What a long deficit costs beyond calories

1. The carrier, not the calories

Think about what actually leaves the plate in week three of a descent. Almost nobody removes an even slice of their diet. They remove the things that are easy to remove: the rice, the bread, the oily fish that felt indulgent, the fruit that was "just sugar", the dairy that bloated them, the red meat that was heavy before sparring. What is left is chicken, greens, eggs and whatever fits under the number.

That is a narrower diet, not just a smaller one, and the position stand written for this sport says so plainly:

"A well-balanced diet may provide sufficient micronutrients, but combat athletes who practice rapid weight-loss or eliminate whole food groups may be at risk of nutrient deficiencies."

Note the two conditions in that sentence. Rapid weight loss, or eliminating whole food groups. Most fight camps do both, in sequence. The elimination starts early because it is painless and the rapid loss finishes late because it has to.

None of that is a diagnosis. It is a description of the conditions under which one becomes more likely, which is a different and weaker claim — and it is the honest one, because almost nobody has drawn blood from a fighter in the middle of a camp to find out.

2. What was actually measured in weight-category athletes

Here is the closest thing this literature has to a direct answer, and it is a small one.

Eleven male NCAA Division I wrestlers, mean age 21.3±1.7 years with 14.9±2.5 years of experience, had their intake recorded by diet record during preseason — not during a fight-week cut — and compared against estimated total energy expenditure. Eight of the eleven, 73%, were eating below their estimated expenditure, with a mean intake of 2,601 kcal. The authors' own sentence on the micronutrient side:

"Intakes for vitamin A, vitamin E, vitamin D, and potassium were below the RDA in at least five out of eleven wrestlers (45%)"

Two things about that finding are load-bearing and get dropped constantly when it is repeated.

The first is that intake below an RDA is not a deficiency. No blood status was measured in that study. An RDA is a population-level intake figure set to cover almost everybody's requirement; an individual eating below it on a given week is not thereby depleted, and someone eating above it is not thereby replete. The measurement tells you the diet narrowed. It does not tell you the athlete did.

The second is that iron was not among the four. In the one weight-category cohort with nutrient-level data, the nutrients that fell short were A, E, D and potassium. That is worth saying because iron is the nutrient fighters buy, and it is not the one this cohort was measurably short of — though the cohort was male, and sex is the single largest moderator in the iron story.

A wider look does not improve the picture. A systematic review of body composition and dietary intake in combat sports reported that across the literature only two studies met energy-intake recommendations and only one met carbohydrate recommendations, with low energy and carbohydrate intake appearing in reference periods as well as pre-competitive ones. We hold that at secondary confidence — the publisher returned a 403 to our fetch and the study counts, sample sizes and sex split could not be confirmed — but it points the same way as everything else: the measured problem in combat athletes is energy and carbohydrate, and the micronutrient story runs downstream of it.

3. Iron, and why it gets the most space

Iron gets the most space here for three reasons: it is the best-evidenced nutrient in this article, it has the clearest performance consequence, and it is the one where acting without a test can hurt you.

Start with the split. Across athlete populations, iron deficiency without anaemia affects roughly 15–35% of female athletes against 5–11% of male athletes. Those are two different disease prevalences in two different populations. They are not one number with a coefficient applied, and nothing in this literature licenses converting between them.

The most careful body of evidence sits on the female side: a systematic review of 23 studies covering 669 female athletes aged 13 to 47, across 16 sports and four performance tiers, with 62% drawn from aerobic-dominant disciplines. Combat sports are barely represented in it, and everything below inherits that limitation.

What that review found, with its conditions attached:

• Iron deficiency in the review was defined as serum ferritin below 40 µg/L, used as the single homogeneous biomarker across studies — and the authors flag that ferritin is an acute-phase protein influenced by exercise-induced inflammation.
• Iron deficiency was associated with a 3–4% decrement in endurance performance across the 23-study set.
• Isokinetic strength and anaerobic power in iron-deficient athletes ranged from −23% to +4%, and supplementation effects from −5% to +9%. Both ranges span zero. That is not a reliable strength effect and must not be reported as one.
• Maximal aerobic capacity effects of deficiency ranged from −6% to +4%; supplementation raised capacity 6–15%, particularly in athletes with serum ferritin below 16 µg/L, across trials running 36 to 126 days.

