LITHIUM in Oratate 1X/2X/3X, GABA
3X, Albumin (USP) 1X/2X/3X. In a base of
not more than USP Glycerine and Purified Saline Solution.
Symmetry is the first FDA registered homeopathic lithium orotate
spray. In combining the highest quality lithium orotate with GABA
and Albumin, HBC has created a formula that is designed to reduce
stress while elevating mental and emotional well-being. Symmetry
may also assist other depression treatments associated with symptoms
of depression, stress, mania as it helps supports the body's ability
to reduce stress for better overall health. The Lithium orotate
used in this formula is the most powerful in its class..
Recommended Daily Allowance for Lithium is 14.6 mgs per day.
There are 140 sprays per 1/2 ounce bottle.
At four sprays per day each bottle of Symmetry should last 35 days.
Stimulating clue hints how lithium works SCIENCE NEWS, MARCH 14, 1998, VOL. 153 BY: J. TRAVIS
Some 50 years ago, Australian physician John Cade observed the
calming effect that lithium had on small animals. After testing
the safety of lithium on himself, Cade ventured to try it on people
suffering from the wild mood swings of manic depression.
Millions of prescriptions later, lithium remains the most popular
choice for treating manic depression, although scientists do not
understand how it quells mania or relieves depression. "It's
still a mystery," says De-Maw Chuang of the National Institute
of Mental Health in Bethesda, Md.
Now, there's a new clue to this riddle. Chuang and his colleagues
have found that lithium protects brain cells from being stimulated
to death by glutamate, one of the many chemicals that transmit messages
in the brain.
The new data suggest that lithium may calm overexcited areas of
the brain or, more provocatively, preserve the life of brain cells
whose presence guards against manic depression.
This finding "potentially contributes a lot to the field,"
says Husseini K. Manji of Wayne State University in Detroit. "If
we could figure out how lithium works, we could theoretically come
up with better drugs and perhaps understand what's going on in manic
depression."
Chuang and his colleagues tested the response of various types
of rat brain cells to glutamate. Many normal cells and cells soaked
in lithium for only a day died from a form of suicide that often
results when this neurotransmitter over-stimulates a brain cell.
Yet rat brain cells soaked in lithium for about a week committed
suicide much more rarely when exposed to glutamate, Chuang's group
reports in the March 3 Proceedings of the National Academy of Sciences.
The effect was seen in cells from several brain regions.
The delay in protection is particularly striking, notes Manji,
since a hallmark of lithium therapy is that it can take a week or
longer to benefit people. Consequently, scientists have been looking
for the long-term actions of lithium on brain cells.
Chuang's team also examined the role of the NMDA receptor, the
cell surface protein that glutamate binds to when it excites a cell.
While cells soaked in lithium for a week had as many NMDA receptors
as untreated cells, the treated cells responded differently.
Normally, activation of the NMDA receptor by glutamate triggers
an influx of calcium ions, setting off a signaling cascade inside
cells. However, cells soaked in lithium for a week let in far less
calcium when exposed to glutamate.
In people with manic depression, lithium may correct a dysfunction
of the NMDA receptor by limiting calcium influx, speculates Chuang.
Both Chuang and Manji also note that a small body of evidence suggests
that people with mania or depression may lose brain cells. Lithium
may thwart that cell death, they say. Indeed, Manji has some evidence
that lithium-treated cells eventually begin to overproduce a protein
that stymies the cell's internal suicide program.
If lithium protects brain cells from death by glutamate over-stimulation,
it may have uses beyond manic depression. This form of cell death
occurs in strokes and in Alzheimer's, Parkinson's, and Huntington's
diseases. Chuang is investigating whether lithium protects mice
from similar neurodegenerative illnesses.
GABA
The brain's chief inhibitory
neurotransmitter
GABA (Gamma-Aminobutryic Acid) is an amino acid that was first discovered
in 1883 in Berlin. Classified as a neurotransmitter, GABA abundantly
present in the brain, and serves as a balancer between excitation
and inhibition. As a neurotransmitter in the central nervous system,
GABA is essential for brain metabolism, aiding in balanced brain
function, especially during episodes of anxiety, stress, depression,
epilepsy, and Parkinson's disease. There are more GABA sites in
the brain than for other neurotransmitters, including dopamine or
serotonin.
How
does GABA work?
As the chief inhibitory neurotransmitter in the brain, GABA exerts
its effects by binding to two distinct receptors, GABA-A and GABA-B.
