Isn’t Iron Ironic?
Iron is a potentially toxic heavy metal, and excessive intake and storage can damage metabolism and promote inflammation, cancer, heart disease, Parkinson’s, Alzheimer’s, MS, diabetes and numerous other degenerative as well as infectious diseases.
Whilst it’s common to be told that iron insufficiency is at the heart of a variety of issues related to aging and disease, experimental evidence continues to show the opposite to be true, and when it comes to maintaining metabolic health, difficulty often lies in ensuring one does not consume and absorb too much.
Blood tests commonly used as evidence of ‘iron deficiency’ can 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 can be predictive of disease outcomes and are an important benchmark for a genuine and accurate determination of metabolic 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, encouraging cancer development.
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 an 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.
Interaction between iron and the polyunsaturated fats (PUFAs) powerfully promotes inflammation, damages metabolic performance, and has been shown to be a cause of degenerative disease, including cancer, MS and alzheimer’s. It is also a significant factor interfering with liver health, preventing the liver from being able to properly carry out many important pro-metabolism and detoxification functions.
Some of the symptoms which are commonly blamed on iron deficiency include fatigue, dizziness or lightheadedness, headache, tongue swelling and inflammation, irregular heartbeats, chest pain, weakness or shortness of breath, irritability, impaired immune function, restless leg syndrome, thinning hair, dry skin, brittle nails, cold extremities, brain fog, poor appetite, depression and anxiety, and of course anemia.
Symptoms such as these often elicit recommendations to increase iron intake with supplements or fortified food items containing excessive amounts of iron, often in the more reactive and dangerous reduced ferrous form.
Realistically, those symptoms mentioned (and many others) blamed on a lack of iron, are often the result of chronic exposure to stress, and the suppression of metabolic energy systems. This includes anemia, which is a common symptom of impaired thyroid function.
Actual iron deficiency anemia (although possible), is unlikely and should be the last suspected cause. In fact, keeping iron stores low can be extremely beneficial for health. Serum ferritin levels have been shown to increase and decrease relative to thyroid function.
The liver plays an important role enabling the effective performance of thyroid energy systems, and the proper removal of excess estrogen from circulation. Excess iron accumulation in the liver interferes with this process, and high estrogen promotes iron absorption, thyroid dysfunction and degenerative disease.
The polyunsaturated fats (PUFAs) are increasingly released out of storage into the system when thyroid function is sub optimal, worsening the inflammatory effects of interactions between estrogen and iron, potentially creating a vicious circle of iron dysregulation which can be difficult to deal with and harmful.
Interactions between estrogen and PUFAs promote the kind of conditions which help to change ‘free’ iron into the far more toxic and reactive reduced ferrous form, making iron more dangerous and damaging.
A diet avoiding the PUFAs and minimizing 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.
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.
Low testosterone has also been shown to increase the risk of anemia, and this makes sense in the context of metabolic suppression, high estrogen relative to progesterone, and an inflammatory state, all of which can be connected to excess iron.
Vitamin A, vitamin K and copper have been demonstrated 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 the inflammatory stress substance, serotonin.
Iron increases serotonin and nitric oxide, and serotonin promotes nitric oxide and estrogen, and all of these things interfere with energy system metabolism and increase the risk of chronic inflammation, thyroid dysfunction and iron dysregulation.
“We concluded that NO is one of the mediators of iron-induced toxicity in proximal tubule cells…”
Elevated iron levels are a risk factor for postmenopausal osteoporosis (PMOP), and it is reasonably common for menopause, chronic inflammation and thyroid dysfunction to go together.
It has been suggested that PMOP is made worse as a result of insufficient estrogen, however this is based largely on the popular belief that menopause is a low estrogen state. In reality, chronic stress, iron dysregulation, thyroid and liver dysfunction, inflammation, and excess estrogen relative to progesterone go hand in hand and promote each other.
Focusing mainly on pro-metabolic foods like milk, cheese, and gelatin to get sufficient protein, and including 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, often misdiagnosed as iron deficiency.
Apart from reducing intake of iron, there are a number of generally safe and easy ways to either lower 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…”
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 PUFAs and excess estrogen (as well as numerous other stress related substances), and as such they can have powerfully synergistic disease protective, anti-aging effects.
Sugar lowers stress hormones and improves energy metabolism, limiting the release of the polyunsaturated free fatty acids and maintaining glycogen stores, helping keep blood sugar levels stable.
Sugar protects against inflammation and thyroid dysfunction, and as such can help to prevent anemia as well as iron dysregulation. Sugar powerfully suppresses cortisol which when high, can also be associated with an inflammatory anemic state.
Diabetes symptoms have been demonstrated to result from interactions between iron, PUFAs, stress substances (including serotonin, nitric oxide and estrogen) as well circulation of bacterial toxins.
Sugar consumption (in the context of a nutritious diet low in iron and the difficult to digest starchy, fibrous, high PUFA foods) rather than being the cause of blood sugar dysregulation symptoms, is likely to be highly protective against them.
Too much iron can promote liver dysfunction, inflammation, estrogen excess, endotoxin issues, increased serotonin, nitric oxide and free fatty acid levels, and all of these things have not only been shown to promote diabetes, but inflammatory disease in general.
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.
Many of the positive effects attributed to 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). Some foods that supply iron, also provide generous amounts of pro-metabolic nutrients, and it is common for the credit for improvement to be incorrectly given to iron. Also harmful effects of iron can take significant time to show up, and are easily misattributed down the track to some other cause.
There are so many ways that too much iron in the system can damage proper thyroid metabolism, it seems ironic (or perhaps a little tragic) that suppressed thyroid function is the predominant cause of the symptoms which so often lead to a recommendation to supplement with iron.
How many of your health issues, rather than having anything to do with iron deficiency, are actually being caused by suppressed thyroid metabolism directly connected to excess iron and PUFAs stored in your body?
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