Lithium Orotate

Almased synergy diet multi protein powder

2009-06-15T13:14:00.000-07:00

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Superiority of Lithium Orotate

2009-06-11T14:39:00.000-07:00

The lithium salt of orotic acid (lithium orotate) improves the specific effects of lithium many-fold by increasing lithium bio-utilization. The orotates transport the lithium to the membranes of mitochondria, lysosomes and the glia cells. Lithium orotate stabilizes the lysosomal membranes and prevents the enzyme reactions that are responsible for the sodium depletion and dehydration effects of other lithium salts. Because of the superior bioavailability of lithium orotate, the therapeutic dosage is much less than prescription forms of lithium. For example, in cases of severe depression, the therapeutic dosage of lithium orotate is 150 mg/day. This is compared to 900-1800 mg of the prescription forms. In this dosage range of lithium orotate, there are no adverse lithium side reactions and no need for monitoring blood serum measurements.17

Raw Thyroid

2009-06-11T12:06:00.000-07:00

Ultra Glandulars Raw Thyroid

Ultra Raw Thyroid is a glandular extract of the endocrine gland responsible for controlling metabolism and growth and may benefit individuals with slow metabolism, low energy, melancholy, cold hands and feet, and restlessness. Ultra Raw Thyroid. Freeze Dried, Glandular Concentrate. The Thyroid Gland is one of the most significant of the endocrine glands, which produces secretions that regulate many basic processes of the body. It lies in the front part of the throat along the windpipe. Reference: Medical and Health Encyclopedia, Volume 13, page 1875. Results are Nutritional Only

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Raw Thyroid Information

Thyroid problems seems to be an ever increasing problem in this country. In my research I have learned that it is possibly a yeast overgrowth condition (known as Candidiasis) that indirectly affects thyroid output, as it can also eventually affect most bodily organs in some way. If you have ever taken antibiotics, steroid medications, been on birth control pills, drink alcohol on a regular basis, are under a lot of stress, or eat a diet high in processed meats, there is a good chance you could have a yeast overgrowth problem. It is estimated that almost everyone in this country has it to some degree. You may want to look into that possibility to see if it may be part of the cause. By the way, if you ask your doctor about Candidiasis don't be surprised if he laughs, scoffs, or says something like, "you would have to have AIDS to have Candidiasis". This is not necessarily true, but is a common opinion in mainstream medicine because most doctors aren't very well educated in this area. To this answer I would direct them to a book written by a colleague of theirs named Dr William Crook, M.D., who wrote "The Yeast Connection". .

Dosage
Take one or more tablets three times a day on an empty stomach for maximum results or as directed by your health care practitioner

Unipolar Disorder

2009-06-10T14:38:00.000-07:00

In addition to its well-recognized benefits in the management of bipolar disorder, trials have conclusively demonstrated that lithium is also an effective treatment for recurrent unipolar depressive illness (recurrent major affective disorder).14-16 Although physicians in Europe have successfully used lithium for this indication for many years, American psychiatrists do not share their appreciation of lithiums safety and effectiveness for conditions other than MDI. Perhaps it is due to a difference in the lithium preparations they have at their disposal.

Mortality-lowering, Anti-suicidal Effect of Lithium

2009-06-09T14:37:00.000-07:00

The mortality of manic-depressive patients is markedly higher than that of the general population. The increased mortality is mainly, but not exclusively, caused by suicide. Studies have shown that the mortality of manic-depressive patients given long-term lithium treatment is markedly lower than that of patients not receiving lithium. The frequency of suicidal acts among treated patients is significantly lower than patients given other antidepressants or carbamazepine. The results of mortality studies are consistent with the assumption that lithium-treatment protects against suicidal behavior. 8-13

Orthodox Treatment

2009-06-08T14:36:00.000-07:00

Hospitalization may be required during an acute phase to control the symptoms. Antidepressant drugs may be given; anticonvulsants (Carbamazepine, Valproic acid, Depakote) may also be used. (These substances deplete body stores of L-carnitine and Taurine. Supplementation with several grams daily of these supplements greatly ameliorates adverse side effects of these drugs).

Lithium, however, is the treatment of choice for recurring bipolar (manic/depressive) illness, serving as an effective mood enhancer in 70-80 percent of bipolar patients.

