Thank you, Drs. Auerbach, DeLoughery, Lim, Rodgers, and Dr. Cifu. I appreciate the opportunity to engage in a collegial exchange on topics such as this.
I am always taken aback when recommendations based on low-level evidence such as these make it into clinical guidelines. Observational studies and surrogate measures, taken out of clinically meaningful context, often lead to correlations that are inconsistent with the principles of evidence-based medicine. To me, high-quality guideline recommendations should imply that we can identify, with an acceptable level of uncertainty, a target population in which implementing a treatment is expected to achieve a desired clinical outcome that exceeds the placebo effect while maintaining an acceptable risk-benefit balance. This should be the foundation of guideline recommendations.
Instead, I see low-level correlations being incorporated into guidelines and subsequently becoming the new standard of care. I would argue that, for a condition as prevalent as iron deficiency in women, it should be easy to demonstrate a clinically meaningful benefit in an adequately powered randomized controlled trial (RCT). If observational studies suggest an impact after only three years in pregnancies complicated by iron deficiency, I would gladly wait three years for a more robust recommendation. Why isn't this being done?
What we are seeing instead is that a low-level recommendation becomes the standard of care, making it virtually impossible to disentangle evidence from correlation. By endorsing such recommendations, we risk ensuring that, as a scientific profession, we will never know whether our interventions truly improved outcomes.
The downside of identifying iron deficiency is that it often triggers a cascade of additional tests and investigations to determine the underlying cause. What is the plan once the cause is identified? Lifelong iron replacement? Oral or intravenous iron? Hormonal therapy? Myomectomy? Hysterectomy? Upper and lower gastrointestinal endoscopy? What are the downstream risks of pursuing this diagnostic pathway?
I believe epidemiologists and population health experts should play a much larger role in developing population-level clinical guidelines precisely because they are trained to address these questions. Yet they are underrepresented.
There is so much garbage and weak evidence that garners high level “guideline recommendations” in my field these days that the use of “guidelines” to justify something instantly triggers the “high” setting on my BS detector.
Interesting post. I agree with the majority here who don't appreciate recommendations based on low-level evidence, observational studies, and surrogate endpoints. From the description in your article, you've made it sound like "iron deficiency without anemia" has a very specific set of symptoms that are frequently being "overlooked" or ignored. Absolutely don't agree. I have seen many women with many of the symptoms you note. Have treated many for low ferritin levels and have definitely NOT seen a good correlation that the woman feels tremendously better once ferritin is within desired range. Maybe the one, very specific symptom would be pica. That I'd believe. But brain fog, musculoskeletal pain, fatigue, etc? No. Sure, there may be overlap and it happens, but not as specifically as pica.
The one area I'd love to see studied in this whole iron deficiency/low ferritin issue: do a RCT to see if screening women for low ferritin levels, then treating them with supplemental iron to reach desired goal range would do anything to decrease the risk of RLS. The difficulty with all of this is the broad age range we'd be dealing with - when does it make sense to check and supplement, etc.
For all of us in medicine, I honestly think we rely too much on "symptoms" and would do better with population level studies and data. Having witnessed the interplay of Mind Body connection, it is quite clear that there are significant number of our population that simply perceive symptoms more readily than others, develop some degree of anxiety regarding these symptoms, present to medical practitioners more readily and thus are tested much more than other people. Even a person who simply feels that a yearly physical or seeing a clinician at least yearly (which we encourage) is going to be tested significantly more than people who just don't pay as much attention to symptoms or recommendations. The longer I practice, the more convinced I am that aside from periodic checks to "know your numbers" (blood pressure, blood sugar, cholesterol) that seeing a health care provider "regularly" does not equate to healthier and longer lives.
Key difficulties here are: 1. the non-specificity of so-called "iron deficiency symptoms", 2. establishing causality between non-specific symptoms and iron deficiency, and 3. defining "normal" ferritin values, especially when number 3 depends on number 2.
This is not to say that iron deficiency does not cause symptoms.
But to be honest I see a similarity here with covid brain fog and so on.
RCTs demonstrating benefits of oral/iv iron in clinically relevant outcomes are paramount, and there are too few/any.
I wanted to mention this in my reply, but feared getting into a parallel discussion.
This is exactly like vitamin D!
We measure something that makes sense in particular contexts, then extrapolate our findings to an entire population, and suddenly everyone is found to be "abnormal."
