Iron Absorption, Hepcidin & Calories

Are you feeling ‘stuck’ with low and/or sub optimal iron levels, despite doing all the common right things? Does it feel like an uphill battle? Keep reading below!

By Noa Deutsch 10 min read
Iron Absorption, Hepcidin & Calories

Happy Thursday👋. A day late this week, I know… That’s the challenge of two posts in one week I suppose. There are new faces around here, which is exciting! If you are new, welcome. I am excited to have you & hope you are taking the time to dive in and go through the archives… If are reading this but haven’t subscribed yet, what are you waiting for?! Join our growing community below 👇

I think it is a well known fact that iron is very important for sports performance, right? Iron is especially important to athletes because of its role in processes like oxygen transport and energy metabolism, but it also happens to be an important requisite component of cytochromes and enzymes within the mitochondria, meaning iron is essential for brain development and cognitive performance.

Its no secret that athletes are at an increased risk of iron deficiency compared with sedentary individuals. Low iron stores can have a negative impact on the capacity for oxygen transport, motivation and cognitive functions like concentration and decision making ability.

But this article isn’t really about a deep dive into iron, it is about potential factors that might affect your ability to increase your iron levels. I have worked with athletes who do everything right. They take iron supplements, eat iron rich foods, mix various nutrients for better absorption, etc but still see no progress…

Are you feeling ‘stuck’ with low and/or sub optimal iron levels, despite doing all the common right things? Keep reading below for a bit of background info and some practical action steps!

Like many high performance athletes, I had issues with iron levels in the past, but not consistently, meaning I was not actually prone to it, it was always a result of other underlying issues. I had several minor issues with iron levels as a teen, which were resolved relatively quickly, but there were two more substantial times when my stores were crazy low: The first one was right before I was eventually diagnosed with Chronic fatigue syndrome (A bit about that here) and the second one was approximately a year after I had a copper IUD inserted. After each of those times, I supplemented with iron for a short duration (1st time was several injections, the second time was pills) and in each case my iron levels went back to my personal normal fairly fast. For reference, my normal levels over the last ~16 years seem to be over 80μg/l, which I consider myself lucky for, as I know many who struggle with very low and/or sub optimal iron levels.

Looking back, whenever I had iron issues, it seemed to be a part of bigger problems, mostly related to chronic under fueling and/or prolonged periods of chronic inflammation (with the exception of the copper IUD, which was an easy to fix ‘external’ problem). Keep reading to learn how that fits with some newer research.

How do we define iron deficiency?

Just so we are all on the same page… Here are the three stages of iron deficiency, with values that have been proposed for athletes (6):

  1. Stage 1 - iron deficiency (ID): iron stores in the bone marrow, liver and spleen are depleted: Ferritin<35 μg/L / haemoglobin >115 g/L / transferrin saturation>16%.
  2. Stage 2 - iron-deficient non-anaemia (IDNA): ferritin<20 μg/L / haemoglobin >115 g/L / transferrin saturation<16%.
  3. Stage 3 - iron-deficient anaemia (IDA): ferritin < 12 μg/L / haemoglobin <115 g/L / transferrin saturation<16%

For reference, I know many athletes who are really happy when their level go over 35μg/L into the ‘normal’ zone, and while that is certainly awesome progress, levels of 35-50μg/L are still considered sub optimal in athletes.

Hepcidin Basics

There has been a growing amount of work around the role of the liver-derived hormone hepcidin in iron metabolism.

While iron is very important, there is such a thing as too much of good thing and iron is a prime example of that. Iron is toxic in excessive quantities, so as a result, the body tightly regulates iron balance through absorption, which is regulated by hepcidin.

High levels of Hepcidin do the following:

  • Lower iron absorption
  • Release iron from storage form into the bloodstream using the iron exporter ferroportin

All of this is done with the goal of reducing iron stores to prevent overload.

What increases Hepcidin levels?

  • Iron overload
  • Chronic infection or Inflammation
  • Chronic or acute high intensity or endurance exercise

What lowers Hepcidin levels?

