While learning about oxalates, I read that oxalates can decrease iron absorption. I will look in to this further.
“In various neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, changes in iron homoeostasis result in altered cellular iron distribution and accumulation. MRI can often identify these changes, thus providing a potential diagnostic biomarker of neurodegenerative diseases. An important avenue to reduce iron accumulation is the use of iron chelators that are able to cross the blood–brain barrier, penetrate cells, and reduce excessive iron accumulation, thereby affording neuroprotection.”
It also reduces zinc. We need zinc. As I’m reading I believe it is not so much an excess of iron as ferritin blood levels are normal or low but somehow it collects in the brain. BBB dysfunction is a likely culprit and protein aggregates play a role. So does the excess iron in the brain cause degeneration or coexist with the degeneration? Arriving on the scene doesn’t definitely make it the perpetrator. So I’m not sure if we should reduce iron or not.
It reduces calcium as well, another very important mineral that causes neurodegeneration
According to this paper, iron but not iron from meat is associated with a greater risk of PD. Vitamin C consumption is associated with less risk which is perplexing bc Vit C increases absorption of iron. ?
Quote:
a 30% increased risk was associated with a diet rich in nonheme iron. This increase in risk was present in those who had low vitamin C intake.
"Although total iron (dietary intake and supplements) was not associated with an increased risk of Parkinson's disease (comparing the top with the bottom quintile of cumulative average intake, relative risk (RR) = 1.10, 95% confidence interval (CI): 0.74, 1.65; Ptrend = 0.84), a modest increase in Parkinson's disease risk was associated with dietary intake of iron alone: After adjustment for possible confounders, the pooled relative risk comparing the highest with the lowest quintile was 1.30 (95% CI: 0.94, 1.80; Ptrend = 0.02) (Table 2). A positive association was found between risk of Parkinson's disease and intake of nonheme iron (for highest vs. lowest quintile of nonheme intake, the pooled RR = 1.27, 95% CI: 0.92, 1.76; Ptrend = 0.02) but not with heme iron (RR = 0.96, 95% CI: 0.68, 1.37; Ptrend = 0.86) (Table 2). We did not find significant heterogeneity of the associations between iron intake and Parkinson's disease risk between men and women (P > 0.2 for all)."
"This was unexpectedly due to a higher risk of Parkinson's disease among participants in both cohorts who consumed large amounts of nonheme iron, whose primary source was fortified grains/cereals." [Emphasis added]
Whole-grain products are not fortified. What gets fortified is white flour. Most likely none of us concerned with this issue are in danger of consumption of excess iron from this source. This pretty much dispositive of the matter. The rest of the story:
I feel moved to inject a note of caution regarding taking these numbers too seriously. This is an observational study. Observational studies do not prove causation. It is easy to get adjusting for confounders wrong – included in my writing here is a study (of eggs) that adjusted for confounders yet missed a crucial one (bacon) and got the conclusion wrong:
A Tale Of Two Studies Leads To A Deeper Understanding Of Cardiovascular Disease
In the matter at hand the unadjusted relative risk is insignificant. The confidence interval of the adjusted relative risks still includes unity which makes me wonder how they come up with the P value of .02. Relative risk of 1.3 seems impressive but observational studies come up with such numbers all the time. I start to pay serious attention when the relative risk/hazard ratio is in excess of 2. For example here, the relative risk of gout due to elevated uric acid (2.4-12x):
Plus, the other lesson in this piece was about how a bunch of people who should have known better got the cause-and-effect relationship between Parkinson's and low uric acid wrong, based on observational studies.
Here, an interventional study of the risk of prostate cancer (2.6x) for ordinary levels of folate supplementation:
You are not trying to dissuade me from my belief that the reason for Japanese longevity is the fact that they speak Japanese, are you? 日本語を勉強するのに時間を無駄にしているとは思わない。
So basically I posted a lousy and misleading paper. I will be more discerning. As I stated above, I wonder if maybe iron is not the culprit. It arrives on the scene bc of BBB permeability which could be caused in part by the processed grains which happen to be fortified with iron.
Is it a fair takeaway that iron from meat is not a problem?
Another puzzle I’m reading about is calcium in the brain which is believed to contribute to degeneration. Should we then maybe consider reducing calcium? Vit D increases calcium. Maybe high dose Vit D may have short term benefits but be a contributor to long term excess calcium in the brain?
