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Microsoft word - dr wright hyperexcretion.rtf
IONIC COBALT REVERSES
By Jonathan V. Wright, M.D.
Tahoma Clinic Foundation
801 S.W. 16th St., Renton, WA 98055
As many readers know, I’ve been prescribing bio-identical sex steroids, including “triple
estrogen”, progesterone, testosterone, and DHEA, since the early 1980s. Usually, bio-
identical hormone replacement (with follow-up visits and laboratory testing as
appropriate) proceeds without problems. For symptomatic women, “hot flashes”, mood
swings, insomnia, depression and other symptoms of declining hormones are relieved,
and life can return to relatively normal.
However, every practitioner who’s prescribed bio-identical hormones for women has
experienced occasional “treatment failures.” In this small percentage of women, despite
carefully escalating doses of triple estrogen1 and accompanying hormones, the “hot
flashes” and other symptoms of menopause aren’t relieved, or are relieved only
In most cases (although certainly not always) these “treatment failures” occur in women
who’ve previously taken Premarin or other non-bio-identical “hormone” replacement. In
frustration, most of these women will return to taking Premarin or other more risky
“hormones”, since “at least they take care of my symptoms”.
Over the years, it’s become obvious that almost all “treatment failures” following bio-
identical hormone replacement have a unique “biochemical signature”. When given an
“average effective treatment dose” of bio-identical estrogens, “treatment failures”
I’ve always followed up bio-identical hormone replacement with laboratory testing to
determine if the dose of each hormone is within physiologic parameters. I’ve used the 24-
hour urine for sex steroids (Meridian Valley Laboratories, www.meridianvalleylab.com)2
to help monitor hormone safety. In addition to the usual measurements of progesterone,
DHEA, and testosterone, I always
want to know the individual and combined levels of
estrone, estradiol, and
estriol3 (E1, E2, E3), as well as levels of androsterone and
etiocholanolone, for all women taking bio-identical hormone replacement.
When tested in this way, nearly all women who don’t respond to bio-identical esrogen
replacement are found to be “hyperexcreting” their estrogens. The combined urinary
levels of E1+E2+E3 resulting from an “average effective treatment dose” are from 50%
to 1800% higher. As a result of estrogen hyperexcretion, apperently very little if any
estrogen remains available to the brain and the rest of the body to quench menopausal
symptoms. As one woman put it: “It feels like my body is just getting rid of every bit of
estrogen supplement I’m putting into it”.
AN INITIAL EAV-AIDED SOLUTION
With the help of EAV technology4 applied by Tahoma Clinic staffers Elizabeth Swinton
and Hetty Hall, we determined a few years ago that the “problem” might involve the liver
and “fat metabolism” (steroids are of course a type of fat). Aided by EAV, we put
together a program that (for most women) slowly improves the liver’s handling of bio-
identical estrogens. Women for whom even “high” doses of triple estrogen (5 to 7½
milligrams daily or more) had been totally ineffective found that these same doses slowly
became more and more effective as they followed the Swinton-Hall program.
The program involved the use of (varying doses and types) of liver-supportive botanicals,
vitamin C, B-complex, gamma-linoleic acid (GLA), vitamin E, bile salts, and pancreatic
enzymes. After several months (usually four to ten) on this program, the previously-
ineffective triple estrogen would become effective, usually fully effective, in relieving
menopausal symptoms. Periodic laboratory evaluation with the 24-hour urinary sex
steroid panel showed combined levels of E1+E2+E3 declining towards normal as
symptom relief improved. For those women determined enough to tolerate several
months of menopausal symptoms in order to avoid Premarin or other non-bio-identical
“hormone” replacement, the program was usually successful.
The biggest problem with this approach was the length of time involved. More women
than not decided that dedication to bio-identical hormones was outweighed by the grief
caused by persistent menopausal symptoms, and returned to Premarin (or other non-bio-
identical “hormones”) simply to eliminate these symptoms.
CYTOCHROMES AND METALS
Along with many other substances, estrogens are metabolized and “detoxified” by
cytochrome p450 (and other) cytochrome enzymes. It seemed logical to hypothesize that
“non-responders” to bio-identical esrogen replacement have “upregulated” cytochrome
enzymes that could be very gradually “downregulated” with the Swinton-Hall program.
