Imagine a group of clinicians on a mission trip to somewhere in the tropics. One day, the well-meaning Samaritans bring some local kids into a sterile looking hut, poke them with needles, examine their blood and find that they are anemic. They give them either a shot of some rust colored liquid or some pills that make them constipated. The kids feel better for a couple of days, but then suddenly they start getting flu-like symptoms and eventually end up with full blown malaria. [1]
What in the hell happened?
First, let’s review microbiology! Malaria is caused by a tiny parasite that reproduces in your blood cells. Malaria steals the iron within the blood cell and uses it to replicate. Once the parasite replicates over and over, it eventually bursts open the blood cells to liberate the baby bugs. Thankfully, your body has evolved mechanisms to prevent the spread of the bug within your system. Your body “hides” iron to prevent the spread of the infection. Hopefully by hiding the iron, you’ll be able to slow down the infection and maybe overcome it. [2] The problem is that when those well-meaning Samaritans gave iron to the kids, they were in fact overriding the evolutionary mechanisms that protect us from infection. [3]
No one expected that the iron deficiency could actually be caused by an underlying infection. Most importantly, supplementation to correct the nutritional deficiency exacerbated the malaria infection. The clinicians were only trying to “move the needle” by supplementing iron and make those numbers look better on paper.
The malaria example is drastic, but many intracellular organisms have evolved strategies for altering your nutrient status. For example, H. pylori creates “wear and tear” in your digestive system, and thus it creates malabsorption of nutrients like B-12. The wear and tear decreases stomach acid production, and thus it makes the stomach cozier for H. pylori to reproduce. The wear and tear of the stomach also causes malabsorption of nutrients like B-12. In lab tests, malabsorption could present as anemia or in extreme cases when the “wear and tear is bad enough, you could have signs and symptoms of an internal bleed. [4] If you merely supplement with vitamin B-12, you are not correcting the underlying cause of the nutritional deficiency, you are just treating the symptom.
Even thyroid function can be a victim to infections! For example, LPS the stuff that makes up the cell membrane of gram negative bacteria, affects thyroid function. In other words, your symptoms of hypothyroidism could be caused by an infection by gram-negative bacteria. [5]
My all-time favorite infection that affects your nutrient status is Lyme Disease. The intracellular organism responsible for Lyme actually downregulates the expression of the Vitamin D Receptor (VDR). This is important because vitamin D has many functions, from anti-inflammatory effects within the body to immune stimulation. Lyme disease actually evolved to disrupt the way our immune system responds to infection! [6]
If you want to learn if you are innapropriatly taking Vitamin D, check out this post by The Robust Human.
The point of this article is to highlight that some nutritional deficiencies might be caused by a clinical or subclinical infection. Having a poor diet is not the only reason we might have a low micronutrient status. I know I sound like a broken record, “Remove Obstacles to Health”.
References:
- Sales MC, de Queiroz EO, Paiva A de A. Association between anemia and subclinical infection in children in Paraíba State, Brazil. Rev Bras Hematol Hemoter. 2011;33(2):96-99. doi:10.5581/1516-8484.20110027.
- Gwamaka M, Kurtis JD, Sorensen BE, et al. Iron deficiency protects against severe Plasmodium falciparum malaria and death in young children. Clin Infect Dis. 2012;54(8):1137-1144. doi:10.1093/cid/cis010.
- Sazawal S, Black RE, Ramsan M, et al. Effects of routine prophylactic supplementation with iron and folic acid on admission to hospital and mortality in preschool children in a high malaria transmission setting: community-based, randomised, placebo-controlled trial. Lancet. 2006;367(9505):133-143. doi:10.1016/S0140-6736(06)67962-2.
- Faller G, Winter M, Steininger H, et al. Decrease of antigastric autoantibodies in Helicobacter pylori gastritis after cure of infection. Pathol Res Pract. 1999;195(4):243-246. doi:10.1016/S0344-0338(99)80041-7.
- Lohuis JA, Verheijden JH, Burvenich C, van Miert AS. Pathophysiological effects of endotoxins in ruminants. 2. Metabolic aspects. Vet Q. 1988;10(2):117-125. doi:10.1080/01652176.1988.9694158.
- Lu R, Wu S, Xia Y, Sun J. The Vitamin D Receptor, Inflammatory Bowel Diseases, and Colon Cancer. Curr Colorectal Cancer Rep. 2012;8(1):57-65. doi:10.1007/s11888-011-0114-1.