from inhibition, activating them; this simultaneously removes the excitation from the OFF bipolar cells, silencing them.

[edit] Discharge patterns

Neurons can be classified according to their electrophysiological characteristics:

Tonic or regular spiking. Some neurons are typically constantly (or tonically) active. Example: interneurons in neurostriatum.
Phasic or bursting. Neurons that fire in bursts are called phasic.
Fast spiking. Some neurons are notable for their fast firing rates, for example some types of cortical inhibitory interneurons, cells in globus pallidus, retinal ganglion cells.^[6]^[7]

[edit] Classification by neurotransmitter production

This section requires expansion.

Neurons differ in the type of neurotransmitter they manufacture. Some examples are

cholinergic neurons - acetylcholine

Acetylcholine is released from presynaptic neurons into the synaptic cleft. It acts as a ligand for both ligand-gated ion channels and metabotropic (GPCRs) muscarinic receptors. Nicotinic receptors, are pentameric ligand-gated ion channels comprised of alpha and beta subunits that bind nicotine. Ligand binding opens the channel causing influx of Na⁺ depolarization and increases the probability of presynaptic neurotransmitter release.

GABAergic neurons - gamma aminobutyric acid

GABA is one of two neuroinhibitors in the CNS, the other being Glycine. GABA has a homologous function to ACh, gating anion channels that allow Cl- ions to enter the post synaptic neuron. Cl- causes hyperpolarization within the neuron, decreasing the probability of an action potential firing as the voltage becomes more negative (recall that for an action potential to fire, a positive voltage threshold must be reached).

glutamatergic neurons - glutamate

Glutamate is one of two primary excitatory amino acids, the other being Aspartate. Glutamate receptors are one of four categories, three of which are ligand-gated ion channels and one of which is a G-protein coupled receptor (often referred to as GPCR). 1 - AMPA and Kainate receptors both function as cation channels permeable to Na⁺ cation channels mediating fast excitatory synaptic transmission 2 - NMDA receptors are another cation channel that is more permeable to Ca²⁺. The function of NMDA receptors is dependant on Glycine receptor binding as a co-agonist within the channel pore. NMDA receptors will not function without both ligands present. 3 - Metabotropic receptors, GPCRs modulate synaptic transmission and postsynaptic excitability. Glutamate can cause excitotoxicity when blood flow to the brain is interrupted, resulting in brain damage. When blood flow is suppressed, glutamate is released from presynaptic neurons causing NMDA and AMPA receptor activation moreso than would normally be the case outside of stress conditions, leading to elevated Ca²⁺ and Na⁺ entering the post synaptic neuron and cell damage.

dopaminergic neurons - dopamine

Dopamine is a neurotransmitter that acts on D1 type (D1 and D5) Gs coupled receptors which increase cAMP and PKA or D2 type (D2,D3 and D4)receptors which activate Gi-coupled receptors that decrease cAMP and PKA. Dopamine is connected to mood and behavior, and modulates both pre and post synaptic neurotransmission. Loss of dopamine neurons in the substantia nigra has been linked to Parkinson's disease.

serotonergic neurons - serotonin

Serotonin,(5-Hydroxytryptamine, 5-HT), can act as excitatory or inhibitory. Of the four 5-HT receptor classes, 3 are GPCR and 1 is ligand gated cation channel. Serotonin is synthesized from tryptophan by tryptophan hydroxylase, and then further by aromatic acid decarboxylase. A lack of 5-HT at postsynaptic neurons has been linked to depression. Drugs that block the presynaptic serotonin transporter are used for treatment, such as Prozac and Zoloft.

[edit] Connectivity

Main article: Synapse

Neurons communicate with one another via synapses, where the axon terminal or en passant boutons (terminals located along the length of the axon) of one cell impinges upon another neuron's dendrite, soma or, less commonly, axon. Neurons such as Purkinje cells in the cerebellum can have over 1000 dendritic branches, making connections with tens of thousands of other cells; other neurons, such as the magnocellular neurons of the supraoptic nucleus, have only one or two dendrites, each of which receives thousands of synapses. Synapses can be excitatory or inhibitory and will either increase or decrease activity in the target neuron. Some neurons also communicate via electrical synapses, which are direct, electrically-conductive junctions between cells.

In a chemical synapse, the process of synaptic transmission is as follows: when an action potential reaches the axon terminal, it opens voltage-gated calcium channels, allowing calcium ions to enter the terminal. Calcium causes synaptic vesicles filled with neurotransmitter molecules to fuse with the membrane, releasing their contents into the synaptic cleft. The neurotransmitters diffuse across the synaptic cleft and activate receptors on the postsynaptic neuron.

The human brain has a huge number of synapses. Each of the 10¹¹ (one hundred billion) neurons has on average 7,000 synaptic connections to other neurons. It has been estimated that the brain of a three-year-old child has about 10¹⁵ synapses (1 quadrillion). This number declines with age, stabilizing by adulthood. Estimates vary for an adult, ranging from 10¹⁴ to 5 x 10¹⁴ synapses (100 to 500 trillion).^[8]

[edit] Mechanisms for propagating action potentials

A signal propagating down an axon to the cell body and dendrites of the next cell.

In 1937, John Zachary Young suggested that the squid giant axon could be used to study neuronal electrical properties.^[9] Being larger than but similar in nature to human neurons, squid cells were easier to study. By inserting electrodes into the giant squid axons, accurate measurements were made of the membrane potential.
The cell membrane of the axon and soma contain voltage-gated ion channels which allow the neuron to generate and propagate an electrical signal (an action potential). These signals are generated and propagated by charge-carrying ions including sodium (Na⁺), potassium (K⁺), chloride (Cl^-), and calcium (Ca²⁺).
There are several stimuli that can activate a neuron leading to electrical activity, including pressure, stretch, chemical transmitters, and changes of the electric potential across the cell membrane.^[10] Stimuli cause specific ion-channels within the cell membrane to open, leading to a flow of ions through the cell membrane, changing the membrane potential.
Thin neurons and axons require less metabolic expense to produce and carry action potentials, but thicker axons convey impulses more rapidly. To minimize metabolic expense while maintaining rapid conduction, many neurons have insulating sheaths of myelin glial cells: oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. The sheath enables action potentials to travel faster than in unmyelinated axons of the same diameter, whilst using less energy. The myelin sheath in peripheral nerves normally runs along the axon in sections about 1 mm long, punctuated by unsheathed nodes of Ranvier which contain a high density of voltage-gated ion channels. Multiple sclerosis is a neurological disorder that results from demyelination of axons in the central nervous system. around their axons. The sheaths are formed by

Some neurons do not generate action potentials, but instead generate a graded electrical signal, which in turn causes graded neurotransmitter release. Such nonspiking neurons tend to be sensory neurons or interneurons, because they cannot carry signals long distances.

[edit] Neural coding

Neural coding is concerned with how sensory and other information is represented in the brain by neurons. The main goal of studying neural coding is to characterize the relationship between the stimulus and the individual or ensemble neuronal responses, and the relationships amongst the electrical activities of the neurons within the ensemble.^[11] It is thought that neurons can encode both digital and analog information.^[12]

[edit] All-or-none principle

The conduction of nerve impulses is an example of an all-or-none response. In other words, if a neuron responds at all, then it must respond completely. The greater the intensity of stimulation does not produce a stronger signal but can produce more impulses per second. There are different types of receptor response to stimulus, slowly adapting or tonic receptors respond to steady stimulus and produce a steady rate of firing. These tonic receptors most often respond to increased intensity of stimulus by increasing their firing frequency, usually as a power function of stimulus plotted against impulses per second. This can be likened to an intrinsic property of light where to get greater intensity of a specific frequency (color) there have to be more photons, as the photons can't become "stronger" for a specific frequency.
There are a number of other receptor types that are called quickly-adapting or phasic receptors, where firing decreases or stops with steady stimulus; examples include: skin when touched by an object causes the neurons to fire, but if the object maintains even pressure against the skin, the neurons stop firing. The neurons of the skin and muscles that are responsive to pressure and vibration have filtering accessory structures that aid their function. The pacinian corpuscle is one such structure; it has concentric layers like an onion which form around the axon terminal. When pressure is applied and the corpuscle is deformed, mechanical stimulus is transferred to the axon, which fires. If the pressure is steady, there is no more stimulus; thus, typically these neurons respond with a transient depolarization during the initial deformation and again when the pressure is removed, which causes the corpuscle to change shape again. Other types of adaptation are important in extending the function of a number of other neurons.^[13]

[edit] History

The term neuron was coined by the German anatomist Heinrich Wilhelm Waldeyer. The neuron's place as the primary functional unit of the nervous system was first recognized in the early 20th century through the work of the Spanish anatomist Santiago Ramón y Cajal.^[14] Cajal proposed that neurons were discrete cells that communicated with each other via specialized junctions, or spaces, between cells.^[14] This became known as the neuron doctrine, one of the central tenets of modern neuroscience.^[14] To observe the structure of individual neurons, Cajal used a silver staining method developed by his rival, Camillo Golgi.^[14] The Golgi stain is an extremely useful method for neuroanatomical investigations because, for reasons unknown, it stains a very small percentage of cells in a tissue, so one is able to see the complete micro structure of individual neurons without much overlap from other cells in the densely packed brain.^[15]

[edit] The neuron doctrine

The neuron doctrine is the now fundamental idea that neurons are the basic structural and functional units of the nervous system. The theory was put forward by Santiago Ramón y Cajal in the late 19th century. It held that neurons are discrete cells (not connected in a meshwork), acting as metabolically distinct units.
Later discoveries yielded a few refinements to the simplest form of the doctrine. For example, glial cells, which are not considered neurons, play an essential role in information processing.^[16] Also, electrical synapses are more common than previously thought,^[17] meaning that there are direct, cytoplasmic connections between neurons. In fact, there are examples of neurons forming even tighter coupling: the squid giant axon arises from the fusion of multiple axons.^[18]
Cajal also postulated the Law of Dynamic Polarization, which states that a neuron receives signals at its dendrites and cell body and transmits them, as action potentials, along the axon in one direction: away from the cell body.^[19] The Law of Dynamic Polarization has important exceptions; dendrites can serve as synaptic output sites of neurons^[20] and axons can receive synaptic inputs.^{[citation needed]}

[edit] Neurons in the brain

The number of neurons in the brain varies dramatically from species to species.^[21] One estimate puts the human brain at about 100 billion ( $1011$ ) neurons and 100 trillion ( $1014$ ) synapses.^[21] Another estimate is 86 billion neurons of which 16.3 billion are in the cerebral cortex and 69 billion in the cerebellum.^[22] By contrast, the nematode worm Caenorhabditis elegans has just 302 neurons making it an ideal experimental subject as scientists have been able to map all of the organism's neurons. The fruit fly Drosophila melanogaster, a common subject in biology experiments, has around 100,000 neurons and exhibits many complex behaviors. Many properties of neurons, from the type of neurotransmitters used to ion channel composition, are maintained across species, allowing scientists to study processes occurring in more complex organisms in much simpler experimental systems.

[edit] Neurological disorders

Main article: Neurology

Charcot-Marie-Tooth disease (CMT), also known as Hereditary Motor and Sensory Neuropathy (HMSN), Hereditary Sensorimotor Neuropathy (HMSN), or Peroneal Muscular Atrophy, is a heterogeneous inherited disorder of nerves (neuropathy) that is characterized by loss of muscle tissue and touch sensation, predominantly in the feet and legs but also in the hands and arms in the advanced stages of disease. Presently incurable, this disease is one of the most common inherited neurological disorders, with 37 in 100,000 affected.
Alzheimer's disease (AD), also known simply as Alzheimer's, is a neurodegenerative disease characterized by progressive cognitive deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioral changes. The most striking early symptom is loss of short-term memory (amnesia), which usually manifests as minor forgetfulness that becomes steadily more pronounced with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), skilled movements (apraxia), recognition (agnosia), and functions such as decision-making and planning get impaired.
Parkinson's disease (also known as Parkinson disease or PD) is a degenerative disorder of the central nervous system that often impairs the sufferer's motor skills and speech. Parkinson's disease belongs to a group of conditions called movement disorders. It is characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia), and in extreme cases, a loss of physical movement (akinesia). The primary symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary symptoms may include high level cognitive dysfunction and subtle language problems. PD is both chronic and progressive.
Myasthenia Gravis is a neuromuscular disease leading to fluctuating muscle weakness and fatigability. Weakness is typically caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated with immunosuppressants, cholinesterase inhibitors and, in selected cases, thymectomy.

[edit] Demyelination

Demyelination is the act of demyelinating, or the loss of the myelin sheath insulating the nerves. When myelin degrades, conduction of signals along the nerve can be impaired or lost, and the nerve eventually withers. This leads to certain neurodegenerative disorders like multiple sclerosis, chronic inflammatory demyelinating polyneuropathy.

[edit] Axonal degeneration

Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute axonal degeneration (AAD), which is rapid separation of the proximal and distal ends within 30 minutes of injury. Degeneration follows with swelling of the axolemma, and eventually leads to bead like formation. Granular disintegration of the axonal cytoskeleton mitochondria in the paranodal regions at the site of injury. Endoplasmic reticulum degrades and mitochondria swell up and eventually disintegrate. The disintegration is dependent on Ubiquitin and Calpain proteases (caused by influx of calcium ion), suggesting that axonal degeneration is an active process. Thus the axon undergoes complete fragmentation. The process takes about roughly 24 hrs in the PNS, and longer in the CNS. The signaling pathways leading to axolemma degeneration are currently unknown. and inner organelles occurs after axolemma degradation. Early changes include accumulation of

[edit] Nerve regeneration

Main article: Nerve regeneration

It has been demonstrated that neurogenesis can sometimes occur in the adult vertebrate brain,^{[citation needed]} and it is often possible for peripheral axons to regrow if they are severed. The latter can take a long time: after a nerve injury to the human arm, for example, it may take months for feeling to return to the hands and fingers.^{[citation needed]}

[edit] References

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^ Spike arrival times: A highly efficient coding scheme for neural networks, SJ Thorpe - Parallel processing in neural systems, 1990
^ Eckert, Roger; Randall, David (1983). Animal physiology: mechanisms and adaptations. San Francisco: W.H. Freeman. pp. 239. ISBN 0-7167-1423-x.
^ ^a ^b ^c ^d López-Muñoz, F.; Boya, J., Alamo, C. (16 October 2006). "Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramón y Cajal". Brain Research Bulletin 70 (4-6): 391–405. doi:10.1016/j.brainresbull.2006.07.010. PMID 17027775. http://www.sciencedirect.com/science/article/B6SYT-4KMYRRC-1/2/b98a884961498c54452886842389ed72. Retrieved 2007-04-02.
^ Grant, Gunnar; Boya, J; Alamo, C (9 January 2007 (online)). "How the 1906 Nobel Prize in Physiology or Medicine was shared between Golgi and Cajal". Brain Research Reviews 55 (4-6): 490. doi:10.1016/j.brainresrev.2006.11.004. PMID 17027775. http://www.sciencedirect.com/science/article/B6SYS-4MSHXWR-1/2/51f3edfd18b81abbd0a9d56e98de6ceb. Retrieved 2007-04-02.
^ Witcher M, Kirov S, Harris K (2007). "Plasticity of perisynaptic astroglia during synaptogenesis in the mature rat hippocampus". Glia 55 (1): 13–23. doi:10.1002/glia.20415. PMID 17001633.
^ Connors B, Long M (2004). "Electrical synapses in the mammalian brain". Annu Rev Neurosci 27: 393–418. doi:10.1146/annurev.neuro.26.041002.131128. PMID 15217338.
^ R. W. Guillery, Observations of synaptic structures: origins of the neuron doctrine and its current status, Phil. Trans. R. Soc. B (2005) 360, 1281–1307 (p 1300).
^ Sabbatini R.M.E. April-July 2003. Neurons and Synapses: The History of Its Discovery. Brain & Mind Magazine, 17. Retrieved on March 19, 2007.
^ Djurisic M, Antic S, Chen W, Zecevic D (2004). "Voltage imaging from dendrites of mitral cells: EPSP attenuation and spike trigger zones". J Neurosci 24 (30): 6703–14. doi:10.1523/JNEUROSCI.0307-04.2004. PMID 15282273.
^ ^a ^b Williams RW, Herrup K (1988). "The control of neuron number". Annual Review of Neuroscience 11: 423–53. doi:10.1146/annurev.ne.11.030188.002231. PMID 3284447.
^ Azevedo FA, Carvalho LR, Grinberg LT, et al. (April 2009). "Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain". The Journal of Comparative Neurology 513 (5): 532–41. doi:10.1002/cne.21974. PMID 19226510.