The review also stages the condition, and the staging is the part a reader should take away:

• IDNA-1: serum ferritin below 30 µg/L with transferrin saturation above 16%.
• IDNA-2: serum ferritin below 20 µg/L with transferrin saturation below 16%.
• IDA-3: haemoglobin below 120 g/L with compromised erythropoiesis.

Those are female-athlete definitions. The haemoglobin cut is a female cut, and every one of those numbers is assay- and laboratory-dependent. They are printed here to show that the condition has stages, not to give anyone a line to measure themselves against.

The authors' own summary of why the staging matters:

"IDNA-1 and -2 athletes do not typically exhibit compromised Hb concentration, thus performance decrements…may become more pronounced in IDA-3 athletes."

In plain terms: you can be iron deficient with a completely normal haemoglobin, and a full blood count alone will not find it. That is the deficiency-without-anaemia distinction, and it is why the assessment is iron studies rather than a routine blood count.

4. Why a fighter loses iron faster than they think

The mechanisms are unglamorous and mostly mechanical. A narrative review lists them as "foot strike hemolysis, thermochemolytic sweat loss, exercise-induced ischemia leading to gastrointestinal iron loss, hematuria," with reduced absorption on top via interleukin-6-driven hepcidin surges. Sweat contributes up to 22.5 µg of iron per litre, which is small next to the other routes — worth knowing, not worth headlining.

Hepcidin is the part that matters in a deficit, because it is the switch that decides how much of what you eat gets absorbed. The mechanism, verbatim from a 2026 study:

"IL-6 level stimulates hepcidin production with the resultant degradation of ferroportin and retention of iron within macrophages and enterocytes, limiting delivery to erythroid precursors."

Hard training raises IL-6. IL-6 raises hepcidin. Hepcidin shuts down absorption and locks iron away inside cells. That happens at the exact point in a camp when intake is lowest, which is why a deficit and a hard training block are a worse combination for iron than either would be alone.

And there is a specific, measured finding about how the cut is done. In the IOC consensus, a three-day low-energy, low-carbohydrate diet produced a 264% increase in hepcidin, against a 69% increase on an isocaloric low-energy higher-carbohydrate diet. That condition must never come off the number: three days, young females, a small sample, an isocaloric comparison. It is not a camp and it is not a fighter. But it is the only direct evidence on this sheet that the composition of a deficit changes iron handling independently of its depth, and carbohydrate is the first thing most fight camps cut.

The consensus also reports that short-term low carbohydrate availability, sometimes without low energy availability, raised bone resorption markers, impaired bone formation markers, and raised post-exercise IL-6 and hepcidin — in studies of six days or fewer, in male endurance athletes, with low-carbohydrate defined as under 3 g/kg body mass per day. Around 3.5 weeks of the same approach in elite endurance athletes impaired bone remodelling markers at rest and up to three hours after exercise.

5. Why the blood test can lie in the direction that reassures

This is the section a fighter with a "normal" result should read twice.

Ferritin is an acute-phase protein. It rises with inflammation. A ferritin drawn the morning after a hard session reads higher than the same athlete's true stores, which means the reassuring result and the depleted athlete can be the same person on the same day.

The clearest demonstration is small and extreme. Seven elite athletes ran an 86.9 km trail race with over 6,500 m of ascent, median duration twelve hours. Serum iron and transferrin saturation fell while hepcidin and ferritin both rose, and their peripheral blood mononuclear cells "behaved as though they were iron-deprived" despite the increased plasma ferritin. Seven people, one extraordinary stimulus, nothing like a fight camp. Use it only for what it demonstrates: a single ferritin value, drawn at the wrong moment, can move in the opposite direction to the thing it is meant to measure.

The IOC's framing solves this, and it is a framing rather than a number:

"Chronically poor or sudden decline in iron studies (eg, ferritin, iron, transferrin) and/or haemoglobin"

A trend. Not one reading. Which means a baseline drawn early in camp, when the athlete is still relatively fresh and still eating, is worth more than a single panel in week ten — and that a result in week ten is close to uninterpretable without the earlier one.

