Nutrients to avoid/take for Thal Minor?

It took awhile, but I found a list I had sent in a private message to another member. This is a general list and there amy be other supplements you choose to add to your regimen.

Thal minor

B-Complex 100   One daily

Vitamin C    200-500 mg daily.
* If your iron level is high, take the lower amount of C
If you bruise easily, take some vitamin C.

Vitamin D   1000-5000 IU daily. Deficiency may require
doses as high as 50,000 IU per week.
*The best thing to do is get your D level checked. Odds
are that 1/2 to 2/3 of people reading this are deficient in
vitamin D. Your level should be minimum 35. Optimum
level is  50-70.  The importance of vitamin D should not
be ignored. D is necessary for the absorption of dozens
of nutrients, including essential minerals.

Vitamin E Natural Complex -Mixed Tocopherols preferred
400-800 IU daily
*Synthetic vitamin E should be avoided. Do NOT take
more than 100 IU daily of synthetic E.
Look for d-alpha tocopherol. Avoid dl-alpha.

Folic acid   1000-5000 mcg daily (1-5 mg)

Calcium/Magnesium  1000/500 mg daily. (Definitely for women and also for men who may need calcium).

L-carnitine may also be considered in thal minors past age 40.

Good info here! Andy, the Vit E. gel cap I am taking now is called Evion and it contains 'Tocopheryl Acetate IP (400mg)'. Does this sound ok?

I can't tell from the info provided if it is natural E. Look for the term d-alpha before tocopherol. D-alpha is natural and dl-alpha is synthetic.

Thank you Andy.

What about in regards to Lipoic Acid and NAC?

I read a post stating ALA and NAC should be avoided?

ParkerLewis:

Reply #18 on: December 03, 2008, 07:35:37 pm

Hi.
I don't think the Alpha lipoic Acid and the NAC content are good ideas for thals,because Alpha lipoic Acid is a potent copper chelator,whereas NAC combines with zinc and copper and can remove them from blood circulation. According to an abstract,the blood levels of copper in both plasma and erythrocytes were higher in the patients (children) with thalassemia than in the controls.This means,we need more copper than normal people,because copper is inwolved in red blood cell production,hemoglobin production and super-oxid dismutase production,which is higher,than in normal persons.It is alos important for iron metabolism.So be careful with the copper...
http://www.ncbi.nlm.nih.gov/pubmed/9656419

Ref:
http://www.thalassemiapatientsandfriends.com/index.php/topic,2164.msg21251/highlight,alpha+lipoic+acid+nac.html#msg21251

It took awhile, but I found a list I had sent in a private message to another member. This is a general list and there amy be other supplements you choose to add to your regimen.

Thal minor

B-Complex 100   One daily

Vitamin C    200-500 mg daily.
* If your iron level is high, take the lower amount of C
If you bruise easily, take some vitamin C.

Vitamin D   1000-5000 IU daily. Deficiency may require
doses as high as 50,000 IU per week.
*The best thing to do is get your D level checked. Odds
are that 1/2 to 2/3 of people reading this are deficient in
vitamin D. Your level should be minimum 35. Optimum
level is  50-70.  The importance of vitamin D should not
be ignored. D is necessary for the absorption of dozens
of nutrients, including essential minerals.

Vitamin E Natural Complex -Mixed Tocopherols preferred
400-800 IU daily
*Synthetic vitamin E should be avoided. Do NOT take
more than 100 IU daily of synthetic E.
Look for d-alpha tocopherol. Avoid dl-alpha.

Folic acid   1000-5000 mcg daily (1-5 mg)

Calcium/Magnesium  1000/500 mg daily. (Definitely for women and also for men who may need calcium).

L-carnitine may also be considered in thal minors past age 40.

There is some confusion in the previous post. Alpha lipoic Acid chelates free iron and free copper, and not the minerals within organs, bones and tissue.

http://lpi.oregonstate.edu/infocenter/othernuts/la/

Metal Chelation: Redox-active metal ions, such as free iron and copper, can induce oxidative damage by catalyzing reactions that generate highly reactive free radicals (24). Compounds that chelate (bind) free metal ions in a way that prevents them from generating free radicals offer promise in the treatment of neurodegenerative and other chronic diseases, in which metal-induced oxidative damage may play a role (25). Both LA and DHLA have been found to inhibit copper- and iron-mediated oxidative damage in the test tube (26, 27), and to inhibit excess iron and copper accumulation in animal models (28, 29).

