• #1 Rubidium
• #2 Fluoride
• #3 Autoimmune Disease:Part 1, Part 2, Part 3
• #4 Shifting Sands of Time: Part 1, Part 2, Part 3
• #5 Allergies: Part 1, Part 2, Part 3
• #6 Menopause
• #7 Osteoporosis
• #8 Breast Cancer
• #9 Cholesterol

For our very first commentary from the Meridianlink Conference Circle, we have chosen to discuss some of the nutritional uses of rubidium that we have observed, at the Balancing Center. Rb is similar to, but heavier than potassium, with a valence of 1+. It is available (for health care professionals only) as a single trace mineral, in a product called Rb-zyme, from Biotics Research Corp P.O. Box 36888, Houston Texas, 77236.

At the Balancing Center, Rubidium, as Rb-zyme from Biotics, is the most frequently requested of all the Biotics trace minerals. Biotics offers a complete array of separate trace minerals, but Rb comes up most often in this practice because we find that many of our clients have a rubidium deficiency, without realizing it.There is not much in the food supply, and whatever there is doesn't show up in foods that most people eat, since it comes mostly in parsnips and turnips. Rubidium, as a necessary trace mineral, is virtually unknown. It has never been publicized, hasn't "hit the press" of the popular health magazines, and it is not available in the Health Stores. As far as I know, very little research has been published, other than to establish rubidium as a factor in cellular membrane regulation.

Even though our clinical experience with rubidium has been quite extensive and well established, over the years, our comments about the biochemical function and clinical requirements of rubidium are not presented here as scientifically established facts. We are presenting these data simply as clinical observations that might be useful for health practitioners who are working with clients in the arena of nutritional balance.

We have found that rubidium, even though it is a very rare trace mineral, is required for the synthesis of an enzyme activator that forms disulfide bridges. When two cysteine molecules join together to form a cystine molecule, they form a bridge that spans across two peptide chains, in order to connect them. For example, disulfide bridges hold the peptide chains of insulin together, so if a certain percentage of insulin molecules are unable to maintain a secure structure, the chains fall apart and are unable to connect with glucose. This would obviously compromise the efficiency of glucose absorption, and create a diabetic effect. Many other molecules also require disulfide bridges, such as the proteolytic enzymes trypsin and chymotrypsin, and without sufficient rubidium, would cause protein digestion to be less than optimal.

Sometimes people can't form those bridges efficiently even with rubidium present, because they're afraid to create bonds. Inadequate sulfide bonding can be an analogy of the fear of emotional bonding, and grief at the lack of connection. If the agreement to disconnect is based upon a past experience, it can sometimes be renegotiated and released by stroking the kidney, heart, and lung meridians, and probably others.

Rubidium appears to encourage the appropriate release of hormone facilitators from the pituitary, as well as regulating the release of fluids from the lachrymal and salivary glands. In face of a rubidium shortage, these secretions are likely to be less abundant. Because rubidium so often serves as a membrane modulator, we have also observed, not surprisingly, that it invites nutrient uptake into hair follicles. A significant shortage could result in hair loss, or hair that was flimsy and dry, even in face of excellent protein and fatty acid nutrients, and abundant thyroxine.

Rubidium is required to activate procollagen hydroxylase so that the collagen fibers can be fully hydroxylated and correctly constructed, and not become too stretchy or too weak to give the joints firm support. Typically it is a corn allergy that creates hyperflexibility by blocking proline synthesis and lysine utilization. Proline synthesis can also be inhibited by high emotional stress level, as well as anti-inflammatory steroid medication, (both create the same bio-chemical effect.) However, for some people, a rubidium shortage might be the significant factor in hyperflexiblity, even if these other issues have been effectively addressed.

We have found that when silicone leaks out from implants, it is likely to intercept rubidium. This might ultimately have significant health effects that would be difficult to identify. Silicone, on the loose, slides slowly through the lymphatic system, and can be released gradually with inositol. In the meantime, this viscous invader appears to capture not only rubidium but also potassium, sodium and lithium---all the minerals with a valence of 1+, seriously interfering with the electrolyte balance, and the enzyme construction that depends upon minerals in that chemical group. Evidently silicone toxicity does not affect minerals with a higher valence, such as calcium or magnesium.

Iron absorption and regulation, according to the literature, is poorly understood. It is known to occur at the membrane of the ileum, and our experience suggests that there is a screening device, which we refer to affectionately as the "iron gate." This consists of a membrane regulator that calls for the exchange of the position of rubidium and selenium within the transfer pores.

So far, we have deduced that iron is regulated in this way: when the iron sensor perceives a shortage of iron in the blood, rubidium stays behind the gate, (at the surface of the lining that is exposed to the capillary bed) and selenium swings to the front of the gate, (toward the surface of the lining of the ileum that is exposed to the nutrient fluid.) This position of selenium invites the iron molecule to separate out of the nutrient broth in the ileum, migrate across the entry pore, and slip into the receptor sites of the capillaries at the back of the pore, and then into the bloodstream. If the sensor perceives that there is already enough iron in the blood, then selenium slides behind the gate, and rubidium comes up to the nutrient surface, and it closes off access to iron. The presence of rubidium at the nutrient surface of the ileum lining prevents further uptake of iron.

If this is true, then we might deduce that in a shortage of rubidium, the absorption of excessive iron could be due to the inability to screen it out, because the iron gate is stuck in the "open" position. In that case selenium would be too abundant at the nutrient surface, and not enough rubidium would be available to trade places and serve as a screen. Iron has an open invitation to continue to enter the bloodstream. In time this would be likely to lead to hemosiderosis.

