Magnesium ...1......2... ...3...
Plasma magnesium levels in a population of psychiatric patients: correlations with symptoms.
Mice selected for low and high blood magnesium levels: a new model for stress studies.
Are age-related neurodegenerative diseases linked with various types of magnesium depletion?
| Neuropsychobiology 1994;30(2-3):73-8 | Related Articles, Books, LinkOut |
Plasma magnesium levels
in a population of psychiatric patients: correlations
with symptoms.
Kirov GK, Birch NJ, Steadman P, Ramsey RG.
Warlingham Park Hospital, UK.
Plasma magnesium levels were tested in a group of 155
psychiatric in-patients with a variety of diagnoses and
were correlated with the severity of their symptoms. We
hypothesized that lower Mg levels would correlate with a
higher degree of anxiety, tiredness and other symptoms
characteristic of Mg deficiency. No such correlations
were observed. However, Mg levels varied widely, with
22.4% below, and 10.4% above the normal range. There was
a strong association for more disturbed and excitable
patients to have abnormal (either high or low) levels. We
speculate that more disturbed patients might have some
abnormality of Mg metabolism with possible therapeutic
implications.
PMID: 7800167 [PubMed - indexed for MEDLINE]
| Physiol Behav 1997 May;61(5):653-8 |
Mice selected for low
and high blood magnesium levels: a new model for stress
studies.
| Magnes Res 1995 Mar;8(1):37-45 | Related Articles, Books, LinkOut |
Inhibition of
mouse-killing behaviour in magnesium-deficient rats:
effect of pharmacological doses of magnesium pidolate,
magnesium aspartate, magnesium lactate, magnesium
gluconate and magnesium chloride.
Bac P, Pages N, Herrenknecht C, Teste JF.
Laboratoire de Pharmacologie, Faculte
de Pharmacie, Chatenay-Malabry, France.
Magnesium deprivation induced interspecific aggressive
behaviour (muricidal behaviour) in rats undoubtedly
attributable to magnesium deficiency since magnesium
chloride, by correcting magnesium deficiency, suppressed
it. Inhibition of magnesium deficiency-induced behaviour
by various magnesium salts should enable the
classification of the therapeutic effects of these salts.
Consequently we compared the effects of various magnesium
salts used therapeutically on the inhibition of the acute
muricidal behaviour induced by magnesium deficiency. All
the magnesium salts used (chloride, pidolate, aspartate,
gluconate, lactate) suppressed the muricidal behaviour.
There was no significant difference in the duration of
the treatment needed to inhibit this comportment for each
of the salts studied. In contrast, significant
differences appeared, concerning the different phases of
muricidal behaviour. Magnesium pidolate significantly
increased the attack latency (P < 0.05). By repeating the
muricidal assays, we showed that magnesium pidolate
treated rats had a muricidal behaviour rate which was
lower than that of the other magnesium salt-treated rat
groups. Consequently, it can be assumed that all the
magnesium salts used had an acute anti-muricidal, perhaps
anti-stress, effect and that magnesium pidolate
presented, on this experimental model the greatest
efficacy.
PMID: 7669506 [PubMed - indexed for MEDLINE]
| 1: Magnes Res 1997 Dec;10(4):339-53 Source |
Are age-related
neurodegenerative diseases linked with various types of
magnesium depletion?
Durlach J, Bac P, Durlach V, Durlach A, Bara M,
Guiet-Bara A.
SDRM, Hopital Saint-Vincent-de-Paul,
Paris, France.
Age-related human neurodegenerative diseases are a
major social and medical problem. It is therefore
logical to take into consideration every theory with an
overall approach to neurodegenerative diseases. This
environmental proposal relies mainly on data concerning
the Western Pacific amyotrophic lateral
sclerosis-Parkinsonism-dementia complex (WP ALS-PD)
considered as 'a prototypal human neurodegenerative
disease' and on extrapolation from it to the bulk of
neurodegenerative diseases (NDD). NDD would be due to
an accelerated ageing process in certain populations of
neurons due to the noxious synergy of (1) increased
environmental slow deleterious factors (such as slow
toxins) and of (2) decreased environmental protective
factors (Mg deficient intake particularly). First, it
was observed that three apparently dissimilar
conditions occurred at extraordinary high rates in the
Guam area: motoneuron disease (ALS), Parkinson's
disease (P) and Alzheimer's-like dementia (D). Next,
several other foci of endemic ALS-PD were found in Asia
and Oceania in three Western Pacific population groups.
