Nader Moradi wrote:
+++++++ Well, drug miasms, toxicity miasms have been posited, and called "miasms" by some--but not discussed in the context of Hahnemannian spirit-like miasms. How amenable they are to later treatment with an isode or other indicated rx(eg in cases of diethylstilbestrol during pregnancy, effects of occupational exposures, poisonous dietary elements, pollution etc) is something I dont know at this point. Such poisoning definitely can cause manifest birth defects--so they either interrupt biochemical processes or engraft energies---are they passed as energetic miasms, or do they merely act as triggering causes to bring latent chronic miasms to the surface....??___________ The difference is between a life force contagion and a biochemical assault. It would seem that the answer could be that the effects are material and gross, and any damage caused is not do to a derangement of vital force in particular. We know that infectious engagements will awaken disease or engraft disease
which can be passed on. Can material biochemicals do this also. It would seem that such damage even when passed on is not in the same category. But even gross substance has an "etheric" component. Prolonged taking of allopathic drugs will respond in some cases to the isode of that drug. Presumably this
++++++ Even degenerative diseases must have a miasmatic base, as they do not come out of nowhere, (and I am sure that is not what Chris was saying, of course). The permutations of miasm complexes in suppressed cases could produce the "degenerative" category perhaps, which does not have stages that resemble the stages of sycosis or syphilis, for example, or any other disease that the parent or precursor NEVER RECOVERED FROM and expelled from their energetic "economy" prior to procreation. The roots of degenerative, "stageless" disease must be taints of the vital force all the same--even if not identified with a KNOWN miasm. This gets back to my point that understanding the chronic diseases is not a finished story. Hahnemann only started it and laid the framework. That in itself was perhaps on the short list of 2 or 3 greatest medical understandings of the last few thousand years (TCM physiology is up there, certainly, but the treatment of disease by similars outstrips TCM
therapeutics, which do not remove miasms).
So this is why I do not find new developments like Sankaran etc to be at all incongrous, and I will discuss this later, though I am sure it will be controversial, which is good, as this is a discussion board
. There are no sacred cows, although the info that Hahnemann gave us is of high quality.
++++ Good reference, comment, and question. Well, nothing too scholarly here, but the drug and toxic exposure-caused diseases, not being borne of life force but of "dead" biochemical forcing functions, may damage DNA, and on longterm use, may engraft a taint on the life force by virtue of their inherent nonphysical basis--even though the contagious and more easily dangerous "noxious fog" of living energy is not present.
1. So, category one would depend on investigation of past drug abuses of the parents and before. In such cases, the nature of the offending drug may yield information about the nature of the disease, and tautopathy may be a useful preamble to treatment.
2. Continuous pathogenic influences--missing dietary elements (eg iodine deficient goiter), lifestyle (eg abuse, lack of love, overwork); local epidemic influences; etc.
3. Diseases only based on chronic miasms (under discussion).
++++Will Taylor theorizes that human papilloma virus is the etiological agent of sycosis and thus the nosode. Your opinion?_________
++++ Oui, si vous plait, bien, bien.
++++ Well, why do you find this so badly misleading---the entire profession for the most part still equates sycosis with gonorrhea, probably erroneously.
Sankaran is just carrying on the mistake---but Thuja and med are still sycotic rx. So his indications will be based on the same understanding of sycosis, though the actual etiological agent is possibly incorrect. In any case, neisseria and the actual etiological agent must bear an intimate relation of some kind--do you not agree. If neisseria is not the infectious agent, then there is some relation to that which IS.