No worries – I have seen much worse. A good example for discussion. Exactly as you point out:
Since the adverse effect, such as it may be, is due to consumption of fortified, i.e. refined, grain products, the observed effect may be a mere association and not a causation. There may be other aspects of consuming refined grain products that may be the real villain. BBB Permeability may be it, but it may be something else – there is no telling from this data.
Indeed this is evidence that consumption of heme iron is okay.
Long-term studies of vitamin D disclose a "bathtub" shaped curve for vitamin D level versus mortality and other health risks. So there is such a thing as too high a vitamin D level, although by far more people are deficient.
That Is if your PD was caused by excessive heavy metals/ high iron.. exposure. I got tested for this and my iron levels have always remained loe to normal...I actually take foliate every day so it'd only work on some PD patients
Long term outcome of PD and other ND diseases is an excess of iron and calcium in that brain. This is not specifically related to what caused the onset. It is due in part by BBB permeability.
Quote:
Clinical trials using iron chelation: Positive experiences validate the use of iron chelation therapy for the treatment of systemic diseases such as thalassemia major, sickle cell disease and cardiomyopathy associated with hereditary hemochromatosis. Recently, iron chelation has been introduced as a new therapeutic concept for the treatment of neurodegenerative diseases that have a component of iron accumulation
the results on the use of chelators for the treatment of neurodegenerative diseases are largely inconclusive. Clinical trials using the iron chelator deferiprone for the treatment of Parkinson’s disease almost unanimously draw the same conclusion: results in slowing disease progression are sufficiently significant to prompt larger studies that might provide clinical benefits to Parkinson’s disease patients (Devos et al., 2014). In this respect, a probe of concept that iron chelation therapy is here to stay is the FAIR PARK II trial, now in the recruiting phase
I do not know the phase or outcome of the study mentioned.
My takeaway is that iron chelators are a possibly viable therapeutic for PD. If chelator are therapeutic then I would think reducing iron intake in the first place or eating substances that reduce absorption could be beneficial.
The reason for the excessive iron is not clear, especially considering how American football and boxing affect the brain. If the excessive iron is caused by brain injury, reducing the iron may need a different approach.
Unfortunately yes it does. This result is due to the fact that folate is very important for cell division, which is why it is essential for expecting mothers to get plenty. For the rest of us the folate from a good diet is enough.
If a person's homocysteine level is high and folate level is low and B12 level is abundant then one could consider supplementation. If so, subsequently measure folate levels to make sure they are not excessive.
Since high folate is strongly associated with several cancers and there is a recognized mechanism of causation, care regarding folate levels is warranted.
PB, cancer feeds on sugar. Wouldn’t eliminating carbs like oats that spike glucose be more important in reducing cancer risk than avoiding Methyl Folate which has so many other benefits?
I mentioned oats specifically bc I know that like me, bears like their oats. I was shocked by how much oats spiked my insulin when I was wearing a monitor. More than berries!
That is very interesting – thank you for sharing. I prepare my breakfast cereal with a modest amount of oatmeal plus abundant doses of sunflower seeds and pistachios (not roasted or salted) and almond milk.
I am aware of getting a sugar rush from sweet things so I try to minimize my consumption of them.
It is true if a person is predisposed to cancer (mutation) or has or has had cancer. I believe we discussed Folate and cancer some time ago. Also, the right form, methyl folate, doesn't pose a danger for cancer. I could be wrong, but isn't it the conclusion of our previous discussion?
That is wrong and it is not the conclusion of any discussion I was involved with. The more effective the form of folate the more dangerous it is with regards the potential to cause cancer.
This is not just an issue for a select group. There is no one who is immune to cancer.
I apologize if you were not involved in that discussion. My memory still serves me well.
I take methyl folate bc for me, increasing methylation is a more immediate concern than reducing cancer risk which can be helped by other means like increasing autophagy.
Bolt, iron chelation for PD? See below
Please, whist is the iron folate connection? What am I missing?
The original post was about iron. 30 years ago I read a study that showed regular blood donators had a lower incidence of all forms of heart disease. Since there's a lot of cardiac disease in my family I started donating blood. I lost count of how much after they gave me a pin for 5 gallons donated. A few years ago I had 100% obstruction of LAD, the largest coronary artery branch in the body. So much for donating. But even when I had the obstruction it didn't affect my daily 10 mile runs.
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