Below is a photo with the list of ingredients of the other supplement I take. I’m aware that some of the composition overlaps with the photo in my previous post
I take them in a haphazardly fashion. Sometimes on the same day, some days alternating and sometimes nothing. I know I I could be overdoing it, so advice and guidance would be great
Thanks
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Noelnoel
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I assume that means 20 milligrams of pyridoxine HCl plus 5 milligrams of pyridoxal-5-phosphate. (If so, why not say it clearly instead of making us do arithmetic to find out?)
I suggest you have a read of my recent post (just over two weeks ago):
Hi, I’ve got no idea who’s right as it’s bit over my head but I’ll read it again tonight and digest it slowly. I thought you might like to see their response out of interest rather than to disprove what you said. Here it is
Thank you for the paper. It makes an interesting read. Firstly, in-vitro studies cannot conclude causation due to their study design. They are purely a means to generate a hypothesis that is to be investigated in animal and human trials. For example in this case the various forms of B6 are tested upon SHSY5Y and Caco-2 cells therefore the findings are relevant to only those cells in an in-vitro setting (rather than to human physiology). SHSY5Y are bone marrow cells and Cacao-2 are cancer cells. I would suggest that these cells are not normally large volume vitamin B6 metabolisers and that in normal circumstances pyridoxine would be metabolised by the liver to P-5-P by the liver before reaching any cell. Furthermore, the human body has millions of cells, genes and enzymes, each which generally have their own specific function but also work synergistically in groups. A fact that cannot be investigated in an in-vitro setting.
The researchers chose to observe the effect on Bax and Caspase-8 enzymes, it would be interesting to read their rationale for the choice, as both enzymes work in apoptosis, it feels a little like they were setting pyridoxine up to fail. However, that aside, Bax also plays a role in mitochondrial function and the activation of p53. Mitochondria are the site of aerobic energy production and p53 is involved in the downregulation of cancer cell activity, so these aspects could be seen as a beneficial finding. What we have to remember, is that in the human body, if the brain required the upregulation of these enzymes it would do so through a series of enzymatic reactions that may involve vitamin B6, yet in this setting the pyridoxine is there without the normal preceding physiology. In fact as the enzymes are considered P-5-P dependant they would not respond in a normal manner to a different molecule, you would expect the opposite which is what happened. In normal human physiology the liver will have transformed pyridoxine to P-5-P if it required activation of those enzymes.
Although this paper was published in 2017, there has not been any further studies to investigate this hypothesis in animals or humans. Nor it is being investigated in active or planned research. I imagine this would be fairly easy to do via biopsy and so could be easily included in research.
All we can conclude from this research is that the effects are specific to solely SHSY5Y and Caco-2 cells when investigated in an in-vitro design. These findings are without the influence of normal human digestion and assimilation, plus normal body function.
The Co-enzyme B Complex provides 20mg of pyridoxine HCl plus 5 mg of pyridoxal-5-phosphate.
Thank you for the paper. It makes an interesting read. Firstly, in-vitro studies cannot conclude causation due to their study design.
The paper doesn’t claim any more than what they did. They say that it indicates – not that it proves anything.
They are purely a means to generate a hypothesis that is to be investigated in animal and human trials. For example in this case the various forms of B6 are tested upon SHSY5Y and Caco-2 cells therefore the findings are relevant to only those cells in an in-vitro setting (rather than to human physiology). SHSY5Y are bone marrow cells and Cacao-2 are cancer cells. I would suggest that these cells are not normally large volume vitamin B6 metabolisers and that in normal circumstances pyridoxine would be metabolised by the liver to P-5-P by the liver before reaching any cell.
I’d have hoped for something with more to back it up than “I would suggest”.
Furthermore, the human body has millions of cells, genes and enzymes, each which generally have their own specific function but also work synergistically in groups. A fact that cannot be investigated in an in-vitro setting.
The researchers chose to observe the effect on Bax and Caspase-8 enzymes, it would be interesting to read their rationale for the choice, as both enzymes work in apoptosis, it feels a little like they were setting pyridoxine up to fail.
Seems odd to allege they were setting up pyridoxine to fail when the study says:
“Cells were exposed to pyridoxine, pyridoxamine, pyridoxal, pyridoxal-5-phosphate or pyridoxamine-5-phosphate for 24h, after which cell viability was measured using the MTT assay.”
Isn’t that what you would do it if you were trying to find out if the various vitamers differ in their effects?
Although this paper was published in 2017, there has not been any further studies to investigate this hypothesis in animals or humans. Nor it is being investigated in active or planned research. I imagine this would be fairly easy to do via biopsy and so could be easily included in research.
The Co-enzyme B Complex provides 20mg of pyridoxine HCl plus 5 mg of pyridoxal-5-phosphate.
Thanks for confirming. I still find the way it expressed on the label somewhat odd. And I am surprised there is no attempt to explain their choice of vitamers and the amounts.
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