Reducing ferritin levels to lower the risk of heart attack and cancer

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Vince

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Ferritin level in blood is an index of body iron stores. Ferritin is elevated in iron overload. A research group looked at The Copenhagen City Heart Study’s data on almost 9,000 people. They found that “stepwise increasing concentrations of ferritin were associated with a stepwise increased risk of premature death overall.”People with a ferritin level of greater than 600 µg/l had a median survival age of 55. Those with a ferritin level of 400 to 599 µg/l lived a median of 72 years; at 200 to 399 µg/l, 76 years and less than 200 µg/l, 79 years.
Total and cause-specific mortality by moderately and markedly increased ferritin concentrations - Research - Rigshospitalet

Men with a ferritin level greater than 200 had 2.2 times the risk of a heart attack than did those with a ferritin level less than 200 µg/l. Many doctors don’t consider 200µg/l to be abnormal.
http://www.healtheiron.com/Websites...cardial_infarction_in_eastern_Finnish_men.pdf
 
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There are five ways to lower iron levels to prevent iron accumulation:

  1. Blood donation is the most effective way to reduce ferritin levels. Some blood banks won’t take your blood if you tell them you have a high ferritin level.
  2. Phlebotomy—some doctors won’t allow you to have a phlebotomy if your ferritin is in the reference range or above.Laboratory reference ranges vary from lab to lab.
  3. Iron Chelation --Quercetin, curcumin, IP6, green tea extract, theaflavin from black tea.
  4. Inhibition of non-heme iron absorption from plant foods. Food and drink that can inhibit iron absorption includes olive oil, tea, coffee, dairy products, eggs, vegetables, walnuts, almonds, peas, chocolate, red wine.
    Dairy products inhibit the absorption of heme iron .Thus eating cheese with a meat meal will hinder iron absorption from meat.
  5. Low iron diet .Avoid foods which are iron fortified.

Vitamin C should not be taken with meals as it increases iron absorption. Don’t drink drinks containing vitamin C with meals. Chicken and fish are lower in iron than beef and pork.





http://circ.ahajournals.org/content/96/10/3300.full

The first graph below shows 10 times the risk.The second graph shows 5 times the risk!

 
Crude and regression-standardized risks of incident atherosclerosis (1990 to 1995) according to ferritin quintiles. The graph below documents dose-response relation between ferritin measurements and risk of early atherogenesis. n=476



Phlebotomy significantly reduced MFFL ferritin levels in iron-reduction compared with control patients Lower iron burden predicted improved outcomes overall and was enhanced by phlebotomy. Controlling iron burden may improve survival and prevent or delay nonfatal myocardial infarction and stroke.

Effect of controlled reduction of body iron stores on clinical outcomes in peripheral arterial disease 66% reduction in events in graph B
 
Healthy people usually absorb about 10% of the iron contained in the food they eat. People with hemochromatosis absorb up to 30% of iron. Over time, they absorb and retain between 5 to 20 times more iron than the body needs.

The association between hemochromatosis and diabetes was first recognized in the late 1800’s.. The damage to the pancreas from excessive iron deposits can cause diabetes, experts say. Even though people have defective hemochromatosis genes from birth, the symptoms usually don’t occur until adulthood. The symptoms associated with hemochromatosis are diverse; however, it sometimes causes no symptoms.

To rid the body of excess iron, people with hemochromatosis are given regular treatments of phlebotomy ( blood removal). The normal iron content of the body is 3 to 4 grams. Hemochromatosis can be diagnosed based on special blood tests. It is best to catch hemochromatosis early. Patients with hemochromatosis may be asymptomatic or may present with general and organ-related signs and symptoms. Excess iron is stored (asymptomatically) in body tissues and patients can get type 2 diabetes, type 1 diabetes or cancer. Primary tumors often develop at body sites of excessive iron deposits.

There are several known mutations in the HFE gene, but presently testing for only three is available: C282Y, H63D, and S65C. When a person has one mutated copy, he or she is called a carrier or heterozygote. When a person has two of the same mutated copies, he or she is called a homozygote. When a person has two different but mutated copies, he or she is called a compound heterozygote.

Most at Risk - C282Y homozygote and the C282Y/H63D compound heterozygote
Moderate Risk- H63D homozygote or other compound heterozygote combinations
Low Risk- C282Y heterozygote (carrier); H63D heterozygote (carrier) or S65C heterozygote (carrier)
The doctors on the Board of Directors of The American Hemochromatosis Society state that transferrin saturation percentage greater than 40% and serum ferritin greater than 150ng/mL could indicate clinical iron overload/iron storage in the body and treatment with phlebotomy (bloodletting) should be considered regardless of DNA test results.