[edit] Sources

Kandel E.R., Schwartz, J.H., Jessell, T.M. 2000. Principles of Neural Science, 4th ed., McGraw-Hill, New York.
Bullock, T.H., Bennett, M.V.L., Johnston, D., Josephson, R., Marder, E., Fields R.D. 2005. The Neuron Doctrine, Redux, Science, V.310, p. 791-793.
Ramón y Cajal, S. 1933 Histology, 10th ed., Wood, Baltimore.
Roberts A., Bush B.M.H. 1981. Neurones Without Impulses. Cambridge University Press, Cambridge.
Peters, A., Palay, S.L., Webster, H, D., 1991 The Fine Structure of the Nervous System, 3rd ed., Oxford, New York

[edit] External links

Wikimedia Commons has media related to: Neuron

IBRO (International Brain Research Organization). Fostering neuroscience research especially in less well-funded countries.
NeuronBank an online neuromics tool for cataloging neuronal types and synaptic connectivity.
High Resolution Neuroanatomical Images of Primate and Non-Primate Brains.
The Department of Neuroscience at Wikiversity, which presently offers two courses: Fundamentals of Neuroscience and Comparative Neuroscience.
NIF Search - Renshaw Cell via the Neuroscience Information Framework
Cell Centered Database - Neuron
NeuroMorpho.Org an online database of digital reconstructions of neuronal morphology.
Immunohistochemistry Image Gallery: Neuron

[hide]

Histology: nervous tissue (TA A14.2.00, GA 9.849)

Neurons

Parts	soma axon (axon hillock, axon terminals, axoplasm, axolemma, neurofibril/neurofilament) dendrite (Nissl body, dendritic spine, apical dendrite, basal dendrite)

Types	bipolar · pseudounipolar · multipolar · pyramidal · Purkinje · granule

Afferent nerve fiber/ Sensory nerve	GSA · GVA · SSA · SVA fibers (Ia, Ib or Golgi, II or Aβ, III or Aδ or fast pain, IV or C or slow pain)

Efferent nerve fiber/ Motor nerve	GSE · GVE · SVE Upper motor neuron · Lower motor neuron (α motorneuron, γ motorneuron)

Termination

Synapses	neuropil · synaptic vesicle Interneuron (Renshaw) · neuromuscular junction · electrical synapse

Sensory receptors	Meissner's corpuscle · Merkel nerve ending · Pacinian corpuscle · Ruffini ending · Muscle spindle · Free nerve ending · Olfactory receptor neuron · Photoreceptor cell · Hair cell · Taste bud

Support

Glial cells	Astrocyte (Radial glia) · Oligodendrocyte · Ependymal cells (Tanycytes) · Microglia

Myelination	CNS: Oligodendrocyte PNS: Schwann cell · Neurolemma · Nodes of Ranvier/Internode · Schmidt-Lanterman incisures

Related connective tissues	epineurium · perineurium · endoneurium · nerve fascicle · meninges

Other

Posterior (Root, Ganglion, Ramus) · Anterior (Root, Ramus) · rami communicantes (Gray, White) · Preganglionic fibers · Postganglionic fibers · Lemniscus · Funiculus · Fasciculus · Decussation · Commissure
Projection fibers · Association fiber · Commissural fiber

M: CNS

anat(s,m,p,4,e,b,d,c,a,f,l,g)/phys/devp/cell

noco(m,d,e,h,v,s)/cong/tumr,sysi/epon,injr

proc,drug(N1A/2AB/C/3/4/7A/B/C/D)

M: PNS

anat(h,r,t,c,b,l,s)/phys/devp

noco/auto/cong/tumr, sysi/epon, injr

proc, drug(N1B)

Retrieved from "http://en.wikipedia.org/wiki/Neuron"

Categories: Neurons | Nervous system | Medical terms

Spiritual Practices: Being Present

2010-04-19T13:52:00.000-07:00

http://bit.ly/dBp9bO

Enhances:
Contentment

Balances/Counters:
Living in past or future

The Basic Practice

Being present in the spiritual life always has a double meaning. There's present, as in here, in attendance. And there's present, as in now, a moment of time. What is the spiritual practice of being present? Being here now.
The world's religions all recommend living in the moment with full awareness. Zen Buddhism especially is known for its emphasis on "nowness." Hindu, Taoist, Jewish, Moslem, Christian, and other teachers urge us to make the most of every day as an opportunity that will not come to us again.

Also under the rubric of being present is the traditional spiritual exercise called practicing the presence of God. This means recognizing that God is here now moving through our everyday activities, no matter how trivial they might seem.

http://www.spiritualityandpractice.com/practices/practices.php?id=3

Why This Practice May Be For You

The contrasts to being present are living in the past and living in the future. We do the former when we hold on to regrets. We constantly review things that have already happened, trying to explain them in terms of our own or someone else's actions. Often this kind of thinking leads to guilt or blaming.

We live in the future when we make assumptions or fantasize about what could happen and then become attached to those expected outcomes. This habit usually results in disappointment. Whether we are consumed with positive expectations (optimism) or negative projections (pessimism), we are not living in the moment.

When you find yourself constantly reacting to your experiences in one of these ways, when you always want to be otherwise and elsewhere, it is time to be present. The companion of this practice is contentment.

+++++++++++++++++++
Sane-and-Sober Today!
http://sane-sober.blogspot.com/
+++++++++++++++++++

Bipolar Disorder ~ NIMH

2010-04-19T10:20:00.000-07:00

http://bit.ly/aaVHFG

Bipolar Disorder

Introduction: Bipolar Disorder

This booklet discusses bipolar disorder in adults. For information on bipolar disorder in children and adolescents, see the NIMH booklet, “Bipolar Disorder in Children and Teens: A Parent’s Guide.”

What is bipolar disorder?

Bipolar disorder, also known as manic-depressive illness, is a brain disorder that causes unusual shifts in mood, energy, activity levels, and the ability to carry out day-to-day tasks. Symptoms of bipolar disorder are severe. They are different from the normal ups and downs that everyone goes through from time to time. Bipolar disorder symptoms can result in damaged relationships, poor job or school performance, and even suicide. But bipolar disorder can be treated, and people with this illness can lead full and productive lives.
Bipolar disorder often develops in a person's late teens or early adult years. At least half of all cases start before age 25.¹ Some people have their first symptoms during childhood, while others may develop symptoms late in life.

Bipolar disorder is not easy to spot when it starts. The symptoms may seem like separate problems, not recognized as parts of a larger problem. Some people suffer for years before they are properly diagnosed and treated. Like diabetes or heart disease, bipolar disorder is a long-term illness that must be carefully managed throughout a person's life.

What are the symptoms of bipolar disorder?

People with bipolar disorder experience unusually intense emotional states that occur in distinct periods called "mood episodes." An overly joyful or overexcited state is called a manic episode, and an extremely sad or hopeless state is called a depressive episode. Sometimes, a mood episode includes symptoms of both mania and depression. This is called a mixed state. People with bipolar disorder also may be explosive and irritable during a mood episode.
Extreme changes in energy, activity, sleep, and behavior go along with these changes in mood. It is possible for someone with bipolar disorder to experience a long-lasting period of unstable moods rather than discrete episodes of depression or mania.

A person may be having an episode of bipolar disorder if he or she has a number of manic or depressive symptoms for most of the day, nearly every day, for at least one or two weeks. Sometimes symptoms are so severe that the person cannot function normally at work, school, or home.

Symptoms of bipolar disorder are described below.

Symptoms of mania or a manic episode include:	Symptoms of depression or a depressive episode include:
Mood Changes A long period of feeling "high," or an overly happy or outgoing mood Extremely irritable mood, agitation, feeling "jumpy" or "wired." Behavioral Changes Talking very fast, jumping from one idea to another, having racing thoughts Being easily distracted Increasing goal-directed activities, such as taking on new projects Being restless Sleeping little Having an unrealistic belief in one's abilities Behaving impulsively and taking part in a lot of pleasurable, high-risk behaviors, such as spending sprees, impulsive sex, and impulsive business investments.	Mood Changes A long period of feeling worried or empty Loss of interest in activities once enjoyed, including sex. Behavioral Changes Feeling tired or "slowed down" Having problems concentrating, remembering, and making decisions Being restless or irritable Changing eating, sleeping, or other habits Thinking of death or suicide, or attempting suicide.

Symptoms of mania or a manic episode include:

Symptoms of depression or a depressive episode include:

Mood Changes

A long period of feeling "high," or an overly happy or outgoing mood
Extremely irritable mood, agitation, feeling "jumpy" or "wired."

Behavioral Changes

Talking very fast, jumping from one idea to another, having racing thoughts
Being easily distracted
Increasing goal-directed activities, such as taking on new projects
Being restless
Sleeping little
Having an unrealistic belief in one's abilities
Behaving impulsively and taking part in a lot of pleasurable,
high-risk behaviors, such as spending sprees, impulsive sex, and impulsive business investments.

Mood Changes

A long period of feeling worried or empty
Loss of interest in activities once enjoyed, including sex.

Behavioral Changes

Feeling tired or "slowed down"
Having problems concentrating, remembering, and making decisions
Being restless or irritable
Changing eating, sleeping, or other habits
Thinking of death or suicide, or attempting suicide.

In addition to mania and depression, bipolar disorder can cause a range of moods, as shown on the scale.

One side of the scale includes severe depression, moderate depression, and mild low mood. Moderate depression may cause less extreme symptoms, and mild low mood is called dysthymia when it is chronic or long-term. In the middle of the scale is normal or balanced mood.

At the other end of the scale are hypomania and severe mania. Some people with bipolar disorder experience hypomania. During hypomanic episodes, a person may have increased energy and activity levels that are not as severe as typical mania, or he or she may have episodes that last less than a week and do not require emergency care. A person having a hypomanic episode may feel very good, be highly productive, and function well. This person may not feel that anything is wrong even as family and friends recognize the mood swings as possible bipolar disorder. Without proper treatment, however, people with hypomania may develop severe mania or depression.

During a mixed state, symptoms often include agitation, trouble sleeping, major changes in appetite, and suicidal thinking. People in a mixed state may feel very sad or hopeless while feeling extremely energized.

Sometimes, a person with severe episodes of mania or depression has psychotic symptoms too, such as hallucinations or delusions. The psychotic symptoms tend to reflect the person's extreme mood. For example, psychotic symptoms for a person having a manic episode may include believing he or she is famous, has a lot of money, or has special powers. In the same way, a person having a depressive episode may believe he or she is ruined and penniless, or has committed a crime. As a result, people with bipolar disorder who have psychotic symptoms are sometimes wrongly diagnosed as having schizophrenia, another severe mental illness that is linked with hallucinations and delusions.

People with bipolar disorder may also have behavioral problems. They may abuse alcohol or substances, have relationship problems, or perform poorly in school or at work. At first, it's not easy to recognize these problems as signs of a major mental illness.

How does bipolar disorder affect someone over time?

Bipolar disorder usually lasts a lifetime. Episodes of mania and depression typically come back over time. Between episodes, many people with bipolar disorder are free of symptoms, but some people may have lingering symptoms.
Doctors usually diagnose mental disorders using guidelines from the Diagnostic and Statistical Manual of Mental Disorders, or DSM. According to the DSM, there are four basic types of bipolar disorder:

Bipolar I Disorder is mainly defined by manic or mixed episodes that last at least seven days, or by manic symptoms that are so severe that the person needs immediate hospital care. Usually, the person also has depressive episodes, typically lasting at least two weeks. The symptoms of mania or depression must be a major change from the person's normal behavior.
Bipolar II Disorder is defined by a pattern of depressive episodes shifting back and forth with hypomanic episodes, but no full-blown manic or mixed episodes.
Bipolar Disorder Not Otherwise Specified (BP-NOS) is diagnosed when a person has symptoms of the illness that do not meet diagnostic criteria for either bipolar I or II. The symptoms may not last long enough, or the person may have too few symptoms, to be diagnosed with bipolar I or II. However, the symptoms are clearly out of the person's normal range of behavior.
Cyclothymic Disorder, or Cyclothymia, is a mild form of bipolar disorder. People who have cyclothymia have episodes of hypomania that shift back and forth with mild depression for at least two years. However, the symptoms do not meet the diagnostic requirements for any other type of bipolar disorder.

Some people may be diagnosed with rapid-cycling bipolar disorder. This is when a person has four or more episodes of major depression, mania, hypomania, or mixed symptoms within a year.² Some people experience more than one episode in a week, or even within one day. Rapid cycling seems to be more common in people who have severe bipolar disorder and may be more common in people who have their first episode at a younger age. One study found that people with rapid cycling had their first episode about four years earlier, during mid to late teen years, than people without rapid cycling bipolar disorder.³ Rapid cycling affects more women than men.⁴

Bipolar disorder tends to worsen if it is not treated. Over time, a person may suffer more frequent and more severe episodes than when the illness first appeared.⁵ Also, delays in getting the correct diagnosis and treatment make a person more likely to experience personal, social, and work-related problems.⁶

Proper diagnosis and treatment helps people with bipolar disorder lead healthy and productive lives. In most cases, treatment can help reduce the frequency and severity of episodes.

What illnesses often co-exist with bipolar disorder?

