The research team, led by Beth Penrose of Charles Darwin University and colleagues at the University of Tasmania and CSIRO, systematically searched three major scientific databases—Scopus, Web of Science, and Google Scholar—following the PRISMA-ScR framework for scoping reviews. From an initial pool of 300 screened articles, they identified 104 peer-reviewed papers containing 109 unique life cycle assessments of feed for cattle, pigs, chickens, fish, and crustaceans. For each study, the reviewers asked a deceptively simple question: did the assessment actually account for the mineral premix that every nutritionist knows is blended into commercial feed? The answer, in the overwhelming majority of cases, was no.

The numbers are striking. Sixty-four percent of the reviewed LCAs excluded mineral supplements entirely from their inventories and impact calculations. The omission was worst in aquaculture, where 84 percent of fish and crustacean studies left minerals out altogether, followed by cattle studies at 73 percent. Chicken and pig studies fared somewhat better, but even there roughly half of the assessments omitted the mineral component. When minerals were included at all, the treatment was often superficial: of the 39 LCAs that did account for mineral supplements, two-thirds relied on proxies—stand-in substances such as calcium carbonate or limestone—rather than modelling the actual premixes specified in the feed formulations. In the end, only 14 of the 109 assessments, about one in eight, modelled the real mineral supplements described in the associated feed profiles.

The choice of proxy matters because mineral requirements vary enormously across species, and a single stand-in cannot capture that diversity. Laying hens, for instance, need nearly four times the calcium that pigs require—roughly 4 percent of the diet versus 0.46 percent—because of the relentless demands of eggshell formation. Iron is a critical supplement for farmed fish yet unnecessary for cattle, which obtain ample iron from forage. Aquatic species complicate the picture further: freshwater fish absorb minerals directly through their gills, saltwater fish take them up through both gills and gut as they drink seawater, and diadromous species such as Atlantic salmon shift their requirements entirely when they migrate from freshwater to ocean pens during production. Dairy cattle are even often deliberately over-supplemented, with National Research Council recommendations suggesting 120 percent of required mineral levels. A uniform limestone proxy flattens all of this biological nuance into a single, misleading number.

Why does the omission matter so much? Because mineral supplements are not grown—they are mined. Ore extraction carries environmental pressures that agricultural and fishery-based feed ingredients do not: land-use change, greenhouse gas emissions, waste rock, soil contamination, and water pollution. Unlike a wheat field or a managed fishery, a mine draws on a finite, non-renewable resource base, and the extraction and processing steps can generate impact intensities far exceeding those of crop production. The review cites greenhouse gas estimates ranging from 774 kilograms of carbon dioxide equivalent per tonne for mono-dicalcium phosphate up to 8,812 for elemental phosphorus, and between 2,000 and 6,120 for zinc mining and processing. Wheat, by comparison, sits at roughly 423 to 735 kilograms of carbon dioxide equivalent per tonne. A kilogram of phosphorus supplement can therefore carry an order of magnitude more embedded emissions than a kilogram of the grain it sits alongside in the feed ration.

Small inclusion rates, multiplied across global production, translate into enormous hidden emissions. The authors illustrate this with two back-of-envelope calculations. United States feedlots used an estimated 83.8 million tonnes of feed in 2025; assuming a phosphorus inclusion of 0.48 percent and the high-end emissions figure for phosphorus mining and processing, phosphorus supplementation alone would account for nearly 72 million tonnes of carbon dioxide equivalent per year. Norwegian salmon farming, which used roughly 1.98 million tonnes of feed in 2020, would add an extra 163,700 tonnes of carbon dioxide equivalent from phosphorus supplements under the same assumptions. These are impacts that, in most published assessments, simply vanish from the ledger.

Aquaculture deserves particular scrutiny because the problem is growing. As the industry moves away from fishmeal and fish oil toward plant-based diets, the demand for supplemental minerals rises, since plant ingredients contain anti-nutritional factors and lower bioavailability of key elements, requiring higher supplementation than older formulations based on marine ingredients. Yet fish and crustacean LCAs were the least likely of any sector to include minerals at all, with 95 percent of studies omitting the mineral component entirely. The sector with the fastest-changing feed composition is, in effect, the one flying blindest.

The review also points to impact pathways that no proxy can capture. Mineral processing introduces environmental pressures with no agricultural analogue—sulfuric acid production during zinc processing, for example, generates impacts entirely absent from feed assessments that exclude or misrepresent minerals. Moreover, the authors mapped the global distribution of mines extracting cobalt, copper, magnesium, manganese, molybdenum, phosphorus, and zinc against terrestrial and marine species richness data, revealing that many mining operations sit in ecologically rich regions. The authors are careful to note that spatial overlap alone does not demonstrate biodiversity loss, but it highlights biodiversity-related exposure risks that are invisible when premixes are excluded or represented by generic limestone. Extraction locations, transport routes, and processing methods all vary widely, and none of that geographic reality survives a proxy-based assessment.