+++ If these are in fact miasms, then why would you require Sankaran to call them something else. I have seen cases cured using his triangulation system using these "miasms"---indicating resonance with the taint via a three legged stool of vital sensation/taxonomy---kingdom--and "miasm". This equation depends on Sankaran's hypothesis that each remedy has a dominant miasm which characterizes it--a new concept and one which still requires definitive proof IMO. But the fact that the system WORKS indicates that Sankaran has developed an understanding through long experience which allows him to differentiate subtler and previously unidentified miasmatic influences---even if previously, so-called "acute" miasms were supposedly not able to engraft and be passed on. If an rx WORKS base on his elaborate and ingenious inferential system, then is this not sufficient proof; or has Sankaran just created, as you imply---a very clever OVERLAY which just HAPPENS to get results? To my mind,
it appears to me provisionally that it is unlikely to get results when the infectious taints have been misidentified, regardless of previous theory which says that "acute" miasms do not linger.
Of course, the acute miasm could be from the PRESENT life, and the susceptibility thereof could be from a complex of chronic miasms. In India, people are more likely to have typhoid or malaria or ringworm than in the west. So his miasms could be identifying susceptibility in the PRESENT life, and his substantiating data is because of his population of cases. All the same, the disease expression in India is the best type of database, generally people who tend to use allopathy less than other populations.
So, we are left with the question---do these so-called "acute" miasms cross the boundary of procreation and were just more subtle than the more florid, staged, and egregious major miasms we have come to see first--or NOT. Is Sankaran identifying only miasms which are from the present life, or has he refined the entire theory of chronic diseases by identifying a more subtle group of miasms....?_________
And--why has he ignored hydrophobia and AIDS heretofore?____________
++++ Can you reference this in Organon or CD for me please, if not too much trouble. As I said, I dont think there are any sacred cows. Just because these were Hahnemann's criteria for whether a miasm was virulent enough to pass on to next generation, does not mean that he was correct. As stated, other miasms may just be more subtle, and his theory was obviously unfinished.
For my understanding, if a client comes with Never Well Since Influenza, and they conceived after that influenza, then the child will have developed under that influence, whether the original disease was a "staged" one or not. I agree that the background of other miasms could account for the susceptibility leading to Never Well since influenza. But the energy of that parent HAD to pass on to the child. Influenza was an "unfinished" disease expression of that parent's immune system. If they received the curative remedy, they would re-experience the symptoms of the flu, and then be free of the miasm. But the child conceived before they got the rx would obtain the taint of that parent's pattern (mixed with that of the other parent.
++++ No. But as I say, I am not convinced that staged diseases are the only ones that can affect the succeeding generations. But I appreciate the discussion, and am learning from it. Sankaran identifies not stages per se in these diseases, but the NATURE of the disease--for example malaria--cyclic intermittent phenomena of attracted danger in the life;; etc. Particularly this malaria one is not covered by any other miasm--this is how Sankaran noted that it did not fit in an existing category. This one is almost certainly passed on to generations beyond--even though it does not pass Hahnemann's "stages" criteria, necessarily. The category "never well since" or "disease x agg" are a form of incompletion of a disease, and evidence of that is recapitulation of that "incomplete disease" in Hering's rule fashion when correct rx is found. These were acute diseases, without stages, but having LINGERING EFFECTS. Conception under such circumstances cannot help but pass on the
taint of even a non-staged disease. We can see the ulcers of tertiary syphilis, for example. But Never Well Since Malaria is more subtle, less obvious. So the fact that a disease is without stages, and usually either resolves or kills the client in a short time, does not mean that it does not have chronic effects, though these effects are not nearly as florid as syphilis, and other insidious bacterial or parasitic infections. So I would challenge the "staged" disease criterion and see if you can prove it to me. _________
So, this is why I say that these miasms that Sankaran is working with are more subtle ---and could represent merely another more refined layer to the theory. Hahnemann caught some of the "big ones"---it appears to me that Sankaran is taking a really good shot at some that are more subtle.
+++ Ok. Would like that. Please also speak to the discussion above without prejudice. What evidence do you have that Influenza never well since, or malaria never well since CANNOT be passed on to the succeeding generation? How could it not be?