The consensus is equally clear about what to order and how to read it:

"Iron studies (iron, ferritin, transferrin, total iron binding capacity) with age-appropriate, sex-appropriate and laboratory-appropriate cut-offs"

Clinical laboratories, the World Health Organization and sports medicine do not use the same ferritin cut-off, and the IOC's instruction is to interpret iron studies against age-appropriate, sex-appropriate and laboratory-appropriate cut-offs. There is no single right number to print, which is the reason this is a conversation with whoever ordered the test.

6. Low iron in a cut is not automatically "the diet"

One more thing the consensus does that an article about deficits should not skip. It lists, under impaired haematological status, the outcomes it associates with REDs — low iron status, increased hepcidin concentrations and response, reduced iron absorption, lower haemoglobin concentration and mass, and a reduced response to altitude training — and then says each of those "can occur in the absence of LEA; therefore a differential diagnosis should always be considered."

Its differential list, verbatim:

"acute or chronic blood loss (eg, menstrual cycle, GI bleeding), RBC destruction (eg, haemolysis, haemoglobinopathy, splenomegaly), poor micronutrient intake (eg, iron, vitamin B12, folate), bone marrow diseases"

Read that as a fighter with a low ferritin and a twelve-week deficit. The deficit is one candidate explanation sitting in a list that also contains gastrointestinal bleeding and bone marrow disease. Deciding it is the diet, buying iron, and feeling slightly better is the route by which a treatable and serious condition gets six months older. That is a clinician's decision tree, and this is the point where the article's job ends and theirs begins. Our piece on low energy availability in combat sports covers how the consensus frames the wider syndrome.

7. The overload problem, which is why "just take some" fails

The common intuition is that iron is a low-risk bet: if you are low it helps, if you are not it does nothing. The measured data says otherwise.

A 2023 review reports 350 ng/mL as a threshold value used for iron overload, and — in 2005 data — that 30% of 88 professional male cyclists and 14% of 42 professional cross-country skiers exceeded it. None of those above the threshold carried HFE mutations, which implicates secondary, acquired overload rather than an inherited condition. That figure appears here as evidence that overload happens in real athlete cohorts, in athletes who look like high-performing endurance competitors rather than patients. It is not a ceiling for anyone to monitor themselves against, and it is not a reason to go and get a ferritin done privately so you can watch a number.

The review's own conclusion is the sentence to keep:

"Iron supplementation should remain medically supervised to prevent secondary overload and associated health consequences."

Put that next to the mechanism from section 4 and the reason self-treatment fails becomes structural rather than cautious. Fatigue in a deficit has many causes. Ferritin is confounded by inflammation in both directions. Absorption is being actively suppressed by hepcidin during hard blocks, so the same intake does not produce the same outcome in two athletes or in the same athlete in two weeks. And the downside is not "wasted money" — it is iron accumulating where it should not.

8. Vitamin D, read honestly from both sides

Vitamin D is where the prevalence data is strongest and the intervention data is weakest, and an article that gives only one of those halves is misleading regardless of which half it picks.

The prevalence half. A 2022 meta-analysis of 51 studies and 5,456 participants found insufficiency — defined as 25(OH)D below 50 nmol/L — in 30% of adult elite athletes (95% CI 22–39%) and 39% of adolescents (95% CI 25–55%). The adult sample was 3,592 participants, mean age 23.3 years, 76% male; the adolescent sample 1,432, mean age 16.4, 56% male. Pooled mean 25(OH)D was 66.4 (SD 30.4) nmol/L in adults and 60.0 (SD 33.6) in adolescents.

And a finding worth stating precisely because the assumption runs the other way:

"no significant difference in prevalence of insufficiency between males versus females RR (1.00; 95% CI 0.79–1.26)"

Vitamin D is not the sex-split nutrient in this article. Iron is.

