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, chelated with an enzyme, in a product called Rb-zyme, from Biotics Research Corp.
At the Balancing Center, we have found that 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 often in this practice because we find that many of our clients have a rubidium deficiency, without realizing it.
There is a varied spectrum of foods that carry it, but whatever there is may not be in foods that many people eat. It comes in Brazil nuts, pecans, sesame and sunflower seeds, potato skins, egg plant, mushrooms, cucumber, avocado, and meat bones. Bone soup is a very rich and delicious source.
The animals, in order to have rubidium in their bone-marrow, would have to have been fed organic food, and to have foraged in clean pastures. To receive rubidium from nuts, seeds, or vegetable, they must all be organic, since genetically modified foods are very depleted in minerals.
The way the herbicide glyphosate (in Roundup,) kills weeds is to prevent them from absorbing minerals. Plants that are genetically modified so that they can withstand the herbicide, by definition are extremely low in minerals, and cannot supply the basic nutritional constituents required to maintain health. Deficiency diseases are becoming rampant, medically unrecognized and often misdiagnosed, a tragic legacy for the millions of people who have been told that this toxic food is safe.
Rubidium, even though it is a necessary trace mineral, is virtually unknown. It hasn’t yet hit the enthusiasm of popular health magazines, hasnt been promoted for the many gifts it can give. Because there is no call for it, it is not available in the health stores. More has been published, recently, other than a paper sent to me by the Biotics Research people years ago, but that earlier one simply documented rubidium as an established factor in cellular membrane regulation, without citing any clinical observations of specific health effects.
At our clinic we are not in a position to do the kind of double-blind testing with animals or with the large number of people that it would require to validate the efficacy of rubidium.
The narrow parameters involved in reductive research that are currently expected by the scientific community to serve as “proof,” may not be the best way to evaluate nutritional information, as that form of inquiry works best under controlled trials where the variables can be carefully eliminated. Because of the infinite variables involved in nutritional testing, the reductive approach to research does not lend itself well to nutritional issues. Well-documented clinical experience may actually be a better way to find out what a nutrient does and how it works, because nutrients work synergistically, not only biochemically but also vibrationally, within a broad interactive context.
Even though our clinical experience has been well-established over the years, these comments are not presented as scientifically established facts, but as clinical information that might be useful for health practitioners, nutritional counselors, or suppliers who are researching and formulating effective supplements. Below are several categories we have found that relate to the health effects of rubidium as a nutrient.
1. We have found that rubidium, as a trace mineral, is required for the synthesis of an enzyme that forms disulfide bridges. When two cysteine molecules join together to form a cystine molecule, they form a bridge that spans across two sections of the molecule, 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 carry glucose. This would obviously compromise the efficiency of glucose absorption, and create a diabetic effect. When that is the only reason for high blood glucose, supplementing rubidium usually clears that up within a few days.
Many other molecules have disulfide bridges, such as the proteolytic enzymes trypsin and chymotrypsin, and without sufficient rubidium, protein digestion would be less than optimal.
On the other hand, sometimes people can’t form those bridges efficiently even with rubidium present, because they’re afraid to create social bonds. Inadequate sulfide bonding can be a psychosomatic expression of the fear of emotional bonding, and grief at the lack of connection. The emotional disconnection might be based upon an unresolved experience from the past, but the outdated emotional charge held by that experience can be renegotiated. When it is updated to current time, it is no longer applicable, and is easily released.
To do this, we locate the age of the client when the event happened, and then trace the meridian pathways that are holding that charge, as of that time. Since the meridians are the messengers of emotional information, as they flow around the body they transfer that information to the physical cells, and sustain cellular communication among the tissues. Tracing the meridians slips away their negative vibrational charge, so this coaxes them into updating and releasing the emotionally charged helplessness that had been sequestered within their vibrational memory.
2. Rubidium, by its action on membrane permeability, 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 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.
3. Rubidium is required to activate procollagen hydroxylase so that the collagen fibers can be hydroxylated and correctly constructed. Otherwise they become too stretchy or too weak to fully support the joints. Typically it is a corn allergy that creates hyper-flexibility by blocking proline synthesis and lysine utilization. Proline synthesis can also be inhibited by a high emotional stress level, as well as by anti-inflammatory steroid medication, since they both create the same effect.