The authors are candid about why these omissions happen. Exact mineral concentrations and chemical forms—whether selenium arrives as sodium selenite or selenomethionine, for example—are often treated as confidential commercial information by feed manufacturers. Data on where ore is mined, how it is transported, and how it is processed are patchy, making it nearly impossible to trace the provenance of minerals in a specific batch of feed. Minerals can also arrive through multiple routes: phosphorus may come from mined rock or from animal bone byproducts, each with different and location-dependent impacts. The reviewers acknowledge that confidential industry LCAs may routinely include minerals, and they invite feed companies to share whether and how they do so.

Still, the authors argue, none of these challenges justifies leaving minerals out altogether. The FAO’s Livestock Environmental Assessment and Performance Partnership published guidance in 2020 advising that vitamin and mineral premixes be included in livestock feed LCAs, with proxies permitted only as a last resort. Life cycle inventory data already exist for the extraction, processing, and transport of many feed-relevant minerals—zinc, for instance, is required by every farmed species in the review, yet it is captured by none of the common proxies and even studies listing it in their inventories often fail to quantify its impacts. The reviewers propose practical fixes: life cycle inventory databases such as EcoInvent could offer proxies that better resemble real mineral inputs; researchers and industry could co-develop a comprehensive, regularly updated database of mineral supplements and their environmental profiles; and supplement suppliers could provide impact data for their premixed products without revealing proprietary formulations. Better collaboration between feed manufacturers, mineral suppliers, and assessment practitioners, the authors conclude, is the key to making the footprints of the world’s farmed animal foods honest, complete, and comparable.

Subject of Research: Representation of mined mineral feed supplements in life cycle assessments of farmed animal production

Article Title: Uncharted links from mining to fed animal systems: a scoping review

Article References: Penrose, B., Zhan, X., Reimer, T., Clawson, G., Amoroso, G., Prasad, S. S., Carter, C. G., Blanchard, J. L., & Cottrell, R. S. (2026). Uncharted links from mining to fed animal systems: a scoping review. npj Sustainable Agriculture, 4(1), Article 82. https://doi.org/10.1038/s44264-026-00193-2

Image Credits: AI Generated

DOI: 10.1038/s44264-026-00193-2

Keywords: life cycle assessment, animal feed, mineral supplements, mining, aquaculture, livestock, sustainability, carbon footprint, phosphorus, zinc, biodiversity, food systems

Androgenetic alopecia, often called male or female pattern hair loss, is the dominant cause of hair thinning worldwide, driven by a genetic sensitivity of hair follicles to dihydrotestosterone, a potent derivative of testosterone. Under its influence, follicles on the scalp gradually miniaturize, producing finer, shorter hairs over successive growth cycles until they eventually stop producing cosmetically meaningful hair at all. Because the condition is so widespread, affecting a large share of men by middle age and a substantial number of women, the market for supplements claiming to restore hair through nutrition has flourished, often citing older, smaller studies that reported altered levels of zinc, copper, or iron in people with hair loss.

The new investigation set out to test that idea at a scale rarely attempted before. The team retrospectively collected patient data from Sichuan Provincial People’s Hospital covering the period from October 2021 to December 2024. Patients diagnosed with androgenetic alopecia formed the experimental group, while healthy individuals served as controls. Serum concentrations of copper, zinc, calcium, phosphorus, magnesium, iron, selenium, manganese, molybdenum, nickel, chromium, cobalt, and lithium were quantified using inductively coupled plasma mass spectrometry, an analytical technique capable of detecting metals and metalloids at extraordinarily low concentrations by ionizing atoms in a plasma torch and sorting the resulting ions by their mass-to-charge ratio.

The statistical analysis, performed with GraphPad Prism 9.0 software, used unpaired t-tests to compare the two groups, with a threshold of P less than 0.05 for significance. Out of the full panel of elements, only four showed statistically significant differences between patients and controls: copper, lithium, calcium, and phosphorus. And even those differences, on close inspection, were modest and clinically unconvincing. Serum copper averaged 897.8 plus or minus 164.2 nanograms per milliliter in the alopecia group versus 922.3 plus or minus 188.2 in the controls, both comfortably inside the reference interval of 240 to 2000 nanograms per milliliter. Serum lithium, measured at 1.20 versus 1.35 nanograms per milliliter, sat far below the upper limit of 200 nanograms per milliliter in both groups.