++++ So the other explanation is that the so-called acute miasms are not what gets passed on to yield a similar susceptibility in the offspring. But the chronic miasms underneath. BUT in the case of malaria, for example, the PATTERN of cyclic intermittent complaints of any kind that Sankaran notes (and I have in a couple of cases that I found using his method)---does NOT BELONG to one of Hahnemann's previously identified miasms. So, again, I feel like you are repeating Hahnemannian dogma, and I would need proof that the more acute diseases are SOMEHOW not able to be passed on energetically in the gametes.
++++ Then I suggest that the acute miasms are not "sacred cows" that do not get passed only because Hahnemann said they did not. I suggest that he just did not have the chance to look at the next level of subtlety that we are just starting to investigate, and which has taken Sankaran some 14 years to get as far as he has. My guess is that there is an "Influenza" miasm as well, for example. How it manifests will be more subtle and require the subtle discernment and miasmatic understanding in order to classify. The number of miasms must be quite large, and epidemiology is the place to look to find ones to investigate. For example, Schistosomiasis is the #1 macroparasitic disease in the world, at least last time I looked with hundreds of millions infected. We do not even have a Bilharziasis miasm identified in homeopathy. WHY NOT? ______________
++++ As said, I am not convinced that hahnemann's requirement of a staged disease does not need renovation. Hydrophobia is a miasm elucidated by Lou Klein quite well, but Rajan has rejected it (I know because I asked about it at a seminar with him around '93 or so). Hydrophobia as a miasm is present in the population, and shows up in particular in many stram, bell, hyos, and lach cases, in particular in children. Animal bites keep happening. Although rabies the florid condition may not occur, an animal bite could be a triggering cause for hydrophobia. In any case, the point is that my working hypothesis is that there is NO ARBITRARY LIMIT to what can be passed on as a result of an UNFINISHED DISEASE, whether it was "acute", chronic, staged or unstaged.
+++++ I agree, and I think it was present in the population well before the disease manifested in humanity, ---even though the disease agent in this case was likely manmade.
+++ I did not say we needed one. But in the cases that DO need the nosode in order to proceed, not having identified the miasm dominant will cause failure. Agree?___
++++ Interesting. If I understand you correctly, Down's syndrome would be defined as a florid miasmatic disease which attacks the affected chromosomes. Whereas conventional thinking sees chromosomal damage as the (unexplained) CAUSAL element in Down's, you are saying it correctly---that a CHARACTERISTIC of Down's syndrome as an energetic, spirit-like miasm or disease is that it CAUSES certain chromosomal damage (eg trisomy 21)--and that this is essentially an indicating symptom, but not a cause. That is good thinking. The cause is a miasm, evidenced by the fact that affected children treated very early can lose most of the limitations the syndrome presents. Which miasm(s) are involved (in present understanding)--and what other as yet undiscovered and uncharacterized miasms could be implicated? (Here is a file on Down's syndrome for you to use to be able to answer this question if it is possible---note I have preserved the original quotes, in which practitioners have used
"mongolism" or "mongols" as a term, and apologize for the offensiveness of the antiquated term):
===============================
DOWNS SYNDROME
•GENERALITIES; DOWNS syndrome: bar-c., carcinosin., des-ac. (DNA), [helium], [lap-gr-m (granite)], lyssin, medorrhinum., morgan., nat-m., [neon], pertussin, phos., puls. sep., syc-co., toxoplasmosis, tuberculinum
-Bar-c (Foubister)
-Carcinosin (Foubister),( Julian)
-Des-ac (DNA) (Julian-“ Mongolism”)
-[Helium] (Scholten-but more for the autistic aspect -1 case only)
-[Lap-gr-m (granite)]- inclusion here based only on the high incidence of Downs syndrome in Connemara granite terrain (a granite generally high in radioactivity-note that terrain remedies (such as Connemara Granite) in British Isles tend to reflect the nature of the people living in the area to a high degree.