The authors call their own estimates conservative, because only 12 of 30 adult studies and 6 of 15 adolescent studies were run in winter or spring — and seasonality is the largest single moderator, with prior work giving a relative risk of around 1.85 for winter or spring measurement, alongside latitude and probably indoor versus outdoor training. Skin pigmentation could not be analysed at all: "few eligible studies reported the race of the participants." That is a gap in the evidence, not a finding about anyone.

You will also meet a figure of 56%. Both numbers can be true at once, and the reason is the threshold: the 2015 meta-analysis reporting 56% inadequacy across 23 studies and 2,313 athletes (76% male) used a cut-off of 25(OH)D below 80 nmol/L, where the 2022 meta-analysis reporting 30% used below 50 nmol/L. Neither figure means anything without the threshold in the same sentence, and the thresholds themselves are contested.

The intervention half. A meta-analysis of 10 randomised controlled trials — 354 athletes randomised, 318 completing — found supplementation reliably raised 25(OH)D versus placebo, mean difference 14.76 nmol/L (95% CI 8.74–20.77, p<0.0001). Combined strength outcomes were not significant: SMD 0.18 (95% CI −0.02 to 0.37, p=0.08), with 1RM bench press at p=0.47, vertical jump at p=0.17 and handgrip at p=0.35. Only quadriceps contraction reached significance, at SMD 0.57 (95% CI 0.04 to 1.11, p=0.04) — a wide interval with a lower bound near zero, one positive among several nulls.

The authors' caution, verbatim:

"with limited available studies for the quantitative synthesis, it cannot warrant significant overall enhancements in muscle strength when athletes attain adequate serum 25(OH)D levels through supplementation"

So: status is measurably low in a large minority of athletes, and the randomised evidence that raising it improves strength in athletes is weak and mostly null. Both halves belong in the same paragraph, which is the reason they are here in one.

The consensus, for its part, names "poor micronutrient intake (eg, calcium and vitamin D)" inside the differential diagnosis for low bone mineral density — an alternative explanation a clinician rules out, alongside hyperparathyroidism, coeliac disease, malignancy, renal disease and anabolic steroid use. That is not an endorsement of supplementation. It is a list of things to exclude.

9. Bone: the part that may not come back

Everything else in this article is, in principle, reversible. You eat again, status recovers, and the cost was temporary. Bone is where that assumption breaks, and it deserves its own section because it is the strongest safety argument the evidence supports.

The IOC reports on a 12-month randomised controlled trial that increased energy intake in exercising females with REDs biomarkers:

"there was a high drop-out rate (57%), and improvement in some (eg, menstrual function resumption in select participants), but not all symptoms (eg, inability to retard bone loss)"

A year. Randomised. Energy deliberately restored. Menstrual function returned for some participants — and bone loss was not retarded. Whatever else that trial shows, it does not show that eating again fixes everything, on the timescale of a year, in the population most studied.

The observational picture is consistent with it. In a clinic-referred retrospective cohort of 82 elite athletes (25 female, 57 male, mean age 23.4±7.6; 56 strength and 26 endurance athletes, with 20 — 24.4% — diagnosed with REDs), the REDs-diagnosed athletes had markedly lower bone mineral density Z-scores than either group. Total hip: strength 2.10±1.06, endurance 1.41±0.70, REDs −0.94±0.81. Lumbar spine: strength 1.60±1.07, endurance 0.64±0.63, REDs −1.65±0.93. Both comparisons at p<0.0001. Within the REDs group, 6 of 19 (31.58%) had a spine Z-score below −2.0, and stress fractures had occurred in 70% of REDs athletes versus 25% of non-REDs (p<0.001). The authors describe "reduced bone formation alongside increased bone resorption," a catabolic bone metabolism.

That cohort is retrospective and clinic-referred — these are athletes who were sent to a clinic, which is not a random sample of anybody — and combat sports are not identified within it. It is an association in a selected group, not a rate a twelve-week cut produces.

