Beware of iron overload — are you getting too much?
—-Important Message—-
Painting it on and watching it grow
She drops to her knees in front of me, naked from the waist up…
I watch as she slowly paints my member with a special mixture…
Her hands are warming it up, as well as her hot breath blowing teasingly on me…
And oh, it feels SO good…her soft hands are rubbing it in from the tip of my shaft to the base of my balls…
And just like that, I’m growing…my member is getting more engorged with every second…
And she is grinning…watching me grow, clapping her hands in excitement.
And then she’s ready to have some fun with my bigger, better member…and so am I!
Just paint it on and watch it grow…
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Here’s what happens to men when they have too much iron
There’s a handful of nutrients that cause blood sugar problems when deficient, yet also a few that do it when in excess.
The nutrients that help all happen to be required for normal insulin signalling in some capacity.
They include magnesium, manganese, chromium, chiro-inositol, and thiamin.
All of these have been found deficient in diabetics and all have been shown, individually, to improve the condition.
On the other hand: the dietary factors known to cause diabetes when IN EXCESS are fewer in number and are, coincidentally, things you’d want to limit anyway.
A main offender is omega-6 fatty acids.
These displace omega-3 fatty acids from cell membranes and lowers basal glucose flux in the process.
There is nothing actually essential about the omega-6 class of “essential fatty acids.”
Another offender is dietary iron.
Although we do actually require some of this, unlike the ω-6 fatty acids, consuming too much can lead to iron overload, excessive free radicals, cancer, and insulin resistance.
There is a wealth of evidence to support this contention, yet there’s a few reasons why it’s generally overlooked.
Most food companies would prefer you not know of the association between iron and diabetes.
And the Big Pharma companies would rather sell you a chemical substance to “correct” it.
Since these business interests are main advertisers of news outlets, you don’t read or hear too much about iron overload.
There’s also something of a “pro-food bias” among news outlets in general, meaning that they’re more likely to talk about the benefits of certain foods than their detriments.
Not many people like to hear that their past choices could’ve been responsible for causing a serious health condition.
Yet the dietary causes of diseases should be known regardless, for their prevention if not reversal.
But of course…since most people wouldn’t accept this association without proof, and nor should they, here is some evidence to the effect:
Although diabetes had long been associated with excessive intake of some foods that happen to be high in iron, the first concrete evidence began emerging in the 1950s…
…when diabetes was found associated with the conditions thalassemia and hemochromatosis.
Thalassemia and hemochromatosis are 2 conditions characterized by iron overload.
Thalassemia is the complete incapacity to synthesize hemoglobin.
This would of course be fatal if left alone, yet frequent blood transfusions can prolong life for decades until the patient ultimately dies of iron overload.
Hemochromatosis is also a genetic condition, and is characterized by a mutation in the HFE gene, which regulates hepcidin.
Hepcidin is normally responsible for balancing body Fe2+ levels by expressing the divalent metal transporter, and ion channel in the intestines that selectively gates iron uptake.
People with hemochromatosis continually absorb Fe2+ in an unregulated manner until clinical iron overload is reached, and then beyond…
The association between hemochromatosis and diabetes became widely known after being reported in 1953.
This association is so strong in fact that diabetes was 1 of the diagnostic features of hemochromatosis in the days before blood tests became routine:
“The diagnosis of hemochromatosis may be suspected clinically when the triad of skin pigmentation, cirrhosis of the liver and diabetes mellitus is present.” —Marble, 1951
Thalassemia is little different.
This condition had been known about for just as long, but case reports of diabetes only began surfacing in the 1960s after blood transfusions had become a viable treatment option.
Perhaps the first formal study of this link surfaced in the 1970s.
It had been reported using glucose tolerance tests that 32% of the patients with thalassemia had either diabetes or impaired glucose tolerance.
And moreover, they were all relatively young in the age range of 9–23.
From this, you could suppose that by the time they’re in their 40s, should they live that long, enough blood would’ve been infused to confer diabetes to most of them.
The converse is also true.
Case reports of diabetes being reversed or improved by the WITHDRAWAL of blood have been reported for nearly just as long (Crosby, 1958).
This observation had been confirmed by newer & larger case-control studies (Valenti, 2007).
Withdrawing blood has even been shown to reduce the risk of new-onset diabetes (Mifuji-Moroka, 2013).
“During the course of treatment the patient’s diabetes was considerably improved.” Crosby, 1958
Besides giving blood, another effective way to reduce iron body stores is via chelation with deferoxamine.
This has, perhaps not surprisingly, also been shown to improve diabetes (Cutler, 1989).
So it would seem as though diabetes is caused by iron overload in general.
This idea only gains credence with every decade of research, and around the turn of the century data from over a thousand subjects further confirmed the link:
Ferritin is the primary iron storage protein and one of the most accurate, convenient, and reliable indicators of whole-body iron status.
This large study was a spin-off of the even larger EPIC Norfolk study of 25,631 people.
Of this giant cohort, the epidemiologists had identified 417 new cases of diabetes after a few years of follow-up.
Each case had initially been matched against 417 controls based on age, sex, and recruitment date, and then again based additionally on BMI.
So this study had initially totalled 1,251 similar subjects comprised of 1 diabetes and 2 control groups, with 1,018 subjects remaining after exclusions for incomplete data.