An infinite number of studies and reviews fail to demonstrate a benefit of vitamin D supplementation. But from emerging evidence to expert recommendations to guidelines, well, this is where we are.
In Quebec, where we have public reimbursement for medications, vitamin D is the #1 medication expenditure. We publicly reimburse something that has a null effect for huge amounts of money (it adds up)!
Costs aside, iron deficiency without anemia is worse because it implies an underlying pathology that needs to be investigated. So imagine the resource expenditure on investigations, follow-up appointments, and treatments if the effect is ultimately found to be null.
Here is a link to the latest on vitamin D for those who are interested:
Calcium, vitamin D, or combined supplementation to prevent fractures and falls: systematic review and meta-analysis.
Current evidence seems correct that old ferritin normals were too low.
The current fad for aggressively treating a lab value is a problem.
I work in Pediatrics, fellowship in Pediatric Heme/Onc, and to read the literature you would believe a two year old who is fussy, having tantrums, not sleeping well, a poor eater, and who after starting day care now has a near constant runny nose obviously has low iron and needs treatment. In my decades doing this, we most often used to call that a normal 2 year old.
The science is minimal at best to show iron is the cause of a long list of nonspecific childhood and teen problems, most being in vitro. Most adult studies are poor quality, and some blinded/placebo studies show no benefit for at least fatigue with IV iron.
The rhetoric about the problems with worldwide iron deficiency is true but not very relevant to the US and Western Europe. Dengue is a serious worldwide health concern, but most I hope would be reluctant to say dengue testing should be routine for anyone in Toronto with a fever.
Perhaps this is a new discovery that millions of children and adults are suffering from low iron, but after decades of cure-alls with vitamin C, zinc, vitamin E, vitamin D, I prefer to not too quickly jump in.
In the absence of a persuasive explanation for iron deficiency, such as in a young blood donor or in a young female with menorrhagia, should individuals with non-anemic iron deficiency be considered for GI studies?
My ferritin was 13 in April. In 2021, it was 4, and my hemoglobin was low, so I did receive an anemia diagnosis then. Now, I am just iron deficient. I have had a colonoscopy, two pelvic ultrasounds, and lots of repeat labs. I have felt lousy since before the ferritin of 4. But, I am also going through perimenopause. It is hard to know what is what. One doctor says a ferritin of 4 is bad but 13 is fine. Another says anything under 50 isn’t optimal. I have zero interest in a transfusion. I try to supplement, but it is difficult to time it around coffee and calcium and other things that inhibit absorption. The lucky iron fish was not for me. Not to mention, I wasted lots of money on iron supplements that ripped my stomach apart. I am also not interested in an IUD, ablation, or hysterectomy.
When a new screening recommendation is proposed I ask myself "What other health issue has to be deprioritized?" Such decisions don't happen in a vacuum and it's not just the screening but what action needs to be taken and how it affects our hematology colleagues. It's a great discussion but the fallout is rarely addressed as deeply as the action.
Nowhere in this post do I see ANY mention of evidence that action based on a diagnosis of asymptomatic iron deficiency (without anemia) changes outcomes.
So im left to wonder about the basis for the enthusiasm of the authors for their advocacy of ferritin-based screening and therapy.
I’m open to some carve-out for subgroups like pregnancy. And I’m not an OB so this might be my ignorance showing. But if the scourge of iron deficiency in pregnancy is as prevalent as the authors suggest, then how has humanity made it this far, thus far?
The authors also claim that “normal ranges” are inaccurate due to the possible inclusion of sickly folk among the “apparently healthy cohort”. But this can be levelled literally towards ANY and ALL lab tests with normal ranges (ie almost all of them). Asymptomatic hyponatremia, anyone?
There is value in your concern about outcomes assessments. But your line sardonically asking how humanity has made it this far seems poorly conceived as humanity has survived many examples of poorly understood and poorly treated health issues. Further, your example of asymptomatic hyponatremia is a poor example for your concern about the determination of "normal" lab values in an "apparently healthy cohort." While there is a legitimate concern about how "healthy" cohorts are established in the determination of "normal" values, an individual with "hyponatremia" would be considered outside of the range of the "apparently health cohort."
I agree that humanity has survived many prior health issues and managed to overcome significant ignorance in the past. Life expectancy increases alone quantitate such progress. But those observations are based on outcome evidence. I’ve yet to see any such evidence in the niche addressed by the authors here. And the burden of proof lies with them.
