Ironing It Out.

Iron Even though it is probably true that getting a small amount of iron from your diet is necessary, it’s important to know that iron is a potentially toxic heavy metal and that excessive amounts can promote cancer, heart disease, Parkinson’s, Alzheimer’s, diabetes and many other degenerative as well as infectious diseases.

“…iron elevation is increasingly reported as a feature of Alzheimer’s disease…these data support…therapeutic strategies that lower brain iron, which have reported beneficial outcomes in Phase II trials of Alzheimer’s and Parkinson’s diseases”

Whilst it is common to be told that iron insufficiency is at the heart of certain problems, experimental evidence is confirming more and more that the opposite is far more accurate, and when it comes to maintaining metabolic health, the real difficulty lies in ensuring that one does not consume and absorb too much.

“…data indicated that high body iron stores…are associated with an increased cancer risk. Other data shows an increased heart attack risk.”

Blood tests commonly used as evidence of a so called ‘iron deficiency’ tend to be diagnostically misleading and fail to accurately measure iron stored inside tissue, thereby not giving a real picture of iron status.

Tissue levels of iron – when properly ascertained – can be predictive of disease outcome and are able to be an important benchmark for a genuine determination of health.

When stores are too high iron tends to accumulate in the liver (as well as in other tissue including the brain and bone marrow) promoting stress and inflammation, interfering with a number of metabolic functions.

“Liver is the major organ for iron storage and has the largest capacity to store excess iron. The measurement of hepatic iron concentration by liver biopsy is the most reliable means to assess body iron storage…”

“The accumulation of iron in the liver would strongly potentiate the development of hepatic tumours…”

Although serum ferritin tests can be somewhat predictive of high iron stores – especially when levels are on the extremely high end – it has been demonstrated that the ratio of ferritin/AST (aspartate transaminase) is a reasonably accurate predictor of liver iron concentration, and is therefore an easier way to determine whether there is iron overload, avoiding more invasive methods such as liver biopsy. Ferritin and transferrin measured together can also help to give a more reasonable picture of actual iron storage status.

“Elevated serum ferritin does not always reflect iron overload…A combination of both parameters expressed as ferritin/aspartate transaminase ratio was highly predictive of tissue iron overload…without exposing the patient to unnecessary risks and costs.”

The interaction between iron and the polyunsaturated fats is a powerful promoter of inflammation, is damaging to metabolic performance and has been shown to be a major cause of degenerative disease, including cancer and alzheimer’s. It is also a significant factor interfering with liver health, preventing it from being able to properly carry out many important functions.

“Increased lipid peroxidation with age is well accepted as an index of age-related increases in oxidative stress…usually attributed to…the vulnerability of lipid molecules to oxidative reactions, due to their unstable double bondings…in the absence of iron, little lipid peroxidation is detected.”

There is no end to the number of symptoms which are popularly blamed upon iron deficiency. These include – but are not limited to – fatigue, dizziness or lightheadedness, weakness or shortness of breath, irritability, impaired immune function, restless leg syndrome, thinning hair, brain fog, depression or anxiety and of course anemia.

As a result of this many people are given the recommendation to increase their intake of iron with supplements or fortified food items containing harmful amounts of iron often in the more reactive and dangerous reduced ferrous form.

Many of the above (as well as other) symptoms erroneously placed upon a lack of iron are far more likely to be the result of chronic exposure to stress of many kinds and the eventual suppression of metabolic function. This includes anemia which is actually a common symptom of under active thyroid metabolism as well as certain types of nutritional deficiency.

Legitimate iron deficiency anemia – although possible – is extremely unlikely and should be the last suspected cause. In fact, keeping iron stores low can be extremely beneficial for health.

The liver plays an important role in effective performance of thyroid energy systems, as well as in the proper removal of excess estrogen. Excess iron accumulation in the liver interferes with this process and high estrogen promotes iron absorption. The polyunsaturated fats are increasingly released into circulation when thyroid function is sub optimal, worsening all of these interactions potentially creating a vicious circle which can be difficult to deal with.

Interactions between increased levels of estrogen and the more highly unsaturated fats promote the kind of conditions which help to change ‘free’ iron into the far more toxic and reactive reduced ferrous form where they then do most of their damage.

A diet avoiding the polyunsaturated fats and minimising excessive intake of high iron foods is a rational approach to improving health and avoiding many kinds of degenerative disease.

A suppressed thyroid metabolism slows digestive function and adds further strain on the liver, and this allows for increasing amounts of bacterial toxins to enter the system causing inflammatory issues. Bacterial endotoxin (LPS) promotes the absorption of iron from food, and excess iron has been shown to interact with these toxins and promote the disease causing effects of endotoxin.

“…we review the evidence that….bacteria are a crucial feature of AD, that their growth in vivo is normally limited by a lack of free iron, and that it is this iron dysregulation that is an important factor in their resuscitation…A consequence of this is that the growing cells can shed highly inflammatory components such as lipopolysaccharides (LPS).”

A small amount of beef or lambs liver once a week has more than enough iron content. Because most cases of anemia are not a genuine reflection of low storage of iron – often being diagnosed on the basis of hemoglobin or red blood cell levels – improving thyroid function (rather than increasing iron intake) is generally all that is required. Vitamin A, vitamin K and copper have also been shown to be effective for improving iron status or different measures of anemia, avoiding an unnecessary increase in iron intake.

Anemia can also be the result of chronic inflammation and so it may not be surprising to discover that iron promotes the release of nitric oxide, a powerful promoter of inflammation and a substance which helps to increase levels of free iron. Reducing iron stores also limits the production of another substance, serotonin, closely tied in with the inflammatory process.

