Minutus

Has anyone here ever worked with anyone diagnosed with alpha-1 antitrypsin deficiency? I have just taken a case and I am not looking for that sort of advice at this time. I am just wondering if anyone has any experience with expectations and prognosis in the long run.
AADT is an “inherited disorder … related to a protein that protects the body from … neutrophil elastase. Neutrophil elastase is released from white blood cells to fight infection, but it can attack normal tissues (especially the lungs) if not tightly controlled by alpha-1 antitrypsin.”
Thanks

Yes.
It is usually an indicator for inherited emphysema state. In fact if measured earlier i life, the emphysema is spotted early before it does a bunch of damage. It usually kicks in by age 40 or before but not as a child.

However it is also low in a severe case of atopy.
So the symptoms may vary accordingly.
Same as with any use of homeopathy.
It depends how good the homeopath is, as to whether their approach will work. It is not to do with the condition present but how it is handled.
A1ATD I presume you mean or?
or not.
Depends on the individual - severe atopy also has very low A1AT.
(Test used for A1AT level is usually electrophoresis on serum or saliva)
I would check what is happening in the body, not just the A1AT level and correlate with age, atopy, symptoms etc.
Namaste,
Irene
--
Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.Furryboots.info
(Info on Feline health, genetics, nutrition & homeopathy)
"Man who say it cannot be done should not interrupt one doing it."

Irene, thank you for this detailed reply. My info was in quotes as I am researching and reacting to the patient’s report of this condition.
If I am understanding what you are saying correctly: atopy could be a cause of lowered or deficient A1ATD just as much as the deficiency might make a person overreact to substances/allergens?
Sherill
From: minutus@yahoogroups.com [mailto:minutus@yahoogroups.com]
Sent: Friday, February 06, 2015 7:57 PM
To: minutus@yahoogroups.com
Subject: Re: [Minutus] AADT
Yes.

It is usually an indicator for inherited emphysema state. In fact if measured earlier i life, the emphysema is spotted early before it does a bunch of damage. It usually kicks in by age 40 or before but not as a child.
However it is also low in a severe case of atopy.

So the symptoms may vary accordingly.
I have just taken a case and I am not looking for that sort of advice at this time. I am just wondering if anyone has any experience with expectations and prognosis in the long run.
Same as with any use of homeopathy.

It depends how good the homeopath is, as to whether their approach will work. It is not to do with the condition present but how it is handled.
AADT
A1ATD I presume you mean or?
is an “inherited disorder …
or not.

Depends on the individual - severe atopy also has very low A1AT.

(Test used for A1AT level is usually electrophoresis on serum or saliva)
related to a protein that protects the body from … neutrophil elastase. Neutrophil elastase is released from white blood cells to fight infection, but it can attack normal tissues (especially the lungs) if not tightly controlled by alpha-1 antitrypsin.”
I would check what is happening in the body, not just the A1AT level and correlate with age, atopy, symptoms etc.
Namaste,

Irene

--

Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.Furryboots.info

(Info on Feline health, genetics, nutrition & homeopathy)
"Man who say it cannot be done should not interrupt one doing it."

Hi Sherill,

There are many ways that A1AT can be deficient. Most of them are genetically inherited. There are about forty different genetic ways (phenotypes) for a person to inherit a low A1AT level.

However a person who has a serious case of atopy (a condition of allergic type in which allergies readily develop to substances) will also have A1AT deficiency, which is then "acquired" A1ATD rather than inherited A1ATD.

The person with acquired deficiency is not born that way, but certain conditions can force them to be atopic (for example, excessive vaccinations , or exposures to multiple toxins) especially if they belong to certain blood types (those which lack A, B or Rh factors for example have highest incidence). Whooping cough vaccine is especially bad as it causes 40% of reecipients to become atopic, though not necessarily severely atopic, unless they have several whooping cough vaccines and/or are O neg nonsecretors or other nonsecretors. (A secretor is a person who secretes their blood type antiogens into their body fluids. IF they do not, they are "nonsecretors" and are more likely to be atopic and severely so.