I was clumsy with the sodium example. The point is that, while we accept lower limit of normal at 135, by the authors’ contention maybe it should be 140 (if only we could have a “truly healthy cohort”). So woe becometh those poor sops who feel well with a Na of 136. I’d also note that there’s no money in fluid restriction.
With the orthorexia we see more nowadays, “ I don’t eat anything that has a face “, to actual fruiterians, just like with twins-studies, go do research on the ones that are more prone to the ferropenia and see how they fare ? Normal is not a term to be used in court …..
From my interpretation of the RCT-level evidence I know, giving iron to non-anemic non-pregnant patients doesn't improve much, at the cost of adverse events (GI if oral iron / IV-related if IV)
This is my issue with population-level screening and lab values in general: Second, while it has been suggested that normal ferritin values should reflect the statistical distribution observed in a general, “otherwise healthy” population, this approach assumes that the reference population is free of underlying pathology.
Recommendations and guidelines are made for the "average person" without knowing whether that "average person" actually had underlying health issues that were not identified. Population lab values do not tell the provider whether they represent the state of health of the patient in front of them.
As a female who has birthed and raised 5 children, I absolutely agree that pregnant women should have their ferritin levels tested, but I disagree that the entire population should. In my opinion, practitioners should be better educated about ferritin levels and be more willing to assess them when the patient's Hgb is "normal" but still feels "off."
Finally, I have concerns with the typical iron replacement products; basically, buy a cast-iron skillet, shave off pieces, and drink them.
I think this is spot on, and gets to the heart of the issue of possible symptomatic iron deficiency, and the idea that frank anemia represents a later manifestation of depleted iron stores.
But the authors kind of lose me a bit when they say that 84% of pregnant women are iron deficient. At what point is that, by definition, normal?
Because of the increased maternal blood volume needed to support the baby and the birthing process, most women are advised to take prenatal vitamins containing iron. However, I suspect (as supported by their data) that the iron supplementation (see my previous comment about the average iron supplement), while maintaining Hgb levels within "normal," is not replenishing iron stores, as measured by ferritin levels. The average ob/gyn does not measure ferritin levels but only hemoglobin and hematocrit.
Balderdash. Where’s the meat? (Pun intended.) all these symptoms are so vague. It sounds like the mitral valve prolapse of this decade. You wanna write guidelines? Do a large placebo controlled randomized double blind study and then replicate it. It will be just like Vitamin D-raise it has much as you want and it won’t do one thing valuable to a patient. In England they call this disease mongering.
I agree with the authors here. As a hematologist, I often see the end result of missing the “borderline” patient, and I do think our ferritin cutoffs are often too conservative. Doing more in medicine is not always better, and iron deficiency still needs to be diagnosed thoughtfully.
But this is a cheap blood test, and treatment is safe, effective, and available over the counter. Waiting for patients to become symptomatic or anemic before acting is reactive medicine. Avoiding morbidity by recognizing early iron deficiency will ultimately save the system $ as well.
Agree entirely on the ferritin (and probably female hemoglobin) cutoffs being too low. Also agree on the point that there are people who are symptomatic or "pre-symptomatic" due to iron deficiency that are currently missed.
Here's a nice little randomized, placebo-controlled study showing a benefit of iron supplementation for women with fatigue, ferritin <50, and hgb > 12. The effect on hematologic markers was most notable on those with hgb 12-13:
At the same, time, I can't see that there is good evidence for universal screening, and certainly not for the cost effectiveness of universal screening.
Study cited has issues: wide confidence interval; no improvement in QOL despite “improvement in fatigue “, only 1-2% of screened population actually presented with fatigue as Chief Complaint, obvious blinding issues with stool color changes /GI sx.
I’d bet a steak dinner it’s more cost effective than 90% of preventative care interventions we currently do. Compare the number of vitamin D levels you see compared to ferritin levels you see in the charts…
Thank you, Drs. Auerbach, DeLoughery, Lim, Rodgers, and Dr. Cifu. I appreciate the opportunity to engage in a collegial exchange on topics such as this.