However, for some people, a rubidium shortage might be the significant factor in hyper-flexibility, even if these other issues had been effectively addressed.
4. We have found that when silicone leaks out from breast implants, it is likely to intercept rubidium. This will have significant health effects that would be difficult to identify. Silicone, on the loose, slides very slowly through the lymphatic system, blocking the usual circulation of the lymph. and it 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 does not affect minerals with a higher valence, such as calcium or magnesium. During the release of silicone by inositol, it would be a good idea to replenish the shortages with additional supplementation. Suggest Himalayan salt or Celtic salt, lithium, potassium, and rubidium.
5. Iron absorption and regulation, according to current literature, is still poorly understood. It is known to occur at the membrane of the ileum, and our experience suggests that there is a screening mechanism which we refer to affectionately as the “Iron Gate.” This consists of a membrane regulator that calls for the exchange of the positions of rubidium and selenium within the access pores of the ileum’s outer membranes.
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 is positioned, within the access pore, at the surface exposed to the nutrient fluid, and selenium swings toward the membrane surface next to the capillary bed. This position of rubidium invites iron molecules to separate out from the nutrient broth in the ileum, enter the access pore, and migrate across the pore toward selenium, at the interface of the capillary bed. Then selenium opens up the outer membrane and releases the iron, which now can enter the receptor sites of the capillaries, and slip into the bloodstream.
When the sensor perceives that there is enough iron in the blood, then selenium slides over to the nutrient surface, and closes off the access to iron. At this interface, selenium does not attract iron into the pore. Rubidium goes over toward capillary bed, but doesnt offer it to the capillary vessels.
If this is true, then we might deduce that when there is adequate rubidium, the absorption of iron is enhanced. As long as rubidium is maintained in that position, and selenium lets it flow across into the capillaries, iron will continue to access the blood. However, unless the regulating signal can shift, in response to high iron saturation, the Iron Gate will be held in the “open” position, and iron will continuously pour into the bloodstream. In time this will lead to hemosiderosis.
On the other hand, if there were a shortage of rubidium, iron couldnt be drawn out of the nutrient broth. Then iron would not gain access to the pore, or proceed to the capillary structure. The Iron Gate would be stuck in the “closed” position. Iron uptake would be diminished, resulting in a form of anemia that would not yield to iron supplements, and would not be related to B12/folic deficiency.
When there is no rubidium available, and only selenium is present, the iron will be refused entry, since rubidium is what invites it in. If selenium were not available, but only rubidium were present, iron would enter the pore but could not be released at the capillary surface, so iron would be unavailable for that reason.
The obvious questions to ask next are: Where is that regulating signal coming from? We think it may be regulated in the thalamus, in the limbic brain. And why is the signal sometimes inaccurate? There might be emotional reasons, there might be a toxin, or a nutrient deficiency. These are questions that would need to be determined and resolved for each person. When the Iron Gate functions optimally, both Se and Rb have to be present, and unless you have access to Biotics Rb-zyme, you would have to eat several Brazil nuts every day.
6. Rubidium facilitates the tryptophan cascade by activating the synthesis of 5-hydroxytryptophan, commonly referred to as 5-HTP. It follows that rubidium would assist the synthesis of adequate serotonin for people who are depressed and not able to maintain adequate serotonin levels. There are several ways to be sure of the synthesis of serotonin: exposure to full-spectrum light, the release of a milk allergy, detoxifying toxins that are blocking the synthesis of the decarboxylase that turns 5-HTP into serotonin, and detoxifying fluoride so that once synthesized, serotonin can reach the receptor sites. However, unless rubidium were there initially, none of the rest of these essential corrections will be helpful.
There are several compounds and pharmaceuticals that access the blood-brain-barrier and interfere with 5-hydroxytryptophan decarboxylase, that should be transforming 5-HTP into serotonin. Any of these substances 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 many pesticides, as well as one of the major over-the-counter antacids, the use of a common hepato.toxic pain reliever, and many commonly prescribed anti.depressents, are all likely to reduce the effectiveness of 5-HTP decarboxylase. Oddly enough, the SSRI anti-depressants, intended to enhance the availability of serotonin, in fact have the effect of blocking not only the synthesis of serotonin, but also other monoamines, i.e. dopamine, nor-epinephrine, and taurine.