Regardless why a person has low A1AT, they will be subject to damage from proteases (enzymes that damage body protein) elastin being one of many. A1At has the job of preventing protease damage from inflammatory enzyme action.
If there is too little, it can not do the job and damage occurs.

In infants wit inherited A1ATD there is liver damage mainly - neonatal hepatitis and infantile chirrhosis.
Followed (added to) by various kinds of lung damage, and you may see asthma, chronic bronchitis or most severely, emphysema.
Inherited Emphysema seldom is clinically seen before age 30 or so, but a blood test for A1AT, will PREDICT (by a very low value) the lung problems to come, and ideally then one would start to remedy the situation before the lung damage set in, in earnest.

Acquired A1ATD will usually be acquired as a baby or child, and also may not show lung issues till much older, ave 30, plus minus 10 yrs. The chronic lung damage types are the same - as the problem is the same - not enough protease inhibitor. But often it is misdiagnosed as asthma, not realizing the lungs are damaged as opposed to constricted.

So you would want to take a good history on the individual and consider that the situation is usually progressive, (especially in inherited A1ATD) with increased damage with increased age.

So basically A1AT is a protease enzyme inhibitor - a chemical that prevents enzyme damage of proteins, and the most vulnerable areas for protease damage are lungs. Emphysema is damage to the alveoli of the lungs so that they collapse and no longer can exchange oxygen. The result is increasing difficulty breathing and getting enough oxygen.

My approach with homeopathy would be to match a remedy to the innate constitutional type in order to restore the epigenetic switches that are permitting the problem. (Or in homeopathy-speak, to restore the vital force to homeostasis.)
I prefer to understand and express, what is really happening in 2015 terms as oppsoed to the best way it could be expressed in Hahnemann's day with the knowledge of that time.
Epigenetic switches are part of the genetic material, but it is a part that can be switched on or off (like a Miasm) - gene switches can be in different positions (technically methylated or acetylated) and that tells the real genes what proteins to make and how much. So if the epigene SWITCH says to make too little A1AT then you need to change that back to the normal switch position.

We know that epigene switch positions CAN be influenced to change. If they are NOT changed, then the issue will be passed on to the next generation. So epigene switches have to do with acquired genetic instructions which can be switched or unswitched (often prediposing an illness issue), as opposed to fixed inherited genes (like having long legs or fat fingers or walking a particular way).

Hope that helps.
Namaste,
Irene
--
Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.Furryboots.info
(Info on Feline health, genetics, nutrition & homeopathy)
"Man who say it cannot be done should not interrupt one doing it."

Irene,

This is very helpful and I will re-read it a few more times. This woman has several factors that you mention and I will consider. She is approaching 30 and she has chronic bronchitis. Was diagnosed “asthma” at age 3. Reaction to 18 month vaccinations, and reacts to MANY substances including seasonal triggers, several foods, and the worst reactions are to allopathic meds… no surprise!

Thanks,

Sherill
From: minutus@yahoogroups.com [mailto:minutus@yahoogroups.com]
Sent: Friday, February 06, 2015 10:41 PM
To: minutus@yahoogroups.com
Subject: Re: [Minutus] AADT
Irene, thank you for this detailed reply. My info was in quotes as I am researching and reacting to the patient’s report of this condition.

If I am understanding what you are saying correctly: atopy could be a cause of lowered or deficient A1ATD just as much as the deficiency might make a person overreact to substances/allergens?
Hi Sherill,
There are many ways that A1AT can be deficient. Most of them are genetically inherited. There are about forty different genetic ways (phenotypes) for a person to inherit a low A1AT level.
However a person who has a serious case of atopy (a condition of allergic type in which allergies readily develop to substances) will also have A1AT deficiency, which is then "acquired" A1ATD rather than inherited A1ATD.
The person with acquired deficiency is not born that way, but certain conditions can force them to be atopic (for example, excessive vaccinations , or exposures to multiple toxins) especially if they belong to certain blood types (those which lack A, B or Rh factors for example have highest incidence). Whooping cough vaccine is especially bad as it causes 40% of reecipients to become atopic, though not necessarily severely atopic, unless they have several whooping cough vaccines and/or are O neg nonsecretors or other nonsecretors. (A secretor is a person who secretes their blood type antiogens into their body fluids. IF they do not, they are "nonsecretors" and are more likely to be atopic and severely so.
Regardless why a person has low A1AT, they will be subject to damage from proteases (enzymes that damage body protein) elastin being one of many. A1At has the job of preventing protease damage from inflammatory enzyme action.