The challenge was to find a more rapid method. A literature review disclosed clinically-
overlooked publications with a direct bearing on this hypothesis.
A “central” part of an apparent solution to “estrogen hyperexcretion” was published in
1977. Maines and Kappas5 pointed out that cytochromes are heme proteins, and that the
rate-limiting enzyme in heme protein formation is gamma-amino levulenic acid
synthetase (ALA synthetase, “ALA-S” in this report). They also noted that the first
enzyme in the degradation of heme proteins is heme oxidase (“HO” in this report). As
they reported, trace metals regulate the formation (and therefore overall activity) of
cytochrome enzymes by simultaneous repression
of ALA-S and de novo induction
Inferring from the laboratory data taken from bio-identical estrogen non-responders, and
from the Maines and Kappas paper, it seemed at least possible that apparent cytochrome
p450 “upregulation” (inferred from estrogen hyperexcretion) might involve the opposite
of the trace metal effect described by Maines and Kappas. The hyperexcretion of the
estrogens (with consequent unavailability to the somatic tissues) might be due to
of ALA-S and/or underactivity
of HO, with consequent excess (or excess
function) of the cytochromes p450. Therefore, it might be possible to reverse this
situation with the use of trace elements.
COBALT, CYTOCHROME P-450, AND GLUTATHIONE
According to Maines and Kappas, of all the trace metals, cobalt has the greatest effect in
the induction of HO synthesis, thus promoting cytochrome p450 degradation and, by
implication, slowing the hyperexcretion (secondary to presumed “hypermetabolization”)
of bio-identical estrogens, and presumably other metabolites.
Others found that cobalt (chloride) simultaneously has another very beneficial effect:
Inducing the formation of considerably more reduced glutathione (GSH). Reprinting
“Treatment of animals with cobaltous chloride caused decreases in hepatic, pulmonary,
and renal cytochrome p-450 and alterations in levels of other components of microsomal
mixed-function oxidases, which can alter the rate of bio-transformation of certain drug
substrates. The treatment also caused a striking, dose-dependent elevation in tissue levels
of reduced glutathione (GSH), within 2 to 8 hours. The effect of cobalt on GSH occurred
in all tested animal species and strains. Actinomycin-D prevented the cobalt stimulated
rise in GSH. Salts of several other divalent metals also produced sharply elevated levels
of hepatic GSH, occurring concomitantly with decreased microsomal content of
These results suggest that pretreatment of animal with cobaltous chloride, or other
divalent metal salts, could alter the disposition of certain toxic, alkylating drug
metabolites not only by decreasing the rate of formation of the reactive metabolites, but
also by increasing theamount of GSH available for the formation of their less reactive,
less toxic, GSH conjugates6. [Emphasis added for obvious reasons.]
Cobalt also has a “bi-phasic” effect on ALA-S, and therefore on heme synthesis,
including the cytochrome p-450 series. It appears to initially inhibit ALA-S, following
which an enhanced rate of ALA-S synthesis occurs7.
From this very brief review, it appears reasonable to infer that cobalt administration
might be of use in slowing the hyperexcretion of estrogens. Of course, this inference
requires the assumption that the effect of cobalt’s HO induction and “first phase” ALA-S
suppression is greater than cobalt’s “second phase” ALA-S induction effect.
DOWN-REGULATED 8-AMINO LEVULINIC ACID
BY COBALT SYNTHETASE
HEME PROTEINS INCLUDING
P450 AND P488
UP-REGULATED HEME OXIDASE
BILIVERDIN AND BILIRUBIN
COBALT AND ESTROGEN HYPEREXCRETION IN MENOPAUSE
A small amount of clinical information accumulated so far indicates that in humans,
cobalt normalizes estrogen hyper-excretion while relieving menopausal symptoms.
Following is preliminary data from a few such cases observed at Tahoma Clinic. A
“typical normal response” case is outlined first for comparison purposes.
“TYPICAL NORMAL RESPONSE”
R.F. is a 48 year old woman whose last menstrual period was four months prior to her
first visit with me at Tahoma Clinic. She has been experiencing increasing “hot flashes”,
night sweats, irritability, insomnia, and mood swings. Although she had an FSH
determination done elsewhere, confirming menopause, she had read about various
options, and had come in for bio-identical hormone replacement therapy.