Substance abuse is very common among people with bipolar disorder, but the reasons for this link are unclear.⁷ Some people with bipolar disorder may try to treat their symptoms with alcohol or drugs. However, substance abuse may trigger or prolong bipolar symptoms, and the behavioral control problems associated with mania can result in a person drinking too much.

Anxiety disorders, such as post-traumatic stress disorder (PTSD) and social phobia, also co-occur often among people with bipolar disorder.^8-10 Bipolar disorder also co-occurs with attention deficit hyperactivity disorder (ADHD), which has some symptoms that overlap with bipolar disorder, such as restlessness and being easily distracted.
People with bipolar disorder are also at higher risk for thyroid disease, migraine headaches, heart disease, diabetes, obesity, and other physical illnesses.^{10, 11} These illnesses may cause symptoms of mania or depression. They may also result from treatment for bipolar disorder.

Other illnesses can make it hard to diagnose and treat bipolar disorder. People with bipolar disorder should monitor their physical and mental health. If a symptom does not get better with treatment, they should tell their doctor.

What are the risk factors for bipolar disorder?

Scientists are learning about the possible causes of bipolar disorder. Most scientists agree that there is no single cause. Rather, many factors likely act together to produce the illness or increase risk.

Genetics

Bipolar disorder tends to run in families, so researchers are looking for genes that may increase a person's chance of developing the illness. Genes are the "building blocks" of heredity. They help control how the body and brain work and grow. Genes are contained inside a person's cells that are passed down from parents to children.

Children with a parent or sibling who has bipolar disorder are four to six times more likely to develop the illness, compared with children who do not have a family history of bipolar disorder.¹² However, most children with a family history of bipolar disorder will not develop the illness.

Genetic research on bipolar disorder is being helped by advances in technology. This type of research is now much quicker and more far-reaching than in the past. One example is the launch of the Bipolar Disorder Phenome Database, funded in part by NIMH. Using the database, scientists will be able to link visible signs of the disorder with the genes that may influence them. So far, researchers using this database found that most people with bipolar disorder had:¹³

Missed work because of their illness
Other illnesses at the same time, especially alcohol and/or substance abuse and panic disorders
Been treated or hospitalized for bipolar disorder.

The researchers also identified certain traits that appeared to run in families, including:

History of psychiatric hospitalization
Co-occurring obsessive-compulsive disorder (OCD)
Age at first manic episode
Number and frequency of manic episodes.

Scientists continue to study these traits, which may help them find the genes that cause bipolar disorder some day.
But genes are not the only risk factor for bipolar disorder. Studies of identical twins have shown that the twin of a person with bipolar illness does not always develop the disorder. This is important because identical twins share all of the same genes. The study results suggest factors besides genes are also at work. Rather, it is likely that many different genes and a person's environment are involved. However, scientists do not yet fully understand how these factors interact to cause bipolar disorder.

Brain structure and functioning

Brain-imaging studies are helping scientists learn what happens in the brain of a person with bipolar disorder.^{14, 15} Newer brain-imaging tools, such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET), allow researchers to take pictures of the living brain at work. These tools help scientists study the brain's structure and activity.

Some imaging studies show how the brains of people with bipolar disorder may differ from the brains of healthy people or people with other mental disorders. For example, one study using MRI found that the pattern of brain development in children with bipolar disorder was similar to that in children with "multi-dimensional impairment," a disorder that causes symptoms that overlap somewhat with bipolar disorder and schizophrenia.¹⁶ This suggests that the common pattern of brain development may be linked to general risk for unstable moods.

Learning more about these differences, along with information gained from genetic studies, helps scientists better understand bipolar disorder. Someday scientists may be able to predict which types of treatment will work most effectively. They may even find ways to prevent bipolar disorder.

How is bipolar disorder diagnosed?

The first step in getting a proper diagnosis is to talk to a doctor, who may conduct a physical examination, an interview, and lab tests. Bipolar disorder cannot currently be identified through a blood test or a brain scan, but these tests can help rule out other contributing factors, such as a stroke or brain tumor. If the problems are not caused by other illnesses, the doctor may conduct a mental health evaluation. The doctor may also provide a referral to a trained mental health professional, such as a psychiatrist, who is experienced in diagnosing and treating bipolar disorder.

The doctor or mental health professional should conduct a complete diagnostic evaluation. He or she should discuss any family history of bipolar disorder or other mental illnesses and get a complete history of symptoms. The doctor or mental health professionals should also talk to the person's close relatives or spouse and note how they describe the person's symptoms and family medical history.

People with bipolar disorder are more likely to seek help when they are depressed than when experiencing mania or hypomania.¹⁷ Therefore, a careful medical history is needed to assure that bipolar disorder is not mistakenly diagnosed as major depressive disorder, which is also called unipolar depression. Unlike people with bipolar disorder, people who have unipolar depression do not experience mania. Whenever possible, previous records and input from family and friends should also be included in the medical history.

How is bipolar disorder treated?

To date, there is no cure for bipolar disorder. But proper treatment helps most people with bipolar disorder gain better control of their mood swings and related symptoms.^18-20 This is also true for people with the most severe forms of the illness.

Because bipolar disorder is a lifelong and recurrent illness, people with the disorder need long-term treatment to maintain control of bipolar symptoms. An effective maintenance treatment plan includes medication and psychotherapy for preventing relapse and reducing symptom severity.²¹

Medications

Bipolar disorder can be diagnosed and medications prescribed by people with an M.D. (doctor of medicine). Usually, bipolar medications are prescribed by a psychiatrist. In some states, clinical psychologists, psychiatric nurse practitioners, and advanced psychiatric nurse specialists can also prescribe medications. Check with your state's licensing agency to find out more.

Not everyone responds to medications in the same way. Several different medications may need to be tried before the best course of treatment is found.

Keeping a chart of daily mood symptoms, treatments, sleep patterns, and life events can help the doctor track and treat the illness most effectively. Sometimes this is called a daily life chart. If a person's symptoms change or if side effects become serious, the doctor may switch or add medications.

Some of the types of medications generally used to treat bipolar disorder are listed on the next page. Information on medications can change. For the most up to date information on use and side effects contact the U.S. Food and Drug Administration (FDA).

Mood stabilizing medications are usually the first choice to treat bipolar disorder. In general, people with bipolar disorder continue treatment with mood stabilizers for years. Except for lithium, many of these medications are anticonvulsants. Anticonvulsant medications are usually used to treat seizures, but they also help control moods. These medications are commonly used as mood stabilizers in bipolar disorder:

Lithium (sometimes known as Eskalith or Lithobid) was the first mood-stabilizing medication approved by the U.S. Food and Drug Administration (FDA) in the 1970s for treatment of mania. It is often very effective in controlling symptoms of mania and preventing the recurrence of manic and depressive episodes.
Valproic acid or divalproex sodium (Depakote), approved by the FDA in 1995 for treating mania, is a popular alternative to lithium for bipolar disorder. It is generally as effective as lithium for treating bipolar disorder.^{23, 24} Also see the section in this booklet, "Should young women take valproic acid?"
More recently, the anticonvulsant lamotrigine (Lamictal) received FDA approval for maintenance treatment of bipolar disorder.
Other anticonvulsant medications, including gabapentin (Neurontin), topiramate (Topamax), and oxcarbazepine (Trileptal) are sometimes prescribed. No large studies have shown that these medications are more effective than mood stabilizers.

Valproic acid, lamotrigine, and other anticonvulsant medications have an FDA warning. The warning states that their use may increase the risk of suicidal thoughts and behaviors. People taking anticonvulsant medications for bipolar or other illnesses should be closely monitored for new or worsening symptoms of depression, suicidal thoughts or behavior, or any unusual changes in mood or behavior. People taking these medications should not make any changes without talking to their health care professional.

Lithium and Thyroid Function

People with bipolar disorder often have thyroid gland problems. Lithium treatment may also cause low thyroid levels in some people.²² Low thyroid function, called hypothyroidism, has been associated with rapid cycling in some people with bipolar disorder, especially women.

Because too much or too little thyroid hormone can lead to mood and energy changes, it is important to have a doctor check thyroid levels carefully. A person with bipolar disorder may need to take thyroid medication, in addition to medications for bipolar disorder, to keep thyroid levels balanced.

Should young women take valproic acid?

Valproic acid may increase levels of testosterone (a male hormone) in teenage girls and lead to polycystic ovary syndrome (PCOS) in women who begin taking the medication before age 20.^{25, 26} PCOS causes a woman's eggs to develop into cysts, or fluid filled sacs that collect in the ovaries instead of being released by monthly periods. This condition can cause obesity, excess body hair, disruptions in the menstrual cycle, and other serious symptoms. Most of these symptoms will improve after stopping treatment with valproic acid.²⁷ Young girls and women taking valproic acid should be monitored carefully by a doctor.

Atypical antipsychotic medications are sometimes used to treat symptoms of bipolar disorder. Often, these medications are taken with other medications. Atypical antipsychotic medications are called "atypical" to set them apart from earlier medications, which are called "conventional" or "first-generation" antipsychotics.

Olanzapine (Zyprexa), when given with an antidepressant medication, may help relieve symptoms of severe mania or psychosis.²⁸ Olanzapine is also available in an injectable form, which quickly treats agitation associated with a manic or mixed episode. Olanzapine can be used for maintenance treatment of bipolar disorder as well, even when a person does not have psychotic symptoms. However, some studies show that people taking olanzapine may gain weight and have other side effects that can increase their risk for diabetes and heart disease. These side effects are more likely in people taking olanzapine when compared with people prescribed other atypical antipsychotics.
Aripiprazole (Abilify), like olanzapine, is approved for treatment of a manic or mixed episode. Aripiprazole is also used for maintenance treatment after a severe or sudden episode. As with olanzapine, aripiprazole also can be injected for urgent treatment of symptoms of manic or mixed episodes of bipolar disorder.
Quetiapine (Seroquel) relieves the symptoms of severe and sudden manic episodes. In that way, quetiapine is like almost all antipsychotics. In 2006, it became the first atypical antipsychotic to also receive FDA approval for the treatment of bipolar depressive episodes.
Risperidone (Risperdal) and ziprasidone (Geodon) are other atypical antipsychotics that may also be prescribed for controlling manic or mixed episodes.

Antidepressant medications are sometimes used to treat symptoms of depression in bipolar disorder. People with bipolar disorder who take antidepressants often take a mood stabilizer too. Doctors usually require this because taking only an antidepressant can increase a person's risk of switching to mania or hypomania, or of developing rapid cycling symptoms.²⁹ To prevent this switch, doctors who prescribe antidepressants for treating bipolar disorder also usually require the person to take a mood-stabilizing medication at the same time.

Recently, a large-scale, NIMH-funded study showed that for many people, adding an antidepressant to a mood stabilizer is no more effective in treating the depression than using only a mood stabilizer.³⁰

Fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), and bupropion (Wellbutrin) are examples of antidepressants that may be prescribed to treat symptoms of bipolar depression.

Some medications are better at treating one type of bipolar symptoms than another. For example, lamotrigine (Lamictal) seems to be helpful in controlling depressive symptoms of bipolar disorder.

What are the side effects of these medications? Before starting a new medication, people with bipolar disorder should talk to their doctor about the possible risks and benefits.

The psychiatrist prescribing the medication or pharmacist can also answer questions about side effects. Over the last decade, treatments have improved, and some medications now have fewer or more tolerable side effects than earlier treatments. However, everyone responds differently to medications. In some cases, side effects may not appear until a person has taken a medication for some time.

If the person with bipolar disorder develops any severe side effects from a medication, he or she should talk to the doctor who prescribed it as soon as possible. The doctor may change the dose or prescribe a different medication. People being treated for bipolar disorder should not stop taking a medication without talking to a doctor first. Suddenly stopping a medication may lead to "rebound," or worsening of bipolar disorder symptoms. Other uncomfortable or potentially dangerous withdrawal effects are also possible.

FDA Warning on Antidepressants
Antidepressants are safe and popular, but some studies have suggested that they may have unintentional effects on some people, especially in adolescents and young adults. The FDA warning says that patients of all ages taking antidepressants should be watched closely, especially during the first few weeks of treatment. Possible side effects to look for are depression that gets worse, suicidal thinking or behavior, or any unusual changes in behavior such as trouble sleeping, agitation, or withdrawal from normal social situations. Families and caregivers should report any changes to the doctor. For the latest information visit the FDA website.

The following sections describe some common side effects of the different types of medications used to treat bipolar disorder.

1. Mood Stabilizers
In some cases, lithium can cause side effects such as:

Restlessness
Dry mouth
Bloating or indigestion
Acne
Unusual discomfort to cold temperatures
Joint or muscle pain
Brittle nails or hair.³¹

Lithium also causes side effects not listed here. If extremely bothersome or unusual side effects occur, tell your doctor as soon as possible.

If a person with bipolar disorder is being treated with lithium, it is important to make regular visits to the treating doctor. The doctor needs to check the levels of lithium in the person's blood, as well as kidney and thyroid function.

These medications may also be linked with rare but serious side effects. Talk with the treating doctor or a pharmacist to make sure you understand signs of serious side effects for the medications you're taking.

Common side effects of other mood stabilizing medications include:

Drowsiness
Dizziness
Headache
Diarrhea
Constipation
Heartburn
Mood swings
Stuffed or runny nose, or other cold-like symptoms.^32-37

2. Atypical Antipsychotics

Some people have side effects when they start taking atypical antipsychotics. Most side effects go away after a few days and often can be managed successfully. People who are taking antipsychotics should not drive until they adjust to their new medication. Side effects of many antipsychotics include:

Drowsiness
Dizziness when changing positions
Blurred vision
Rapid heartbeat
Sensitivity to the sun
Skin rashes
Menstrual problems for women.

Atypical antipsychotic medications can cause major weight gain and changes in a person's metabolism. This may increase a person's risk of getting diabetes and high cholesterol.³⁸ A person's weight, glucose levels, and lipid levels should be monitored regularly by a doctor while taking these medications.

In rare cases, long-term use of atypical antipsychotic drugs may lead to a condition called tardive dyskinesia (TD). The condition causes muscle movements that commonly occur around the mouth. A person with TD cannot control these moments. TD can range from mild to severe, and it cannot always be cured. Some people with TD recover partially or fully after they stop taking the drug.

3. Antidepressants

The antidepressants most commonly prescribed for treating symptoms of bipolar disorder can also cause mild side effects that usually do not last long. These can include:

Headache, which usually goes away within a few days.
Nausea (feeling sick to your stomach), which usually goes away within a few days.
Sleep problems, such as sleeplessness or drowsiness. This may happen during the first few weeks but then go away. To help lessen these effects, sometimes the medication dose can be reduced, or the time of day it is taken can be changed.
Agitation (feeling jittery).
Sexual problems, which can affect both men and women. These include reduced sex drive and problems having and enjoying sex.

Some antidepressants are more likely to cause certain side effects than other types. Your doctor or pharmacist can answer questions about these medications. Any unusual reactions or side effects should be reported to a doctor immediately.

