Rubidium, Unknown but Essential
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 emzyme, in a product called
Rb-zyme, from Biotics Research Corp P.O. Box 36888, Houston Texas,
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 bones, would have to have been fed organic food, and to have foraged in clean pastures.The nuts, seeds, and vegetables 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 believe that this toxic food is safe.
Rubidium, as a necessary trace mineral, is virtually unknown. It has never been publicized, hasn't "hit the press" of the popular health magazines. Because there is no call for it, it is not available in the health stores. As far as we know, very little research has been published, other than a paper sent to me by the Biotics Research people many years ago, that simply documented rubidium as an established factor in cellular membrane regulation, but 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 nutritent 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, our comments about the biochemical function of rubidium are not presented here as scientifically established
facts. We are presenting these data simply as the result of long-term clinical observation.
This is being presented as information that might be useful
for health practitioners who are working with clients as nutritional counselors, and for suppliers who are researching and formulating efficient and 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, even though it is a rare 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 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 carry glucose. This would obviously compromise the efficiency
of glucose absorption, and create a diabetic effect. If that is the only reason for high blood glucose, supplementing rubidium usually clears that up within a few days.
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.
On the other hand, sometimes
people can't form those bridges efficiently even with rubidium
present, because they're afraid to create 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 would be based upon an unresolved experience from the past, but the out-dated 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, sustaining cellular communication among the tissues. Tracing the meridians slips away their negative vibrational charge, so we can coax them into updating and releasing the emotional helplessness that had been sequestered within their vibrational memory.
2. Rubidium, by its action on membrane permeabiity,
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.
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 fully support the joints. Typically it is a corn
allergy that creates hyperflexibility 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-flexiblity, 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 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. After the release of silicone by inositol, it would be favorable to replenish the shortages with additional supplmentation, Himalayan salt or Celtic salt, lithium, potasssium, 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 position of rubidium and selenium within the access pores of the ileum's outer membrane.
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 of 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, it enters the receptor sites of the capillaries, and slips into the bloodstream.
If the sensor perceives that there is already enough iron in the blood, then selenium slides to the nutrient surface, and closes off access to iron. At this interface, selenium does not attract iron into the pore. Rubidium goes over toward capillary bed, but since the nutrient surface isn’t sending iron through, it would be unable to draw the iron across and offer it to the capillary bed.
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 has an open invitation to continuously pour into the bloodstream. In time this will lead to hemosiderosis.
On the other hand, if there were a shortage of rubidium, it wouldn’t draw enough iron out of the nutrient broth. Then iron would not be able to 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 B-12/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 hypothalamus. 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 both of them are abundant in Brazil nuts.
facilitates the tryptophan cascade by activating the synthesis of 5-hydroxytryptophan, commonly referred to as 5-HPT. It follows that rubidium would assist the synthesis of adequate serotonin for people who are 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 enzyme that turns 5-HTP into serotonin, and detoxifying fluoride so that once synthesized, serotonin can reach the receptor sites. However, unless rubidium is there initially, none of the rest of these essential corrections will be helpful.
There are several
compounds and pharmaceuticals that can access the blood-brain-barrier and interfere with 5-hydroxytryptophan decarboxylase,
the enzyme that transforms 5HTP into serotonin. 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 many pesticides, as well as one
of the 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 all the other mono-amines, i.e. dopamine, nor-epinephrine, and taurine. This guarantees that any attempt to gradually withdraw from these pharmaceuticals will be extremely difficult, since the normal transmitters that the body uses to maintain an up-beat mood would be 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 these medications, a health practitioner who can muscle-test you could tell you how your body responds to them.
While we could identify the opinion of your body-consciousness with muscle-testing, we would not ask you to stop them. We always recommend that all pharmaceuticals must be maintained unless they are phased out by your doctor. We could support you nutritionally in a way that would minimize their side effects, however, and this would kindle your ablity to synthesize the transmitters you need. In that case, you would be able to make your own decarboxylase enzymes, even when you continue the drugs. Once you establish these neurotransmitters by your own internal process, 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 casade, 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 seratonin, 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.
On the other hand there might be an entirely
different reason for a shortage of thrombocytes, a.k.a. "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 bonemarrow! 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. Along with that there is often 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 these hormones can enter the blood stream sufficiently.
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 very 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 anaesthesia.Then the acetyl radicals and the choline molecules cannot be reassembled quickly enough to sustain the muscle.
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.