Bipolar Disorder

2009-06-08T14:35:00.000-07:00

Bipolar Disorder
Bipolar disorder is a severe mood disorder characterized by manic or depressive episodes that usually cycle back and forth between depression and mania. The depressive phase is characterized by sluggishness (inertia), loss of self-esteem, helplessness, withdrawal and sadness, with suicide being a risk. The manic phase is characterized by elation, hyperactivity, over-involvement in activities, inflated self-esteem, a tendency to be easily distracted, and little need for sleep. In either phase there is frequently a dependence on alcohol or other substances of abuse. The disorder first appears between the ages of 15 and 25 and affects men and women equally. The cause is unknown, but hereditary and psychological factors may play a role. The incidence is higher in relatives of people with bipolar disorders. A psychiatric history of mood swings, and an observation of current behavior and mood are important in the diagnosis of this disorder.

Lithium Orotate The Unique, Safe Mineral with Multiple Uses

2009-06-08T14:32:00.000-07:00

Lithium is a mineral with a cloudy reputation. It is an alkali metal in the same family as sodium, potassium and other elements. Although lithium is highly effective in the treatment of manic depressive illness (X4 DI), its pharmaceutical (prescription) versions, lithium carbonate and lithium citrate, must be used with caution. The reason for the caution with prescription lithium is because lithium in these forms is poorly absorbed by the cells of the body — and it is within the cells that lithiums therapeutic effects take place. Lithium ions are believed to act only at particular sites on the membranes of intracellular structures like mitochondria and lysosomes.

Consequently, because of this poor intracellular transport, high dosages of pharmaceutical forms of lithium must be taken in order to obtain a satisfactory therapeutic effect. Unfortunately, these therapeutic dosages cause blood levels to be so high that they border on toxic levels. Consequently, patients taking prescription lithium must be closely monitored for toxic blood levels. Serum lithium and serum creatinine levels of prescription lithium-treated patients should be monitored every 3-6 months.

Toxic effects of lithium may include hand tremors, frequent urination, thirst, nausea, and vomiting. Even higher doses may cause drowsiness, muscular weakness, poor coordination, ringing in the ears, blurred vision, and other symptoms.

There has been concern that long-term lithium treatment may damage kidney function, but data in this regard are equivocal. Renal insufficiency without a known cause has occurred in the general population, and the incidence of renal failure among manic-depressive patients not treated with lithium remains unknown.

Most patients treated with lithium are also taking other medications, and it is just as likely that the few known cases of renal failure in patients taking lithium were due to other medications that they were simultaneously taking.2-5

Nevertheless, with potential side effects like this, why in the world would anyone want to take lithium? It is because lithium has been found to be one of the most effective treatments for manic-depressive illness (bi-polar disorder).

by Ward Dean, M.D. and Jim English

Lithium Orotate and Alcoholism

2009-06-05T13:18:00.000-07:00

Lithium orotate in the treatment of alcoholism and related conditions.
Alcohol. 1986 Mar-Apr;3(2):97-100. Sartori HE.
The subjects were 42 alcoholic patients (33 males and 9 females) who were treated with lithium orotate during an alcohol rehabilitation program in a private clinical setting for at least six months. They derive from a total number of 105 patients who received this treatment initially, while the remainder discontinued the treatment within six months. The data were collected from a private practice record and the follow-up varied between six months and 10 years. The 42 patients studied displayed a multitude of complaints in addition to chronic alcoholism. These included liver dysfunction, seizure disorders, headaches, hyperthyroidism, affective disorders. Meniere's syndrome, liver and lung cancers. Thirty-six of the 42 patients studied had been hospitalized at least once for the management of their alcoholism. Lithium orotate was given, 150 mg daily, with a diet low in simple carbohydrates and containing moderate amounts of protein and fat. In addition, calcium orotate (for hepatic involvement), magnesium orotate, bromelaine, and essential phospholipids (for cardiac problems), and supportive measures were instituted, if required. Lithium orotate proved useful as the main pharmacologic agent for the treatment of alcoholism. Ten of the patients had no relapse for over three and up to 10 years, 13 patients remained without relapse for 1 to 3 years, and the remaining 12 had relapses between 6 to 12 months. Lithium orotate therapy was safe and the adverse side effects noted were minor, i.e., eight patients developed muscle weakness, loss of appetite or mild apathy. For these patients, the symptoms subsided when the daily dose was given 4 to 5 times weekly.

Lithium orotate

2009-06-04T13:16:00.000-07:00

Lithium orotate, is a lithium salt of pyrimidinecarboxylic acid and lithium. It is available as the monohydrate, LiC₅H₃N₂O₄·H₂O^[1].