  • High iron requirements
  • When iron stores are very low

Iron status and hepcidin changes

Baseline iron status seems to play an important role in the regulation of hepcidin. Larger iron baseline stores mean a larger post exercise hepcidin response.

On the other hand, lower iron stores can cause a downregulation of hepcidin to improve iron absorption (9) - Its all a protective mechanism - It’s pretty smart, the human body! Those with not low, but still suboptimal iron levels (35-50μg/L) are at risk the most, because their post exercise hepcidin levels will be elevated, which will compromise absorption of dietary iron, making it hard to go past the sub optimal ‘slump’. This is an important point of consideration as to why so many athletes seem to be ‘stuck’ in those not low but still sub optimal levels for prolonged periods of time!

Its fairly basic knowledge that hard training promotes inflammation and depletes glycogen and one of the consequences is increases in Interleukin-6 (IL-6), which in turn leads to an increase in hepcidin, which reduces iron absorption and might contribute to the decline in iron status often seen after hard training sessions.

Hepcidin levels are significantly elevated at 3, 6 and 24 hours after exercise, so hard, frequent training sessions increase the risk of iron deficiency and/or have an impact on iron absorption (8).

Nutrients and Hepcidin

Can various nutrients have an effect on hepcidin? Maybe… Sadly, we don’t seem to know enough about that at this time.

Vitamin D - There is mixed research around the effect of vitamin D supplementation. There has been some evidence suggesting that vitamin D supplements can affect hepcidin levels in non athletes. On the other hand, a different research paper showed no affect on hepcidin in athletes, potentially due to research limitations, but most likely due to the fact that vitamin D levels were already sufficient in the athletes taking part in that study.

Carbohydrate intake - Its fairly basic knowledge that hard training promotes inflammation and depletes glycogen and one of the consequences is increases in Interleukin-6 (IL-6), which in turn leads to an increase in hepcidin. Acute post exercise carbohydrate intakes does not seem to have an effect on IL-6 and hepcidin responses (11), but overall low muscle glycogen stores may increase hepcidin levels after training (4, 7). There is a lot more research to be done in this area!

Iron supplements - Acutely increase hepcidin production, so lower doses (ie. 40-80 mg Fe) and avoiding twice-daily supplementation can maximize absorption. The duration of the hepcidin response supports supplementing every other day, in addition to the fact that it may be easier on the stomach, depending on the supplement and the individual.

Overall caloric intake - This is an interesting one, and newer research is starting to emerge, mostly in military populations undergoing heavy training loads. A 2021 study (1) found that energy deficit during training increased hepcidin levels, negatively affecting iron absorption compared with energy balance, meaning that making sure you are maintaining appropriate energy balance to supports your training is important to prevent iron level and absorption woes (not to mention a whole lot of other issues… see intro to RED-S article).

Those with reduced overall caloric intake are likely not able to get enough iron from diet alone. Sadly, it could be a chicken vs egg scenario as low iron stores are known to decrease appetite and impair metabolic efficiency (and affect thyroid function, too), all leading to potentially eating even less, making it harder to break the cycle. The area is lacking in research right now, but the little evidence we do have on both caloric and carbohydrate availability is compelling and I am sure more studies are being done (or planned) as I write this.

For the Women

Female athletes are more at risk of iron deficiency due to menstruation, especially those with heavy bleeding. The menstrual cycle influences cytokine production, causing inflammation at different times within the cycle, which in turn influences the hepcidin response.

Testosterone has been reported to have a suppressive effect on hepcidin, while the effect of female sex hormones estrogen and progesterone (and their synthetic forms estradiol and progestogens) are less clear. There is some evidence the effect of estrogen on hepcidin is similar to that of testosterone, but there isn’t enough research around that and there are too many factors influencing it, in particular birth control use (ie. the pill). There is even less we know about the role of progesterone (and its synthetic form progestogens) on iron metabolism (6)

Next week’s publication is all about training with the menstrual cycle, so I will gather more resources to provide more information on this then.

Takeaway messages / In Practice

The moment you have all been waiting for (unless you just scrolled straight here 😂🤔 ) - What can you actually do with all this information if your end goal is to increase your iron stores?!