The consensus's own bone indicators are worth knowing for the shape of them rather than the numbers:

"Pre-menopausal females and males <50 years old: BMD Z-score <−1 at the lumbar spine, total hip or femoral neck or decrease in BMD Z-score from prior testing"

Sex- and age-conditioned, and the trend counts as much as the level — the same structure as the iron guidance. For younger athletes the framing changes again: the adolescent indicator covers a decrease from prior testing that "can occur from bone loss or inadequate bone accrual." Failing to build bone is a distinct harm from losing it, and it is the relevant one for a teenager. This matters because a survey of 70 judoka found that 95.7% reported rapid weight loss, "typically beginning between ages 13 and 16 years" — exactly the window in which the skeleton is being built. No source here measured micronutrient status or bone in adolescent fighters, so that overlap is a mechanism with no combat-sport data behind it, and we are not going to pretend otherwise. Our companion piece on bone health in combat athletes goes further into the skeletal side.

10. The threshold everyone quotes, quoted properly

You will be given a number at some point: 30 kilocalories per kilogram of fat-free mass per day, offered as the line below which things go wrong. The consensus that made the figure famous does not endorse it. Its actual sentence:

"While a universal cut-off of 30 kcal/kg FFM/day as a threshold of LEA leading to some REDs outcomes in females is debated, such a cut-off or range at which males experience REDs-related symptoms is even less understood, but appears to be lower (eg, ~9 to 25 kcal/kg FFM/day)."

Debated. Not advocated — and the distinction is not pedantry, because the sentence is routinely repeated with the meaning reversed. The consensus adds that "there are risks in setting a definitive clinical threshold of EA due to many moderating factors," and elsewhere notes that the figure was derived from short-term laboratory studies in a small sample of sedentary females.

Two consequences follow for this article. The first is that the male range is not a coefficient-adjusted version of the female one. They are separate estimates from separate and much thinner literatures — the consensus states that only 20% of original REDs studies from 2018 to 2022 included male athletes. Nothing about sex differences in this field is closable with a multiplier, in either direction.

The second is that nothing downstream of a disputed threshold is a target either. Not an energy-availability figure, not a ferritin value, not a vitamin D level. If the anchor number is contested by the body that published it, a number derived from it cannot be treated as a floor a fighter manages themselves to.

11. B vitamins, zinc and magnesium: where marketing outruns evidence

This section is short because the evidence is.

The position stand written for combat sports puts it this way, in a sentence that is awkward in the original and is quoted exactly rather than tidied:

"Although micronutrients are considered essential for optimum health, their ability to function as ergogenic aids is unlikely, mainly when overt deficiency was present before vitamin and mineral supplementation."

Which is to say: correcting a real deficiency can restore function; adding nutrients to someone who is not deficient is not an ergogenic strategy.

B12 and folate appear in the IOC's differential for impaired haematological status — again, as things to rule out, not as things to take. Beyond that, the claims thin out fast. ZMA formulations are widely marketed for recovery, testosterone and "energy"; what evidence exists does not support performance benefit, and any testosterone effect appears confined to individuals who were already deficient. We hold that at low confidence because the literature on it is dominated by secondary and consumer sources rather than trials, and we would rather say that than dress it up. The same applies to the frequently repeated line that deficiencies in B2, B5 and B6 have minimal effect on performance — plausible, poorly sourced, and reported here as such.

Zinc, magnesium and the B vitamins have no strong athlete trial base in this article at all. That absence is itself the finding, and it should be read against how confidently these are sold.

What does have data is the pattern of use. Among 198 supplement-using athletes (105 female, 93 male; 44 collegiate at mean age 22.07±2.06 and 154 masters at mean age 40.19±11.05), collegiate males took more vitamin A, folate and magnesium than females; masters females took more calcium than males; powerlifters led on zinc and swimmers on iron. Self-reported, cross-sectional, no combat sports in the sport list, and no blood status measured in anyone. The authors' closing line is the honest summary of what is unknown:

"Further research should examine both dietary and micronutrient supplement intake among Collegiate and Masters Athletes to examine the extent that athletes exceed the Recommended Dietary Allowances."

Supplement use in athletes is patterned by sport and by sex. Whether it is patterned by need is a question the data cannot answer.

12. Should you just take a multivitamin?

It is the question everyone actually asks, and the same position stand contains both halves of the answer.