After history and physical examination, initial quantities of bio-identical hormone
replacement were prescribed on a 28 day cycle, including “triple estrogen” 2.5 milligrams
on “days 1-25”, progesterone 25 milligrams on “days 12-25”, and DHEA 15 milligrams
every day. [“Triple estrogen” is a combination of estrone (10%), 17-b estradiol (10%),
and estriol (80%).] She was advised to have follow-up 24-hour urinary steroid
determination done in 60 days or after her symptoms subsided, whichever came first. She
was advised (as usual) that the urine specimen should be collected during a day when she
was using all three replacement hormones.
Approximately 10 weeks later, she reported that nearly all the above noted symptoms
were gone with the exception of occasional insomnia. Her urinary estrogens were:
Micrograms Per 24 Hours
· Postmenopausal normal range, total estrogens = 0-60 micrograms/24 hours
· Progesterone and DHEA were also within the expected range.
In my experience with hundreds of women relieved of menopausal symptoms with 2.5
milligrams Triple Estrogen daily (along with progesterone, DHEA, and in many cases
testosterone), the usual range of total estrogens has been from 90-180 micrograms/24
The data in this first case were collected by my colleague at Tahoma Clinic, Davis
RW is a 49 year old white woman with a prior history of chronic fatigue syndrome. In
December 1997, she saw Dr. Lamson concerning menopausal symptoms, including
moderately severe hot flashes, insomnia, and anxiety. She collected a 24 hour urine
specimen, upon which a comprehensive steroid determination was performed, and
reported in January 1998. Estrogens were reported as:
Micrograms Per 24 Hours
She was started on Triple Estrogen [E1:E2:E3/10:10:80], 1.25 milligrams daily with no
ensuing symptom relief. Triple Estrogen was then increased to 2.5 milligrams daily.
While still using the 2.5 milligram daily dosage of triple estrogen, she collected another
24-hour urine specimen, upon which the same steroid determinations were performed.
Micrograms Per 24 Hours
Along with her continuing Triple Estrogen, RW then started cobalt supplementation with
“Meira” cobalt “beads” (20 micrograms ionic cobalt per bead, DSD International,
Phoenix; see below). She used 20-25 beads daily, a total of 400-500 micrograms daily.
Two weeks later, she reported her hot flashes and other menopausal symptoms ceased for
the first time. However, she also reported that if she skipped a daily dose of cobalt, her
hot flashes promptly returned, only to disappear with resumption of the cobalt.
Slightly over a month after starting the cobalt, she reported that on another “skipped
dose” occasion, she not only had return of hot flashes, but “spotting”. The spotting
continued at a low level for two weeks, even though the hot flashes ceased as before with
As she has continued cobalt (along with the Triple Estrogen at 2.5 milligrams daily, taken
on a 25/28 day cyclic basis) she had no further hot flashes. She gradually became able to
omit the occasional cobalt dosage without recurrence of hot flashes.
After 10 weeks of supplemental cobalt along with the continuing triple estrogen, her 24-
hour steroid analysis yielded the following estrogen values:
Micrograms Per 24 Hours
As noted above, this estrogen total is within the anticipated range for postmenopausal
women supplemented with 2.5 milligrams of Triple Estrogen daily.
The data in this and the next case were collected by my former Tahoma Clinic colleague
Joni Olehausen, N.D., (now in Minnesota), and her patients J.S. and J.K.
