|Image 1: You better pump iron than "bleed iron" if you want to do something for your health.|
Donate blood or not, is that the question?
Other than most previous studies, in which scientists had simply discovered a telling association (not even a clear-cut correlation) between glucose resistance / diabetes and the amount of stored iron (ferritin) in the bodies of their mostly obese subjects (Rajpathak. 2009), Houschyar et al. actually set out to test their hypothesis that there is a mechanistic explanation for the striking associations in a randomized controlled trial, involving 25 to 70 year old patients with presumed metabolic syndrome, who had been recruited through advertisements and general (family) practices and complied to at least three of the following criteria
- abdominal adiposity as defined by a waist circumference >1020 mm in (menmen; >880 mm (women);
- low levels of high-density lipoprotein cholesterol, i.e. HDL-C < 40 mg/dL (men), <50 mg/dL (women)
- hypertriglyceridemia indicated by blood triglyceride level >150 mg/dL
- elevated blood pressure of >130/85 mmHg
- impaired glucose homeostasis with fasting plasma glucose >110 mg/dL
|Figure 1: Phlebotomy protocol used in the study by Houschyar et al.|
- iron reduction group, with subjects donating blood at on day 1 and day 28 of the 6 week study period, and the
- control group, who were offered phlebotomy at the end of the 6-week study period, to ensure compliance (after all, many had applied because they hoped to see improvements in response to the treatment)
"Phlebotomy, anyone?" If this was the question your answer should be "YES" if...
... you suffer from high blood pressure, have high blood glucose levels or an undesirable high density to low density lipoprotein (HDL / LDL) ratio, because - as the data in figure 2 goes to show - all those parameters could improve significantly, when you are "550-800ml of blood lighter" ;-)
|Figure 2: Change in parameters related to blood pressure, glucose homeastasis, iron and lipoprotein metabolism in active and control arm of the phlebotomy study at the end of the 6-week study period (Houschya. 2012)|
Causality, statistics and why it always comes full circle to the liver in the real world
Just because a thing has a name, it does not necessarily exist; and as a physicist I'd rather believe in the existence of the Higgs-Boson than in the causal, and not simply corollary involvement / subsequent development of something Dongiovanni et al. refer to as the "dysmetabolic iron overload syndrome" (Dongiovanni. 2011). A syndrome, the 'diagnosis' of which has no real-world significance whatsoever, as its own pathogenesis (i.e. how tis "bad health" effects come about) is intricately entwined with the development of non-alcoholic fatty liver disease (NAFLD) and the liver's subsequent inability to store, release and manage not just iron, but also glucose, lipoproteins (HDL, LDL) and the whole cytochrome P450 enzymatic cascade which keeps your hormones in balance (Gautier. 2011).
Tea and iron levels: For the average Western iron deficiency may not be so much of an issue, but in the developed world and subgroups of our society with suboptimal, not so say insufficient, iron intake, the consumption of large quantities of tea could well turn a marginal into a full blown deficiency (Temme. 2002). On the other hand, an increase in tea consumption and the subsequently reduced iron absorption from the gut could probably reduce the average sedentary meat eater's risk of developing "iron overload" or at least highish iron levels.This is something the "dysmetablic iron overload syndrome" has in common with another syndrome, you know which? Right! The "metabolic syndrome" - so, if we A begets B and A begets C, will B disappear when we take care of C? No, and guess what: That's exactly what the Houschyar study confirmed. The hilarious reductions in blood pressure, blood glucose and above all HOMA-IR, which were all "statistical significant", but left the study participants still obese, still diabetic and still metabollically messed up were not just without physiological relevance, they are also a necessary not even physiological, but simply physical consequence of the loss of blood. Especially the HOMA-IR, the long term measure of blood glucose loses all its value, when you simply remove the "old" glycated blood cells 2 weeks before the last measurement and thus increases the relative abundance of "fresh" not yet glycated blood cells over baseline.
You Could Be Just as Lean, But More Muscular Without ALA"!) and supplemental zinc or ZMA (see "Metabolic Syndrome after 120 Days on 2x RDA of Zinc"), by the way ;-)
- Dongiovanni P, Fracanzani AL, Fargion S, Valenti L. Iron in fatty liver and in the metabolic syndrome: a promising therapeutic target. J Hepatol. 2011 Oct;55(4):920-32. Epub 2011 Jun 28.
- Gautier A, Lainé F, Massart C, Sandret L, Piguel X, Brissot P, Balkau B, Deugnier Y, Bonnet F. Liver iron overload is associated with elevated SHBG concentration and moderate hypogonadotrophic hypogonadism in dysmetabolic men without genetic haemochromatosis. Eur J Endocrinol. 2011 Aug;165(2):339-43. Epub 2011 Jun 6.
- Houschyar KS, Ludtke R, Dobos GJ, Kalus U, Brocker-Preuss M, Rampp T, Brinkhaus B, Michalsen A. Effects of phlebotomy-induced reduction of body iron stores on metabolic syndrome: Results from a randomized clinical trial. BMC Med. 2012 May 30;10(1):54. [Epub ahead of print]
- Merkel D, Huerta M, Grotto I, Blum D, Rachmilewitz E, Fibach E, Epstein Y, Shpilberg O. Incidence of anemia and iron deficiency in strenuously trained adolescents: results of a longitudinal follow-up study. J Adolesc Health. 2009 Sep;45(3):286-91.
- Rajpathak SN, Crandall JP, Wylie-Rosett J, Kabat GC, Rohan TE, Hu FB. The role of iron in type 2 diabetes in humans. Biochim Biophys Acta. 2009 Jul;1790(7):671-81. Epub 2008 May 3.
- Temme EH, Van Hoydonck PG. Tea consumption and iron status. Eur J Clin Nutr. 2002 May;56(5):379-86.