"Nonetheless, studies have highlighted that consuming a multivitamin can help athletes meet their daily micronutrient needs, which are higher compared to the general population."

Read what that says: meet intake needs. It does not say improve performance, and the same document — quoted in the previous section — says ergogenic effect is unlikely in the absence of overt deficiency. Both sentences are from the same authors, and they are consistent.

So the honest position is narrow. A multivitamin is plausible insurance against a narrowed diet. It is not a performance aid: no trial in the evidence assembled for this article shows a multivitamin improving athletic performance in a non-deficient athlete. An older trial of three months of multivitamin and mineral supplementation reportedly found no ergogenic effect on running performance in trained athletes, and a 2025 systematic review of randomised trials in elite athletes found consistent benefit for caffeine and sport-specific benefit for beta-alanine, with multivitamins not among the supplements showing consistent performance benefit — both of those are second-hand here, neither full text was retrieved, and we flag them rather than lean on them.

And it is not a substitute for the test. A multivitamin does not tell you whether your ferritin is falling, and taking one does not make the question go away. If the concern that sent you to the shelf was iron, the multivitamin is the wrong object entirely: the right one is an appointment.

13. Anything you take is your problem under the rules

If a deficiency is confirmed and something is prescribed, there is a second layer of risk that has nothing to do with physiology.

The 2026 WADA Prohibited List is the current List, in force since 1 January 2026; WADA revises it annually, publishing in October to take effect the following January. According to USADA's advisory on it, "For 2026, there is only one instance where a substance or method changes from permitted to prohibited (see section M.1 below)" — that instance being blood and blood-component withdrawal. Carbon monoxide is introduced separately as another change in 2026, with "the non-diagnostic use of carbon monoxide (CO) was added as a new section, M 1.4". Other reported 2026 changes — esters of prohibited steroids clarified as prohibited, pegmolesatide added as an EPO-mimetic example, an updated inhaled salmeterol dosing interval, and cell components including nuclei, mitochondria and ribosomes added under gene doping — come from national anti-doping agency summaries rather than the List itself, and we could not retrieve the primary WADA PDF.

On supplements specifically, USADA's language is qualitative and we are going to keep it that way: "any supplement an athlete chooses could contain dangerous, illegal or banned ingredients." We will not print a contamination percentage. The widely circulated "one in ten supplements is contaminated" comes from a testing laboratory's own marketing page, a competing search surfaces a range of 12% to 58% with no primary study behind it either, and both are ungroundable as stated.

Third-party certification reduces the risk and does not remove it. USADA states that "Using an NSF Certified for Sport® product significantly reduces, but does not necessarily eliminate, the chance of testing positive," and that if an athlete tests positive and establishes the source as a contaminated certified product, they "could get a much-reduced sanction, but there likely would still be a consequence." USADA currently recognises NSF Certified for Sport as the programme best suited for athletes to reduce supplement risk; other schemes exist and are used by other bodies. Informed Sport, run by LGC, describes itself as sampling, analysing and clearing every certified batch before sale and calls this "the highest level of assurance currently available to athletes" — that is the company's own description of its own programme. NSF states its programme screens for more than 270 substances on the WADA list plus substances banned by major professional leagues; also the company's own copy, though the USADA recognition half of it is corroborated by USADA itself.

Certification lowers the risk of a contaminated supplement. It does not transfer responsibility: under strict liability a contaminated certified product yields a reduced sanction, not none. If you compete under a testing programme, the substance that fixes your deficiency is a decision to make with your doctor and with whoever handles your anti-doping compliance. Our article on banned substances and supplement risk covers that side in detail.

14. What a monitoring plan looks like — and what it is not

Put the pieces in order and the practical shape is a monitoring plan, not a supplement plan.

Intake narrows before status falls. The wrestler cohort shows the first step: the diet gets smaller and narrower, four nutrients drop below the RDA in nearly half the squad, and nobody is deficient yet. That is the window in which a food log is genuinely useful, because it shows what left the plate. It is also the limit of what a food log can do — it records intake, and intake is not status.