For the most up-to-date information on medications for treating bipolar disorder and their side effects, please see the online NIMH Medications booklet.

Should women who are pregnant or may become pregnant take medication for bipolar disorder?

Women with bipolar disorder who are pregnant or may become pregnant face special challenges. The mood stabilizing medications in use today can harm a developing fetus or nursing infant.³⁹ But stopping medications, either suddenly or gradually, greatly increases the risk that bipolar symptoms will recur during pregnancy.⁴⁰

Scientists are not sure yet, but lithium is likely the preferred mood-stabilizing medication for pregnant women with bipolar disorder.^{40, 41} However, lithium can lead to heart problems in the fetus. Women need to know that most bipolar medications are passed on through breast milk.⁴¹ Pregnant women and nursing mothers should talk to their doctors about the benefits and risks of all available treatments.

Psychotherapy In addition to medication, psychotherapy, or "talk" therapy, can be an effective treatment for bipolar disorder. It can provide support, education, and guidance to people with bipolar disorder and their families. Some psychotherapy treatments used to treat bipolar disorder include:

Cognitive behavioral therapy (CBT) helps people with bipolar disorder learn to change harmful or negative thought patterns and behaviors.
Family-focused therapy includes family members. It helps enhance family coping strategies, such as recognizing new episodes early and helping their loved one. This therapy also improves communication and problem-solving.
Interpersonal and social rhythm therapy helps people with bipolar disorder improve their relationships with others and manage their daily routines. Regular daily routines and sleep schedules may help protect against manic episodes.
Psychoeducation teaches people with bipolar disorder about the illness and its treatment. This treatment helps people recognize signs of relapse so they can seek treatment early, before a full-blown episode occurs. Usually done in a group, psychoeducation may also be helpful for family members and caregivers.

A licensed psychologist, social worker, or counselor typically provides these therapies. This mental health professional often works with the psychiatrist to track progress. The number, frequency, and type of sessions should be based on the treatment needs of each person. As with medication, following the doctor's instructions for any psychotherapy will provide the greatest benefit.

For more information, see the Substance Abuse and Mental Health Services Administration web page on choosing a mental health therapist.

Recently, NIMH funded a clinical trial called the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). This was the largest treatment study ever conducted for bipolar disorder. In a study on psychotherapies, STEP-BD researchers compared people in two groups. The first group was treated with collaborative care (three sessions of psychoeducation over six weeks). The second group was treated with medication and intensive psychotherapy (30 sessions over nine months of CBT, interpersonal and social rhythm therapy, or family-focused therapy). Researchers found that the second group had fewer relapses, lower hospitalization rates, and were better able to stick with their treatment plans.⁴² They were also more likely to get well faster and stay well longer.

NIMH is supporting more research on which combinations of psychotherapy and medication work best. The goal is to help people with bipolar disorder live symptom-free for longer periods and to recover from episodes more quickly. Researchers also hope to determine whether psychotherapy helps delay the start of bipolar disorder in children at high risk for the illness.

Visit the NIMH Web site for more information on psychotherapy.

Other treatments

Electroconvulsive Therapy (ECT)—For cases in which medication and/or psychotherapy does not work, electroconvulsive therapy (ECT) may be useful. ECT, formerly known as "shock therapy," once had a bad reputation. But in recent years, it has greatly improved and can provide relief for people with severe bipolar disorder who have not been able to feel better with other treatments. Before ECT is administered, a patient takes a muscle relaxant and is put under brief anesthesia. He or she does not consciously feel the electrical impulse administered in ECT. On average, ECT treatments last from 30–90 seconds. People who have ECT usually recover after 5–15 minutes and are able to go home the same day.⁴³
Sometimes ECT is used for bipolar symptoms when other medical conditions, including pregnancy, make the use of medications too risky. ECT is a highly effective treatment for severely depressive, manic, or mixed episodes, but is generally not a first-line treatment.

ECT may cause some short-term side effects, including confusion, disorientation, and memory loss. But these side effects typically clear soon after treatment. People with bipolar disorder should discuss possible benefits and risks of ECT with an experienced doctor.⁴⁴
Sleep Medications—People with bipolar disorder who have trouble sleeping usually sleep better after getting treatment for bipolar disorder. However, if sleeplessness does not improve, the doctor may suggest a change in medications. If the problems still continue, the doctor may prescribe sedatives or other sleep medications.

People with bipolar disorder should tell their doctor about all prescription drugs, over-the-counter medications, or supplements they are taking. Certain medications and supplements taken together may cause unwanted or dangerous effects.

Herbal Supplements

In general, there is not much research about herbal or natural supplements. Little is known about their effects on bipolar disorder. An herb called St. John's wort (Hypericum perforatum), often marketed as a natural antidepressant, may cause a switch to mania in some people with bipolar disorder.⁴⁵ St. John's wort can also make other medications less effective, including some antidepressant and anticonvulsant medications.⁴⁶ Scientists are also researching omega-3 fatty acids (most commonly found in fish oil) to measure their usefulness for long-term treatment of bipolar disorder.⁴⁷ Study results have been mixed.⁴⁸ It is important to talk with a doctor before taking any herbal or natural supplements because of the serious risk of interactions with other medications.

What can people with bipolar disorder expect from treatment?

Bipolar disorder has no cure, but can be effectively treated over the long-term. It is best controlled when treatment is continuous, rather than on and off. In the STEP-BD study, a little more than half of the people treated for bipolar disorder recovered over one year's time. For this study, recovery meant having two or fewer symptoms of the disorder for at least eight weeks.

However, even with proper treatment, mood changes can occur. In the STEP-BD study, almost half of those who recovered still had lingering symptoms. These people experienced a relapse or recurrence that was usually a return to a depressive state.⁴⁹⁴⁹ Scientists are unsure, however, how these other illnesses or lingering symptoms increase the chance of relapse. For some people, combining psychotherapy with medication may help to prevent or delay relapse.⁴² If a person had a mental illness in addition to bipolar disorder, he or she was more likely to experience a relapse.

Treatment may be more effective when people work closely with a doctor and talk openly about their concerns and choices. Keeping track of mood changes and symptoms with a daily life chart can help a doctor assess a person's response to treatments. Sometimes the doctor needs to change a treatment plan to make sure symptoms are controlled most effectively. A psychiatrist should guide any changes in type or dose of medication.

How can I help a friend or relative who has bipolar disorder?

If you know someone who has bipolar disorder, it affects you too. The first and most important thing you can do is help him or her get the right diagnosis and treatment. You may need to make the appointment and go with him or her to see the doctor. Encourage your loved one to stay in treatment.

To help a friend or relative, you can:

Offer emotional support, understanding, patience, and encouragement
Learn about bipolar disorder so you can understand what your friend or relative is experiencing
Talk to your friend or relative and listen carefully
Listen to feelings your friend or relative expresses-be understanding about situations that may trigger bipolar symptoms
Invite your friend or relative out for positive distractions, such as walks, outings, and other activities
Remind your friend or relative that, with time and treatment, he or she can get better.

Never ignore comments about your friend or relative harming himself or herself. Always report such comments to his or her therapist or doctor.

Support for caregivers

Like other serious illnesses, bipolar disorder can be difficult for spouses, family members, friends, and other caregivers. Relatives and friends often have to cope with the person's serious behavioral problems, such as wild spending sprees during mania, extreme withdrawal during depression, poor work or school performance. These behaviors can have lasting consequences.

Caregivers usually take care of the medical needs of their loved ones. The caregivers have to deal with how this affects their own health. The stress that caregivers are under may lead to missed work or lost free time, strained relationships with people who may not understand the situation, and physical and mental exhaustion.

Stress from caregiving can make it hard to cope with a loved one's bipolar symptoms. One study shows that if a caregiver is under a lot of stress, his or her loved one has more trouble following the treatment plan, which increases the chance for a major bipolar episode.⁵⁰ It is important that people caring for those with bipolar disorder also take care of themselves.

How can I help myself if I have bipolar disorder?

It may be very hard to take that first step to help yourself. It may take time, but you can get better with treatment.
To help yourself:

Talk to your doctor about treatment options and progress
Keep a regular routine, such as eating meals at the same time every day and going to sleep at the same time every night
Try to get enough sleep
Stay on your medication
Learn about warning signs signaling a shift into depression or mania
Expect your symptoms to improve gradually, not immediately.

Where can I go for help?

If you are unsure where to go for help, ask your family doctor. Others who can help are listed below.

Mental health specialists, such as psychiatrists, psychologists, social workers, or mental health counselors
Health maintenance organizations
Community mental health centers
Hospital psychiatry departments and outpatient clinics
Mental health programs at universities or medical schools
State hospital outpatient clinics
Family services, social agencies, or clergy
Peer support groups
Private clinics and facilities
Employee assistance programs
Local medical and/or psychiatric societies.

You can also check the phone book under "mental health," "health," "social services," "hotlines," or "physicians" for phone numbers and addresses. An emergency room doctor can also provide temporary help and can tell you where and how to get further help.

What if I or someone I know is in crisis?

If you are thinking about harming yourself, or know someone who is, tell someone who can help immediately.

Call your doctor.
Call 911 or go to a hospital emergency room to get immediate help or ask a friend or family member to help you do these things.
Call the toll-free, 24-hour hotline of the National Suicide Prevention Lifeline at 1-800-273-TALK (1-800-273-8255); TTY: 1-800-799-4TTY (4889) to talk to a trained counselor.

Make sure you or the suicidal person is not left alone.

Citations

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22. Kupka RW, Nolen WA, Post RM, McElroy SL, Altshuler LL, Denicoff KD, Frye MA, Keck PE, Jr., Leverich GS, Rush AJ, Suppes T, Pollio C, Drexhage HA. High rate of autoimmune thyroiditis in bipolar disorder: lack of association with lithium exposure. Biol Psychiatry. 2002 Feb 15;51(4):305-311.
23. Bowden CL, Calabrese JR, McElroy SL, Gyulai L, Wassef A, Petty F, Pope HG, Jr., Chou JC, Keck PE, Jr., Rhodes LJ, Swann AC, Hirschfeld RM, Wozniak PJ, Group DMS. A randomized, placebo-controlled 12-month trial of divalproex and lithium in treatment of outpatients with bipolar I disorder. Arch Gen Psychiatry. 2000 May;57(5):481-489.
24. Calabrese JR, Shelton MD, Rapport DJ, Youngstrom EA, Jackson K, Bilali S, Ganocy SJ, Findling RL. A 20-month, double-blind, maintenance trial of lithium versus divalproex in rapid-cycling bipolar disorder. Am J Psychiatry. 2005 Nov;162(11):2152-2161.
25. Vainionpaa LK, Rattya J, Knip M, Tapanainen JS, Pakarinen AJ, Lanning P, Tekay A, Myllyla VV, Isojarvi JI. Valproate-induced hyperandrogenism during pubertal maturation in girls with epilepsy. Ann Neurol. 1999 Apr;45(4):444-450.
26. Joffe H, Cohen LS, Suppes T, McLaughlin WL, Lavori P, Adams JM, Hwang CH, Hall JE, Sachs GS. Valproate is associated with new-onset oligoamenorrhea with hyperandrogenism in women with bipolar disorder. Biol Psychiatry. 2006 Jun 1;59(11):1078-1086.
27. Joffe H, Cohen LS, Suppes T, Hwang CH, Molay F, Adams JM, Sachs GS, Hall JE. Longitudinal follow-up of reproductive and metabolic features of valproate-associated polycystic ovarian syndrome features: A preliminary report. Biol Psychiatry. 2006 Dec 15;60(12):1378-1381.
28. Tohen M, Sanger TM, McElroy SL, Tollefson GD, Chengappa KN, Daniel DG, Petty F, Centorrino F, Wang R, Grundy SL, Greaney MG, Jacobs TG, David SR, Toma V. Olanzapine versus placebo in the treatment of acute mania. Olanzapine HGEH Study Group. Am J Psychiatry. 1999 May;156(5):702-709.
29. Thase ME, Sachs GS. Bipolar depression: pharmacotherapy and related therapeutic strategies. Biol Psychiatry. 2000 Sep 15;48(6):558-572.
30. Sachs GS, Nierenberg AA, Calabrese JR, Marangell LB, Wisniewski SR, Gyulai L, Friedman ES, Bowden CL, Fossey MD, Ostacher MJ, Ketter TA, Patel J, Hauser P, Rapport D, Martinez JM, Allen MH, Miklowitz DJ, Otto MW, Dennehy EB, Thase ME. Effectiveness of adjunctive antidepressant treatment for bipolar depression. N Engl J Med. 2007 Apr 26;356(17):1711-1722.
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38. Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, Keefe RS, Davis SM, Davis CE, Lebowitz BD, Severe J, Hsiao JK. Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. N Engl J Med. 2005 Sep 22;353(12):1209-1223.
39. Llewellyn A, Stowe ZN, Strader JR, Jr. The use of lithium and management of women with bipolar disorder during pregnancy and lactation. J Consult Clin Psychol. 1998 59(Suppl 6):57-64.
40. Viguera AC, Whitfield T, Baldessarini RJ, Newport J, Stowe Z, Reminick A, Zurick A, Cohen LS. Risk of recurrence in women with bipolar disorder during pregnancy: prospective study of mood stabilizer discontinuation. Am J Psychiatry. 2007 Dec;164(12):1817-1824.
41. Yonkers KA, Wisner KL, Stowe Z, Leibenluft E, Cohen L, Miller L, Manber R, Viguera A, Suppes T, Altshuler L. Management of bipolar disorder during pregnancy and the postpartum period. Am J Psychiatry. 2004 Apr;161(4):608-620.
42. Miklowitz DJ, Otto MW, Frank E, Reilly-Harrington NA, Wisniewski SR, Kogan JN, Nierenberg AA, Calabrese JR, Marangell LB, Gyulai L, Araga M, Gonzalez JM, Shirley ER, Thase ME, Sachs GS. Psychosocial treatments for bipolar depression: a 1-year randomized trial from the Systematic Treatment Enhancement Program (STEP). Arch Gen Psychiatry. 2007 Apr;64(4):419-426.
43. Pandya M, Pozuelo L, Malone D. Electroconvulsive therapy: what the internist needs to know. Cleve Clin J Med. 2007 Sep;74(9):679-685.
44. Mental Health: A Report of the Surgeon General. U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health. 1999.
45. Nierenberg AA, Burt T, Matthews J, Weiss AP. Mania associated with St. John's wort. Biol Psychiatry. 1999 Dec 15;46(12):1707-1708.
46. Henney JE. From the Food and Drug Administration: Risk of Drug Interactions With St John's Wort. JAMA. 2000 Apr 5;283(13):1679.
47. Stoll AL, Severus WE, Freeman MP, Rueter S, Zboyan HA, Diamond E, Cress KK, Marangell LB. Omega 3 fatty acids in bipolar disorder: a preliminary double-blind, placebo-controlled trial. Arch Gen Psychiatry. 1999 May;56(5):407-412.
48. Freeman MP, Hibbeln JR, Wisner KL, Davis JM, Mischoulon D, Peet M, Keck PE, Jr., Marangell LB, Richardson AJ, Lake J, Stoll AL. Omega-3 fatty acids: evidence basis for treatment and future research in psychiatry. J Consult Clin Psychol. 2006 Dec;67(12):1954-1967.
49. Perlis RH, Ostacher MJ, Patel JK, Marangell LB, Zhang H, Wisniewski SR, Ketter TA, Miklowitz DJ, Otto MW, Gyulai L, Reilly-Harrington NA, Nierenberg AA, Sachs GS, Thase ME. Predictors of recurrence in bipolar disorder: primary outcomes from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). Am J Psychiatry. 2006 Feb;163(2):217-224.
50. Perlick DA, Rosenheck RA, Clarkin JF, Maciejewski PK, Sirey J, Struening E, Link BG. Impact of family burden and affective response on clinical outcome among patients with bipolar disorder. Psychiatr Serv. 2004 Sep;55(9):1029-1035.

