3 replies to this topic

[Dorian Grey]

This paper (see attached pdf below) from William R. Ware PhD from JOM, the Journal of Orthomolecular Medicine is interesting, as it gives various ferritin thresholds associated with disease.  Scroll down to "Association and Thresholds of Ferritin Levels and the Risk of Various Diseases" (page 3).  

 

The author points out, not only is the upper limit of the normal range for ferritin set by most labs dangerously high, but 50% averages may also be associated with some ferrotoxic diseases.  

 

The "Ferritin Thresholds for Benefit in Iron Lowering Studies" found on page 4 documents the benefits of iron reduction and guidelines for optimal iron homeostasis.  Interesting in this area is the benefit of a single blood donation for glucose tolerance, even in those with relatively low ferritin (average 75).  

 

The author does not mention this, but every blood donation causes a brief (several days) but drastic drop in hepcidin, the bodies master iron transport hormone. This drop opens the floodgates for iron transport within the body, and may help re-balance iron loading in tissues.  This supports the hypothesis blood ferritin may not be accurately indicative of iron loading of various tissues within the body, and even those without alarmingly elevated ferritin may benefit from occasional whole blood donation.  The iron is in the red cells, so plasma and platelet donors do not get this benefit.  

 

Annual or bi-annual bloodletting may have a substantial effect in health and longevity, particularly for those who live in countries where iron fortification is the norm. The post war baby-boom generation has been the first to live their entire lives under iron fortification, and though we're living longer, chronic disease is running quite rampant.  

 

Attached Files

•  FerritinThresholdsandDisease.pdf   238.58KB   22 downloads

[misterE]

Yes. Iron is a mineral that accumulates in the body. Iron also oxidizes and gives off lots of nasty free-radicals. Women are known to suffer from less heart-disease and diabetes than men... until menopause; when their risks increase to that of men. Researchers think it's due to menstruation and the loss of iron from the body. Men obviously don't have this advantage, so it is recommended to donate-blood and eat a plant-based diet low in heme-iron to prevent over-accumulation of iron. Iron tends to zap the body of anti-oxidants and is known to accumulate in and damage the beta-cells of the pancreas, leading to diabetes and oxidation of LDL-cholesterol.

[HighDesertWizard]

Among the most significant issues faced by the Longevity Science Movement (LSM) today is this...

• NF-kB Signaling, aka, Expression, is the single most significant independent variable driving aging. And its inhibition has been shown to increase survival probability.

• It is a confounding variable for virtually all other "independent" variables purported to drive the aging process.

• And, in this case, Ferritin is just another example of how NF-kB Signaling appears as a confounding independent variable driving aging.
  • ​Ferritin functions as a proinflammatory cytokine via iron-independent protein kinase C zeta/nuclear factor kappaB–regulated signaling in rat hepatic stellate cells
• Is the pro-aging impact of Ferritin independent of the impact of NF-kB signaling?
  • Where is the study showing that Ferritin DOES have a pro-aging impact independent of the impact of NF-kB?

Because, time and again, variables purported to be "independent" drivers of aging turn out to have their actual impact on aging confounded by NF-kB signaling, it seems to me that NF-kB Signaling must be considered the single most significant independent variable driver of aging.

 

A few questions for all you scientists out there... You know, I'm just a software engineer and I really don't know much. I don't have any of that post-high school, expensive science education you all have. You know, the education that makes you all so much smarter than I am.

 

So, um, hmm, let me try to put these questions delicately...

 

You folks, know, right, that it's important to distinguish between two variables that may confound each other as independent variables?

 

Did they cover that in something like Biology 101 in college?

 

And, a follow up, question, if you don't mind... Why is that a software engineer, like me, is consistently the only person who brings up the NF-kB as confounding variable dimension on aging?

 

Why aren't some of you doing some of this heavy lifting?

 

Um... Are you folks living in the same universe of scientific studies that I'm living in?

 

If you are, I have a request for you...

 

Please take off the blindfold you've got over one eye that causes you not to notice the importance of NF-kB.

 

If it too much to ask that you actually do a little reflection about this issue?

 

Thank you in advance for listening.

 

Sincerely,

 

HDW

 

 

 

-----

 

I've pasted in the table of contents from the study I've linked to above...

 

Contents
 

1. Introduction 3
2. NF-κB Signaling Pathway 3
2.1 IKK Complex 5
2.2 IκB Proteins 5
2.3 NF-κB Transcription Factors 5
2.4 Canonical and Noncanonical Signaling 6
3. NF-κB Activation in Ageing 7
4. Monitoring NF-κB Activity During Ageing 9
5. NF-κB Signaling in Ageing 10
5.1 NF-κB Lessons From Progeroid Animal Models 11
5.2 NF-κB Secretory Phenotype 15
5.3 NF-κB and Apoptosis 17
5.4 NF-κB and Cellular Senescence 17
5.5 NF-κB and Telomeres 18
5.6 Immunosenescence 18
5.7 NF-κB Crosstalk with Other Ageing Regulators 19
5.8 NF-κB and Metabolism 22
5.9 NF-κB in Age-Associated Pathologies 23

5.10 NF-κB in Cell Reprogramming and Stem Cells Biology
5.11 Fat Inflammatory Paradox
5.12 NF-κB and Microbiota
6. NF-κB and Cancer
7. NF-κB as a Biomarker of Ageing
8. Rejuvenation Approaches Based on NFkB Inhibition
9. Conclusions
Acknowledgments
References

 

[Dorian Grey]

Ferritin is the best indicator of excess iron accumulation we have, though it can give a false positive when systemic infection is present or inflammation is high.  Transferrin saturation should rule out or confirm ferritin's initial indication. 

 

Ferritin itself isn't particularly evil as it binds iron within its protein shell, but it can & does leak.  Xanthine Oxidaise (for instance) liberates iron from ferritin, & it is this free labile iron (the labile iron pool) that causes damage through fenton chemistry.  

 

https://www.scienced...027510703001623

 

High ferritin (triple digits) combined with TSAT (transferrin saturation) in the upper third of normal range is like having leaky barrels of toxic waste stashed in various tissues throughout the body.  

 

The Hydroxyl Radical is perhaps the most destructive force in cellular physiology, and your independent variable from NF-kB.

 

https://www.research...lth_and_Disease

 

More on Ferrotoxic Disease Here: http://www.longecity...isease-omnibus/

 

Avoid this if you can!  

Edited by Dorian Grey, 07 February 2018 - 12:28 AM.