The way you cut changes the biology, not just the arithmetic. Cutting carbohydrate hardest, which almost every camp does because it is the easiest lever, is the condition under which hepcidin rose 264% in that three-day comparison in young females. Less absorbed, at the moment least is eaten. If you want to see how the weight cut interacts with the rest of camp, that is one of the mechanisms.

Test the trend, early, with someone who can read it. A baseline in week one and a comparison later tells a clinician something a single panel in week ten cannot. The IOC's phrasing is "chronically poor or sudden decline in iron studies," and a decline needs two points. The sample timing matters too: a normal ferritin drawn the morning after a hard session is not evidence of adequacy.

Let the person who ordered the test decide what happens next. That is not a disclaimer bolted onto the end — it is what the evidence in this article actually supports. Cut-offs differ between laboratories and between clinical and sports-medicine practice, the differential for a low result includes conditions far more serious than a deficit, overload is documented in real athlete cohorts, and anything taken carries strict liability under the anti-doping rules. Nothing in that list is improved by a fighter picking a number.

And nothing here overrides a physician or a registered dietitian who has seen you. If a clinician has already tested you and made a plan, that plan wins over anything on this page.

What we could not verify

• The whole timeframe of this article is an evidence gap. No study we located measured micronutrient blood status in female combat athletes through an actual weight cut, and nothing measured anything across twelve weeks. The nearest evidence is a three-day carbohydrate manipulation, studies of six days or fewer, a 3.5-week low-carbohydrate protocol, a single race day and a 12-month trial in exercising females. Twelve weeks in a fighter is the reader's situation and nobody has measured it.
• Women in combat sports are barely measured at all. The wrestler cohort is 11 men. The judo survey is 17 women out of 70, by questionnaire, with no blood markers. The REDs bone cohort is 25 women out of 82 with combat sports unidentified. The female iron review is female-only but 62% aerobic-dominant sports.
• Adolescents and amateurs are absent. Rapid weight loss reportedly begins at 13 to 16 in judo and the consensus has a separate adolescent bone indicator covering inadequate accrual, but no source here measured micronutrient status in adolescent fighters. Every cohort in this article is collegiate, national or elite; none describes an amateur cutting weight around a full-time job.
• Any supplement contamination percentage. "One in ten supplements is contaminated" comes from a testing laboratory's marketing page; a competing claim of 12% to 58% is equally unsourced to a primary study. Both are ungroundable as stated, so we used USADA's qualitative language instead.
• The WHO's ferritin cut-off for iron deficiency. We saw it reported only second-hand and did not retrieve the WHO document, so the value does not appear here. It is mentioned only to make the point that the cut-offs disagree between bodies.
• A haemochromatosis prevalence figure. A commonly repeated prevalence for people of northern European descent traces only to a 2004 commentary abstract in our search and was not confirmed, so it does not appear as a number.
• Stress fracture reductions from dairy intake. An observational cohort of 125 female distance runners reportedly found large reductions associated with skim milk and a high-dairy dietary pattern. The fetch was blocked, it is female distance runners rather than combat athletes, and it would be an association in any case. We did not print the figures.
• A binge-eating rate from the judo survey. The retrieved text reported two irreconcilable figures in different places. We did not print either.
• A combat-sports systematic review's study counts, and its line about women needing stricter protection of energy availability, iron, calcium and vitamin D. The publisher returned a 403; we saw only a search summary and have flagged it as secondary wherever it appears.
• A REDs case study in an elite muaythai athlete was blocked by a captcha and never retrieved. Nothing from it appears here.
• The primary WADA 2026 Prohibited List PDF. The WADA page returned nothing to our fetch. All 2026 List detail here comes from USADA and national anti-doping agency summaries, and anyone citing a specific List clause should open the WADA document directly.
• Calcium intake in combat athletes. No measured data was located. The calcium story here is bone-outcome data plus a differential-diagnosis mention, not measured intakes in fighters.