The GABA-A receptors form a Cl- channel. The binding of GABA to
GABA-A receptors increases the Cl- conductance of presynaptic neurons.
The anxiolytic drugs of the benzodiazepine family exert their soothing
effects by potentiating the responses of GABA-A receptors to GABA
binding. The GABA-B receptors are coupled to an intracellular G-protein
and act by increasing conductance of an associated K+ channel. Several
amino acids have distinct excitatory or inhibitory effects upon
the nervous system. The amino acid derivative, g-aminobutyrate,
also called 4-aminobutyrate, (GABA) is a well-known inhibitor of
presynaptic transmission in the CNS, and also in the retina. The
formation of GABA occurs by the decarboxylation of glutamate catalyzed
by glutamate decarboxylase (GAD). GAD is present in many nerve endings
of the brain as well as in the b-cells of the pancreas. Neurons
that secrete GABA are termed GABAergic.
What does that mean?
What this means is that rather than stimulating neurons to fire,
GABA balances neuronal activity, and is
therefore associated with both muscle relaxation, as well as mental
states of calm, serenity, and symmetry.GABA basically acts as an
inhibitory transmitter, keeping the brain and body from going into
"overdrive." Supplementation of GABA seems to be quite effective
for anxiety disorders as well as insomnia (especially the type of
insomnia where racing thoughts keep the individual from falling
asleep). Hence, those suffering from depression exacerbated by anxiety
might want to consider taking this supplement.
An example of how GABA helps alleviate depression.
When people use alcohol, and or drugs (Heroin, cocaine, ecstasy,
marijuana . . . ) they do not feel depressed. They can not feel
their depression. They have temporarily masked by flooding their
brain with artificial opiods. When the drugs wear off, the depression
returns. But, NOT exactly at the same point of use. Why? Because
their GABA level remains temporarily high. The brain has been tricked
into thinking its natural opiod level is high. Symmetry works to
provide the brain and the body with the necessary nutrients that
it needs to produce and keep opiod and GABA neurotransmitter levels
up. Studies with oral administration of sodium valproate (an enhancer
of endogenous GABA activity) and the muscle relaxant Baclofen (an
agonist* of the GABA B receptor) demonstrate their ability
to stimulate increased HGH levels.
Agonist.* 1. Any molecule that improves the activity of a
different molecule; e.g., a hormone, which acts as an agonist when
it binds to its receptor, thus triggering a biochemical response.
2. A drug that both binds to receptors and has an intrinsic effect.
How does GABA enhance sleep?
Studies have shown that GABA increases the body’s sleeping cycle
and patients reported much more vivid dreams. A good night’s sleep
leads to more energy throughout the day. More energy feelings of
vigor are common side effects of supplementing with GABA
Research has shown that GABA plays a key role in anxiety and sleep
by potentially counteracting the excitatory effects of glutamate.
Recent evidence suggests a very important role for GABAeric agents
in the treatment of anxiety disorders like generalized anxiety disorder
(GAD), social anxiety disorder (SAD), posttraumatic stress disorder
(PTSD) both for modulating anxiety and also for treating the sleep
disturbances that are inherent to these disorders.
What about GABA & alcohol?
In the absence of alcohol (left), GABA
opens GABAA receptor chloride (Cl-) channels and inhibits neurotransmission.
Alcohol enhances the effect of GABA (middle),
allowing more Cl- to flow into the cell and producing more inhibition.
In alcohol dependence (right), both GABA
and alcohol have smaller effects on GABA receptors. This results
in less Cl- influx and more activation of neurons that may underlie
anxiety and seizure susceptibility in alcohol dependence and withdrawal.
What's this about GABA and eyesight?
GABAC receptors are expressed in many brain regions, with prominent
distributions on retinal neurons, suggesting these receptors play
important roles in retinal signal processing.
Recent studies indicate GABAc receptors are present on various other
types of retinal neurons. GABAc receptor mediated responses have
been recorded from cone-driven horizontal cells in catfish (Dong
et al., 1994; Kaneda et al., 1997), cone photoreceptors (Picaud
et al, 1998), and some types of ganglion cells (Zhang and Slaughter,
1995). GABAc responses are particularly prominent in bipolar cells
of every species examined thus far (Feigenspan et al., 1993; Qian
and Dowling, 1995; Lukasiewicz et al., 1994; Lukaisiewicz and Wong,
1997; Qian et al., 1997; Nelson et al., 1999), and both immunocytochemistry
and in situ hybridization studies indicate GABAc receptors are present
on bipolar cells (Qian et al., 1997; Enz et al., 1995, 1996; Koulen
et al., 1997). It appears that these receptors play an important
role in shaping signal transmission from bipolar cells to third
order neurons in the retina.