J.S. is a 63 year old woman. She had been on bio-identical hormone replacement therapy
for approximately three years. She was still having night sweats and difficulty sleeping,
as well as difficulty with memory and concentration. Twenty-four hour urinary estrogens
Micrograms Per 24 Hours
Following this, she was continued on triple estrogen 2.5 milligrams. Approximately six
months later, she was advised to start 20-25 Meira cobalt beads daily. Eleven weeks later,
Micrograms Per 24 Hours
JK is a 52 year old woman with symptoms of hypothyroidism and menopause, the latter
including night sweats, vaginal dryness, anxiety, irritability, mood swings. Her last
menstrual period was four months previously
She was already taking “Bi-estrogen” (Estriol 1 milligram, estradiol 250 micrograms)
twice daily, along with Provera 2.5 milligrams8, daily. Her sex hormones were evaluated
with the 24-hour urine for sex steroids with the result below:
Micrograms Per 24 Hours
Menopausal symptoms continued. On a return visit, six months later, she was advised to
start on Meira cobalt beads, 20-25 beads daily, while continuing her bio-identical
estrogens. Ten weeks later, her estrogens were as follows:
Micrograms Per 24 Hours
Although her total estrogens had not yet diminished to a more expected range, except for
continuing sleeping difficulty, her menopausal symptoms were improved. Unfortunately,
she has not followed up since Dr. Olehausen left for a clinic directorship in Minnesota.
(In both Case 2 and Case 3, although total estrogen excretion declined dramatically
following the ingestion of ionic cobalt, the relative proportion of estriol as a fraction of
total excreted estrogens also declined dramatically. Many readers familiar with the work
of Henry Lemon, M.D., recognize that a larger percentage of estriol is likely advisable as
a “target”. This will addressed in a future posting.)
The data in this case were colllected by my Tahoma Clinic colleagues Joni Olehausen
N.D., David Steele M.D., and their patient S.T.
S.T. is a 46 year old woman first seen with problems of depression, mood swings, night
sweats, and insomnia. Two years previously she had undergone hysterectomy with
bilateral ovariectomy, and at the time of first consultation was using only a non-
prescription “progesterone cream”. (She was taking no bio-identical estrogens or
estrogenic hormones of any kind. Her 24-hour urinary estrogens were:
Micrograms Per 24 Hours
On follow-up she was started on 3 milligrams triple estrogen daily, along with
progesterone 50 milligrams, DHEA 30 milligrams, and testosterone 5 milligrams.
Four months later there had been no symptomatic improvement. Follow-up 24 hour
urinary steroid analysis was done; her 24-hour urinary estrogens were:
Micrograms Per 24 Hours
Notably, her DHEA and progesterone levels were within anticipated physiologic limits,
but testosterone was supraphysiologically elevated to 125.5 milligrams/24 hours (pre-
supplemented testosterone level 28.5 milligrams/24 hours, unsupplemented women’s
Her symptoms continued as before. Without alteration of hormone supplementation,
cobalt supplementation was begun. Eight weeks later (just before this report was written),
Micrograms Per 24 Hours
Progesterone and DHEA remained within the physiologic range; testosterone was still
supraphysiologic, but declined to 71.8 micrograms/24 hours. Symptoms were partially
improved, but some of that improvement was attributed to an adjustment in thyroid
supplementation made by another practitioner.
She has been advised to continue all hormone supplementation (and cobalt) unchanged,
and to repeat her test in another 2 to 4 months.
In contrast to the women reported in “cases 1-3”, this individual had estrogen
hyperexcretion “on her own” without any known ingestion of exogenous estrogens. As
noted below, one wonders about “environmental estrogen” exposure with consequent
“upregulation” of the cytochrome p450 series.
The use of low-dose ionic minerals was introduced (as were many innovations in mineral
therapeutics) by John A. Myers, M.D., who practiced in Baltimore. He developed barely-
visible negatively-charged “ion-transfer” resin beads, which were then coated with
positively-charged electrostatically-adherent minerals. Approximately 20 micrograms of
each mineral adheres to a single bead, making this delivery system more suitable for trace
The ion-transfer beads are placed on the tongue, where the mineral is nearly-
instantaneously dissolved in body fluids and subsequently absorbed. Although the ion-
transfer beads are not digestible, it’s advisable to scrape them off the tongue after a
minute or two. Since the beads coated with cobalt initially have a deep purple color, it’s
quite obvious after they’re scraped off that the cobalt is gone.