-Lyssin-(S.K Banerjea, Calcutta)
-Medorrhinum-“a near specific”-(Foubister) “Mongols are helped very much by Med”-(Blackie) “Mongolism of children; with history of gonorrhoea in parents; with characteristic symptoms of medorrhinum.” (Mathur)
-Morgan- (Patterson)
-Nat-m (Foubister)
-[Neon] (Scholten-not confirmed)
-Pertussin (Julian)
-Phos-(Foubister)
-Puls (Priestman)
-Sepia (Foubister)
-Sycotic co -(Voisin)
-Toxoplasmosis (Julian)
-Tuberculinum-(Foubister)
===================================================================
*Blackie: “Mongols are helped very much by Medorrhinum. All Mongols like light.”
*Foubister:
Backward and Mentally Defective Children
It is very well worthwhile to consider homoeopathic treatment in the case of backward children and the fairly high - grade mentally defective. Obviously the prognosis ultimately depends on the pathology. Mongols cannot be altered basically but constitutional treatment, apart from a minority who presumably have a primitive brain formation, enables the mongol to accept some education. Nearly all mongols benefit definitely, physically and mentally, by receiving constitutional homoeopathic treatment. Medorrhinum is a near specific, Carcinosin, Sepia, Baryta carb. and other remedies may be required. Medorrhinum is a near specific, Carcinosin, Sepia, Baryta carb. and other remedies may be required.”
•Treatment of Mongols:
Old homoeopaths thought that Medorrhinum was the only remedy. But in our experience Carcinosin, Natrum muriaticum, Phosphorus, Sepia are useful. Rest depends on individual makeup.
1. Select the proper remedy.
2. Vit A and D should be given side by side.
Potency of vitamin 6 - 30 may also be used. Vit E also help.
Calendula off. 200 potency also helps, it affects Vit. A. Vit mixture 6
So treatment consists 1. Constitutional and 2. Vit. Potency.
•Medorrhinum, Carcinosin, Sepia, Tuberculinum bovinum, Natrum muriaticum: Constitutional remedies for mongols.
*Priestman: Mongols have usually Catarrh, they tend to be overweight. Pulsatilla and Medorrhinum most indicated.
----------------------------
I also append an article on the observed types of chromosomal damage in Downs to help you develop your theories about its miasmatic origin so you can inform us further on this topic
Until next installment
Andy
http://www.nas.com/downsyn/benke.html
==================================
Risk and Recurrence Risk of Down Syndrome
Paul J. Benke, M.D., Ph.D. Director, Clinical Genetics
Virginia Carver, Ph.D. Prenatal Diagnosis Program
Roger Donahue, Ph.D Director, Cytogenetics Laboratory
Genetics Division, Department of Pediatrics
University of Miami School of Medicine Miami, Fla. 33101 USA
October 1995
Children with Down Syndrome (DS) account for one of every 800 births. The risk of chromosome disorders like DS, trisomy 13 and trisomy 18 increases with
maternal age. The incidence of DS at birth is lower at age 20 (1/1600) than at age 35 ( 1/370), but many more younger women have children than older women. So
most (75-80%) DS children are born to younger women. If a couple has a child with DS, there is usually an increased risk for a second affected child.
Genetic Forms of DS
All individuals with DS have extra chromosome 21 material. There are 3 genetic mechanisms for trisomy
21. The first and most common, is called non-disjunction, where there is an entire extra chromosome 21 in
all cells. A chromosome study (karyotype) of trisomy 21 is shown in Fig. 1.
Figure 1
The second is mosaic DS, where trisomy 21 cells are mixed with a second cell line, usually "normal" (46,XX or 46,XY). Individuals with this form of DS are frequently
a bit milder in their presentation, depending on the proportion of normal cells.
The third is a translocation DS, about 3-5% of the total, where part or all of chromosome 21 is translocated to another chromosome, usually 14. Translocation DS does
not vary with age. Children with translocation DS are indistinguishable from individuals with the usual form of DS.