Fig. 7 illustrates some examples of bipolar cells isolated from
white perch retina. These bipolar cells keep their morphology when
isolated in culture. They usually have a pear-shaped cell body from
which several dendrites and one axon extends. The GABA responses
of bipolar cells in white perch retina have both transient and sustained
components, indicating both GABAA and GABAc receptors are present
as shown in Fig. 8. The transient component can be selectively blocked
by the co-application of bicuculline, leaving a more sustained response.
Thus, the electrophysiological and pharmacological properties of
GABAc receptors on bipolar cells are very similar to those of GABAc
receptors on rod-driven horizontal cells (Qian and Dowling 1995;
Lukasiewicz et al., 1994; Feigenspan and Bormann, 1994).
Different kinetic properties of GABAA and GABAc
receptors suggest that they play different roles in mediating inhibition
on bipolar cell terminals (Qian et al., 1997; Lukasiewicz and Shields,
1998). Furthermore, various subtypes of bipolar cells exhibit different
proportions of GABAA and GABAc receptors. For example, in the rat
retina, there is a clear difference in the contribution of GABAA
and GABAc receptors to rod and cone bipolar cells (Euler and Wassle,
1998). In white perch too, different morphological types of bipolar
cells exhibit different proportions of GABAc receptor mediated components
(Qian and Dowling, 1995). These results strongly suggest that different
subtypes of bipolar cell utilize various mixtures of GABAA and GABAc
receptors to perform different activities and help create the variety
of functional pathways through the retina.
Because of the presence of multiple GABA receptors on retinal neurons,
it is sometimes difficult to isolate the contributions of each receptor.
Recent studies on ganglion cell responses reveal some interesting
features of GABAc receptors in retinal information processing. For
example, activation of GABAc receptors leads to more transient light
responses in ganglion cells (Dong and Werblin, 1998) and the delayed
inhibition mediated by GABAc receptors is thought to play a major
role in shaping edge-enhancement of ganglion cell receptive fields
(Jacobs and Werblin, 1998). The bipolar cell to ganglion cell synapse
is probably heavily influenced by inhibitory amacrine feed forward
or feedback synapses and these appear to be via primarily GABAc
receptors.
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Albumin Albumin has several essential physiologic
functions in the human body.
Definition: \Al*bu"min\, n. (Chem.)
A thick, viscous nitrogenous substance, which is the chief
and characteristic constituent of white of eggs and of the
serum of blood, and is found in other animal substances, both
fluid and solid, also in many plants. It is soluble in water
and is coagulated by heat and by certain chemical reagents.
Albumin is the protein of the highest concentration
in plasma responsible for transporting many small molecules. (Calcium,
progesterone, drugs . . . ) It is also of prime importance in maintaining
the oncotic pressure of the blood (Keeping the fluid from leaking
out into the tissues. When administered intravenously albumin increases
total blood volume by drawing fluid from the extravascular tissues.).
Unlike small molecules such as sodium and chloride, the concentration
of albumin in the blood is much greater than it is in the extracellular
fluid. Albumin is synthesized by the liver, therefore decreased
serum albumin may be caused by liver disease. It can also result
from kidney disease, which allows albumin to escape into the urine.
Albumin has been shown to offer therapeutic advantages in shock,
acute liver failure, burns, hypoproteinemia, adult respiratory distress
syndrome, cardiopulmonary bypass, neonatal hemolytic disease, renal
dialysis, acute nephrosis, erythrocyte resuspension, acute peritonitis,
pancreatitis, mediastinitis and cellulitis. Adverse reactions to
albumin are rare. Decreased albumin may also be explained by malnutrition
or a low protein diet.*
Albumin is also called albuminate, plasbumin, buminate, albutein
and albuminar. It is prepared as a sterile solution, contains no
preservatives and is treated to prevent transmitting viruses. The
elimination half life of serum albumin is twenty days. The U.S.
Food and Drug Administration (FDA) regulates its preparation, distribution
and use.
What is albumin?