This in no way means that  Alpha lipoic Acid is harmful. It helps to prevent the oxidative damage that these free metal ions cause.

Hi Andy, how about the debate that we should take Folate supplements (natural) instead of Folic Acid (the synthetic form).  I read on another forum that folic acid is not readily absorbed and that it could be dangerous in high doses.  Folate instead comes from the natural source and is safe in higher doses.  What's your take on this?

Here is a link to an article about this:

http://www.holisticchineseherbs.com/weston-price-2/the-problem-with-folic-acid-supplements-and-why-you-should-avoid-fortified-foods/

I always favor natural supplements over synthetic. Most synthetic supplements have little if any value, and some may be harmful when used long term.  Vitamin C may be the exception because it is simple ascorbic acid. I also suggest avoiding fortified foods as much as possible. Much of these so-called supplements that end up in foods are nothing more than industrial waste and by-products. Synthetic vitamin E falls into this category, as does iron. Iron filings can actually be separated from some cereals with a magnet.

Try to get as many nutrients from your diet by eating real whole foods and when you use supplements, go natural.

There is some confusion in the previous post. Alpha lipoic Acid chelates free iron and free copper, and not the minerals within organs, bones and tissue.

http://lpi.oregonstate.edu/infocenter/othernuts/la/
This in no way means that  Alpha lipoic Acid is harmful. It helps to prevent the oxidative damage that these free metal ions cause.

Hi Andy,
Can you underline this statement? Where is the proof that ALA only chelates free copper and iron and that the statement by Mr.Lewis is not right?
ALA is a potent chelator and a important part in Andrew Cutlers Anti Mercury Protocol for example,because it removes Mercury and other heavy metals from the cells,tissue and other body parts. It is in some way comparable to DMSA,DMPS,EDTA and other Chelators,which are also able to chelate from organs and body's store. You can google that,if you want.
http://en.allexperts.com/q/Pharmacy-1407/2009/8/Chelation-therapy-ALA.htm
There is also a german PDF (sorry for that),where you can see,that DMPS is able to destroy enzymes and grab the mercury/zinc/mercury/heavy metal from its binding place. You can see that in figure 2. You can also see in figure 3,that copper is also chelated by DMPS and in figure 6 that DMPS chelates in Liver,Tissues and other organs. According to Dr.Cutler, Alpha Lipoic Acid is much stronger affecting tissues and special organs(brain,liver,but not kidney) as DMPS.
http://www.labor-bayer.de/publikationen/11_DrBayer-DMPS-2008.pdf
ALA is also able to bound complexes with ferritin bound iron in vivo (in human).It is able to destroy the iron body's store so the effect is not only limited to chelate free iron. you can see that in this pdf (english/ page 463)
http://www.thorne.com/altmedrev/.fulltext/7/6/456.pdf

I think,ALA whereas Nac is absolutely able to lower serum copper and ceruloplasmin levels in human as mentioned in the link below.
http://www.cancerfoundation.com/roleofcopper.html
Free Copper levels imo has nothing to do with serum copper or ceruloplasmin (copper bound to enzyme,which is also a potent antioxidant by itself) levels. It is the question if this copper is necessary or not in Thalassemia,because of its importance in hemoglobin synthesis and iron metabolism. I don't know,whether AlA is necessary in Thalassemia Treatment or better avoided,but i think it is not as black and white (good,bad,right,wrong)as we think it is. Even High Doses of Vitamin C (≤1500mg/day) are able to lower copper levels in humans,because of an antagonism.
http://www.ajcn.org/content/37/4/553.abstract

The vitamin C study is outdated. http://lpi.oregonstate.edu/infocenter/minerals/copper/index.html

Vitamin C

Although vitamin C supplements have produced copper deficiency in guinea pigs (7), animals requiring dietary vitamin C, the effect of vitamin C supplements on copper nutritional status in humans is less clear. Two small studies in healthy young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C. In one study, vitamin C supplementation of 1,500 mg/day for two months resulted in a significant decline in ceruloplasmin oxidase activity (8). In the other study, supplements of 605 mg of vitamin C/day for three weeks resulted in decreased ceruloplasmin oxidase activity, although copper absorption did not decline (9). Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status.

