“A beautiful head of hair is biological peacocking, the original form of peacocking, bragging to everyone around you that you have extra ATP the way some people buy Lambos and boats to show off their extra cash. “
Thanks for making a technical topic so fun to read!
Thanks for these articles on iron, very interesting! I have this annoying bedtime routine where almost every night when I lay down to sleep I have a window of say 20 minutes where I almost fall asleep and then wake back up and then cant go back to sleep for a very long time. My body is then very very restless with restless legs and raising thoughts. Happens often, Im sometimes wondering if this has to do with iron...as well as I get irritated and achey gums almost every time I eat and I cant connect it to a certain food.
If we did think we might be deficient, even if we're eating a lot of red meat, and have restless leg stuff happening since October, what is the best way to supplement? A health friend gave me iron bisglycinate (I think that's what is was) and I tried a few capsules a few days in a row and all I experienced was the inability to eat. Just made me feel nauseous. Thank you for any comments.
I’ve recently reintroduced raisins into my diet - not sure if it’s the extra iron or the extra high glycemic carbs, but certainly experiencing a lot more energy and accomplishing more each day!
As to whether that is mainly reversing the process of continuing to lose hair, versus the regrowth of hair, it probably depends on whether the follicle cells are still alive or there is sufficient stem cells to replenish them.
Forgive my ignorance, is iron overload too much iron in the blood and/or elsewhere but not in the cells or where it actually needs to be? Or am I misunderstanding it?
And if that is correct, is iron overload a functional iron deficiency and if so what is the difference? Just trying to sort out iron deficiency and iron overload functionally speaking cause I might have the wrong notion of overload but searching has not helped me get clarity.
What do you make of the conflicting role of cysteine on rescuing keritinocytes from iron deficiency.
If cysteine increases ferritin and hydrogen sulfide, and hydrogen sulfide releases iron from ferritin, wouldn't the chelator also chelate the iron released by cysteine.
And yet this can't be true if the keritinocytes were able to synthesize DNA from the iron released from ferritin. I'm just curious if you have a hypothesis for what is happening beyond what you have written here.
My favorite sentence:
“A beautiful head of hair is biological peacocking, the original form of peacocking, bragging to everyone around you that you have extra ATP the way some people buy Lambos and boats to show off their extra cash. “
Thanks for making a technical topic so fun to read!
Thanks for these articles on iron, very interesting! I have this annoying bedtime routine where almost every night when I lay down to sleep I have a window of say 20 minutes where I almost fall asleep and then wake back up and then cant go back to sleep for a very long time. My body is then very very restless with restless legs and raising thoughts. Happens often, Im sometimes wondering if this has to do with iron...as well as I get irritated and achey gums almost every time I eat and I cant connect it to a certain food.
If we did think we might be deficient, even if we're eating a lot of red meat, and have restless leg stuff happening since October, what is the best way to supplement? A health friend gave me iron bisglycinate (I think that's what is was) and I tried a few capsules a few days in a row and all I experienced was the inability to eat. Just made me feel nauseous. Thank you for any comments.
Iron deficiency protocol forthcoming.
I’ve recently reintroduced raisins into my diet - not sure if it’s the extra iron or the extra high glycemic carbs, but certainly experiencing a lot more energy and accomplishing more each day!
Do you know if hair loss caused by iron deficiency is reversible?
The two trials and animal experiment show it is.
As to whether that is mainly reversing the process of continuing to lose hair, versus the regrowth of hair, it probably depends on whether the follicle cells are still alive or there is sufficient stem cells to replenish them.
Forgive my ignorance, is iron overload too much iron in the blood and/or elsewhere but not in the cells or where it actually needs to be? Or am I misunderstanding it?
And if that is correct, is iron overload a functional iron deficiency and if so what is the difference? Just trying to sort out iron deficiency and iron overload functionally speaking cause I might have the wrong notion of overload but searching has not helped me get clarity.
Thanks in advance.
What do you make of the conflicting role of cysteine on rescuing keritinocytes from iron deficiency.
If cysteine increases ferritin and hydrogen sulfide, and hydrogen sulfide releases iron from ferritin, wouldn't the chelator also chelate the iron released by cysteine.
And yet this can't be true if the keritinocytes were able to synthesize DNA from the iron released from ferritin. I'm just curious if you have a hypothesis for what is happening beyond what you have written here.
I was able to find a copy of the study. It seems the cysteine was administered after the cell was depleted of iron, not concurrent with chelation.
Here is the relevant excerpt, for those that are curious:
By analyzing in the interplay of cysteine supplementation and
cellular iron status in the regulation of cytokeratin expression, we
found that the simultaneous exogenous supplementation of both
cysteine and iron results in a further increase of keratins levels. As
well as cysteine, intracellular iron seems to be another key factor
in regulating keratins expression in epidermal tissues [Hirobe,
2009]. Indeed, we have shown that a cellular iron deficiency status
by desferrioxamine-mediated metal chelation negatively affects
keratins expression. This effect can be explained according to the
special role played by iron, particularly in cells endowed with a
very high proliferative activity, as an essential component of
fundamental biochemical activities. One of the most surprising
findings emerging from our study is that cysteine supplementation seems able to revert the adverse effect of iron deficiency on
cellular keratin expression. One of the reasons may lie in the
regulatory role of this amino acid on protein biosynthesis and
turnover. As reported for keratins, cysteine availability leads to
a synthesis induction of many other proteins, including those
involved in iron metabolism. Indeed our results have shown a
significant cysteine-induced up-regulation of TfR-1, ferritin and
IRP1, among the most important cellular proteins required for the
maintenance of iron homeostasis. This induction is particularly
detectable after 24 h of cysteine treatment, and mainly concerns
the TfR-1, required for iron intake into the cell. The TfR-1 overexpression at the cell membrane allows metal entry, thereby
restoring iron content. The concomitant increase in ferritin
protein—the major regulator of the cellular iron content—may
allow safe storage of any excess iron, thus limiting the potential
oxidative stress induction by free iron within cells. In fact, by
acting as a buffer against iron deficiency and iron overload,
ferritin provides protection against oxidative stress. This result is
consistent with the estimation of the cellular free iron content,
showing no substantial changes in labile iron pool (LIP) following
cysteine supplementation, and a trend toward a recovery of LIP
when cysteine was administered in iron depleted cells. LIP is
fundamental in preserving cellular biochemical activities since it
represents the catalytic and redox-active iron; its level must be
maintained within a limited range that assures the iron supplies
for the cell and prevents iron excess causing oxidative damage
[Kakhlon and Cabantchik, 2002]. Consequently, as evidenced by
the recovery of the keratin levels in iron depleted cells, the
restoration of iron homeostasis following treatment with cysteine
should occur without creating cellular dangerous pro-oxidant
conditions. This is an important endpoint. Actually, these findings
further reinforce the idea of a regulatory role in protein synthesis
for cysteine, in conjunction with its antioxidant protective
functions