Calcium and phosphorus told a similar story of technical significance without clinical meaning. Some individuals in the control group had serum calcium values exceeding the reference interval of 80 to 100 micrograms per milliliter, but the proportion of out-of-range results was similar in both groups, indicating no meaningful association with hair loss. Phosphorus levels remained within the reference interval of 25 to 200 micrograms per milliliter in more than 99 percent of participants in both arms of the study. In other words, the elements that reached statistical significance did so on the strength of a very large sample size, which can detect tiny shifts that would go unnoticed in smaller cohorts, rather than because of any dramatic biological divergence.

Perhaps most striking was what did not differ at all. Zinc, the element most frequently blamed for hair loss in popular nutrition discourse, showed no statistically significant difference between patients and healthy controls. Neither did magnesium, iron, manganese, molybdenum, nickel, selenium, chromium, or cobalt. This null result carries particular weight because zinc and iron have been the focus of numerous earlier investigations, some of which reported lower serum levels in people with various forms of hair loss, fueling a persistent belief that supplementation could slow or reverse the process. The new data, drawn from a far larger patient population, undercut that assumption for androgenetic alopecia specifically.

The authors draw a direct practical conclusion: because serum trace element levels in patients with androgenetic alopecia fall within reference intervals and do not differ meaningfully from those of healthy individuals, routine screening of serum trace elements in these patients is not recommended. That recommendation, if adopted widely, could reshape clinical practice. Dermatologists frequently order panels of micronutrient tests when patients present with pattern hair loss, partly to reassure anxious patients and partly because historical literature suggested deficiencies might contribute. Each panel costs money, delays diagnosis, and can lead to unnecessary supplementation, which is not always harmless. Excess selenium, for example, has been linked in animal studies to changes in hair structure, and indiscriminate zinc supplementation can interfere with copper absorption.

The biology of why trace elements became suspects in the first place is not entirely unreasonable. Zinc participates in hundreds of enzymatic reactions, including processes central to the hair follicle cycle, and severe zinc deficiency is a documented cause of hair loss in conditions such as acrodermatitis enteropathica. Iron deficiency anemia is associated with diffuse hair shedding. Copper is a cofactor for enzymes involved in cross-linking keratin, and experimental work has explored copper-binding peptides in tissue remodeling. Selenium-dependent enzymes protect follicles from oxidative stress. The follicle, one of the most metabolically active structures in the human body, plausibly depends on an adequate mineral supply, which is precisely why the absence of measurable serum differences in this study is informative: the problem in androgenetic alopecia is not supply but signaling.

That signaling problem is hormonal and genetic. Follicles in the scalp of susceptible individuals express androgen receptors and the enzyme 5-alpha reductase, which converts testosterone into dihydrotestosterone. In these follicles, dihydrotestosterone binding to the androgen receptor triggers a cascade that shortens the growth phase of the hair cycle and progressively miniaturizes the follicle. Recent research has even traced how miniaturization depletes follicular stem cells through mechanosensory signals involving calcium flux and inflammatory mediators, an intracellular pathway entirely independent of how much calcium circulates in the serum. Approved treatments, including topical minoxidil and oral finasteride, act on vascularization and hormone conversion respectively, not on nutrition, and their efficacy reflects the true nature of the disease.

None of this means nutrition is irrelevant to hair health in general. Diffuse shedding can accompany crash dieting, malabsorption disorders, or genuine deficiencies, and clinicians should still investigate those contexts. But the distinction matters: androgenetic alopecia is a genetically programmed, hormone-driven process, and this study provides the strongest evidence yet that a blood test for minerals will not reveal anything useful about it. For the millions of people spending money on mineral supplements in the hope of regrowing a receding hairline, the message from this large, carefully measured dataset is blunt and liberating at once. The minerals are there. The hair loss has other causes, and future progress will come from targeting the hormonal and molecular machinery of the follicle itself rather than the chemistry of the bloodstream that feeds it.

Subject of Research: Serum trace element concentrations in patients with androgenetic alopecia compared with healthy controls

Article Title: A study on the serum trace element concentration in patients with androgenetic alopecia

Article References: Sun, H., Luo, J., & Xie, C. (2026). A study on the serum trace element concentration in patients with androgenetic alopecia. Archives of Dermatological Research, 318(1), Article 486. https://doi.org/10.1007/s00403-026-04967-z

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04967-z

Keywords: androgenetic alopecia, trace elements, serum copper, zinc, hair loss, inductively coupled plasma mass spectrometry, micronutrients, dermatology, clinical screening, mineral supplements, hair follicle, case-control study