What does iron in your blood have to do with Parkinson’s? This was the question in the back of my mind when I signed up for “Haptoglobin and iron study” via the Michael J. Fox Foundation research registry. (Psst….Have you signed up? They need non-Parkis too as controls.) Well, let’s connect the theoretical dots:
- Parkinson’s is a disease of dying dopamine cells.
- Free radicals can lead to cell death.
- Increased iron in the brain can result in “neurodegeneration” (cell death) by causing free radicals.
Side note for those of us who haven’t had human biology for a while: What the heck is a free radical? It always sounds like a Berkeley protester to me. To grossly simplify, a free radical is reactive oxygen or reactive nitrogen, results of chemical processes in the body. Free radicals are neutralized by antioxidants (you know, that good stuff you get from kale…). Too much bad stuff (say, Twinkies, pesticides, sleepless nights), not enough kale, and the antioxidants are overwhelmed: your body gets “oxidative stress”. Skin starts wrinkling, cells start dying, and kale starts to look good to you.
The emphasis on getting your antioxidants through fruits and vegetables helps to explain the rather odd junction (to me anyway) between a naturopathic university and Parkinson’s research. Bastyr University, a respected naturopathic university here in Seattle, has facilitated several PD research projects, including this one.
Although elevated “free iron” in the brain has been associated with PD and neurodegeneration in some studies, this research study has found that Parkinson’s patients have lower “serum iron” than the general population.
Wait a minute — higher free iron is bad but lower serum iron is bad too….? When I asked the lead researcher, Dr. Paola Costa-Mallen, how this could make sense, she responded, “We still don’t have an answer to your question, ‘why is one lower and bad, and one other higher and bad’. We will need to investigate all the iron-binding proteins involved to understand this.” Oh, and just to complicate things further, Dr. Costa-Mallen also wrote me that there are two competing hypotheses: one is that abnormally high iron in the brain can lead to neurodegeneration, the other that abnormally LOW iron in the brain may predispose to PD. Whew — you start to see how complex Parkinson’s research is, and why we need smart researchers like Dr. Costa-Mallen.
The second objective of this research was whether the lower iron correlated with a haptoglobin phenotype. Haptoglobin is a hemoglobin-binding protein that exists in three major phenotypes (varieties). Haptoglobin phenotype 2-1 has previously been associated with increased PD risk, and sure enough, the first round of this study concluded that “PD cases had lower serum iron than controls and in particular among subjects with phenotype 2-1.” But don’t run out and get your phenotype tested quite yet. Nearly half the population (48%) has this phenotype. So simply having this phenotype is not a clear biomarker for Parkinson’s.
And the third objective was whether the phenotype 2-1 reduced the protective benefit of smoking. Huh? Yes, smoking is good for you, at least as far as PD is involved: “Among the environmental factors that affect risk of PD, tobacco smoking has been consistently found to confer a protective effect, with a reduction of PD risk by about 50%, among cigarette smokers as compared to non-smokers.” The study concluded that the “protective effect of smoking on PD risk… (was) weakest among subjects with phenotype 2-1.”
You will notice I am referring to conclusions from a published study. I asked Dr. Costa-Mallen why she was still recruiting. She responded that “there is a lot more work to be done” to tease out other blood iron parameters, and analyze the questionnaire data. (I filled out a lengthy questionnaire about diet, relatives, pesticide exposure, etc., etc. This is pretty typical for PD research to ask for lifestyle information, since the theory is that environment plays a role in PD.)
Dr. Costa-Mallen’s not just recruiting new research subjects, but also additional research funds. In an email to me, she wrote, “In order to elucidate whether or not low blood iron is “bad” for you and increases the risk of Parkinson’s disease and speeds up the progression of Parkinson’s disease, especially in persons genetically predisposed, we will need to investigate other parameters related to iron metabolism, and we need larger study populations. ”
How did I turn out? The study is going to collect more samples from PD patients and controls before testing for phenotypes, so I don’t know if have the 2-1 phenotype. But all my blood tests are normal – no anemia, I guess. I’m hoping this means I can avoid kale a little longer. (For the record, I eat LOTS of spinach — works for Popeye, works for me.)