Trisomy 21
An extra whole chromosome 21 in all cells examined is found in about 92 per cent of all DS individuals. This is shown in Figure 1. DS is common enough that it may
appear that there is an excess cluster or hot spot when several DS children are born in the same area, but this is just chance and statistical variation.
As far as we know, there is no relationship between DS and diet, drugs, economic status, or life style. Some evidence suggests that it is a little more common in families
with Alzheimer's disease in one or more older family members.
Non-disjunction results from unequal chromosome division, usually in the mother's egg production. This is the form of DS that increases in incidence with increased
maternal age. But DS is so common, it is not rare in young parents.
If a couple has a child with DS, the risk is higher for the next pregnancy (1/100). Obviously, this means that the risk is 99% that the next child will NOT have DS. If
the risk is already 1/220 at birth, the risk at age 37, the risk is usually estimated as twice the risk for age. Risks for amniocentesis results are higher because half to
three-quarters of DS fetuses die before birth of natural causes.
The risk of DS does not appear increased in siblings of trisomy 21 individuals.
Prenatal testing is always recommended for couples who are worried about a second affected child. But prenatal testing procedures may not be for everyone, since they
are expensive and many parents may not want to know or act on the information.
The testing is more than 99 per cent reliable in most genetic centers, only rarely is there a sampling of maternal cells, failure of cells to grow or bacterial or yeast
contamination.
Mosaic Trisomy 21
A mosaic DS child has two populations of cells, the trisomy 21 cells, and a second cell line, usually normal. This form is 2-4 % of the DS population. The physical
features may be milder in these individuals, particularly if there is a large proportion of normal cells.
It was once thought that the unequal chromosome division of mosaic DS takes place early after fertilization, and is a defect in mitotic cell division. However, CVS
studies have shown that a fetus with 47 (XX or XY) + 21 chromosomes can lose an extra 21 chromosome in some cells, providing an alternate mechanism for the
mosaic result. Thus, Mosaic DS may also be related to maternal age. This also means that an increased recurrence risk is theoretically possible, and prenatal studies for
subsequent pregnancies would be recommended.
Translocation Trisomy 21
In 3 - 4% of DS the extra chromosome 21 is permanently attached to another =chromosome causing a translocation. "Translocation" refers to one type of rearrangement
of chromosomal material; in DS almost all translocations are Robertsonian translocations, named for Dr. Roberts, an Australian chromosome expert who originally
described this type of translocation.
A Robertsonian translocation is formed when one chromosome 21 attaches to another chromosome, forming a single new, chromosome. The recipient chromosome is
usually chromosome 14 and the combination of 2 chromosomes is called a fourteen, twenty one translocation, written t(14;21) or t(14q21q). The q refers to the long
arm of a chromosome. Here, the long arm of 21 is attached to the long arm of 14.
Karyotypes with a Robertsonian translocation can be balanced or unbalanced. Individuals who have one 21, one 14, and a t(14;21)
are balanced: there is no extra or missing chromosomal material. Here there are 45 instead of the usual 46 chromosomes. The one
translocation chromosome now carries the original 2 chromosomes. A translocation DS karyotype is shown in Figure 2.
Figure 2
Down syndrome results when there are two chromosomes 21, one 14, and one t(14q21q) because this combination has 3 chromosomes 21, a trisomy 21 by a different
genetic mechanism. Sometimes, a Robertsonian translocation is formed between a 21 and a chromosome other than a 14. There are Robertsonian translocations
between 13 and 21; 15 and 21; and 21 and 22. The recurrence risks for DS for balanced carriers with these other translocations is taken to be the same as that for the
t(14;21).
In about one-fourth of translocation DS individuals, the translocation is inherited. When it runs in families, the carriers are usually unaware they have a translocation
because there are no problems for the balanced translocation carrier. Only with the birth of a DS child or DS fetus by miscarriage, does the couple find out one parent
is a translocation carrier.