http://www.ncbi.nlm.nih.gov/pubmed/12565812

In the present study we examined the in vivo effects of lipoic acid treatment on Fe metabolism in cultured lens epithelial cells, and found that LA decreases Fe uptake from transferrin, increases Fe deposition into ferritin and increases the concentration of this protein. When administered together with ascorbic acid, lipoic acid changes the characteristic heavy to light chain ratio of ferritin makeup. The decreased Fe uptake and increased storage diminishes the size of the cytosolic highly reactive Fe pool (LIP). These changes are associated with increased cell resistance to H(2)O(2) challenge. Therefore, LA may reduce the risk of Fe induced oxidative damage and also might be useful as a treatment of Fe overload.

This suggests a protective effect as the amount of iron sequestered in ferritin rises when ALA and vitamin C are used together.

It is a mistake to assume that because an agent removes the toxic free minerals in the body, that they will also have a negative effect on the minerals the body needs. Free metals are a certain danger and free minerals stored in tissue are the last place your body will look for them when it needs them. The body is designed to get its nutrients through dietary absorption and not by stores that should not be there in the first place. This is why supplements are so important, because your body will use what it can get from your gut but will not necessarily pull nutrients out of "storage".

By the way, I have taken doses of vitamin C for over 30 years much higher than what was used in that study and have never tested low for any mineral, other than iron and that was after severe blood loss.

Hi Andy.
No,this study is not outdated.Why should it be? It is even quoted by the LPI.The Rest is in my opinion a incorrect interpretation by the Paulus Linus Institute and not a fact.There isn't a word in "my" study that mentioned that there wasn't an adversely effect found.On the contrary this study mentioned crystal clear:
http://www.ajcn.org/content/37/4/553.abstract

Although observed effects occurred within physiological ranges of normal values, this study confirms that a high ascorbic acid intake is antagonistic to copper status of men as has been demonstrated in laboratory animals.

So copper status is lowered within physiological ranges.
Another aspect to think of is that this studies were time limited,so it is possible that copper status fall below that ranges with a longer period of intake. It should be also clear that the reference range can not mean an optimal status for an individual. I think a reduction in enzyme activity by Vitamin C for example s not a point that should be ignored.

Serum ceruloplasmin activity was significantly reduced (p less than 0.01) at every data point throughout the ascorbic acid supplementation period

Ceruloplasmin is also an important part in Thalassemia,because of its role in preventing iron-induced oxidative damage.
http://www.ncbi.nlm.nih.gov/pubmed/21315066

Andy,
You can see in the links i posted,that chelators are able to lower body stores which,in my opinion, are not able to be restored by a higher rate of absorption simultaneously in every case. You can see this effect even for Vitamin C. A higher rate of absorption must balance out the the depletion effects of the chelators. A significant balance in serum parameters must be recognized,but this is not the case. Only after 20 days you can recognize a significant increase of copper parameters after depletion to compensate this effect.

Furthermore there was a significant increase (p less than 0.01) in serum copper concentration 20 days after the supplementation period.

 
Ceruloplasmin has nothing to do with free copper. It represents the bound copper in the plasma. A significant reduction means inevitably a reduction in bound,maybe needed copper status in plasma and serum.
In the linked PDF Lyn Patrick,ND mentioned:

ALA is also able to form complexes with ferritin-bound iron both in vitro and in vivo.59 ALA has the ability to displace protein or vitamin C bound to iron and bind to Fe2+. DHLA can facili- tate the release of iron from the ferritin molecule and bind iron.41

http://www.thorne.com/altmedrev/.fulltext/7/6/456.pdf (p.456-457)
You can see the direct effect of bound,not free iron by Lipoic Acid here:

Molecular aspects of the removal of ferritin-bound iron by DL-dihydrolipoate.
Bonomi F, Cerioli A, Pagani S.