Lithium orotate is generally marketed as a dietary supplement used in small doses to treat conditions including stress, manic depression, alcoholism, ADHD and ADD, aggression, PTSD, Alzheimer's and to improve memory. It has controversially been promoted as an alternative to lithium carbonate. In this compound, lithium is non-covalently bound to an orotate ion, rather than to a carbonate or other ion. Lithium orotate is sold under a wide variety of brand names and is available at some drugstores and health food stores.

Although a few psychiatrists prescribe lithium orotate to their patients, it is most often naturopaths and other alternative health practictioners who recommend this drug to their patients.

Systematic (IUPAC) name of Lithum orotate

2009-06-03T13:14:00.000-07:00



Lithium orotate
Systematic (IUPAC) name
?
Identifiers
CAS number	5266-20-6
ATC code	?
PubChem	23686432
Chemical data
Formula	C₅H₃LiN₂O₄
Mol. mass	162.03
Pharmacokinetic data
Bioavailability	?
Metabolism	?
Half life	?
Excretion	?
Therapeutic considerations
Pregnancy cat.	?
Legal status	OTC
Routes	Oral

Selling Lithium

2009-06-03T13:12:00.000-07:00

So, we already know why lithium orotate is sold as a dietary supplement (selling it as the drug it obviously is would incur the wrath of the FDA). But look at the marketing that some of these vendors use. For example, the horribly named Find Serenity Now:

Serenity™ is an all-natural, effective mood enhancer. It promotes a natural balance to moods and emotions. Serenity™ does not lower energy levels and has no known side effects. Serenity™ changes peoples’ lives for the better every single day.

…

A key step in producing Serenity™ is our advanced ‘Micro Vortex Enteric Coating’. This is a required process of Urban Nutrition’s authentic formula, ensuring that the stomach acids are by-passed so the Orotate can carry the natural Lithium and release it within the cells where it is utilized as a trace mineral in the body.

The combination of the Orotate mineral carrier and our Micro Vortex Enteric Coating manufacturing process make Serenity™ a natural & effective product. This provides optimal absorption and there is little or NO excess lithium left in the body. Research has demonstrated that this does NOT raise the lithium levels in the blood at all or in any significant way. Therefore, toxic levels of Lithium are not an associated problem with Serenity™.

You’ve seen the total extent of research into lithium orotate. Do you think these claims reflect the facts in any way? But that’s OK, because Serenity™ can help you if you have occasional mood swings, could use a boost in your spirits, your marriage suffers from unstable emotions, you’d like a natural mood enhancer, you long to find the person you deserve to be, or even if PMS or menopause feels like a curse.

No mention of actual medical disorders there, so that’s all right then. Still, I do have one question: Who the hell takes lithium in order to find the person they “deserve to be”?

Another lithium orotate supplement Symmetry Homeopathic Spray from HBC Protocols™ seems a little more bold in its claims to:

Oh, that bit about being FDC/NDC (National Drug Code) Registered? That’s a bit of regulatory fluff. The FDA maintains a database of drug products. It publishes a database of prescription drugs and insulin products (which Symmetry, being neither, doesn’t appear on). You submit your product’s data to the FDA and they give you a number. Implying that this is some kind of mark of approval is like me saying that the UK government approves of me because hey, I have a national insurance number.

No, I’m not sure what makes it a homeopathic spray either.

They also say:

If you cannot tolerate higher doses of lithium due to side effects you might try replacing it with lithium orotate. It requires no blood tests and side effects are pretty much non-existent. It is non-prescription and even at lower doses is just as effective as much higher doses of the prescription forms of lithium.

Strong claims, especially given the incredibly limited amount of evidence for lithium orotate. And isn’t it kind of irresponsible to recommend that people who are taking lithium (who will almost certainly have been prescribed it) should switch from an approved form of the drug to a form that was last studied with any seriousness in the 1970’s?

Lithium Orotate: Just a dietary supplement, not a drug at all, oh no.

2009-06-03T12:29:00.000-07:00

This is one of the more irresponsible things I’ve seen recently:

Lithium. As a dietary supplement.

Lithium is a – perhaps the – mood stabiliser used in the treatment of bipolar disorder. It’s been used to treat mania since the 1970’s and is widely prescribed today. People who have been prescribed lithium usually have regular blood tests, because too much lithium can cause kidney damage and do bad things to the thyroid. Lithium’s useful and has saved lives, but it’s not a drug that should be treated lightly.

So how come it’s being sold like a multi-vitamin?