A carrier parent can have a chromosomally normal child, or a child who is a balanced carrier like the parent, or a DS child.
Curiously, the chance that such a couple will have another DS child depends on which parent is the carrier. When the
mother is a balanced carrier of a t(14;21), there is about a 12% risk for another DS child to be born in each subsequent
pregnancy. When the father is the carrier, the observed risk drops to about 3% for DS. The reason for this difference in
risks is not at all clear. A balanced translocation karyotype is shown in Figure 3.
Figure 3
In about three-fourths of translocation DS neither parent is a carrier, and a mutation in the germ cells of one parent has caused the translocation. No one knows what
causes these mutations. In cases of a new, or de novo, Robertsonian translocation, the risk of a couple producing a second DS is low, estimated to 2-3 %. There are rare
instances of recurrence on record, and prenatal testing in subsequent pregnancies should be considered.
One might think that translocation DS accounts for most of the cases occurring in younger ("age-independent") mothers but the evidence shows this is not true.
Translocation DS occurs with about equal frequency in younger and older women.
There are other rare translocations leading to DS. One is a Robertsonian translocation between two chromosomes 21, t(21;21); this has a 100% risk for DS when
transmitted by a carrier parent. Also rare is a non-Robertsonian translocation formed by the union of two 21's such that the translocation forms a mirror image of the
normal 21.
Finding professionals with a positive outlook and who have personal knowledge of the potential and the accomplishments of individuals with DS will be a big help in
dealing with the DS child. No matter what the genetic mechanism, some DS children do better than others.
Prenatal Testing
Maternal serum alpha feto-protein (MSAFP) is measured by a blood test in the pregnant woman at 15-18 weeks of gestation. AFP is made in the fetal liver, and some
escapes into the maternal circulation. It is widely used as a screening test for a DS fetus. MSAFP and at least 1 other screening test (see below) are recommended for
all pregnancies not having amniocentesis by the American College of Obstetrics, and the American College of Medical Genetics. MSAFP testing is based on the fact
that DS fetuses tend to be a little smaller on average, have smaller placentas, and thus secrete less MSAFP and other materials, which are determined in the serum of the
pregnant woman. Factors that affect this test include gestational age, maternal weight, diabetes and ethnicity.
MSAFP screening is not a definitive test. If the MSAFP test is low it suggests the risk of a DS fetus equal to the risk of a woman age 35, and prenatal
testing/chromosome studies are suggested if the parents want this information. If MSAFP alone is tested, 20 per cent of DS fetuses will test low. If MSAFP and
human chorionic gonadotrophin (HCG) are determined, 50 - 60 % of DS fetuses will be identified. If MSAFP, HCG and estradiol (E2) are tested, 60 -70 % of DS
fetuses will be identified. Some HCG testing employs a beta subunit but this is not widespread.
A positive screening test suggests only that the risk of DS is increased, and the definitive testing of amniocentesis is indicated.
Some ultrasonographers can determine suggestive findings of DS by changes in the neck, or heart. This is not yet confirmed or in wide spread use. Ultrasounds can be
normal in a DS fetus.
Prenatal testing can be done at 10 - 11 wks by chorion villus biopsy (CVS). Earlier testing is thought to be associated with a small risk of fetal limb damage. The CVS
test is done earlier and is usually more rapid than amniocentesis. There is a small chance of maternal cell contamination and a 1/100 risk of miscarriage after the
procedure.
Amniocentesis, a sampling of the amniotic fluid surrounding the fetus, is routinely done at 14-16 wks. Amniocentesis testing for chromosome disorders is 99.8 per
cent reliable for chromosome number, and there is a risk of miscarriage (usually 1/250 or less) after the procedure.
The advantages/disadvantages of prenatal testing is an individual matter, and should be discussed with a geneticist or obstetrician experienced with the procedures.