I am always taken aback when recommendations based on low-level evidence such as these make it into clinical guidelines. Observational studies and surrogate measures, taken out of clinically meaningful context, often lead to correlations that are inconsistent with the principles of evidence-based medicine. To me, high-quality guideline recommendations should imply that we can identify, with an acceptable level of uncertainty, a target population in which implementing a treatment is expected to achieve a desired clinical outcome that exceeds the placebo effect while maintaining an acceptable risk-benefit balance. This should be the foundation of guideline recommendations.
Instead, I see low-level correlations being incorporated into guidelines and subsequently becoming the new standard of care. I would argue that, for a condition as prevalent as iron deficiency in women, it should be easy to demonstrate a clinically meaningful benefit in an adequately powered randomized controlled trial (RCT). If observational studies suggest an impact after only three years in pregnancies complicated by iron deficiency, I would gladly wait three years for a more robust recommendation. Why isn't this being done?
What we are seeing instead is that a low-level recommendation becomes the standard of care, making it virtually impossible to disentangle evidence from correlation. By endorsing such recommendations, we risk ensuring that, as a scientific profession, we will never know whether our interventions truly improved outcomes.
The downside of identifying iron deficiency is that it often triggers a cascade of additional tests and investigations to determine the underlying cause. What is the plan once the cause is identified? Lifelong iron replacement? Oral or intravenous iron? Hormonal therapy? Myomectomy? Hysterectomy? Upper and lower gastrointestinal endoscopy? What are the downstream risks of pursuing this diagnostic pathway?
I believe epidemiologists and population health experts should play a much larger role in developing population-level clinical guidelines precisely because they are trained to address these questions. Yet they are underrepresented.
Absolutely.
Well said. I agree.
There is so much garbage and weak evidence that garners high level “guideline recommendations” in my field these days that the use of “guidelines” to justify something instantly triggers the “high” setting on my BS detector.
Show me RCT evidence, or stop wasting my time.
Interesting post. I agree with the majority here who don't appreciate recommendations based on low-level evidence, observational studies, and surrogate endpoints. From the description in your article, you've made it sound like "iron deficiency without anemia" has a very specific set of symptoms that are frequently being "overlooked" or ignored. Absolutely don't agree. I have seen many women with many of the symptoms you note. Have treated many for low ferritin levels and have definitely NOT seen a good correlation that the woman feels tremendously better once ferritin is within desired range. Maybe the one, very specific symptom would be pica. That I'd believe. But brain fog, musculoskeletal pain, fatigue, etc? No. Sure, there may be overlap and it happens, but not as specifically as pica.
The one area I'd love to see studied in this whole iron deficiency/low ferritin issue: do a RCT to see if screening women for low ferritin levels, then treating them with supplemental iron to reach desired goal range would do anything to decrease the risk of RLS. The difficulty with all of this is the broad age range we'd be dealing with - when does it make sense to check and supplement, etc.
For all of us in medicine, I honestly think we rely too much on "symptoms" and would do better with population level studies and data. Having witnessed the interplay of Mind Body connection, it is quite clear that there are significant number of our population that simply perceive symptoms more readily than others, develop some degree of anxiety regarding these symptoms, present to medical practitioners more readily and thus are tested much more than other people. Even a person who simply feels that a yearly physical or seeing a clinician at least yearly (which we encourage) is going to be tested significantly more than people who just don't pay as much attention to symptoms or recommendations. The longer I practice, the more convinced I am that aside from periodic checks to "know your numbers" (blood pressure, blood sugar, cholesterol) that seeing a health care provider "regularly" does not equate to healthier and longer lives.
As a psychiatrist treating low ferritine proves to be an excellent first line intervention, be it placebo or not
Key difficulties here are: 1. the non-specificity of so-called "iron deficiency symptoms", 2. establishing causality between non-specific symptoms and iron deficiency, and 3. defining "normal" ferritin values, especially when number 3 depends on number 2.
This is not to say that iron deficiency does not cause symptoms.
But to be honest I see a similarity here with covid brain fog and so on.
RCTs demonstrating benefits of oral/iv iron in clinically relevant outcomes are paramount, and there are too few/any.
This subject reminds me of the "Vitamin D pandemic" - https://www.nejm.org/doi/full/10.1056/NEJMp1608005
Thank you for bringing up vitamin D.
I wanted to mention this in my reply, but feared getting into a parallel discussion.
This is exactly like vitamin D!
We measure something that makes sense in particular contexts, then extrapolate our findings to an entire population, and suddenly everyone is found to be "abnormal."