Sources

Sourced to

1. International Society of Sports Nutrition position stand: nutrition and weight cut strategies for mixed martial arts and other combat sports — Ricci AA, Evans C, Stull C et al., Journal of the International Society of Sports Nutrition, 2025;22(1):2467909. DOI 10.1080/15502783.2025.2467909, PMID 40059405
2. 2023 International Olympic Committee's (IOC) consensus statement on Relative Energy Deficiency in Sport (REDs) — Mountjoy M, Ackerman KE, Bailey DM, Burke LM, Constantini N, Hackney AC, Heikura IA, Melin A, Pensgaard AM, Stellingwerff T, Sundgot-Borgen JK, Torstveit MK, Jacobsen AU, Verhagen E, Budgett R et al., British Journal of Sports Medicine, 2023;57(17):1073–1097. DOI 10.1136/bjsports-2023-106994, PMID 37752011
3. Nutrient Intake, Performance, and Body Composition of Preseason Wrestlers — Coapstick GJA, Barry AM, Levesque CL, Shoemaker ME, International Journal of Exercise Science, 2024;17(2):517–530. DOI 10.70252/DJES3022, PMID 38665328
4. Iron deficiency, supplementation, and sports performance in female athletes: A systematic review — Pengelly M, Pumpa K, Pyne DB, Etxebarria N, Journal of Sport and Health Science, 2025;14:101009. DOI 10.1016/j.jshs.2024.101009, PMID 39536912
5. The IRONy in Athletic Performance — Kardasis W, Naquin ER, Garg R et al., Nutrients, 2023;15(23):4945. DOI 10.3390/nu15234945, PMID 38068803
6. Long-distance trail running induces functional iron deficiency driven by inflammation — Tobiasch AK et al., Blood Advances, 2026;10(17):5836–5846. DOI 10.1182/bloodadvances.2025019105, PMID 42085607
7. Prevalence and novel risk factors for vitamin D insufficiency in elite athletes: systematic review and meta-analysis — Harju T, Gray B, Mavroedi A, Farooq A, Reilly JJ, European Journal of Nutrition, 2022;61(8):3857–3871. DOI 10.1007/s00394-022-02967-z, PMID 35882673
8. Effects of vitamin D3 supplementation on strength of lower and upper extremities in athletes: an updated systematic review and meta-analysis of randomized controlled trials — Han Q et al., Frontiers in Nutrition, 2024;11:1381301. DOI 10.3389/fnut.2024.1381301, PMID 38860160
9. Prevalence of Vitamin D Inadequacy in Athletes: A Systematic Review and Meta-Analysis — Farrokhyar F, Tabasinejad R, Dao D et al., Sports Medicine, 2015;45(3):365–378. DOI 10.1007/s40279-014-0267-6
10. Impact of Relative Energy Deficiency in Sport (REDs) on Bone Health in Elite Athletes: A Retrospective Analysis — von Brackel FN, Munzinger R, Bartosik M et al., Journal of Cachexia, Sarcopenia and Muscle, 2025;16(5):e70082. DOI 10.1002/jcsm.70082, PMID 41030229
11. Micronutrient supplement intakes among collegiate and masters athletes: a cross-sectional study — Nichols QZ, Ramadoss R, Stanzione JR, Volpe SL, Frontiers in Sports and Active Living, 2023;5:854442. DOI 10.3389/fspor.2023.854442
12. Rapid Weight Reduction in Judo: Dietary Practices and Short-Term Health Effects — Staśkiewicz-Bartecka W, Ziomek P, Dobkowska-Szefer D, Malchrowicz-Mośko E, Tomaszewski P, Nutrients, 2025;17(24):3964. DOI 10.3390/nu17243964, PMID 41470908
13. Supplement Risk and NSF Certified for Sport — United States Anti-Doping Agency, supplement risk guidance for athletes
14. Athlete Advisory: What's New on the 2026 WADA Prohibited List? — United States Anti-Doping Agency, advisory on the List in force from 1 January 2026
15. Body Composition and Dietary Intake of Combat Sports Athletes: A Systematic Review — Nutrients, 2026;18(6):884. DOI 10.3390/nu18060884 — held at abstract level; the publisher returned a 403 to our fetch
16. Micronutrient deficiency in athletes and inefficiency of supplementation: is low energy availability a culprit? — Performance Enhancement & Health, 2020 — held at abstract level; full text not retrieved

Read next