Albumin is a protein (single polypeptide, 585 amino acids) manufactured
by the liver, (9-12g/day) it is also a powerful antioxidant. It
is a major source of sulphydryl groups, these "thiols"
scavenge free radicals (nitrogen and oxygen species). It may also
be an important free radical scavenger in sepsis. (In sepsis there
is an increased rate of albumin loss into the tissues - this is
probably related to increased capillary membrane permeability).
What does albumin do?
Albumin is also involved in between fifty and one hundred biological
functions. Our body’s main transport system, it moves vitamins,
minerals, hormones, fatty acids, and other essential substances
to their destinations. Other functions include maintaining the "osmotic
pressure" that causes fluid to remain within the blood stream
instead of leaking out into the tissues.
Why is albumin important?
1. Binding and transport. There are actually
four binding sites on albumin and these have varying specificity
for different substances.Competitive binding of drugs may occur
at the same sit or at different sites (conformational changes) [eg.
warfarin and diazepam]. The drugs that are important for albumin
binding are: warfarin, digoxin, NSAIDS, midazolam, thiopentone.
The relevence of a low albumin and drug binding is unknown.
2. Maintenance of colloid osmotic pressure.
Albumin is responsible for 75 - 80 % of osmotic pressure.Starling's
equation: Transcapillary Flow = k [(Pcap + p i) - (Pi + p cap )]
Remember that albumin is the main protein both in the plasma and
in the interstitium and it is the COP gradient rather than the absolute
plasma value that is important: this is what distinguishes hypoalbuminaemia
derived from redistribution (capillary leak) from that of pure full
body deficiency.
3. Free radical scavenging. Albumin is
a major source of sulphydryl groups, these "thiols" scavenge
free radicals (nitrogen and oxygen species). Albumin may be an important
free radical scavenger in sepsis.
4. Platelet function inhibition and antithrombotic
effects. The anticoagulant and antithrombotic effects of
albumin are poorly understood this may be due to binding nitric
oxide radicals inhibiting inactivation and permitting a more prolonged
antiaggregatory effect. In diabetes, glycosylated albumin may increase
the incidence of thrombotic events and atherosclerosis.
5. Effects on vascular permeability.
In sepsis there is an increased rate of albumin loss into the tissues
- this is probably related to increased capillary membrane permeability.
Which diseases cause albumin to be too low?
Liver disease, kidney disease, and malnutrition are the major causes
of low albumin. A diseased liver produces insufficient albumin.
Diseased kidneys sometimes lose large amounts of albumin into the
urine faster than the liver can produce it (this is termed nephrotic
syndrome). In malnutrition there is not enough protein in the patient's
diet for the liver to make new albumin. The British Heart Study,
published in the British medical journal The Lancet in 1989, followed
7,735 middle-aged British men for 9.2 years, finding that men with
the lowest albumin levels had the highest rates of death from a
plethora of causes.
What is a normal level of albumin?
The normal value depends on the laboratory running the test. Most
labs consider roughly 3.5 to 5 grams per deciliter to be normal.
What happens if it gets too low?
In a healthy person with normal nutrition, the liver will simply
manufacture more and the level will normalize. If albumin gets very
low swelling can occur in the ankles (edema) and fluid can begin
to accumulate in the abdomen (ascites) and in the lungs (pulmonary
edema).
Why does albumin fluctuate so much?
Albumin levels are also dependant on the state of hydration of the
body. A person that is deficient of water ("dry") because
of dehydration will have an artificially low albumin level. This
returns to normal when the dehydration is corrected. Albumin fluctuates
so widely because it is very sensitive to changes in hydration of
the body.
What causes serum albumin to decrease?
1. Decreased synthesis 2. Increased catabolism [ very slow ] 3.
Increased loss: Nephrotic syndrome, exudative loss in burns, hemorrhage,
gut loss, redistribution: hemodilution, ncreased capillary permeability
(Increased interstitial albumin) decreased lymph clearance.
What are the consequences of decreased plasma
albumin?
1. Decreased ligand binding. 2. Decreased plasma colloid pressure:
decreased colloid oncotic pressure, and oedema formation. The formation
of oedema is determined by: the rate of fluid flux. The clearance
of fluid by lymphatics.
* HBC Protocols strongly believes that medical
information is best conveyed to patients by their licensed healthcare
providers. The materials presented here should be considered supplemental
to that information. Should you have any questions, please consult
your healthcare provider.
18 References:
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In the 