An infinite number of studies and reviews fail to demonstrate a benefit of vitamin D supplementation. But from emerging evidence to expert recommendations to guidelines, well, this is where we are.
In Quebec, where we have public reimbursement for medications, vitamin D is the #1 medication expenditure. We publicly reimburse something that has a null effect for huge amounts of money (it adds up)!
Costs aside, iron deficiency without anemia is worse because it implies an underlying pathology that needs to be investigated. So imagine the resource expenditure on investigations, follow-up appointments, and treatments if the effect is ultimately found to be null.
Here is a link to the latest on vitamin D for those who are interested:
Calcium, vitamin D, or combined supplementation to prevent fractures and falls: systematic review and meta-analysis.
BMJ. 2026;393. doi: https://doi.org/10.1136/bmj-2025-088050 (Published 20 May 2026).
Current evidence seems correct that old ferritin normals were too low.
The current fad for aggressively treating a lab value is a problem.
I work in Pediatrics, fellowship in Pediatric Heme/Onc, and to read the literature you would believe a two year old who is fussy, having tantrums, not sleeping well, a poor eater, and who after starting day care now has a near constant runny nose obviously has low iron and needs treatment. In my decades doing this, we most often used to call that a normal 2 year old.
The science is minimal at best to show iron is the cause of a long list of nonspecific childhood and teen problems, most being in vitro. Most adult studies are poor quality, and some blinded/placebo studies show no benefit for at least fatigue with IV iron.
The rhetoric about the problems with worldwide iron deficiency is true but not very relevant to the US and Western Europe. Dengue is a serious worldwide health concern, but most I hope would be reluctant to say dengue testing should be routine for anyone in Toronto with a fever.
Perhaps this is a new discovery that millions of children and adults are suffering from low iron, but after decades of cure-alls with vitamin C, zinc, vitamin E, vitamin D, I prefer to not too quickly jump in.
In the absence of a persuasive explanation for iron deficiency, such as in a young blood donor or in a young female with menorrhagia, should individuals with non-anemic iron deficiency be considered for GI studies?
Absolutely
My ferritin was 13 in April. In 2021, it was 4, and my hemoglobin was low, so I did receive an anemia diagnosis then. Now, I am just iron deficient. I have had a colonoscopy, two pelvic ultrasounds, and lots of repeat labs. I have felt lousy since before the ferritin of 4. But, I am also going through perimenopause. It is hard to know what is what. One doctor says a ferritin of 4 is bad but 13 is fine. Another says anything under 50 isn’t optimal. I have zero interest in a transfusion. I try to supplement, but it is difficult to time it around coffee and calcium and other things that inhibit absorption. The lucky iron fish was not for me. Not to mention, I wasted lots of money on iron supplements that ripped my stomach apart. I am also not interested in an IUD, ablation, or hysterectomy.
So, here I am. Chronically exhausted.
When a new screening recommendation is proposed I ask myself "What other health issue has to be deprioritized?" Such decisions don't happen in a vacuum and it's not just the screening but what action needs to be taken and how it affects our hematology colleagues. It's a great discussion but the fallout is rarely addressed as deeply as the action.
Nowhere in this post do I see ANY mention of evidence that action based on a diagnosis of asymptomatic iron deficiency (without anemia) changes outcomes.
So im left to wonder about the basis for the enthusiasm of the authors for their advocacy of ferritin-based screening and therapy.
I’m open to some carve-out for subgroups like pregnancy. And I’m not an OB so this might be my ignorance showing. But if the scourge of iron deficiency in pregnancy is as prevalent as the authors suggest, then how has humanity made it this far, thus far?
The authors also claim that “normal ranges” are inaccurate due to the possible inclusion of sickly folk among the “apparently healthy cohort”. But this can be levelled literally towards ANY and ALL lab tests with normal ranges (ie almost all of them). Asymptomatic hyponatremia, anyone?
There is value in your concern about outcomes assessments. But your line sardonically asking how humanity has made it this far seems poorly conceived as humanity has survived many examples of poorly understood and poorly treated health issues. Further, your example of asymptomatic hyponatremia is a poor example for your concern about the determination of "normal" lab values in an "apparently healthy cohort." While there is a legitimate concern about how "healthy" cohorts are established in the determination of "normal" values, an individual with "hyponatremia" would be considered outside of the range of the "apparently health cohort."