On the other hand, if there were a shortage of selenium, iron might not be able to gain access to the capillary structure. The transfer pores would be guarded by rubidium, and would remain closed. In that case, iron uptake would be less than optimal, resulting in a form of anemia that would not yield to iron supplements, and would not be related to B-12/folic deficiency. Oddly enough, if there is no rubidium available at all, and only selenium is present, the iron will also be refused entry. Possibly rubidium, stationed at the rear position of the regulatory pore, serves as a sort of magnetic-like draw that pulls the iron in. Both Se and Rb have to be present for the "iron gate" to work.

It is well known that molybdenum is an important trace mineral for facilitating iron uptake, but instead of acting upon the ileum's capillary bed, it appears to catalyze the entry of iron into the target cells after the iron has already been absorbed into the bloodstream.

Rubidium facilitates the tryptophan cascade. It follows that rubidium would assist the synthesis of adequate serotonin for people who are not able to maintain serotonin levels, even when they get enough full-spectrum light, and even if they release the milk allergy or the toxins that are blocking the synthesis of 5-hydroxytryptophan decarboxylase, and even if they are not deactivating their serotonin with fluoride.

There are several compounds and pharmaceuticals that can access the blood-brain-barrier and interfere with 5-HTP decarboxylase, and any of them have the potential for creating a serotonin shortage. This would cause not only chemically mediated depression but the insomnia that accompanies it, since melatonin is derived from serotonin.

Our observation is that DDT and other pesticides, as well as one of the over-the-counter antacids, and the excessive use of a common hepato-toxic pain reliever, and two commonly prescribed anti-depressents, are all likely to reduce the effectiveness of 5-HTP decarboxylase. Oddly enough, several of the anti-depressants intended to enhance or maintain serotonin in fact have the effect of blocking its synthesis, and a couple of them actually contain fluoride. We are not in a position to point out what these are, in this context, but if you are taking any of these medications, they can be identified for you during your appointment. While we would not ask you stop them, we can support your body nutritionally in ways that will minimize their side effects, so that you would be able to synthesize your decarboxylase enzymes even if you continue the drugs.

If you can derive this neurotransmitter from tryptophan within your own internal process, it will be abundant, accurate, and comfortably harmonious within your brain biochemistry. A little silica will help the serotonin to convert to melatonin, and very likely this will give you a good night's sleep. If these suggestions don't help with sleep, you may be harboring night fears and hypervigilance, and these fears can often be released with bioenergy balancing.

Five steps for deriving your own serotonin

1. Check for the presence of adequate tryptophan, and rubidium availability.

2. Release the heavy metals, pesticide or herbicide residue that may be blocking the synthesis of 5-HTP.

3. Release the milk allergy and other toxins that are preventing the synthesis of the enzyme 5-HTP-decarboxylase.

4. Release any fluoride residue with DMAE that may be preventing serotonin from reaching the receptor sites, and creating chemically mediated depression.

5. Be sure you have exposure to full sunshine---without dark glasses---at least a few minutes on a sunny a day, or use Ott lights, or other forms of full-spectrum lighting.

Since rubidium is required for the proper synthesis of serotonin, then it must also be a requirement for the correct synthesis of thrombocytes, although from an emotional perspective, there might be an entirely different reason for a shortage of thrombocytes, a.k.a. "platelets."

We had a client, now in her forties, who had dropped her platelet count at the age of 24. She said she had been working as a waitress at that time, and to her dismay she dropped a tray full of little plates that were holding fancy desserts. The limbic brain got the message, and produced a physical expression of this trauma by dropping the platelet synthesis in the marrow! In her case, even if rubidium had been offered as a supplement, it couldn't have been utilized until the trauma had been released by tracing her kidney meridian.

People sometimes keep out minerals because MINERAL can be translated in the limbic brain's pun-making word-processor as MEN ARE ALL mean, unkind, violent, scary, alcoholic, etc. and we're not going to let them in. This is a fear that women sometimes come up with, based upon past experiences. If the charge on the old experiences can be released, then new options that engage adult self-empowerment can come in. Helpless fear can be released through the tracing of the sex/circulation meridians, bladder, kidney, sometimes stomach meridians. To find out which ones, you would have to muscle test or use your pendulum.

Although this is usually a woman's issue, we also had a male client whose body refused to absorb minerals. His subconscious message was that MEN ARE ALL expendable. This belief came from his experience in the Air Force during the Vietnam war. It caused significant trace mineral rejection that persisted from then on. After we released his terror by lightly stroking his governing and central vessels, and then his bladder and kidney meridians, his body-consciousness indicated that he would allow rubidium (and all the other traces) to access his blood stream fully, and be utilized effectively.

One of the most recent surprises we have been finding is that rubidium is required at the post-synaptic membrane of the motor endplate. Without it, the acetylcholine cannot gain abundant access to the other side, and so cannot transmit information quickly enough to support continuing endurance of the muscles. This has not been verified by enough clients to establish it as an informal "discovery" as of this writing, but I will check this out over time, to see if it comes up as a consistent connection. If not, I will erase this paragraph!

If anyone out there has more information on the nutritional uses of rubidium, its role in the regulation of membrane access, or enzyme synthesis, or any other metabolic consideration such as its possible role in correcting amino acid cascade errors, let us know.

Comments about this article are welcome, and will be posted here if you request it.

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None of the statements in this commentary have been reviewed or approved by the FDA nor by any recognized scientific forum for evaluation, and none of the statements in this commentary are intended to offer treatment for any disease. If you have a health problem, see your doctor.