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How to increase serotonin in the human brain without drugs via Young

2010-04-18T21:54:00.000-07:00

http://bit.ly/crVRmt

Simon N. Young

Editor-in-chief, Journal of Psychiatry and Neuroscience, and Department of Psychiatry, McGill University, Montréal, Que.

Medical subject headings: serotonin, exercise, phototherapy, food, depression, happiness

For the last 4 decades, the question of how to manipulate the serotonergic system with drugs has been an important area of research in biological psychiatry, and this research has led to advances in the treatment of depression. Research on the association between various polymorphisms and depression supports the idea that serotonin plays a role, not only in the treatment of depression but also in susceptibility to depression and suicide.

The research focus here has been on polymorphisms of the serotonin transporter, but other serotonin-related genes may also be involved.^1–5 In the future, genetic research will make it possible to predict with increasing accuracy who is susceptible to depression. Much less attention has been given to how this information will be used for the benefit of individuals with a serotonin-related susceptibility to depression, and little evidence exists concerning strategies to prevent depression in those with such a susceptibility. Various studies have looked at early intervention in those with prodromal symptoms as well as at population strategies for preventing depression.^6–11 Obviously, prevention is preferable to early intervention; moreover, although population strategies are important, they are ideally supplemented with preventive interventions that can be used over long periods of time in targeted individuals who do not yet exhibit even nonclinical symptoms. Clearly, pharmacologic approaches are not appropriate, and given the evidence for serotonin's role in the etiology and treatment of depression, nonpharmacologic methods of increasing serotonin are potential candidates to test for their ability to prevent depression.

Another reason for pursuing nonpharmacologic methods of increasing serotonin arises from the increasing recognition that happiness and well-being are important, both as factors protecting against mental and physical disorders and in their own right.^12–14 Conversely, negative moods are associated with negative outcomes. For example, the negative mood hostility is a risk factor for many disorders. For the sake of brevity, hostility is discussed here mainly in relation to one of the biggest sources of mortality, coronary heart disease (CHD). A meta-analysis of 45 studies demonstrated that hostility is a risk factor for CHD and for all-cause mortality.¹⁵ More recent research confirms this. Hostility is associated not only with the development of CHD but also with poorer survival in coronary artery disease (CAD) patients.¹⁶ Hostility may lead to decreased social support and social isolation,¹⁷ and low perceived social support is associated with greater mortality in those with CAD.¹⁸ Effects are not just limited to CHD. For example, the opposite of hostility, agreeableness, was a significant protective factor against mortality in a sample of older, frail participants.¹⁹

The constitution of the WHO states “Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.”²⁰ This may sound exaggerated but positive mood within the normal range is an important predictor of health and longevity. In a classic study, those in the lowest quartile for positive emotions, rated from autobiographies written at a mean age of 22 years, died on average 10 years earlier than those in the highest quartile.²¹ Even taking into account possible confounders, other studies “found the same solid link between feeling good and living longer.”¹²²² increased incidence of depression,²³ increased suicide²⁴ and increased mortality²⁵ up to 2 decades later. Positive emotions protected against these outcomes. A recent review including meta-analyses assessed cross-sectional, longitudinal and experimental studies and concluded that happiness is associated with and precedes numerous successful outcomes.²⁶²⁷ Low social support is associated with higher levels of stress, depression, dysthymia and posttraumatic stress disorder and with increased morbidity and mortality from a host of medical illnesses.²⁷ In a series of recent studies, negative emotions were associated with increased disability due to mental and physical disorders, Mood may influence social behaviour, and social support is one of the most studied psychosocial factors in relation to health and disease.

Research confirms what might be intuitively expected, that positive emotions and agreeableness foster congenial relationships with others.²⁸^,²⁹ This in turn will create the conditions for an increase in social support.

Several studies found an association between measures related to serotonin and mood in the normal range. Lower platelet serotonin₂ receptor function was associated with lower mood in one study,³⁰ whereas better mood was associated with higher blood serotonin levels in another.³¹ Two studies found that greater prolactin release in response to fenfluramine was associated with more positive mood.³²^,³³ The idea that these associations indicate a causal association between serotonin function and mood within the normal range is consistent with a study demonstrating that, in healthy people with high trait irritability, tryptophan, relative to placebo, decreased quarrelsome behaviours, increased agreeable behaviours and improved mood.³⁴ Serotonin may be associated with physical health as well as mood. In otherwise healthy individuals, a low prolactin response to the serotonin-releasing drug fenfluramine was associated with the metabolic syndrome, a risk factor for heart disease,³⁵ suggesting that low serotonin may predispose healthy individuals to suboptimal physical as well as mental functioning.

Nonpharmacologic methods of raising brain serotonin may not only improve mood and social functioning of healthy people — a worthwhile objective even without additional considerations — but would also make it possible to test the idea that increases in brain serotonin may help protect against the onset of various mental and physical disorders. Four strategies that are worth further investigation are discussed below.

The article by Perreau-Linck and colleagues³⁶ (page 430 of this issue) provides an initial lead about one possible strategy for raising brain serotonin. Using positron emission tomography, they obtained a measure of serotonin synthesis in the brains of healthy participants who underwent positive, negative and neutral mood inductions. Reported levels of happiness were positively correlated and reported levels of sadness were negatively correlated with serotonin synthesis in the right anterior cingulate cortex. The idea that alterations in thought, either self-induced or due to psychotherapy, can alter brain metabolism is not new. Numerous studies have demonstrated changes in blood flow in such circumstances. However, reports related to specific transmitters are much less common. In one recent study, meditation was reported to increase release of dopamine.³⁷³⁶ is the first to report that self-induced changes in mood can influence serotonin synthesis. This raises the possibility that the interaction between serotonin synthesis and mood may be 2-way, with serotonin influencing mood and mood influencing serotonin. Obviously, more work is needed to answer questions in this area. For example, is the improvement in mood associated with psychotherapy accompanied by increases in serotonin synthesis? If more precise information is obtained about the mental states that increase serotonin synthesis, will this help to enhance therapy techniques? The study by Perreau-Linck and colleagues

Exposure to bright light is a second possible approach to increasing serotonin without drugs. Bright light is, of course, a standard treatment for seasonal depression, but a few studies also suggest that it is an effective treatment for nonseasonal depression³⁸ and also reduces depressed mood in women with premenstrual dysphoric disorder³⁹ and in pregnant women suffering from depression.⁴⁰ The evidence relating these effects to serotonin is indirect. In human postmortem brain, serotonin levels are higher in those who died in summer than in those who died in winter.⁴¹ A similar conclusion came from a study on healthy volunteers, in which serotonin synthesis was assessed by measurements of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the venous outflow from the brain.⁴² There was also a positive correlation between serotonin synthesis and the hours of sunlight on the day the measurements were made, independent of season. In rats, serotonin is highest during the light part of the light–dark cycle, and this state is driven by the photic cycle rather than the circadian rhythm.⁴³^,⁴⁴ The existence of a retinoraphe tract may help explain why, in experimental animals, neuronal firing rates, c-fos expression and the serotonin content in the raphe nuclei are responsive to retinal light exposure.^44–48 In humans, there is certainly an interaction between bright light and the serotonin system. The mood-lowering effect of acute tryptophan depletion in healthy women is completely blocked by carrying out the study in bright light (3000 lux) instead of dim light.⁴⁹

Relatively few generations ago, most of the world population was involved in agriculture and was outdoors for much of the day. This would have resulted in high levels of bright light exposure even in winter. Even on a cloudy day, the light outside can be greater than 1000 lux, a level never normally achieved indoors. In a recent study carried out at around latitude 45° N, daily exposure to light greater than 1000 lux averaged about 30 minutes in winter and only about 90 minutes in summer⁵⁰ among people working at least 30 hours weekly; weekends were included. In this group, summer bright light exposure was probably considerably less than the winter exposure of our agricultural ancestors. We may be living in a bright light–deprived society. A large literature that is beyond the scope of this editorial exists on the beneficial effect of bright light exposure in healthy individuals. Lamps designed for the treatment of seasonal affective disorder, which provide more lux than is ever achieved by normal indoor lighting, are readily available, although incorporating their use into a daily routine may be a challenge for some. However, other strategies, both personal and institutional, exist. “Light cafes” pioneered in Scandinavia have come to the United Kingdom,⁵¹ and an Austrian village that receives no sunshine in the winter because of its surrounding mountains is building a series of giant mirrors to reflect sunlight into the valley.⁵² Better use of daylight in buildings is an issue that architects are increasingly aware of. Working indoors does not have to be associated with suboptimal exposure to bright light.

A third strategy that may raise brain serotonin is exercise. A comprehensive review of the relation between exercise and mood concluded that antidepressant and anxiolytic effects have been clearly demonstrated.⁵³ In the United Kingdom the National Institute for Health and Clinical Excellence, which works on behalf of the National Health Service and makes recommendations on treatments according to the best available evidence, has published a guide on the treatment of depression.⁵⁴ The guide recommends treating mild clinical depression with various strategies, including exercise rather than antidepressants, because the risk–benefit ratio is poor for antidepressant use in patients with mild depression. Exercise improves mood in subclinical populations as well as in patients. The most consistent effect is seen when regular exercisers undertake aerobic exercise at a level with which they are familiar.⁵³ However, some skepticism remains about the antidepressant effect of exercise, and the National Institute of Mental Health in the United States is currently funding a clinical trial of the antidepressant effect of exercise that is designed to overcome sources of potential bias and threats to internal and external validity that have limited previous research.⁵⁵

Several lines of research suggest that exercise increases brain serotonin function in the human brain. Post and colleagues⁵⁶⁵⁷ showed that exercise increased tryptophan and 5-HIAA in rat ventricles. More recent studies using intracerebral dialysis have shown that exercise increases extracellular serotonin and 5-HIAA in various brain areas, including the hippocampus and cortex (for example, see^58–60). Two different mechanisms may be involved in this effect. As reviewed by Jacobs and Fornal,⁶¹ motor activity increases the firing rates of serotonin neurons, and this results in increased release and synthesis of serotonin.⁶² In addition, there is an increase in the brain of the serotonin precursor tryptophan that persists after exercise.⁶³ measured biogenic amine metabolites in cerebrospinal fluid (CSF) of patients with depression before and after they increased their physical activity to simulate mania. Physical activity increased 5-HIAA, but it is not clear that this was due to increased serotonin turnover or to mixing of CSF from higher regions, which contain higher levels of 5-HIAA, with lumbar CSF (or to a combination of both mechanisms). Nonetheless, this finding stimulated many animal studies on the effects of exercise. For example, Chaouloff and colleagues

The largest body of work in humans looking at the effect of exercise on tryptophan availability to the brain is concerned with the hypothesis that fatigue during exercise is associated with elevated brain tryptophan and serotonin synthesis. A large body of evidence supports the idea that exercise, including exercise to fatigue, is associated with an increase in plasma tryptophan and a decrease in the plasma level of the branched chain amino acids (BCAAs) leucine, isoleucine and valine (see⁶⁴^,⁶⁵ for reviews). The BCAAs inhibit tryptophan transport into the brain.⁶⁶ Because of the increase in plasma tryptophan and decrease in BCAA, there is a substantial increase in tryptophan availability to the brain. Tryptophan is an effective mild hypnotic,⁶⁷ a fact that stimulated the hypothesis that it may be involved in fatigue. A full discussion of this topic is not within the scope of this editorial; however, it is notable that several clinical trials of BCAA investigated whether it was possible to counter fatigue by lowering brain tryptophan, with results that provided little support for the hypothesis. Further, exercise results in an increase in the plasma ratio of tryptophan to the BCAAs before the onset of fatigue.⁶⁴^,⁶⁵ The conclusion of these studies is that, in humans, a rise in precursor availability should increase serotonin synthesis during and after exercise and that this is not related to fatigue, although it may be related to improved mood. Whether motor activity increases the firing rate of serotonin neurons in humans, as in animals, is not known. However, it is clear that aerobic exercise can improve mood.

As with exposure to bright light, there has been a large change in the level of vigorous physical exercise experienced since humans were hunter-gatherers or engaged primarily in agriculture.⁶⁸ Lambert⁶⁸ argued that the decline in vigorous physical exercise and, in particular, in effort-based rewards may contribute to the high level of depression in today's society. The effect of exercise on serotonin suggests that the exercise itself, not the rewards that stem from exercise, may be important. If trials of exercise to prevent depression are successful, then prevention of depression can be added to the numerous other benefits of exercise.

The fourth factor that could play a role in raising brain serotonin is diet. According to some evidence, tryptophan, which increases brain serotonin in humans as in experimental animals,⁶⁹ is an effective antidepressant in mild-to-moderate depression.⁶⁷^,⁷⁰ Further, in healthy people with high trait irritability, it increases agreeableness, decreases quarrelsomeness and improves mood.³⁴ However, whether tryptophan should be considered primarily as a drug or a dietary component is a matter of some dispute. In the United States, it is classified as a dietary component, but Canada and some European countries classify it as a drug. Treating tryptophan as a drug is reasonable because, first, there is normally no situation in which purified tryptophan is needed for dietary reasons, and second, purified tryptophan and foods containing tryptophan have different effects on brain serotonin. Although purified tryptophan increases brain serotonin, foods containing tryptophan do not.⁷¹ This is because tryptophan is transported into the brain by a transport system that is active toward all the large neutral amino acids and tryptophan is the least abundant amino acid in protein. There is competition between the various amino acids for the transport system, so after the ingestion of a meal containing protein, the rise in the plasma level of the other large neutral amino acids will prevent the rise in plasma tryptophan from increasing brain tryptophan. The idea, common in popular culture, that a high-protein food such as turkey will raise brain tryptophan and serotonin is, unfortunately, false. Another popular myth that is widespread on the Internet is that bananas improve mood because of their serotonin content. Although it is true that bananas contain serotonin, it does not cross the blood–brain barrier.