Focusing on pro metabolic foods like milk, cheese, gelatin and shellfish to get sufficient protein, and plenty of carbohydrate from sweet ripe fruits, fruit juice, honey and white sugar is a good way to reduce iron intake and an effective method for avoiding many of the thyroid related symptoms mentioned, including anemia, commonly misdiagnosed as iron deficiency.

Apart from a limited intake of iron there are a number of generally safe and easy ways to either reduce iron stores or protect against some of the dangerous effects of iron in the body. These include regular use of aspirin, vitamin E, supplementation with glycine and taurine, certain kinds of antibiotics as well as occasional blood donation.

“In conclusion, our results suggest that ASA [aspirin] may chelate endogenous hepatic iron…”

“…results suggest that glycine could be a beneficial agent against iron mediated toxicity in hepatocytes.”

Many of the things which have been shown to protect against the toxicity of iron are also known to protect against the inflammatory and thyroid suppressive impact of the circulating polyunsaturated fats as well as the dangers of too much estrogen and numerous other stress related substances, and as such they can have powerfully synergistic disease protective and anti-aging effects.

Sugar is known to suppress the stress hormones and improve metabolism, limiting the release of the polyunsaturated free fatty acids and maintaining glycogen stores, helping keep blood sugar levels stable. As a result it is an important factor protecting against anemia as well as the dangers of excess iron. Sugar powerfully suppresses cortisol which when high can also be associated with an inflammatory anemic state.

Diabetes is another disease which is now being understood to be the result of the interaction between excess iron, polyunsaturated fats, stress substances and bacterial toxins and consequently sugar, rather than being causitive, is (in combination with a nutritious diet low in iron and the difficult to digest starchy, fibrous and high pufa foods) likely to be highly protective.

“High-fat diets and iron overload are associated with insulin resistance, modified hepatic lipid and iron metabolism and increased mitochondrial dysfunction and oxidative stress.”

“…excess iron may diminish glucose utilization…and lead to a shift from glucose to fatty acid oxidation…”

Regularly consuming coffee with the consumption of foods high in iron can possibly help to limit excessive absorption. As vitamin C may be able to increase the absorption of iron, it is probably a good idea to avoid drinking things like orange juice together with meat if you are attempting to lower iron stores.

Positive effects associated with iron supplementation can be explained as the short term response of the body to the introduction of a stress promoting substance (for example causing an increase in red blood cells or hemoglobin) and because the harmful effects can take significant time to show up, they are later easily misattributed to some other cause.

How many of your health issues, rather than having anything to do with iron deficiency, are likely related to excess iron as well as polyunsaturated fats stored within your body?

Read more here

Pathological mechanisms of hepatic tumour formation in rats exposed chronically to dietary hexachlorobenzene.

Ferritin levels in the cerebrospinal fluid predict Alzheimer’s disease outcomes and are regulated by APOE

Modulation of age-related alterations of iron, ferritin, and lipid peroxidation in rat serum

High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men.

Association Between Body Iron Stores and the Risk of Acute Myocardial Infarction in Men

Estimating iron overload in patients with suspected liver disease and elevated serum ferritin.

Effects of vitamin A supplementation on nutritional status of iron in healthy adults.

Iron induces hepatocytes death via MAPK activation and mitochondria-dependent apoptotic pathway: beneficial role of glycine.

T cell lipid peroxidation induces ferroptosis and prevents immunity to infection

Aspirin intake and the use of serum ferritin as a measure of iron status.

Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide

Effects of excess dietary iron and fat on glucose and lipid metabolism.

Taurine supplementation reduces oxidative stress and protects the liver in an iron-overload murine model

Iron dependence of tryptophan hydroxylase activity in RBL2H3 cells and its manipulation by chelators.

Iron chelation by cranberry juice and its impact on Escherichia coli growth.

Iron metabolism, free radicals, and oxidative injury.

A Bacterial Component to Alzheimer’s-Type Dementia Seen via a Systems Biology Approach that Links Iron Dysregulation and Inflammagen Shedding to Disease

Iron, free radicals and cancer.

Iron chelation as a possible mechanism for aspirin-induced malondialdehyde production by mouse liver microsomes and mitochondria.

Involvement of splenic iron accumulation in the development of nonalcoholic steatohepatitis in Tsumura Suzuki Obese Diabetes mice

Aspirin intake and the use of serum ferritin as a measure of iron status.

Most free-radical injury is iron-related: it is promoted by iron, hemin, holoferritin and vitamin C, and inhibited by desferoxamine and apoferritin.

Iron-Chelating Activity of Tetracyclines and Its Impact on the Susceptibility of Actinobacillus actinomycetemcomitansto These Antibiotics

Iron and Diabetes Risk

Relation of iron stores to oxidative stress in type 2 diabetes.

Dietary iron intake, body iron stores, and the risk of type 2 diabetes: a systematic review and meta-analysis

Body iron stores and risk of type 2 diabetes: results from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study

An update on iron chelation therapy

A novel method for assessing the role of iron and its functional chelation in fibrin fibril formation: the use of scanning electron microscopy.

Body iron metabolism and pathophysiology of iron overload

Iron Accumulation with Age, Oxidative Stress and Functional Decline

Anemia in male patients with cushing’s syndrome before and after cure

Effects of iron deficiency on serotonin uptake in vitro by rat brain synaptic vesicles.

Nitric oxide and iron: effect of iron overload on nitric oxide production in endotoxemia.

Serum ferritin as a marker of thyroid hormone action on peripheral tissues.

Iron supplements: the quick fix with long-term consequences

Characteristics of anemia in subclinical and overt hypothyroid patients.

Role of iron in carcinogenesis: cancer as a ferrotoxic disease.

Cerebral quantitative susceptibility mapping predicts amyloid-β-related cognitive decline.


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