Oh, Dr. Nieper

For the answer we have to go back to the 1970’s and a German doctor called Hans Nieper. Nieper, who died in 1998, was known for his controversial methods of treating cancer, multiple sclerosis and heart disease. using large doses of vitamins, minerals and various extracts, he theorised that combining drugs with specific acids – which he called “mineral transporters” – could more effectively deliver the drug in the patient’s body.

Many drugs need to be in the form of a salt to be stable. Lithium, the kind that actual doctors prescribe, is usually in the form of lithium carbonate. The lithium molecule is combined with a molecule of carbonic acid, to form lithium carbonate. It would be unwise to take pure lithium as adding lithium to water results in what chemists like to call a “brisk exothermic reaction”. To put it another way, you’d end up with no tongue.

The orotate form of lithium replaces the carbonic acid with orotic acid. Nieper believed that combining a mineral like lithium with orotic acid would mean that the drug would be released only inside cells. His own description of this process can be found here.

Saying that Nieper’s approach is outside the mainstream is a little like saying that Las Vegas is on the outskirts of New York. In 1990 the US Office of Technology Assessment prepared a report for Congress on unconventional cancer treatments. Four years before, the FDA had banned the importing of drugs produced by Dr. Nieper:

More than 75 misbranded and unapproved drugs prescribed by Nieper have been detected in mail and personal baggage importations. These are directed to patients who may have been referred to the Nieper clinic by promotional groups in Wisconsin and California, including the recently established Hans A. Nieper Foundation. FDA has advised these groups that they should correct any materials they send out that suggest drugs prescribed at the Nieper clinic can be legally shipped to the United States.

The American Cancer Society reports that the Nieper cancer therapies include the discredited amygdalin (laetrile) and such other unproved substances as Iscador, fresh cell therapy and wobe-mugos enzyme. The American Heart Association says the drugs reportedly used for his cardiovascular treatments include bromelain, carnitine, selenium, magnesium orotate and potassium orotate—for which “there are no significant data indicating that any of these drugs are efficacious.” The American College of Cardiology strongly warns against any use of unapproved drugs for treatment of cardiovascular disease, adding that lithe FDA review process has done much to protect the American people from exposure to unsafe and ineffective drugs.”

And the National Multiple Sclerosis Society advises that the calcium products, including calcium aminoethyl phosphate or CaEAP, frequently prescribed as part of an expensive program of massive drug intake and special diets “has not been demonstrated to be effective in controlled experiments. II The German Multiple Sclerosis Society, according to its counterpart here, strongly advises against the treatment methods of Dr. Nieper.

In a 1981 advisory, the National Multiple Sclerosis Society emphasized that “when a physician makes a claim of producing a clinical improvement in MS, that physician has a moral and professional responsibility to prove scientifically the specificity of the treatment.” Nieper had by then been making claims about multiple sclerosis for more than a decade and had not yet—and still has not—been willing or able to demonstrate the effectiveness of his therapies to other scientists.

(from Quackwatch)

This is, incidentally, why in the USA lithium orotate is marketed as a dietary supplement rather than a drug. Since 1994, the FDA has (by law) regulated dietary supplements as foods rather than drugs. Whereas a drug has (in theory at least) to be shown to be safe and effective in order to be legal, dietary supplements are banned only if they’re shown to be unsafe. Marketing lithium orotate as a dietary supplement is clearly nonsensical and mendacious, it’s the same drug in lithium orotate as in lithium carbonate, the only possible difference is in how the drug is metabolised in the body.

Symmetry Homeopathic Spray Ingredients

2009-05-25T08:16:00.000-07:00

Symmetry Homeopathic Spray Ingredients

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).

Fig. 7. Examples of solitary white perch bipolar cells in culture.

Fig. 8. GABA elicited responses from isolated white perch bipolar cells. The membrane currents elicited by GABA application (left) contain both transient and sustained components, indicating both GABAA and GABAc receptors are present. In the pesence of bicuculline, GABAA receptor activitys is inhibited, revealing sustained GABA responses mediated by GABAc receptors (right).

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.

References

Albrecht, B.E., Breitenbach. U., Stuhmer, T., Harvey, R.J. and Darlison, M.G. (1997) In situ hybridization and reverse transcription-polymerase chain reaction studies on the expression of the GABA(C) receptor rho1- and rho2-subunit genes in avian and rat brain. Eur. J. Neurosci. 9, 2414-2422.

Amin, J. and Weiss, D. S. (1996) Insights into the activation mechanism of r1 GABA receptors obtained by coexpression of wild type and activation-impaired subunits. Proc. R. Soc. 263, 273-282.