α-Lactalbumin, a minor constituent of milk, is one protein that contains relatively more tryptophan than most proteins. Acute ingestion of α-lactalbumin by humans can improve mood and cognition in some circumstances, presumably owing to increased serotonin.⁷²^,⁷³ Enhancing the tryptophan content of the diet chronically with α-lactalbumin is probably not practical. However, increasing the tryptophan content of the diet relative to that of the other amino acids is something that possibly occurred in the past and could occur again in the future. Kerem and colleagues⁷⁴ studied the tryptophan content of both wild chickpeas and the domesticated chickpeas that were bred from them in the Near East in neolithic times. The mean protein content (per mg dry seed) was similar for 73 cultivars and 15 wild varieties. In the cultivated group, however, the tryptophan content was almost twice that of the wild seeds. Interestingly, the greater part of the increase was due to an increase in the free tryptophan content (i.e., not part of the protein). In cultivated chickpeas, almost two-thirds of the tryptophan was in the free form. Kerem and colleagues⁷⁴ argue that there was probably selection for seeds with a higher tryptophan content. This is plausible, given another example of an early strategy to increase the available tryptophan content of an important food source. Pellagra is a disorder caused by niacin deficiency, usually owing to poverty and a diet relying heavily on corn (maize), which has a low level of niacin and its precursor tryptophan. Cultures in the Americas that relied greatly on corn used alkali during its processing (e.g., boiling the corn in lime when making tortillas). This enhanced the nutritional quality of the corn by increasing the bioavailability of both niacin and tryptophan, a practice that prevented pellagra.⁷⁵ The Europeans transported corn around the world but did not transport the traditional alkali-processing methods, thereby causing epidemics of pellagra in past centuries. Breeding corn with a higher tryptophan content was shown in the 1980s to prevent pellagra⁷⁶; presumably, it also raised brain serotonin. In a recent issue of Nature Biotechnology, Morris and Sands⁷⁷ argue that plant breeders should be focusing more on nutrition than on yield. They ask, “Could consumption of tryptophan-rich foods play a role in reducing the prevalence of depression and aggression in society?” Cross-national studies have reported a positive association between corn consumption and homicide rates⁷⁸ and a negative association between dietary tryptophan and suicide rates.⁷⁹ Although the idea behind such studies is interesting, any causal attribution must remain speculative, given the possible confounds. Nonetheless, the possibility that the mental health of a population could be improved by increasing the dietary intake of tryptophan relative to the dietary intake of other amino acids remains an interesting idea that should be explored.

The primary purpose of this editorial is to point out that pharmacologic strategies are not the only ones worthy of study when devising strategies to increase brain serotonin function. The effect of nonpharmacologic interventions on brain serotonin and the implications of increased serotonin for mood and behaviour need to be studied more. The amount of money and effort put into research on drugs that alter serotonin is very much greater than that put into non-pharmacologic methods. The magnitude of the discrepancy is probably neither in tune with the wishes of the public nor optimal for progress in the prevention and treatment of mental disorders.

Footnotes

Competing interests: None declared.

Correspondence to: Dr. Simon N. Young, Department of Psychiatry, McGill University, 1033 Pine Ave. W., Montréal QC H3A 1A1; fax 514 398-4370; Simon.Young@mcgill.ca

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077351/
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The Placebo Effect: How to Use Your Mind-Body Connection for Healing via Deepak Chopra

2010-03-02T11:14:00.000-08:00

http://bit.ly/9WvlMK

In an earlier post, I raised the question of the mind healing the body. We know that this is possible because of the placebo effect, in which patients obtain relief even though the doctor has given them only a sugar pill, an injection of saline solution or some other innocuous substance. The placebo effect, contrary to widespread suspicion, is a "real" cure. Pain is diminished; symptoms are alleviated. But it depends upon deception. The doctor knows that he is giving a harmless substance; the patient doesn't.

So the issue comes down to triggering the mind-body connection without being deceived. Is there a way for each person to influence his body consciously? We do this all the time, of course. You can't lift a finger, throw a baseball or drive a car without translating a mental intention into a physical response. But when it comes to disease symptoms, the mind-body connection feels weak or nonexistent. Every sick person wants to get well. How can the mind help?

There are four conditions that would insure a stronger mind-body connection during illness, and all are inter-connected:

* The mind contributes to getting well.
* The mind doesn't contribute to getting sick.
* The body is in constant communication with the mind.
* This communication benefits both the physical and mental aspects of being well.

When the placebo effect works, it's clear all four aspects are involved. The patient's mind cooperates with the treatment and trusts it. The body is aware of this trust. There is open communication, and as a result, cells throughout the body participate in a healing response. The healing system as a whole is incredibly complex and all but impossible to explain as a whole. We only know parts of how it operates, such as our knowledge of antibodies and the immune response to infection.

How to use your mind to deal with illness

Yet somehow, for all its complexity, the healing system can be triggered by a simple intention of the mind. To be your own placebo, then, requires the same conditions that apply in a classic placebo response:

* You trust what is happening.
* You deal with doubt and fear.
* You don't send conflicting messages that get tangled with each other.
* You have opened the channels of mind-body communication.
* You let go of your intention and let the healing system do its work.

Clearly, everyone finds it easy to let go when a problem is small, such as a cut finger or a bruise. The mind isn't interfering with doubts and fears. But both play a major role in serious illness, which is why a practice like meditation or going to group counseling can be a great help. Sharing your anxiety with others in the same position is one way to begin to clear them.

It's also helpful to follow your instincts. Most of us deal with illness through misleading processes like wishful thinking and denial. Our fears lead us into the blind alleys of false hope. In such cases, the mind isn't really alert to what the body is saying, or vice versa. The atmosphere is clouded. To trust what your body is telling you implies that you will take action to give it what it wants. Each body wants different things at any given moment, but at the very least our bodies do best without tobacco, alcohol, excessive medications and various chemical adulterants.

How to become more aware of your body

One way to become more aware of your body is to sit quietly with your eyes closed and simply feel the body. Let any sensation come to the surface. Don't respond to the sensation, whether pleasant or unpleasant. Relax and be aware of it. Notice where the sensation is coming from. There won't be one sensation or feeling only. You will find that your awareness goes from place to place, one moment noticing your foot or your stomach, your chest or your neck.

This simple exercise is like a mind-body reconnection. Too many people are in the habit of not paying attention to anything but the grossest signals from their bodies, like extreme pain, stiffness or discomfort. What you want to do is to increase your sensitivity and your trust at the same time. Your body knows at a subtle level where disease and discomfort are. It sends signals at every moment, and these are not to be feared. Even if you consciously ignore what is happening in your cells, there is a level of conscious information that is being exchanged just below the level of awareness.

Indeed every cell in the body knows, through chemical messengers, what every other cell is doing. By bringing your conscious mind into the loop, you are adding to this communication. How? The body operates through two compatible aspects of the nervous system. One is involuntary and takes care of every process that doesn't need your awareness. The other is voluntary, meaning that it responds to your awareness. These two aspects of the mind/brain are connected. You can switch from one to the other.

For example, if you are stuck in traffic and feeling stressed, your heart rate can increase involuntarily. Yet you can also choose to go running, which increases your heart rate as the result of your intention. We know from research experiments that advanced yogis can alter involuntary responses at will, such as lowering their heart rate and breathing to very low levels or increasing skin temperature in a very precise way. As it happens, you and I have the same abilities, although we don't consciously use them. You can be led through an exercise to make a spot on the palm of your hand grow warmer, and it would happen even though you have never used that ability before.

One can venture that the placebo effect falls into the same category. It's a voluntary response we could use if only we learned to. The healing system seems to be involuntary. You don't have to think in order to heal a cut or a bruise. Yet the fact that some patients can make their own pain go away when given a sugar pill they think is aspirin implies, very strongly, that intention makes a difference in healing. We aren't talking about positive thinking, but a deeper mind-body connection.

One final note: Because this is a public forum read by all kinds of people with all kinds of health issues, let me be clear. I am not—repeat not—advising anyone to stop conventional medical treatment or to reject medical help. The placebo effect remains mysterious, and this article is exploring that mystery, not giving you a how-to for self-cure.

Keep Reading

How to be your own placebo
Start listening to your body's signals

Deepak Chopra is the author of more than 50 books on health, success, relationships and spirituality, including his current best-seller, Reinventing the Body, Resurrecting the Soul, and The Ultimate Happiness Prescription, which are available now. You can listen to his show on Saturdays every week on SiriusXM Channels 102 and 155.

http://www.oprah.com/spirit/Use-Your-Mind-Body-Connection-to-Heal/2
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Sane-and-Sober Today!
http://sane-sober.blogspot.com/
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Why It's Better to Have a Mind Than a Brain by Deepak Chopra

2010-03-02T11:08:00.000-08:00

http://bit.ly/d96Ws1

First, Deepak Chopra explained how you can be your own placebo and ways to use your mind-body connection for healing. Now, get his take on the difference between the mind and the brain and which one you need to heal before you can treat depression.

I've decided to continue to write about the mind. In particular, the point must be made that we are not our brains. We are our minds, a rich, alive, constantly changing mystery. The brain carries out what the mind wants. To mistake the brain, a lump of proteins, sugar and water, for a mind is a drastic mistake.

But it also happens to be the mistake of choice for modern science. It will help the mind side of the debate to read the recent cover story in Newsweek, which proclaimed, in stark terms, "Antidepressants don't work."

The support for this bold and disturbing claim comes from previous articles in scientific journals, where the whole rationale for giving a pill to treat depression was undermined. First, when a patient comes to the doctor complaining of mild to moderate depression (the kind most commonly encountered, as opposed to the crippling disorder known as severe chronic depression), for up to 50 percent of people, the standard antidepressants offer no improvement. Some studies indicate that the placebo effect is just as reliable and offers just as much relief as these medications.

Yet for the mind-brain debate, it's another research finding that stands out. The brains of depressed people aren't different from the brains of undepressed people. It has long been assumed that depressed brains are deficient in two vital neurotransmitters called serotonin and dopamine. Taking an antidepressant was supposed to rectify this imbalance. But studies indicate that the genes responsible for the secretion and regulation of neurotransmitters are the same in depressed people as they are in undepressed people.

Which means that your brain may be used to being depressed. It may even be used to a chemical imbalance of some sort. But to focus solely on the brain is to miss major causes of depression that are mental instead. Think of the experiences that can make a person depressed, meaning someone with a mind:

* Outside stress
* Personal crisis
* Grief
* Physical illness
* Sudden life changes
* Accidents and unforeseen setbacks
* Loss of job or money
* Personal insecurity
* Failure
* Bad parenting
* Low self-esteem
* Negative religious beliefs leading to guilt and shame
* Other causes of guilt and shame
* Rejection in love
* Being around other depressed people, particularly family members
* The X factor

This is a long list. Even if we discount some undiscovered cause (the X factor), the mind is faced with the complexity of life, and numerous experiences can engender depression. If I tell you that you've just been fired, it's not your brain that will make you depressed. It's a sudden jolt of devastating bad news. Nobody knows why some people convert bad experiences into depression while others don't. It is equally true, after all, that the glass is half empty and half full. Studies show that when shown neutral photos of various people and situations, depressed people habitually see them as negative, disappointing, sad and unlikely to lead to a positive outcome.

Are antidepressants helpful?

Thus, depression has a large circular component of response and habit. A person learns to respond to ordinary situations by being depressed, and once learned, this response becomes a habit that reinforces itself. The habit of depression is as hard to break as addiction. And in both cases one hears the cry: "I can't help it. I have to be this way. This is me." Telling someone that they are prisoners of their sick or damaged brains only reinforces this belief and the circle of depression.

Those who focus on the brain seem to be right that habitual responses form neural pathways that constantly reinforce the same depressed reaction. These pathways are like ruts in the road that a wagon wheel falls into automatically. But brain researchers are misguided to ignore the mind. That's like saying that the road made its own ruts.

I've said enough to provoke scorn from the materialists and outrage among some depressed people, who accuse me of saying that they have caused their condition. I am robbing them of hope. I am saying nothing of the sort, however. Severe depression requires medical treatment of the most intensive kind. Millions of people testify that antidepressants have relieved their suffering. Nobody is trying to counter such testimony. Nobody is offering despair in place of hope.

But the research that has undermined antidepressants cannot be wished away. In many ways, the brain has been a cop-out for the therapeutic community. Instead of undertaking long, expensive cognitive therapy that tries to get to the bottom of why a person is depressed, how much easier is it to write a prescription? This despite the fact that talk therapy has proven to work in cases of mild to moderate depression. But Prozac, the first billion-dollar drug, seemed to cut the Gordian knot.

Going the route of antidepressants, behind all the hype and the millions spent by drug companies to boost their products, was always far from perfect. There were side effects. There was drug tolerance, which causes a medication to become less effective over time. There was the stark reality that antidepressants only relieve symptoms; they were never a cure. Finally, the same research that undermined the efficacy of antidepressants also found that taking them doesn't aid with other therapies used at the same time.

I'm not deliberately painting a dismal picture. The drug route leads to its own dead end (discounting, once again, those who are actually helped). Let's keep exploring the use of psychotropic medications. It would be naive to believe that America is going to abandon a belief system that puts materialism ahead of everything else. But discounting the mind while constantly referring everything to the brain is folly. It defies common sense, for reasons we will go into in the next post.

Keep Reading
How to be your own placebo

The placebo effect: How to use your mind-body connection for healing

Deepak Chopra is the author of more than 50 books on health, success, relationships and spirituality, including his current best-seller, Reinventing the Body, Resurrecting the Soul, and The Ultimate Happiness Prescription, which are available now. You can listen to his show on Saturdays every week on SiriusXM Channels 102 and 155.
From Oprah.com on Tuesday, March 2, 2010
© 2010 Harpo Prod

http://www.oprah.com/spirit/Why-Its-Better-to-Have-a-Mind-Than-a-Brain
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Sane-and-Sober Today!
http://sane-sober.blogspot.com/
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Year of the Tiger meets St. Valentine’s Day

2010-02-12T18:57:00.001-08:00

http://bit.ly/dBPEAc

Year of the Tiger meets St. Valentine's Day

David Bebee, Record staffAstrologer Bryan Trussler will be doing a talk on the Chinese new year.

February 12, 2010

By Valerie Hill, Record staff

KITCHENER — Does the fact that Chinese New Year's falls on the same day as Valentine's Day this year portend of great things to come for those romantic souls? Well, it's all in the stars.

This Chinese New Years trumpets the beginning of the Year of Tiger, and like its namesake, the upcoming year can be temperamental and unpredictable. Much like romance.

The Year of the Tiger's formal name is Geng Yin and is the third sign in the Chinese zodiac. This new year will begin on Valentine's Day, Feb. 14, and replaces the Year of the Ox.

Bryan Trussler, professional astrologer and consultant as well as a teacher, said this month's transition from the Year of the Ox to that of the tiger can be tumultuous as both animals are so different: one steadfast and stentorian, the other all instinct, unpredictable, watching and waiting to pounce. Tigers are to be carefully watched.