This depletion guarantees that any attempt to withdraw from these pharmaceuticals will be extremely difficult, since the normal transmitters that the body uses to maintain an up-beat mood would have been almost entirely deactivated. The depression would be overwhelming, worse than it had been before starting the drugs.
We are not in a position to point out what these drugs are, in this context, but if you are taking medications, a health practitioner who can muscle-test you could tell you how your body responds to them, so you could then make some better choices.
While we could identify the inhibiting medications by muscle-testing, we would not suggest that you stop them. We always recommend that medications must be maintained, unless they are phased out by your doctor. We would support you nutritionally in a way that could minimize their side effects, however, and this would kindle your ability to synthesize the transmitters you need, even if you continue the drugs
In that case, you would be able to make your own decarboxylase enzymes by your own internal process, and with your doctor’s guidance you will have an easier time gradually letting go of the drugs.
When you can derive serotonin and melatonin from your own tryptophan cascade, they will be abundant, accurate, and comfortably harmonious. 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 some unprocessed night fears and hypervigilance, and these fears can often be released with bioenergy balancing.
Five steps for deriving your own serotonin:
a. Check for the presence of adequate tryptophan, and rubidium availability.
b. Release any heavy metals, pesticide or herbicide residues that may be blocking the synthesis of 5-HTP.
c. Release the milk allergy that could be preventing the synthesis of the enzyme 5-HTP-decarboxylase.
d. Release any fluoride residue with DMAE, to free up the receptor sites that would otherwise prevent the utilization of serotonin, creating chemically mediated depression.
e. Be sure you have exposure to full sunshine—without dark glasses—at least ten minutes on a sunny a day, or use Ott lights, or other forms of full-spectrum lighting.
7. Since rubidium is required for the proper synthesis of serotonin, then it must also be a requirement for the correct synthesis of thrombocytes, a.k.a.“Platelets” On the other hand there might be an entirely different reason for a shortage of platelets. We have seen them fall dangerously low in face of a mycoplasmic infection, so in that case the body-consciousness would select an herbal or mushroom formula that could open up the biofilm where the mycoplasma is sequestered. This would reveal the culprit to the normal action of the immune system, and the body would be able to take care of the platelets on its own.
We had a client, now in her forties, who had low platelets. The reason was not biochemical, nor was it due to a toxin, it came up as an emotional issue. Her muscle-testing indicated that the level of platelets dropped at the age of 24. “Oh,” she said, “That’s funny, I was working as a waitress at that time, and to my intense embarrassment I dropped a tray full of little plates that were holding many small fancy desserts! It was a disaster, and a complete mess.” Her limbic brain processed this trauma “dropping the little plates” with a psychosomatic reflection, by inhibiting the synthesis of platelets in her bone-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 meridians.
8. When there is a thyroxine shortage, sometimes this is due to the lack of stimulus from thyroid stimulating hormone, TSH, from the pituitary. Ordinarily when there is low TSH, this indicates a high amount of thyroxine. If the TSH is low and the thyroxine is also low, then we need to look at the pituitary. We might see that there is also a diminished release of ACTH, GH, and the hormones FSH and LH that stimulate the release of estrogen and progesterone. Rubidium is a requirement for the correct permeability of the pituitary membrane so that all these hormones can enter the blood stream sufficiently. Along with rubidium, check for a cord at the sixth chakra, or a pituitary tumor, or the intention not to “see” psychically.
9. One of the most recent surprises we have been finding is that rubidium, along with calcium, is required at the membranes of the synaptic nobs, to open upon command and release acetylcholine, so it can float across the synaptic gap and access the motor endplate, to initiate muscle movement.
Without rubidium and calcium, the acetylcholine cannot gain fast access to the other side, and so cannot transmit information quickly enough to support continuing endurance of the muscles. The result is that the muscles are perceived as strong at first, but for some reason are very easily fatigued. This role of rubidium has not been verified by enough clients to establish it as an informal “discovery,” as of this writing, but considering its role as a membrane regulator, it sounds likely.
Another reason for the rapid fading of muscle strength that we have observed occurs when choline acetyltransferase within the synaptic knob is being inhibited by a toxin. Sometimes it is left.over anesthesia. Then the acetyl radicals and the choline molecules cannot be reassembled quickly enough to sustain the muscle. This difficulty is known as Myasthenia Gravis.
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.