Myers’ ion transfer beads are still sold by DSD International of Phoenix, Arizona, under
the “Meira” brand name. In addition to cobalt, silver, chromium, copper, manganese,
zinc, calcium, magnesium, sodium, and potassium are available. (I am not in any way
In this application, symptomatic women who hyperexcrete estrogen are advised to use 20
to 30 beads (400-600 micrograms) daily until symptoms subside and laboratory tests
normalize. At present, it’s anticipated that the cobalt supplement can be discontinued
once the cytochrome enzymes have been “downregulated” to an apparent normal level of
activity. If symptoms return, laboratory evaluation can easily detect “recurrent
hyperexcretion (and apparent “re-current cytochrome p450 up-regulation) and cobalt can
According to a current major textbook9 concerning minerals: “Cobalt has a low order of
toxicity in all species studied, including humans.” A study of children in 28 institutions
scattered across the United States found that unsupplemented dietary cobalt ingestion
ranged from 300 to 1770 micrograms daily10. However, other investigators have
published data concerning daily cobalt intakes ranging from 6 micrograms to 580
micrograms daily11,12,13,14. Well-known trace mineral researcher Henry Schroeder
estimated the daily intake of Americans to be at the upper end of this range, at 160 to 580
Even though cytochromes are heme proteins whose synthesis can be diminished by cobalt
and other trace minerals (as noted above), cobalt does not decrease hemoglobin synthesis.
Cobalt is a well-known hematopoetic whose effect is apparently brought about through
increased renal synthesis of erythropoetin. However, the quantities of cobalt required to
achieve a hematopoetic effect are large, 20 to 30 milligrams (20,000 to 30,000
micrograms) daily, amounts well beyond any reported daily dietary intake. At this dosage
range, toxic manifestations including thyroid hyperplasia, myxedema, and congestive
Specifically discussing the role of cobalt in the synthesis of hemoglobin, cytochrome p-
450, and other liver proteins, Tephly and Hibbein wrote:
“Cobalt chloride administration to rats stimulates erythropoesis, but inhibits the
synthesis of hepatic microsomal p-450….No effect on NADPH-cytochrome c reductase
activity was observed….cobalt treatment of rats has no effect on hepatic protein synthesis
over the course of these experiments, cobalt administration may be valuable as a tool for
studying the role(s) of p-450 in various biological reactions16.”
From the above data, it seems reasonable to infer:
A small minority of women have “upregulated” estrogen-metabolizing enzymes,
Ionic cobalt “downregulates” these enzymes and “normalizes” the “upregulated
enzymes”. In doing so, ionic cobalt enables normalization of bio-identical
hormone metabolism, with co-incident symptom relief.
Many questions remain. These include (but are not limited to):
Does “upregulation” of cytochrome p450 (and possibly other) enzymes mean more
total enzymes, hyperactivity of a “normal” number of enzymes, or some
Is cobalt-mediated “downregulation” simply a matter of lessening total enzyme
synthesis, as described by Maines and Kappas, or is there a component of
Which substances induce significant cytochrome p450 “upregulation”?
At least a partial answer to this last question is probably “Premarin” and other
“conjugated equine estrogens”, as a preponderance of cases so far have been former
Premarin users. My (non-statistically verified) impression is that more cases occur among
longer-term Premarin users. However, estrogen hyperexcretion in response to physiologic
dosage of bio-identical estrogen has also been observed in women who’ve not taken any
known exogenous estrogens, as in Case 4 above.
A second strong possibility carries the general descriptor of “environmental estrogens”.
These include (but are likely not limited to) components of plastics, pesticides, solvents,
detergents, and dioxins. If the exogenous, non-bio-identical but “natural” estrogens
contained in Premarin are associated with “upregulation” of cytochromes, it’s likely that
a sufficient quantity (whatever that might be) of one or more “environmental estrogens”
Stretching this line of thought a little further, it might reasonably be asked: “Since
Premarin is a known carcinogen for a small number of women, but not all, and since it’s
very likely that “environmental estrogens” are also carcinogens for a small number of
women (and perhaps men), but not all, could estrogen hyperexcretion, either in response
to physiologic dose bio-identical estrogen replacement, or with no known cause, be a
“Most of the time, increased mitochondrial oxidative activity and cytochrome p450
content are desirable since for most drugs and some carcinogens, “oxidation” and
“detoxification” are the same thing. By contrast, for a small group, “oxidation” and
“activation” are the true synonyms. “Activation” means these metabolites may in some
cases be more dangerous to cells than their parent compounds.”
“Depletion of cellular heme proteins including cytochromes p450 and p448 should not
always be viewed as augmenting toxicity; in some cases, this depletion is preventing the
formation of toxic metabolites.”