"They are the predator," said the Kitchener astrologer. He points out that in the U.S., previous years of the tiger brought unexpected upheavals such as Watergate, the Monica Lewinsky scandal, the Cuban missile crises and the Iran/Contra crises.

"In Canada, not so much," he said of our milder political climate, though everyone should still be wary. "Expect to be blindsided, out of left field." When it comes to love in the year of the tiger, there could be more energy, and more conflict. "The tiger likes nothing better than a good fight. They'll get what they want."

Trussler warns, the year of the tiger can signal flared tempers and conflict, not a good combination particularly if you are trying to woo someone. On the plus side, tigers are courageous and the year should be met with happiness and a smile, and, above all, don't criticize others. Such a positive beginning for the new year could set the standard for the next 12 months.

In a broader sense, the year of the tiger can signal variable weather such as late snowfalls, lots of wind and early thaws, said Trussler. "In the States, they could have a bumper crop of tornadoes."

Politically, the tiger can bring early elections but with little real change to the country, even if Canada ends up with a different party running the government. At home, the tiger wards off fire, thieves and ghosts.

Trussler holds a master's degree in religion and culture from Wilfrid Laurier University and developed his interest in astrology in 1987, attracted by both its history and complex characters. To understand Chinese astrology, he suggests conjuring an image of a compass containing circles within circles. An inner circle is broken into dawn and noon, dusk and night. The next circle contains the four seasons, followed by a circle representing the four elements: fire, water, metal and wood. The 12 animal signs show up on the zodiac in one of the largest, outer circles. Each animal has a particular temperament, which is then reflects what is to come.

At the heart of all this is the Taoist philosophy, the theory of Yin Yang, which are two opposing principles leading to changes in the universe. The Year of the Tiger symbolizes the female Yin energy, opposite of the Yang male energy of the dragon.

Both Chinese New Year's and Valentine's share the colour red as a powerful symbol of good luck and happiness and both holidays can be seen as a time of renewal and of love, a time for sharing. Frances Tse of the Central Ontario Chinese Cultural Centre in Kitchener, said that in China, young people often go the temple on Valentine's where they give a wish of love, while lighting incense.

Tse's friends, Peter Chieh and his wife Shiao-Yu, said that in China, Valentine's Day has about the same meaning as it does in North America, a time when young lovers get together for a special day though in China they tend to stroll outdoors in nature. They said there is also a similar, though more ancient holiday, based on the legend of the seventh daughter of the Emperor of Heaven.

According to legend, the daughter left her father's side to marry a lowly human cow header and raise children. Upon discovery, the young woman was forced to return to her heavenly paradise. Her poor husband implored the father to reunite the couple and he agreed to just one day a year, thereafter celebrated as the 7th Goddess Day. The holiday falls on the seventh day of the seventh lunar month in the Chinese calendar, which is usually in the summer months. "A lot of people like to get married on that day," said Shiao-Yu.

Love in China when the Chiehs were children is very different than today, said the couple. During the era of their parents, many young people would have been married off according to a matchmaker's recommendation and the matchmaker was often just a family friend, not a professional. The young couple would have to be from families of equal social standing. Love never entered into the equation.

Even as he was growing up, public affection was frowned upon. "It was quite reserved," Peter said. "You were not allowed to touch each other."

Today, he said, Chinese couples chose their own partners and tend to marry later in life after finishing their education and embarking on a career though it's not unusual to have friends and family members make recommendations, given young people are too busy to search on their own.

"It's different than in the West," he said. "In China, they partner for life. It's a serious matter. You have to be there for each other, you have to work for each other. Divorce is not common."

vhill@therecord.com

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Unidos Venceremos! United We Will Win!
~Peta~de~Aztlan~ Sacramento, California, Amerika
Email: peter.lopez51@yahoo.com

http://twitter.com/Peta_de_Aztlan @Peta_de_Aztlan

http://www.facebook.com/Peta51

http://help-matrix.ning.com/

"Those who make peaceful revolution impossible, make violent revolution inevitable."
~ President John F.Kennedy ~ Assassinated November 22, 1963
c/s

Prescription narcotics cause more deaths than both heroin and cocaine

2010-01-02T06:53:00.001-08:00

http://bit.ly/4Mh7wK

Prescription narcotics cause more deaths than both heroin and cocaine

Wednesday, December 23, 2009

by Mike Adams, the Health Ranger

(NaturalNews) On the heels of the sudden death of celebrity actress Brittany Murphy (http://www.naturalnews.com/027781_Brittany_Murphy_drugs.html ), people are once again raising the question of just how dangerous prescription drugs might really be.

Some are arguing, however, that street drugs are the real danger, not prescription drugs. But the following study demonstrates why prescription drugs are far more dangerous than illegal recreational drugs.

According to a new study conducted by physicians at St. Michael's Hospital and the Institute for Clinical Evaluative Sciences (ICES) in Toronto, the number of deaths due to prescription opioid use has doubled between 1991 and 2004. Following the introduction of oxycodone into Toronto's drug formulary in 2000, there has been a 500% increase in deaths due to the drugs.

Researchers reviewed over 7,000 files from the Office of the Chief Coroner in Ontario and found that between the years of 1991 and 2004, oxycodone prescriptions increased by more than 850 percent, representing about one-third of the opioid prescriptions given in 2006. (This is the largest prescription increase among all opioid drugs.)

Following the addition of this drug into the provincial drug benefit plan in 2000, deaths from opioid usage rose by 41 percent. Shockingly, deaths from prescription opioids like oxycodone were far greater than deaths from heroin. The vast majority of people who died from opioids had visited their doctor and received a prescription for the drug within a month of their death.

The total number of opioid-related deaths in Toronto in 2004 is estimated to be 27.2 per million people. Study authors said they hope to shed light on the tremendous dangers associated with prescription opioid drugs.

Coked up on prescription smack

It's the dirty little secret of the pharmaceutical industry: More people are killed by prescription opioids than all those killed by heroin and cocaine combined. And that probably even includes all the shootings of gang bangers in northern Mexico.

Prescription drug abuse is now more common than street drug abuse -- by far! And yet Big Pharma rakes in huge profits from all the patient addictions to their opioids. And by "opioids", what I mean is narcotics. They are, in fact, one and the same.

So of all the drug addicts in America today, you can divide them into two camps:

1) People addicted to street drugs.

2) People addicted to prescription drugs.

The people in group #1 (street drugs) are taken to jail where they are given prison sentences. People in group #2 (prescription drugs) are taken to their doctor where they are given prescription refills. It's all really the same narcotics, it's just that one group is legal and the other is illegal.

And what really determines whether a particular narcotic is legal or illegal? Whether or not Big Pharma profits from it. If Big Pharma makes money off the narcotics, they're considered legal.

Big Pharma, you see, earns tens of billions of dollars each year from drug addicts. And just by coincidence, it turns out that their prescription narcotics are extremely addicting, guaranteeing repeat business. The business model is so dang lucrative, you might think they were drug dealers...

Why do you think the main sponsors for the Partnership For A Drug-Free America are the drug companies themselves? It's because Big Pharma is trying to eliminate the competition. By keeping up the so-called "War on Drugs" front, the pharmaceutical industry can make sure it dominates the market for narcotics. After all, if you're going to feed narcotics to a nation full of junkies, why not make a hefty profit on it? That's the thinking of drug companies, it seems, as they have done basically zilch to effectively stem the abuse of their own prescription narcotics.

Much like the tobacco companies, drug companies secretly want people to be addicted to their products.

Sources for this story include:

Deaths related to narcotic pain relievers have doubled since 1991: Study

http://www.eurekalert.org/pub_releases/2009-12/smh-drt120109.php

Deaths from opioid use have doubled, 5-fold increase in oxycodone deaths

http://www.eurekalert.org/pub_releases/2009-12/cmaj-dfo120109.php

About the author: Mike Adams is a natural health researcher and author with a passion for sharing empowering information to help improve personal and planetary health He has authored and published thousands of articles, interviews, consumers guides, and books on topics like health and the environment, reaching millions of readers with information that is saving lives and improving personal health around the world. Adams is a trusted, independent journalist who receives no money or promotional fees whatsoever to write about other companies' products. In 2007, Adams launched EcoLEDs, a manufacturer of mercury-free, energy-efficient LED lighting products that save electricity and help prevent global warming. He's also a successful software entrepreneur, having founded a well known email marketing software company whose technology currently powers the NaturalNews email newsletters. Adams volunteers his time to serve as the executive director of the Consumer Wellness Center, a 501(c)3 non-profit organization, and practices nature photography, Capoeira, Pilates and organic gardening. Known on the 'net as 'the Health Ranger,' Adams shares his ethics, mission statements and personal health statistics at www.HealthRanger.org

http://www.naturalnews.com/027794_narcotics_addiction.html

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Venceremos Unidos! Education for Liberation!

Peter S. López, Jr. aka~Peta

Email: peter.lopez51@yahoo.com

http://twitter.com/Peta_de_Aztlan

<>+<>+<>+<>+<>+<>+<>+<>+<>+<>+<>>+<>+<>
Key Recovery Links:
http://prorecovery.blogspot.com/

http://casa-12steps.blogspot.com/

http://groups.yahoo.com/group/CASA-12-Steps-Program/
<>+<>+<>+<>+<>+<>+<>+<>+<>+<>+<>>+<>+<>

HumanE-Liberation-Party~http://help-matrix.ning.com/

c/s

FYI: A Homeless Success Story!

2009-12-29T18:12:00.001-08:00

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Gracias ~ I will pass it on!

Venceremos Unidos! Education for Liberation!

Peter S. López, Jr. aka~Peta

Email: peter.lopez51@yahoo.com

http://twitter.com/Peta_de_Aztlan

From: Cottage Housing Inc. <jwalten@cottagehousing.org>
To: peter.lopez51@yahoo.com
Sent: Tue, December 29, 2009 1:20:29 PM
Subject: A Homeless Success Story!

from the streets to self-sustainability

A Homeless Success Story!

My daughter and I arrived at Quinn Cottages without much furniture but with lots of hope. We didn't just get a place to live; we also found a new beginning.

I write to ask for a donation that would give other families the same opportunity.

I was homeless before coming into this Cottage Housing program, and my life was about drug addiction, welfare dependence and criminal behavior. I dropped out of school and was a terrible mom for my daughters. I had been in and out of jail for receiving stolen property, grand theft auto, burglary, drug possession, and check fraud. I could not imagine being a productive member of society, holding a job and supporting my family. I felt like I was stuck and didn't think there was any way out.

The worst part of being in prison was when my children called saying they wanted me to come home but I couldn't.

Right then I knew if I didn't change, I was going to spend the rest of my life in prison or soon end up dead. I wanted something better and knew I needed to do something different but didn't know what or how.

Cottage Housing gave me the opportunity to create the life I have today. The program gave me the chance to develop living skills I'd never learned --- like how to be a parent ... balance a checkbook ... stay sober. It also helped me to be around others who were committed to making changes in their lives.

For the first time, I had a sense of direction toward the goals that made me the woman I am today. I took positions of responsibility within the program where I learned how to be accountable - not to the staff, but to myself.

I'm now employed at the place I went to for help, extending to others the same opportunities offered to me. Some program participants say: "you can't possibly understand what I've been through", but when they see I've been there and hear what has happened since, they think: if she can do it, I can too.

Thanks to people like you investing in Cottage Housing, more than six hundred formerly homeless people have successfully graduated from Quinn Cottages and Serna Village with housing secure, income stabilized and sobriety intact. I am proud that this year's exiting participants achieved a 90.2% graduation rate - our highest ever!

I came up with the phrase: "we're going from tax-taker to tax-maker". I save myself and other taxpayers over $100,000 every year I stay out of prison, keep my kids out of foster care, remain employed and off welfare. Unlike 70% who return to California prisons - which have the highest recidivism rate in the nation - I haven't been in trouble since getting off parole.

I have a wonderful life and my future has no limits. I completed my human services degree in chemical dependency at American River College, and am securing certification in addiction counseling. I've been sober for eleven years, breaking the cycle of addiction, unemployment and dysfunction within my family.

My daughters have learned from my experience without following in my footsteps, and won't have to go through what I did to get where I am today. It took me too long to realize there is enjoyment in life ... we all face hard times, but it's not hard all the time.

Please make one of your gifts during this holiday season a financial donation to the program that helped me become the contributing member of society I always wanted to be.

In appreciation,

Cynthia Hunt, Alumna & Program Manager

Quinn Cottages

Donate Now!

Quinn Cottages and Serna Village are healing residential communities
where homeless people help themselves - and each other-
in their transition from the streets to self-sustainability.

The project's +75% graduation rate is made possible through partnership
between Cottage Housing Inc. and Mercy Housing California,
the construction and property manager,
and through collaboration with numerous community allies.

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FYI:[Progressive Recovery Today!] On Our Spiritual Liberation Program: via Peter ...

2009-12-14T11:05:00.001-08:00

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Comment: Take it for what it is worth to you. It you do not have

any 'issues', just remember that if you wear your halo too tight

you can get a headache! ;->~

Venceremos Unidos! Education for Liberation!

Peter S. López, Jr. aka~Peta

Email: peter.lopez51@yahoo.com

http://twitter.com/Peta_de_Aztlan

HumanE-Liberation-Party~http://help-matrix.ning.com/

c/s

From: ~Peta-de-Aztlan~ <peter.lopez51@yahoo.com>
To: peter.lopez51@yahoo.com
Sent: Sun, December 13, 2009 8:47:16 AM
Subject: [Progressive Recovery Today!] On Our Spiritual Liberation Program: via Peter ...

Post: Saturday, December 12, 2009

CASA is a progressive recovery group based upon the original 12-Steps spiritual program first made popular by Alcoholic Anonymous in order to help drunken alcoholics achieve long-term lasting sobriety. The two co-founders of A.A. were Bill Wilson (1895 –1971) and Dr. Bob Smith (1879–1950). The founding date of A.A. in June 1935 is based upon Dr. Bob's last drink of beer. He remained sober until his death in 1950 from colon cancer and was an avowed Christian man of God without reservations.

On the other hand, though Bill Wilson remained sober from alcohol, despite death bed requests for whiskey, he had other 'issues'. He saw a Jungian psychotherapist from 1945 to 1949 for severe bouts of depression; took LSD in a designed medical situation in 1956 and several times more up to 1959; had a female business associate who received a lifelong 10% of his book royalties with suspicions of infidelity to his wife Lois (founder of Al-Anon); and had a life long interest in esoteric spiritualism and the occult, including séances. He seemed to be in search of new alternative cures for alcoholism. In his own unique controversial way, Brother Bill was a genius as a social engineer, especially with the worldwide success of A.A. and its basic 12-Steps program.