This means that patients' treatment should not be based on genetic test results alone whether positive or negative. The DNA test is a powerful tool to help us find people at risk; 85-98% of patients with clinical iron overload have the hemochromatosis mutations, however, the most important point to remember is that excess iron needs to be evaluated and treated.Dr.William Crosby, the late well known hemochromatosis physician and researcher, declared that if a patient has demonstrated excess iron then they are in danger of organ damage and premature death.
Untitled Document
 
Objective:
Endothelial dysfunction, secondary to systemic inflammation and oxidative stress, is known to play a major role in the development and progression of atherosclerosis. It is hypothesized that the lower incidence of coronary artery disease in the premenopausal period in females when compared with males is associated with regular menstrual blood loss. We investigated whether regular blood donation (BD) is associated with improved endothelial function in healthy adult males.
Methods:
Fifty young healthy male volunteers volunteers with a mean age of 30±6 years without overt cardiovascular disease were enrolled to participate in serial consecutive BDs. Serum iron levels as oxidative stress parameters, flow-mediated dilatation (FMD) for endothelial function, 24-h mean diastolic blood pressure for peripheral vascular resistance identification, and high-sensitivity C-reactive protein (hs-CRP) levels as systemic inflammatory markers were evaluated before and after BD. This study used a prospective observational cohort design. Patients with cardiovascular and inflammatory diseases were excluded.
Results:
BD was found to improve FMD steadily and significantly when compared with the baseline (mean±SD: 9.9%±3.8%, 10.44%±3.9%, 10.65%±3.9%, and 10.75±3.9%, respectively, p=0.15, p=0.02, p=0.006 as compared with the baseline). A steady decrease was identified in hs-CRP levels after serial BDs, although this decrease was not statistically significant in the all phases (2.96±3.3 mg/L, 2.26±1.5 mg/L, and 2.12±1.5 mg/L, respectively, p=0.829, p=0.558). The 24-h mean diastolic blood pressures were significantly lower in the chronic phase (77±9 mm Hg, 75±7 mm Hg, and 72±8 mm Hg, respectively, p=0.50, p=0.003), whereas there was no significant change in iron levels in the acute and chronic phases (66±32 mg/dL, 72±43 mg/dL, and 68±33 mg/dL, respectively, p=1.000, p=1.000).
Conclusion:
The results of the study indicate that regular BD improves endothelial function. (Anatol J Cardiol 2016; 16: 154-8)

Regular blood donation improves endothelial function in adult males
 
RE: the first post, because this wasn't an interventional study we need to consider the possibility that people with elevated ferritin may have something else going on that increases their CVD risk in other ways unrelated to iron, e.g. excessive red meat consumption (trans and saturated fats, TMAO). There are also studies showing that people who give blood live longer than those who don't, but of course people who give blood are more likely to be healthier than the general population.

Ferritin is a more expensive test than a standard CBC with hemoglobin and hematocrit. Does anyone know if hemoglobin/hematocrit is sufficient to see if "iron overload" is happening? E.g. could you have "too high" ferritin but normal hemoglobin and hematocrit?

Inhibition of non-heme iron absorption from plant foods. Food and drink that can inhibit iron absorption includes olive oil, tea, coffee, dairy products, eggs, vegetables, walnuts, almonds, peas, chocolate, red wine.

Looks like my coffee addiction may be helping me here!
 
Thanks for posting Vince. I have hemochromatosis and I have been wondering where to maintain ferritin. This study has great info that the upper levels of the accepted range are to be avoided. This is another good example of where the 'normal' or acceptable range for blood work is not the best guide. I was maintaining under 200 but I have decided to be closer to the 50 to 100 range.

XQFQ - I don't think Ferritin test is that expensive. It was (decades ago) part of the standard blood work but due to abuses and fraud (I was told/read), it was removed. Everyone should check it occasionally, particularly men. IMO, hemoglobin/hematocrit is not suffficient to check ferritin level or iron overload. If I recall correctly my hemoglobin/hematocrit were in range but ferritin was very high.
 
Ferritin level in blood is an index of body iron stores. Ferritin is elevated in iron overload. A research group looked at The Copenhagen City Heart Study’s data on almost 9,000 people. They found that “stepwise increasing concentrations of ferritin were associated with a stepwise increased risk of premature death overall.”People with a ferritin level of greater than 600 µg/l had a median survival age of 55. Those with a ferritin level of 400 to 599 µg/l lived a median of 72 years; at 200 to 399 µg/l, 76 years and less than 200 µg/l, 79 years.
Total and cause-specific mortality by moderately and markedly increased ferritin concentrations - Research - Rigshospitalet

Men with a ferritin level greater than 200 had 2.2 times the risk of a heart attack than did those with a ferritin level less than 200 µg/l. Many doctors don’t consider 200µg/l to be abnormal.
http://www.healtheiron.com/Websites...cardial_infarction_in_eastern_Finnish_men.pdf
 
That’s interesting. Ferritin can be quickly elevated due to infection or inflammation. Would this make ferritin more of a marker for inflammation as opposed to the ferritin being the cause for increased mortality? If the subjects also had horrible diets and did not exercise setting off a chronic inflammatory cascade......this could also increase cardiovascular events. They would more than likely live with an elevated ferritin level.
 
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