If there is too little, it can not do the job and damage occurs.
In infants wit inherited A1ATD there is liver damage mainly - neonatal hepatitis and infantile chirrhosis.

Followed (added to) by various kinds of lung damage, and you may see asthma, chronic bronchitis or most severely, emphysema.

Inherited Emphysema seldom is clinically seen before age 30 or so, but a blood test for A1AT, will PREDICT (by a very low value) the lung problems to come, and ideally then one would start to remedy the situation before the lung damage set in, in earnest.
Acquired A1ATD will usually be acquired as a baby or child, and also may not show lung issues till much older, ave 30, plus minus 10 yrs. The chronic lung damage types are the same - as the problem is the same - not enough protease inhibitor. But often it is misdiagnosed as asthma, not realizing the lungs are damaged as opposed to constricted.
So you would want to take a good history on the individual and consider that the situation is usually progressive, (especially in inherited A1ATD) with increased damage with increased age.
So basically A1AT is a protease enzyme inhibitor - a chemical that prevents enzyme damage of proteins, and the most vulnerable areas for protease damage are lungs. Emphysema is damage to the alveoli of the lungs so that they collapse and no longer can exchange oxygen. The result is increasing difficulty breathing and getting enough oxygen.
My approach with homeopathy would be to match a remedy to the innate constitutional type in order to restore the epigenetic switches that are permitting the problem. (Or in homeopathy-speak, to restore the vital force to homeostasis.)

I prefer to understand and express, what is really happening in 2015 terms as oppsoed to the best way it could be expressed in Hahnemann's day with the knowledge of that time.

Epigenetic switches are part of the genetic material, but it is a part that can be switched on or off (like a Miasm) - gene switches can be in different positions (technically methylated or acetylated) and that tells the real genes what proteins to make and how much. So if the epigene SWITCH says to make too little A1AT then you need to change that back to the normal switch position.
We know that epigene switch positions CAN be influenced to change. If they are NOT changed, then the issue will be passed on to the next generation. So epigene switches have to do with acquired genetic instructions which can be switched or unswitched (often prediposing an illness issue), as opposed to fixed inherited genes (like having long legs or fat fingers or walking a particular way).
Hope that helps.

Namaste,

Irene

--

Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.Furryboots.info

(Info on Feline health, genetics, nutrition & homeopathy)
"Man who say it cannot be done should not interrupt one doing it."

You are Welcome
I would suggest going gluten free and low/no starch at least, and maybe avoiding high saponin foods and using lots of antioxidants and benefivial fats....all so as to lower the inflammation level.

Irene
--
Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.Furryboots.info
(Info on Feline health, genetics, nutrition & homeopathy)
"Man who say it cannot be done should not interrupt one doing it."

The a neat thing about lower the inflammation level is that you don't need to consult with someone to know whether it works. The pain goes away. Experiment with this and that. Perhaps you don't need 'xyz', you don't need to pay for it. Perhaps you try 'abc' and discover that it takes the pain away.

Roger Bird
________________________________

To: minutus@yahoogroups.com
From: minutus@yahoogroups.com
Date: Sat, 7 Feb 2015 22:48:36 -0800
Subject: Re: [Minutus] AADT

You are Welcome

I would suggest going gluten free and low/no starch at least, and maybe avoiding high saponin foods and using lots of antioxidants and benefivial fats....all so as to lower the inflammation level.

Irene