As time went on more and more people saw the 12-Steps program as appropriate for the treatment of a variety of disorders: drug addiction, gambling, obesity, sexual promiscuity and other sufferings of the soul. Thus, there are now many groups who use the 12-Steps to address specific problems and various issues in question. The 12-Steps offer a set of spiritual principles and general guidelines for good character building, getting rid of major character defects and being aware of personal shortcomings. Plus, it helps improve our relationships and communications with others by using basic humane spiritual principles for all our social interactions; making appropriate amends to those we have wronged; and the on-going maintenance of conscious awareness as to how we work with people on a daily basis. Learn from past mistakes to prevent future ones. What comes around goes around; karma creates karma.

For progressive recovery, sobriety is the central starting gate for sober living but we need to continue to advance spiritual growth, not get strung out on recovery and think going to recovery meetings and sitting silent is enough. We need to clearly understand the deeper origins of addiction in order to root out its symptoms out of our lives for good. We must change our old evil ways into new ways of being genuine, honest and 'for real'. Create good order out of confused chaos. As a mature, functional and responsible adult, be centered in a good healthy balance with high level of self-esteem, self-love and self-respect.

We should strive to be liberated beings involved in a spiritual liberation program. Be liberated and free from all forms of oppression and self-oppression, including the affliction of drug addiction and the insane vicious circle that comes with it. There is no good addiction. The addict does not know when to stop and when enough is enough. All indulgence in addiction is being out of balance, self-destructive and harmful to our well-being. There are relative differences between use, abuse and addiction, but casual use easily develops into hard core addiction in a cunning, powerful and baffling way.

Addiction is an obvious sign of Obsessive Compulsion Disorder (OCD). The drug addict is obsessed about a drug to alter his consciousness. He has a mad compulsion to indulge in it when it is at hand that he cannot control. At times the addict will switch to another drug or suffer cross addiction. He can become addicted to medication that often takes him back to his original drug of choice. Hard core addiction is a manifestation of obvious mental illness and deeper spiritual sickness. The 'dope fiend' finds it impossible to really live a normal healthy life with its rewards and responsibilities. Live life on life's terms one day at a time and be prepared for its ups and downs. A good healthy life is lived in pursuit of the best in life, true spiritual liberty and inner happiness, not in paranoid fear.

As a recovering addict, continue to work in a three-stage spiritual healing process of daily sobriety, continued recovery and spiritual growth. Do not dwell on the past with all its guilt trips and sad shames. Do not forget key lessons learned from past experiences. Remember the past to clearly see today, but do not try to live in the past. Neither should we have endless anxiety about the future filled with worries that shows a lack of faith in the Creator and the dynamic healing process. The past is over, the future has not arrived. It is HOW we are really being HERE NOW that matters the most to us today.

Let your being be in a spiritual realm on a natural high, being happy with your progress and with you being you. Live in harmony with the Creator, your inner self and others you care about in your life. If you are without joy and never comfortable in your own skin, then there is something dreadfully wrong with the way you are being. A severe relapse or even a short slip is a sign of continued sickness and a weak phony program without a spiritual foundation. The spiritual foundation of our program should be an undying faith in the Creator, not traditional anonymity.

Ask the right questions, find your own answers, figure stuff out on your own and come to your own conclusions in your own mind. It is ultimately a spiritual journey that you must travel on your own. Others can walk along with you, but you alone must be brave and walk your own journey, no one else can walk it for you. If spiritual healing is to come true, it is up to you. We hold regular meetings together for group support, to listen and learn, to heal and help and to share our "experience, strength and hope". Nevertheless, you must develop your own spiritual liberation program in a way that works best for you. Work your own program for your own life, for your own self-interest and your personal survival. It is your program!

Ultimately, the addict is a creature divorced from his own best survival interests, from the workings of his own inner soul and from conscious communion with the Creator. His soul has lost its original soul intention for being on Mother Earth: spiritual liberty!

"The fastest spiritual growth will always be through following your inner guidance in the moment, not in following some external ideal. Spiritual unfoldment always has to develop from precisely as you are and where you are right now.
~ Deepak Chopra ~ http://www.intent.com/deepakchopra/profile

To know and love others is good; to know and love your true soul is enlightenment.

c/s

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● Progressive Recovery Today!
http://prorecovery.blogspot.com/

● CASA 12-Steps Program Blog
http://casa-12steps.blogspot.com/

● CASA 12-Steps Program Yahoo Group
http://groups.yahoo.com/group/CASA-12-Steps-Program/
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Posted By ~Peta-de-Aztlan~ to Progressive Recovery Today! at 12/13/2009 08:47:00 AM

Echo ~ NATIVE AMERICAN CODE OF ETHICS ~

2009-12-08T11:14:00.001-08:00

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http://www.networkaztlan.com/indigenous.html

Echo ~ NATIVE AMERICAN CODE OF ETHICS ~

1. Rise with the sun to pray. Pray alone. Pray often. The Great Spirit will listen, if you only speak.

2. Be tolerant of those who are lost on their path. Ignorance, conceit, anger, jealousy and greed stem from a lost soul. Pray that they will find guidance.

3. Search for yourself, by yourself. Do not allow others to make your path for you. It is your road, and yours alone. Others may walk it with you, but no one can walk it for you.

4. Treat the guests in your home with much consideration. Serve them the best food, give them the best bed and treat them with respect and honor.

5. Do not take what is not yours whether from a person, a community, the wilderness or from a culture. It was not earned nor given. It is not yours.

6. Respect all things that are placed upon this earth - whether it be people or plant.

7. Honor other people's thoughts, wishes and words. Never interrupt another or mock or rudely mimic them. Allow each person the right to personal _expression.

8. Never speak of others in a bad way. The negative energy that you put out into the universe will multiply when it returns to you.

9. All persons make mistakes. And all mistakes can be forgiven.

10. Bad thoughts cause illness of the mind, body and spirit. Practice optimism.

11. Nature is not FOR us, it is a PART of us. They are part of your worldly family.

12. Children are the seeds of our future. Plant love in their hearts and water them with wisdom and life's lessons. When they are grown, give them space to grow.

13. Avoid hurting the hearts of others. The poison of your pain will return to you.

14. Be truthful at all times. Honesty is the test of ones will within this universe.

15. Keep yourself balanced. Your Mental self, Spiritual self, Emotional self, and Physical self - all need to be strong, pure and healthy. Work out the body to strengthen the mind. Grow rich in spirit to cure emotional ails.

16. Make conscious decisions as to who you will be and how you will react. Be responsible for your own actions.

17. Respect the privacy and personal space of others. Do not touch the personal property of others - especially sacred and religious objects. This is forbidden.

18. Be true to yourself first. You cannot nurture and help others if you cannot nurture and help yourself first.

19. Respect others religious beliefs. Do not force your belief on others.

20. Share your good fortune with others. Participate in charity.

http://www.networkaztlan.com/indigenous.html

c/s

Venceremos Unidos! Education for Liberation!

Peter S. López, Jr. aka~Peta

Email:peter.lopez51@yahoo.com

http://twitter.com/Peta_de_Aztlan

HumanE-Liberation-Party~http://help-matrix.ning.com/

c/s

Friday Night~from Peter in 501

2009-11-27T21:11:00.001-08:00

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Thank you for the Office and Cell Numbers left on my door. I must of been taking a shower ~ I rarely take the time for baths anymore since the bath fiasco.

Yesterday afternoon I got a call from my Supervisor at Salvation Army ~ Natasha Perez ~ and she said they had an abundance of food left. She was thinking of sharing stuff with residents here, BUTTT I could not contact anyone in the office. I suggested they share with the Union Gospel Mission. I work on Saturdays and will see what is up tomorrow.

I am getting a few people at the CASA Talking Circle on Wednesdays at
6 PM and sometimes a couple from here in this building. One evening no one showed up so I just sat there for an hour and read my book.

I will keep being there for now. It would be good to distribute the CASA Notice to the next building and have it posted somewhere.

See Attachment

It would be good if we had a general Community Bulletin Board for people. So many of the tenants here seem to be isolated away from each other in their own apartments. After my work day at Sally's I have learned to greatly appreciate the solitude of my loneliness and I rarely have any visitors here, except maybe my Brother Bobby sometimes.

I just hope none of the residents here has a melt down because they failed to reach out to anyone outside their apartment for help.

If it continues to be OK with you I will keep doing them, at least through the Holidays and if my schedule is good for it.

Matthew 18:20
For where two or three are gathered together in my name, there am I in the midst of them.

Education for Liberation!
Peter S. López, Jr. aka~Peta
Office: 916/442-0331 x3051
CASA: 916/346-4483
Email: peter.lopez51@yahoo.com
http://twitter.com/Peta51

Stress Weight Gain

2009-11-26T10:28:00.001-08:00

http://joegoldfarb.com/health/stress-weight-gain

Stress Weight Gain

Posted: November 21st, 2009 | Author: Joe | Filed under: Positive Thinking, health | 1 Comment »

Who doesn't want to lose weight? Many people go to gyms daily and take an assortment of diets towards that goal and fail to reach it. We all know someone who stopped a diet or gym visits for one reason (excuse) or another. Yet there is a factor at play in weight gain much stronger than any fast food or lack of using workout machines. That factor is psychological. The mind, the perception of one's relationship to their environment causes one to gain weight. Let me explain.

The number of Americans that overweight and obese is increasing. In fact, more than one-third of women between the ages of 20 and 74 are not overweight but obese. Interestingly, the majority of these women are African or Mexican American.

Diet and food are quickly to blame for the weight problem. In truth, this is a factor. Not only are peoples food choices unwise but poor neighborhoods generally have higher store food prices with less fruits and vegetables than other neighborhoods. Thus eating cheap fast food becomes a bargain relative to calorie/cost ratio. This same reason applies to other food choices such as pastas, cheap fatty meats, and so forth. A strong argument for the minority weight problem is the lack of healthy neighborhood food choices. Adding fuel to this position is the lack of parks, walking and biking paths.

Interestingly, eating poor quality foods leading to weight gain is not the whole picture. An interesting study emerged from Stanford University. Two rat groups both ate the same type and amount of food. The group of rats that were subjected to stress gained weight.

More studies emerged, one from London I believe that showed lower ranking employees tended to be overweight while high ranking employees, managers, and executives are not .

This was confirmed by a study of wild baboons in Africa. Baboons with lower social ranking in the troop had higher levels of stress hormones in their blood. These stress hormones have previously been linked to weight gain around the midsection. Some of the low ranking baboons were indeed fat. The alpha baboons in the troop had no stress hormones in their blood and no extra weight. Wild baboons in regards to social ranking and fat deposits matched the London employee study. The research on stress weight gain has cross-species proof.

Esteem

This brings us back to the African Americans and Mexican Americans who constitute the majority of obese Americans. Minorities tend to be located in low income neighborhoods. Existing low on the economic scale puts everyone who has money and power above. Without money one may feel trapped by bills and unable to move or lacking a voice and power and feel insignificant to society. One may have feel they have no other option than to be employed in a dead end job to make ends meet, pay bills and put food on the table for their children. This raises stress. This will cause weight gain. As proved with baboons and low status employees, feeling a lack of power harms the body by releasing stress hormones that add weight to the midsection. Prolonged stress leads to depression.

Weight gain not only occurs with certain food intake and a lack of exercise but also from stress caused from low social status. If you can entertain humor here, making yourself feel worthless will certainly cause a cascade of behavioral and hormonal changes that will cause you to pack on the pounds. Surely you will not employ this as a weight gaining method but rather as a learning tool to better understand how your relationship to your social environment has on your well-being. Depression, anxiety, and other stress related disorders are symptoms of a misaligned inner and outer relationship to reality. Weight gain is a physical manifestation of this.

This same relationship you have with your social environment dictates your overall view of reality. Those that are under stress will not think clearly, will have mental fog and will have a weak, continuous deteriorating relationship with the external world. When this happens opportunities for growth presented by the Universe is missed or not created due to the weak relationship, whichever position you feel is metaphysically correct.

When suck in the mud only one thing get's you out. To rise above your limited physical environment requires a change in your thinking first. Engage in an abundance mindset. Let go to the old mindset of scarce resources. When you change your thinking a shift of inner power occurs. This power shift is key to rise from the bottom to the top and all it requires is a perceptional change of reality. As long as you continue to put yourself in powerless situations your health will suffer.

Let's get back to the low-tiered employees and the baboons. Remember the studies showed the alphas in both groups as the fit and healthy members. Be active. Eat healthy. But first think like a winner for all things begin with thought.

I end with the motto: change your mind, change your world.

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Education for Liberation! Venceremos Unidos!
Peter S. López, Jr. aka~Peta
Email: peter.lopez51@yahoo.com
http://twitter.com/Peta51
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Come Together! Join Up! Seize the Time!
http://groups.yahoo.com/group/Humane-Rights-Agenda/
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http://groups.yahoo.com/group/NetworkAztlan_News/
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http://groups.yahoo.com/group/THIRD-WORLD-NEWS/
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Sane-and-Sober Today!

Neuron - Wikipedia, the free encyclopedia

Neuron

From Wikipedia, the free encyclopedia

Contents

[edit] Overview

[edit] Anatomy and histology

[edit] Histology and internal structure

[edit] Classes

[edit] Structural classification

[edit] Polarity

[edit] Other

[edit] Functional classification

[edit] Direction

[edit] Action on other neurons

[edit] Discharge patterns

[edit] Classification by neurotransmitter production

[edit] Connectivity

[edit] Mechanisms for propagating action potentials

[edit] Neural coding

[edit] All-or-none principle

[edit] History

[edit] The neuron doctrine

[edit] Neurons in the brain

[edit] Neurological disorders

[edit] Demyelination

[edit] Axonal degeneration

[edit] Nerve regeneration

[edit] References

[edit] Sources

[edit] External links

Spiritual Practices: Being Present

Bipolar Disorder ~ NIMH

Bipolar Disorder

Introduction: Bipolar Disorder

What is bipolar disorder?

What are the symptoms of bipolar disorder?

How does bipolar disorder affect someone over time?

What illnesses often co-exist with bipolar disorder?

What are the risk factors for bipolar disorder?

Genetics

Brain structure and functioning

How is bipolar disorder diagnosed?

How is bipolar disorder treated?

Medications

Other treatments

What can people with bipolar disorder expect from treatment?

How can I help a friend or relative who has bipolar disorder?

Support for caregivers

How can I help myself if I have bipolar disorder?

Where can I go for help?

What if I or someone I know is in crisis?

Citations

For more information on bipolar disorder

Reprints:

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How to increase serotonin in the human brain without drugs via Young

The Placebo Effect: How to Use Your Mind-Body Connection for Healing via Deepak Chopra

Why It's Better to Have a Mind Than a Brain by Deepak Chopra

Year of the Tiger meets St. Valentine’s Day

Prescription narcotics cause more deaths than both heroin and cocaine

FYI: A Homeless Success Story!

FYI:[Progressive Recovery Today!] On Our Spiritual Liberation Program: via Peter ...

Echo ~ NATIVE AMERICAN CODE OF ETHICS ~

Friday Night~from Peter in 501

Stress Weight Gain

Stress Weight Gain