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Sorry, but as I said, I didn’t have them (I think there were 2), so I didn’t pay too much attention, but I did feel a little guilty saying EVERYONE should take B12. I believe I read about one on, is it NIH or NIMH website?, or some other med site like that. The other was an ailment that has to to with the digestive tract, especially the colon, I’m pretty sure. Or maybe the bladder, I think I was looking up Interstitial Cystitis because I had been looking at marshmallow root tea on Amazon, and a lot of people used it that had IC. So, I googled and looked and followed links, and it could be IC, or one of the dozen or more other diseases that had links — now you know why I don’t know which disease it was…and why my house never gets cleaned. Sorry I can’t be of more help, but I definitely know I saw the warning(s) against B12.


HF says

Hi Annf, Re B12 side effects. There are some possible side effects, but are rare. This site should help: http://vitamins.lovetoknow.com/Vitamin_B12_Injections_Side_Effects


Thanks for the link. Maybe it was only Leber’s, but I could have sworn it was two, not one. Weird thing about the site, all the side effects were the same things that B12 helps. Maybe it’s because the list is from CyanoCobalamin. It could be the Cyanide that is causing the problems, not the B12.

Lisa Bloomquist says

The exact same article could be written about magnesium. Just replace “Vitamin B12” with magnesium, and, well, same article. You could say the same about thiamine too – another B vitamin.

When are people, doctors in particular, going to start looking at what depletes cellular minerals and B vitamins? When you start looking at a bigger picture, you might actually find some culprits. The culprits are the pharmaceutical industry. One, of probably many, class of drugs that depletes magnesium, B vitammins and iron – and causes mitochondrial damage / oxidative stress – is fluoroquinolone antibiotics (cipro/ciprofloxacin, levaquin/levofloxacin, avelox/moxifloxacin and floxin/ofloxacin). But doctors give them out like candy despite the 43 PAGE warning label.

Here is a great article about how fluoroquinolones are a risk factor for type-2 diabetes – http://www.medical-hypotheses.com/article/S0306-9877(14)00217-5/fulltext A similar one could be done for all of the diseases mentioned at the top of this article.


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by Kathleen Millar

Peer Reviewed Open Access

“I found a job!” Rose snapped open a can of beer and quickly reached for my glass to catch the foam that poured down its sides. It was a quiet Sunday afternoon in Jardim Gramacho, the sprawling neighborhood at the base of Rio de Janeiro’s garbage dump. Rose and I lounged on overturned wooden crates outside her house, in a yard that was brown and barren except for a few scattered plastic bottles and tin cans. I first met Rose in 2008 while conducting research on the life projects of the roughly two-thousand laboring poor, known as catadores, who collect and sell recyclables on Rio’s dump for a living. Her husband, Carlos, often helped me heave my burlap sacks of wet cardboard onto the back of a buyer’s flatbed truck, and the two of them occasionally hung out at the bar in front of my house. Like other catadores, Rose had insisted many times that she would leave the garbage if she could: “The dump is pure suffering.” “In the garbage, there is no future.” Seu Marcão, a rather eccentric catador who had worked on the dump for over twenty years, would spontaneously shout over the clamor of unloading trucks, “Pay to enter and pray to leave!” an expression taken from the Portuguese-translated title of the horror film, The Funhouse. These were the common refrains of catadores.

Rose’s new job, however, meant more than an exit from the garbage dump. For the first time in her life, she had acquired employment with a signed worker ID ( carteira assinada ), a document guaranteeing a minimum wage, benefits, and the recognition of a regularly employed worker in Brazil. She told me that she would receive the equivalent of two monthly minimum-wages—as much if not more than she was presently making on the dump. She would be cleaning the house of a couple who lived a relatively short twenty-minute bus-ride away, and she was due to start that Monday. After Rose shared the good news, I lifted my glass to propose a toast to her new work. No, not just work ( trabalho ), she corrected me—this was a job ( emprego ).

I was therefore surprised when, after a few weeks, I asked Rose how she was finding her new job and she replied with a brush of her hand, “Oh, I quit.” Rose’s employer insisted that she stay at work until seven o’clock in the evening even though she easily finished all of her cleaning tasks by two in the afternoon. The requirement to remain at work, while not working, struck Rose as absurd. Her three children would already be dismissed from school and she would rather be home with them.

A few days later I saw Rose back on the dump. She waved to me from across a pile of recently unloaded waste—balancing a barrel of plastics on her right shoulder as she carefully stepped through mud that oozed puddles from the drizzling rain.

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doi: 10.1101/cshperspect.a006957 Copyright © 2012 Cold Spring Harbor Laboratory Press; all rights reserved

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Somatic recombination of TCR genes in immature thymocytes results in some cells with useful TCR specificities, but also many with useless or potentially self-reactive specificities. Thus thymic selection mechanisms operate to shape the T-cell repertoire. Thymocytes that have a TCR with low affinity for self-peptide–MHC complexes are positively selected to further differentiate and function in adaptive immunity, whereas useless ones die by neglect. Clonal deletion and clonal diversion (Treg differentiation) are the major processes in the thymus that eliminate or control self-reactive T cells. Although these processes are thought to be efficient, they fail to control self-reactivity in all circumstances. Thus, peripheral tolerance processes exist wherein self-reactive T cells become functionally unresponsive (anergy) or are deleted after encountering self-antigens outside of the thymus. Recent advances in mechanistic studies of central and peripheral T-cell tolerance are promoting the development of therapeutic strategies to treat autoimmune disease and cancer and improve transplantation outcome.

T cells recognize pathogen fragments in the context of surface MHC molecules on host cells. As such, they have the potential to do enormous damage to healthy tissue when they are not appropriately directed, that is, when they respond to self-antigens as opposed to foreign antigens. T lymphocyte tolerance is particularly important, because it impacts B-cell tolerance as well, through the requirement of T cell help in antibody responses. Thus, failure of T-cell tolerance can lead to many different autoimmune diseases. The tolerance of T cells begins as soon as a T-cell receptor is formed and expressed on the cell surface of a T-cell progenitor in the thymus. Tolerance mechanisms that operate in the thymus before the maturation and circulation of T cells are referred to as “central tolerance.” However, not all antigens that T cells need to be tolerant of are expressed in the thymus, and thus central tolerance mechanisms alone are insufficient. Fortunately, additional tolerance mechanisms exist that restrain the numbers and or function of T cells that are reactive to developmental or food antigens, which are not thymically expressed. These mechanisms act on mature circulating T cells and are referred to as “peripheral tolerance.”

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T lymphocytes arise from circulating bone-marrow-derived progenitors that home to the thymus. After T lineage commitment and expansion, T-cell receptor (TCR) gene rearrangement ensues and gives rise to either γδ or αβ progenitors at the CD4 and CD8 double-negative (DN) stage. A small number of αβ committed DN cells give rise to a large number of CD4 and CD8 double-positive (DP) thymocytes, and somatic recombination of TCR genes results in a remarkably broad repertoire of distinct αβ TCRs with random specificity. The TCR affinity for self-peptide–major histocompatibility complex (MHC) determines a thymocyte’s fate from this point forward ( Fig. 1 ). DP thymocytes expressing TCRs that do not bind self-peptide–MHC complexes die by neglect. Those with a low affinity for self-peptide–major histocompatibility complex MHC complexes differentiate to CD4 or CD8 single-positive (SP) thymocytes—so-called positive selection. However, those with high-affinity TCR for self-peptide–MHC complexes represent a potential threat to the health of the animal, and various mechanisms operate to ensure tolerance to self, including clonal deletion, clonal diversion, receptor editing, and anergy.

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