I agree that humanity has survived many prior health issues and managed to overcome significant ignorance in the past. Life expectancy increases alone quantitate such progress. But those observations are based on outcome evidence. I’ve yet to see any such evidence in the niche addressed by the authors here. And the burden of proof lies with them.
I was clumsy with the sodium example. The point is that, while we accept lower limit of normal at 135, by the authors’ contention maybe it should be 140 (if only we could have a “truly healthy cohort”). So woe becometh those poor sops who feel well with a Na of 136. I’d also note that there’s no money in fluid restriction.
Thank you for your reply.
With the orthorexia we see more nowadays, “ I don’t eat anything that has a face “, to actual fruiterians, just like with twins-studies, go do research on the ones that are more prone to the ferropenia and see how they fare ? Normal is not a term to be used in court …..
From my interpretation of the RCT-level evidence I know, giving iron to non-anemic non-pregnant patients doesn't improve much, at the cost of adverse events (GI if oral iron / IV-related if IV)
This is my issue with population-level screening and lab values in general: Second, while it has been suggested that normal ferritin values should reflect the statistical distribution observed in a general, “otherwise healthy” population, this approach assumes that the reference population is free of underlying pathology.
Recommendations and guidelines are made for the "average person" without knowing whether that "average person" actually had underlying health issues that were not identified. Population lab values do not tell the provider whether they represent the state of health of the patient in front of them.
As a female who has birthed and raised 5 children, I absolutely agree that pregnant women should have their ferritin levels tested, but I disagree that the entire population should. In my opinion, practitioners should be better educated about ferritin levels and be more willing to assess them when the patient's Hgb is "normal" but still feels "off."
Finally, I have concerns with the typical iron replacement products; basically, buy a cast-iron skillet, shave off pieces, and drink them.
I think this is spot on, and gets to the heart of the issue of possible symptomatic iron deficiency, and the idea that frank anemia represents a later manifestation of depleted iron stores.
But the authors kind of lose me a bit when they say that 84% of pregnant women are iron deficient. At what point is that, by definition, normal?
Because of the increased maternal blood volume needed to support the baby and the birthing process, most women are advised to take prenatal vitamins containing iron. However, I suspect (as supported by their data) that the iron supplementation (see my previous comment about the average iron supplement), while maintaining Hgb levels within "normal," is not replenishing iron stores, as measured by ferritin levels. The average ob/gyn does not measure ferritin levels but only hemoglobin and hematocrit.
"Both sides saw misogyny in the other’s view."
For God's sake, people. Get over yourselves.
Balderdash. Where’s the meat? (Pun intended.) all these symptoms are so vague. It sounds like the mitral valve prolapse of this decade. You wanna write guidelines? Do a large placebo controlled randomized double blind study and then replicate it. It will be just like Vitamin D-raise it has much as you want and it won’t do one thing valuable to a patient. In England they call this disease mongering.
“Opening a rich vein” is an interesting word choice here. Much appreciated.
😉
I agree with the authors here. As a hematologist, I often see the end result of missing the “borderline” patient, and I do think our ferritin cutoffs are often too conservative. Doing more in medicine is not always better, and iron deficiency still needs to be diagnosed thoughtfully.
But this is a cheap blood test, and treatment is safe, effective, and available over the counter. Waiting for patients to become symptomatic or anemic before acting is reactive medicine. Avoiding morbidity by recognizing early iron deficiency will ultimately save the system $ as well.
Agree entirely on the ferritin (and probably female hemoglobin) cutoffs being too low. Also agree on the point that there are people who are symptomatic or "pre-symptomatic" due to iron deficiency that are currently missed.
Here's a nice little randomized, placebo-controlled study showing a benefit of iron supplementation for women with fatigue, ferritin <50, and hgb > 12. The effect on hematologic markers was most notable on those with hgb 12-13:
https://www.cmaj.ca/content/184/11/1247
At the same, time, I can't see that there is good evidence for universal screening, and certainly not for the cost effectiveness of universal screening.
Study cited has issues: wide confidence interval; no improvement in QOL despite “improvement in fatigue “, only 1-2% of screened population actually presented with fatigue as Chief Complaint, obvious blinding issues with stool color changes /GI sx.
I’d bet a steak dinner it’s more cost effective than 90% of preventative care interventions we currently do. Compare the number of vitamin D levels you see compared to ferritin levels you see in the charts…