These comments imply that the answer to this question may be “yes”. If so, dietary-range
cobalt supplementation may help prevent estrogen-related cancers
in women whose
exposure to Premarin and “environmental estrogens” results in “upregulation” of the
cytochrome p450 system with consequent estrogen hyperexcretion.
A clue to the strength of this “cobalt may prevent estrogen-related cancer” hypothesis is
found in data concerning a parallel situation: carbon tetrachloride hepatotoxicity.
Carbon tetrachloride is a known hepatotoxin whose toxicity depends on the “activation”
of free radical metabolites17. This activation is mediated by the cytochrome p450 system,
and is decreased by cobalt pretreatment18.
“The administration of cobaltous chloride to rats produced a selective dose-dependent
decrease in the cytochrome p450 component of the microsomal electron transport system.
A concomitant of this alteration….was a refractoriness to the carbon tetrachloride-
induced elevation in serum glutamic oxaloacetic transaminase (SGOT), serum
glutamicpyruvic transaminase (SGPT), serum isocitric dehydrogenase, (ICDH), and the
decrease in hepatic microsomal glucose-6-phosphatase activity. Cobaltous chloride
pretreatment alos decreased the intensity of micro-somal diene conjugation absorption
observed after carbon tetrachlorideadministration.”
If cobalt decreases the “activation” of carbon tetrachloride into toxic metabolites through
it’s effects on the cytochrome p450 system, it’s possible that it also reduces the
“activation” of estrogens into toxic and perhaps carcinogenic metabolites. It’s also
possible that the simultaneous GSH-generating effect of cobalt would help neutralize
“activated” estrogen metabolites, also reducing the risk of cancer.
Reverses bio-identical estrogen replacement failure
May help reduce the risk of estrogen-related and “environmental estrogen”-related
1 In this report, “triple estrogen” is 80% estriol, 10% estradiol, 10% estrone. 2 Indeed I am a consultant for Meridian Valley Labs 3 Remember Henry Lemon? For those who don’t, there will be a posting on the
importance of monitoring certain steroid metabolites in the future. Hint: estriol is the
“detoxified metabolite” of 16a-hydroxyestrone.
4 EAV, Electroacupuncture According to Voll, sometimes termed MSA (Meridian Stress
5 Maines MD, Kappas A. Metals as regulators of heme metabolism.
6 Sasame HA, Boyd MR. Paradoxical effects of cobaltous chloride and salts of other
divalent metals on tissue levels of reduced glutathione and microsomal mixed-function
J Pharm Exp Ther 1978;205(3):718
7 Maines MD, Janousek V, Tomio JM, Kappas A. Cobalt inhibition of synthesis and
induction of gamma-aminolevulinate synthase in liver.
8, there was no known explanation for the previous physician’s prescription of two bio-
identical estrogens along with the non-bio-identical medroxyprogesterone (Provera)
9 Smith RM, Cobalt
, page 174, in Mertz, W, ed., Trace Elements in Human and Animal
Nutrition, 5th edition, Academic Press, San Diego, 1987 (the most recent edition)
10 Murthy GK, Rhea U, Peeler, JT. Environ Sci Technol 1971;5:436-442 11 Harp MJ, Scoular FI. J Nutr 1952;47:67-72 12 Schroeder HA, Nason AP, Tipton IH. J Chron Dis 1967;20:869-890 13 Tipton IH, Stewart PL, Martin PG. Health Phys 1966;12:1683-1689
14 Yamagata N, Kurioka W, Shimuzu T. J Radiat Res 1963;4:8-15 15 Smith RM, ibid.,
p. 173 16 Tephly TR, Hibbein P. The effect of cobalt chloride administration on the synthesis of
hepatic microsomal cytochrome p-450
Biochem Biophys Res Comm 1971;42(4):589
17 Recknagel RO, Glende R. Carbon tetrachloride hepatotoxicity: an example of lethal
CRC Critical Reviews in Toxicology 1973;2:263-297
18 Suarez KA, Bhonsle P. The relationship of cobaltous chloride-induced alterations of
hepatic microsomal enzymes to altered carbon tetrachloride hepatotoxicity.
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