Dipartimento di Scienze Molecolari Agroalimentari, Università degli Studi di Milano, Italy.
Abstract
The removal of ferritin-bound iron by the physiologic dithiol DL-dihydrolipoate was studied over the pH range 5.5-9.0. A novel method was devised for the determination of iron removal, making it possible to study the actual release of iron from ferritin, regardless of the oxidation state or complexation form. The overall iron-removal process appears to depend upon a balance between the deprotonation of the dithiol and the protolytic dissolution of the iron core inside the ferritin molecule. The amount of iron removed at equilibrium increases with the pH, at any of the dihydrolipoate/ferritin iron ratios tested. The formation of the binuclear iron-dithiol complex [Fe2(dihydrolipoate)3]-3 is not strictly required for iron mobilization, but it seems to affect the efficiency of the dithiol in iron mobilization by providing a stable complexation form for the released iron outside the ferritin protein shell. Comparison of the release of ferritin-bound iron by free and immobilized dihydrolipoate indicates that mobility of the dithiol is mandatory for the removal process to take place.

So we have two studys here,one says there is a negative effect on iron bound ferritin even in vivo as mentioned by Lyn Patrick and we have got the opposite. I don't know which one is right,but i know that we shouldn't discuss about effects on free metals only.  

By the way, i have taken high doses of vitamin c for one year only and had a copper deficiency,including anemia within the anemia..;)  

Was your copper level tested before supplementing with C? What is anemia within anemia (Hb levels change regularly and are affected by something as simple as level of hydration during the test)? What other supplements were you taking? Did you at anytime take iron or zinc supplements?

When you state "in your opinion" what gives your opinion more validity than the cited research in the Pauling article?
I repeat

Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status.

I truly do not understand much of your argument. Yes, ALA affects how much iron is bound in ferritin. Why is this a negative? It is not, as the iron that cannot harm is bound in ferritin.

Your comment

so it is possible that copper status fall below that ranges with a longer period of intake.

has no scientific basis. You cannot jump to that assumption. Only a study that demonstrated that supposition would prove it.

Chelation drugs do remove some trace minerals along with iron and this is well established. Testing for copper and zinc levels are already recommended. Iron, copper and zinc all affect the levels of the others and this is well recognized and in the guidelines for treatment, this is taken into account. Copper, zinc, and selenium are all recommended supplements.

I don't see support for your arguments in the documents you cite. If anything, I see great evidence of the importance of ALA. I am not the only one. Oakland has been doing a study on Alpha-lipoic acid (LA), enhanced with acetyl-L-carnitine and its value in fighting oxidative stresses in thalassemia, as the therapy shows incredible promise. http://www.chori.org/Current_News/2008/08_Mar_Lal.html

In the end I am puzzled at what you think will happen if a thal takes ALA. I see no negative but plenty of positive.

Hi Andy,
My opinion is in my opinion more valid,because the cited research by LPI isn't a research,but a summary of studies done,which i read completely...;) This has nothing to do with new scientific results or anything else. It is just a secondary source.I quoted one of the primary sources here and it says clearly that the Vitamin C supplementation affected copper status.
So why the statement of the LPI should be accepted as a fact? This statement isn't true.Period

Serum ceruloplasmin activity was significantly reduced (p less than 0.01) at every data point throughout the ascorbic acid supplementation period.A similar but nonsignificant trend was observed for serum copper...Although observed effects occurred within physiological ranges of normal values, this study confirms that a high ascorbic acid intake is antagonistic to copper status of men as has been demonstrated in laboratory animals.

It think,it should be allowed to assume that a higher intake for a longer time could induce a classic copper deficiency. This is the case for a high zinc intake for a long time,so this could be the case for a high vitamin C intake.The antagonistic effect is proven. There is another study which supports this assumption.

Young male Hartley guinea pigs were fed a basal diet, or a basal diet and supplemented daily with vitamin C, p.o. Pharmacologic doses (25 mg per 100 g BW per day) of vitamin C resulted in two-to-three-fold decreases in liver copper, when compared with those receiving normal (0.5 mg per 100 g BW per day) intakes

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7429759


You wrote in a previous post,that ALA only chelates free iron and free copper and couldn't affect body stores/bound metals. So this is a good and safe effect for everybody and Parkerlewis is wrong.
This is argument is not true,because it has a proven effect on ferritin-bound iron and is able to build complexes with the bound-iron and move it outside the protein shell. This is a negative effect,because it is a iron removal process and that iron isn't bound to ferritin any longer. That is the point.
The Statement by Dr Lal is about Thalassemia in connection with iron overload,but Thalassemia isn't equate with iron overload. What about people with low copper and/or iron status? Did you read the statement of the cancer foundation that ALA and NAC are able to lower copper status and are recommended to just do that?