Boue-Grabot, E., Roudbaraki, M., Bascles, L., Tramu, G., Bloch, B. and Garret, M. (1998) Expression of GABA receptor rho subunits in rat brain. J. Neurochem. 70, 899-907.

Calvo, D. J., Vazquez, A. E. and Miledi, R. (1994) Cationic modulation of r1-type g-aminobutyrate receptors expressed in Xenopus oocytes. Proc. Natl. Acad. Sci. USA 91, 12725-12729.

Chang, Y, Amin, J. and Weiss, D. S. (1995) Zinc is a mixed antagonist of homomeric r1 g-aminobutyric acid-activated channels. Mol. Pharmacol. 47, 595-602.

Chang, Y. and Weiss, D. S. (1999) Channel opening locks agonist onto the GABAC receptor. Nat. Neurosci. 2, 219-225.

Cutting, G.R., Lu, L., Zoghbi, H., O'Hara, B.F., Kasch, L.M., Montrose-Rafizader, C., Donovan, D.M., Shimada, S., Antonarakis, S.E., Guggino, W., Uhl, G.R. and Kazazian, H.H.Jr. (1991) Cloning of the g-aminobutyric acid (GABA) rho 1 cDNA: a GABA receptor subunit highly expressed in the retina. Proc. Natl. Acad. Sci. USA 88, 2673-2677.

Cutting, G.R., Curristin, S., Zoghbi, H., O'Hara, B., Selden, M.F. and Uhl, G.R. (1992) Identification of a putative gamma-aminobutyric acid (GABA) receptor subunit rho2 cDNA and colocalization of the genes encoding rho2 (GABRR2) and rho1 (GABRR1) to human chromosome 6q14-q21 and mouse chromosome 4. Genomics 12, 801-806.

Dong, C. J. and Werblin, F. S. (1994) Dopamine modulation of GABAC receptor function in an isolated retinal neuron. J. Neurophysiol. 71, 1258-1260.

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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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[2] Nieper HA. The anti-inflammatory and immune-inhibiting effects of calcium orotate on bradytrophic tissues. Agressologie. 1969;10(4):349-57. Available as article #CM14 from the A. Keith Brewer International Science Library at (608) 647-6513 or on the Web .
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[6] Moruzzi G, Viviani R, Marchetti M. Orotic acid as a "growth factor" for chickens and its relation to vitamin B12 and methionine [in German]. Biochem Z. 1960;333:318-27.
[7] Pasquali P, Landi L, Caldarera CM, Marchetti M. Effects of orotic acid on dihydrofolate dehydrogenase and on tetrahydrofolate-dependent enzymes in the chick liver. Biochim Biophys Acta. 1968;158(3):482-4.
[8] OäSullivan WJ. Orotic acid. Aust N Z J Med. 1973;3(4):417-22.
[9] Connolly GP, Duley JA. Uridine and its nucleotides: biological actions, therapeutic potentials. Trends Pharmacol Sci. 1999;20(5):218-25. [Abstract ]
[10] Dodin G, Lalart D, Dubois JE. Role of magnesium cations in the yeast orotate phosphoribosyltransferase catalyzed reaction. Mechanism of the inhibition by Cu++ and Ni++ ions. J Inorg Biochem. 1982;16(3):201-13. [Abstract ]
[11] Donohoe JA, Rosenfeldt FL, Munsch CM, Williams JF. The effect of orotic acid treatment on the energy and carbohydrate metabolism of the hypertrophying rat heart. Int J Biochem. 1993;25(2):163-82. [Abstract ]
[12] Ferdinandy P, Fazekas T, Kadar E. Effects of orotic acid on ischaemic/reperfused myocardial function and glycogen content in isolated working rat hearts. Pharmacol Res. 1998;37(2):111-4. [Abstract ]
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[15] Jellinek H, Takacs E. Morphological aspects of the effects of orotic acid and magnesium orotate on hypercholesterolaemia in rabbits. Arzneimittelforschung. 1995;45(8):836-42. [Abstract ]
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[17] Dewar AJ, Reading HW. Effect of lithium administration on RNA metabolism in rat brain. Psychol Med. 1971;1(3):254-9.
[18] Nieper HA. Recalcification of bone metastases by calcium diorotate. Agressologie. 1970;11(6):495-502. Available as article #CA21 from the A. Keith Brewer International Science Library at (608) 647-6513 or on the Web .

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