These included the Chamorro people in Mariana Islands
(Guam and Rota), the Auyu and Jakai people of West New
Guinea and the Japanese residents of the Kii peninsula
(Honshu island). The post-Second World War decline of
the occurrence of WP ALS-PD in all three high incidence
disease foci coupled with the absence of demonstrable
heritable or transmissible factors had led to focus the
search for the cause of this degenerative disease on
nontransmissible environmental factors that are
disappearing as the susceptible population groups
acculturate to modern way. Epidemiologic study has
shown that preference for traditional Chamorro food is
the only one of 23 tested variables significantly
associated with an increased risk for PD. An early
suggestion incriminated the toxic seed of the false
sago palm (Cycas circinalis L) which was used in
traditional food and medicine. Laboratory investigation
of cycad seed revealed the presence of various toxins
and particularly of an 'unusual' non protein aminoacid:
L-BMAA (beta-N-methylamino-L-alanine), an excitotoxic
aminoacid. This slow toxin presents some structural
similarity to another 'unusual' excitotoxic aminoacid:
L-BOAA (beta-N-oxalyl-amino-L-alanine), an exogenous
neurotoxin present in the grass pea (Lathyrus sativus)
whose excessive consumption may cause lathyrism. The
excitotoxicity of both L-BMAA and L-BOAA mainly
concerns non-NMDA receptors. The neurotoxicity of these
aminoacids varies with experimental models failing to
induce an experimental model akin to WP ALS-PD or
displaying many of the motor-system and behavioral
changes of WP ALS-PD. It may be due to the presence of
physiological levels of bicarbonate or of various toxic
cofactors: bio-organic such as cycasin or inorganic
such as pollutant metals e.g. aluminum or manganese,
together with the lack of protective factors (e.g.
calcium and magnesium deficiencies). Combined Al
intoxication with Ca-Mg deficiencies is a reasonable
model to investigate the pathogenesis of
neurodegenerative diseases and eventually to screen
their treatments. It may also be considered as a model
of magnesium deficit, but it does not concern simple
magnesium deficiency reversible with mere oral
physiological magnesium supplementation. Magnesium
deficiency cannot result in neurodegenerative disease.
Combined Al intoxication with Ca-Mg deficiencies is not
reversible through physiological oral magnesium
supplementation. It therefore constitutes a type of
experimental magnesium depletion model, instrumental in
the investigation of the pathogenesis of magnesium
depletion and in the screening of its still unknown
possible treatments. (ABSTRACT TRUNCATED)
Publication Types:
PMID: 9513930 [PubMed - indexed for MEDLINE]
Source
CALCIUM AND MAGNESIUM
Calcium and magnesium are extremely important minerals that are often out of balance in persons with thyroid disease. Imbalances of these minerals can result in very rapid heart rate, low heart rate, and irregular heart rate. Thyroid function itself is most likely controlled by the ratio of these minerals.
Most people with thyroid disease find that they have to supplement calcium and magnesium. Supplementing these minerals in the correct ratio can make a huge improvement in the symptoms. However, supplementing them in the wrong ratio can make symptoms worse. To further complicate the situation, the correct ratio of cal/mag changes as you recover from thyroid disease.
I have struggled a very long time with finding the right cal/mag ratio for myself. Well after recovering from hyperthyroidism, swinging back hypo, and then getting normal again, I had many months of fast, irregular heart rate that was often initiated by strenuous exercise. Because magnesium had been an important factor in reducing my heart rate when I was hyper, I would take a cal/mag supplement in a 1:1 ratio or take 400-800 mgs of magnesium only to correct this problem. Usually I would have this irregular heart rate throughout the night but would be recovered by morning.
I experimented with potassium and found that taking 800-1200 mgs of potassium before my night time basketball often prevented the irregular heart rate and began thinking that I was potassium deficient. One time I grabbed an unlabeled baggie that I thought was potassium and took 6 capsules before playing. I had extreme irregular heart rate that lasted all night. I later discovered that I had mistakenly taken magnesium.
This was very strange to me because magnesium had been my savior for such a long time. Whenever I had high heart rate when I was hyper, magnesium would slow my heart, usually within 20-30 minutes. So I was wondering, "Why doesn't it work now?" I began to think that the manufacturer had made a mistake and there was a problem with the product.
Eventually the answer came in a sudden insight. I was lying awake at night with my heart beating very irregular and fast. Paying close attention to my heart, I realized that my heart was not just irregular and fast, it was beating very weakly. I noted that this was in stark contrast to the time when I was hyper. Then my heart was beating fast and irregular, but very strong.
The insight was that it was the strength of my heart beat and not the speed and irregularity that was the key. I thought back on how calcium is the mineral that is responsible for the heart contracting and magnesium is responsible for the heart relaxing.
During hyperthyroidism, magnesium is low and calcium is high. This imbalance is the result of other mineral imbalances (copper, zinc, iron, etc.), but the effects on the heart rate are direct effects of a calcium/magnesium imbalance. This can be demonstrated by taking a magnesium supplement or a cal/mag supplement with much higher magnesium than the usual 2:1 cal/mag ratio when your heart rate is high. This intake of more magnesium will slow the heart rate temporarily. However, as we have seen, the body can't maintain normal magnesium levels in the blood if copper is low. So until copper is replenished, extra magnesium is needed on a constant basis to control the rapid heart rate.