Upon dividing all subjects into 5 subgroups based on serum ferritin levels, they had found that the most extreme group had a sevenfold increased risk of developing diabetes, as assessed retroactively.
In other words, serum ferritin over 300 ng⁄ml has a very high predictive power when it comes to diabetes.
This was confirmed later using serum hepcidin, another sensitive biomarker for iron, in 1,391 subjects with metabolic syndrome (Martinelli, 2012).
A hint towards the mechanism was reported by Korean scientists who found that adiponectin, a strongly antidiabetic hormone, correlates more with serum ferritin than with:
Age, sex, body mass index, diastolic blood pressure, triglycerides, HDL-cholesterol, fasting blood glucose, fasting insulin, HOMA‑IR, or C‑reactive protein (Ku, 2009).
“The ferritin concentration was the most powerfully associated with serum adiponectin.” ―Ku, 2009
Adiponectin is an antidiabetic hormone because it increases the activity of pyruvate dehydrogenase in muscle (McAinch, 2009), at least in part.
And also because it inhibits gluconeogenesis in the liver (Zhou, 2005).
This inverse association between ferritin and adiponectin has since been confirmed repeatedly in human adipose tissue removed for bariatric surgery (Gabrielsen, 2012).
This was also noted in tissue samples from 245 Spanish subjects (Moreno–Navarrete, 2014), and then again from 46 French ones (LeBars, 2016).
The idea that adiponectin is downregulated in response to iron, and not the other way around, is supported by other biomarkers of iron status — e.g. hepcidin, transferrin, transferrin receptor — also being strongly correlated (LeBars, 2016).
And this is not simply because foods high in iron are generally associated with ω-6 fatty acids or anything to that effect.
This is because rats fed diets with escalating levels of iron, all else being equal, also show progressively lower serum adiponectin and cellular adiponectin mRNA (Gabrielsen, 2012).
This was attributed to changes in the acetylation status of FOXO-1, the only other transcription factor besides PPARγ known to transcribe for the adiponectin gene.
This seems plausible because FOXO-1 is known to be activated by SIRT-1 in response to increased NAD+ levels (Qiao, 2006).
And that cellular NAD+ is decreased by hydroxyl radicals (Jayasena, 2007).
Iron is a well-known generator of hydroxyl radicals through the Fenton reaction.
What is meant by “oxidative stress” is essentially an increase in superoxide, hydrogen peroxide, and/or hydroxyl radicals inside the cell.
There are many ways to induce this and they all lead to a depletion of FOXO-1 activity (Subauste, 2006).
Although not mentioned by Gabrielsen, I’ve confirmed that the FOXO-1 gene also has an iron response element.
This adds another plausible mechanism behind the iron-induced reduction of adiponectin.
Yet the prodiabetic effect of iron probably isn’t limited to just adiponectin.
Iron overload has also been shown to lower the retention of chromium (Sargent, 1979), and also limit the uptake of manganese through the divalent metal transporter (Fitsanakis, 2010).
And as it turns out, the hypoxia-inducible factor-1α (HIF-1α) also plays a role in iron-induced diabetes:
This study used human hepatocytes, mouse hepatocytes, whole rats, and the iron chelator deferoxamine.
They had demonstrated by using Western blot, Northern blot, and PCR that removing iron from the cells led to an increase in: HIF-1α, the glucose transporter-1, and the insulin receptor.
“Iron depletion increased insulin receptor activity, whereas iron supplementation had the opposite effect.” ―DonGiovanni, 2008
It was shown previous to this point that HIF-1α transcribes for many things including glucose transporter-1 (Chen, 2001), 3 separate glycolytic enzymes (Semenza, 1994), and VEGF.
Hypoxia-inducible factor-1α is also inactivated by iron, a fairly well-known effect (Nandal, 2011).
For this reason these results aren’t only believable but are even expected.
Incidentally, it is this reduction of HIF-1α that’s thought responsible for the delayed wound healing in diabetics via reduced VEGF (Bento, 2011).
If that weren’t enough, both iron restriction and phlebotomy have been shown to upregulate HIF-1α and increase insulin levels (Minamiyama, 2010).
Other evidence of the importance of HIF-1α is that it’s been found to be lowered in β-cells taken from diabetics (Gunton, 2005).
And polymorphisms is the gene which encodes it is associated with diabetes risk (Nagy, 2009).
And almost unbelievably, hypoxia itself — which activates HIF-1α — has even been shown to improve insulin resistance (Tian, 2016).
Additional confirmation comes from using a different iron chelator, FBS0701, in a study that’d translated into the complete normalization of glucose tolerance in leptin-deficient mice (Cooksey, 2010).
And conversely, the simple addition of iron to the rodent diet of course results in diabetes (DonGiovanni, 2013).
So no matter how it’s accomplished, either through restriction or addition, the group having lower iron levels has invariably better glucose control.
So it would seem that iron is associated with diabetes without exception.
There is so much evidence that you could fill an entire book about just this, yet the association would become so obvious after only a few pages that nobody would bother reading the entire thing.
But to add further support to this link, as if it needed any, streptozotocin has been shown to increase liver iron by 215% (Wang, 2014).
This perhaps finally explains why streptozotocin, along with alloxan, it’s been the go-to substance for inducing experimental diabetes since the late ’60s.
—-Important Message for Men With Blood Sugar Problems—-
Why does this special breakfast help reverse blood sugar problems?
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