The key to understanding the effects of calcium and magnesium on the heart is this: Calcium is needed for muscles to contract and magnesium is needed for muscles to relax. The heart muscles are like all muscles. Calcium causes heart contraction; magnesium causes heart relaxation.
If magnesium is low, as during hyperthyroidism, and calcium is adequate, the heart contracts normally but the relaxation phase is shortened and incomplete. If the normal heart contracts for .5 seconds and relaxes for .5 seconds, we have a 1.0 second cycle which translates into a 60 beats per minute heart rate. If magnesium is low and the relaxation phase is shortened to .25 seconds, then the complete cycle is .75 seconds, which translates to a 80 beats per minute heart rate (60 seconds divided by .75 seconds). As you can see, as magnesium gets more depleted, the relaxation phase shortens and the heart rate increases.
When I was experiencing the irregular heart rate, what was happening was that it was calcium that was low and not magnesium. When calcium is low, the contraction phase is shortened while the relaxation phase remains normal. If the contraction phase shortens to .25 seconds and the relaxation phase stays at .5 seconds, the heart rate also increases to 80 beats per minute. If you just looked at the increase in rate, you might, as I did, think that magnesium was deficient.
The key to the insight that it was calcium that was deficient was the observation that the heart rate was weak. A weak heart rate means that calcium is deficient and the contraction phase is weak and short. This results in an increase in heart rate and also an irregular heart rate because some contractions are missed entirely. Contrast this to a magnesium deficiency where the heart rate is irregular because some of the relaxations are missed.
Once I reached this insight, it all became so simple. I was amazed that I had continued to make the same mistake over and over again. The key mental block for me was that I thought that magnesium always slowed and regulated the heart rate. Once I thought through the whole process of how calcium and magnesium affect the heart, I realized that a calcium deficiency can also lead to a fast and irregular heart rate.
With this new insight, I switched my cal/mag ratio to 2:1. I had been mixing a 1:1 ratio supplement with a 2:1 supplement which resulted in a ratio of about 3:2. However with the addition of extra magnesium or extra 1:1 cal/mag after basketball, I probably had about a 1:1 overall ratio.
Once I switched to a 2:1 ratio, the heart irregularity completely disappeared and hasn't occurred in months. I found that the cal/mag ratio is the key. However along the way to this discovery I ran across some other interesting information.
As I was struggling through this irregular heart rate problem, I found that two things often helped the situation: potassium and vitamin B-5. Potassium often helped and I think the reason for this is that potassium and magnesium are antagonistic minerals. Since I was essentially suffering from too much magnesium (or too little calcium), the potassium helped because it reduced the metabolic effect of the magnesium (or assisted the metabolism of calcium). I think this is important, particularly for persons with hypothyroidism, because they need a higher calcium to magnesium ratio. A potassium deficiency could prevent the cells from getting enough calcium which is an activator in the cellular response to thyroid hormone.
The other discovery was that vitamin B-5 is important in preventing irregular heart rate. If B-5 gets deficient, it seems to have an effect on the calcium/magnesium metabolism so that calcium doesn't work as well. A B-5 deficiency has similar effects to a calcium deficiency. I don't know why this happens, but I now realize that it's important when supplementing B complex vitamins to always make sure that you are taking as much B-5 as any of the other B vitamins. For example, if you are supplementing with high amounts of niacin (for headaches or other reasons), be aware that you will need to increase B-5 to the same amount or a little greater to prevent a disturbance of the cal/mag ratio which could result in irregular heart rate.
One other discovery in all this was that by not taking enough calcium and taking too much magnesium, another of my teeth died. I developed an extreme tooth ache which led to another root canal. For dental and bone health, don't maintain a high magnesium/calcium ratio past the point where you need it.
Remember that balancing calcium and magnesium won't correct thyroid problems. You'll need to correct the other minerals like copper, zinc, iron, selenium, chromium, manganese, etc. to achieve this. Calcium and magnesium get out of balance because of these other nutritional problems. However, getting your calcium/magnesium balance corrected is essential for normalizing heart rate, preventing dental decay and osteoporosis, and preventing muscle cramps (too little magnesium).
In summary, to balance calcium and
magnesium keep these points in mind: a normal person need
a cal/mag ratio of about 2:1; a hyper needs more
magnesium and a hypo needs more calcium, but these ratios
need to be constantly adjusted as you approach normality;
irregular heart rate can be a sign of either too little
calcium or too little magnesium; the key to knowing
whether you need calcium or magnesium is the strength of
the heart beat, not the speed or the irregularity--if
it's too strong, take more magnesium and if it's too
weak, take more calcium.
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