The research team worked with 160 five-month-old, first-time pregnant does, each weighing around 2.84 kilograms on average. The animals were randomly divided into four groups: one received plain drinking water, while the other three received L-carnitine dissolved in their water at concentrations of 100, 200 or 300 milligrams per liter. Crucially, the supplementation began as soon as pregnancy was confirmed, roughly ten to twelve days after mating, and continued through the entire gestation and lactation periods. This design allowed the researchers to capture what they call carry-over effects, meaning benefits passed from mother to offspring through the placenta before birth and through milk afterward, rather than effects of the compound fed directly to the young.

L-carnitine is a naturally occurring molecule with a very specific job inside the body: it shuttles long-chain fatty acids across the inner mitochondrial membrane so they can be burned for energy through a process called beta-oxidation. Without enough of it, cells struggle to convert fat into usable fuel. It also plays supporting roles in glucose metabolism, helping activate the enzyme pyruvate dehydrogenase so that sugar breakdown products can enter the energy-generating Krebs cycle, and it can spare the amino acids lysine and methionine for protein synthesis. Because fetal and newborn animals synthesize very little carnitine on their own, they depend almost entirely on what their mothers supply through the placenta and, later, through milk.

The results were striking, particularly at the highest dose. Newborn kits whose mothers received 300 milligrams of L-carnitine per liter of water showed the highest individual body weights at 21 days of age and the greatest average daily gain over the first three weeks of life, outperforming both the unsupplemented control group and the lower-dose groups. Litter sizes also trended upward in the supplemented groups, with the mid-dose group showing the largest litters at weaning age. In practical terms, the offspring of supplemented mothers were simply growing faster, a sign that energy was flowing more efficiently from mother’s milk into growing tissue.

Blood analyses of the neonates, conducted during weeks one, two and three of life, revealed what was happening beneath the surface. Serum glucose concentrations were significantly elevated in the highest-dose group across all three weeks, which the authors interpret not as a warning sign but as evidence of improved energy availability and metabolic flexibility. When growth is accelerating and thyroid activity is rising, higher circulating glucose more likely reflects better nutrient delivery and more efficient carbohydrate oxidation than any metabolic dysfunction. Cholesterol and triglyceride levels, by contrast, were largely unaffected, suggesting the compound was fine-tuning energy use without disrupting lipid handling.

Two liver enzymes, aspartate aminotransferase and alanine aminotransferase, told an equally encouraging story. These enzymes leak into the bloodstream when liver cells are stressed or damaged, so lower levels generally indicate a healthier liver. In the highest-dose group, both enzymes dropped significantly during the later weeks of the study compared with controls. The researchers attribute this hepatoprotective effect to L-carnitine’s ability to keep mitochondrial fat burning running smoothly, preventing fat from accumulating inside liver cells and reducing the production of reactive oxygen species that can destabilize cell membranes.

Perhaps the most telling hormonal shift involved the thyroid. Triiodothyronine, or T3, the biologically active thyroid hormone that drives oxygen consumption, thermogenesis and protein synthesis, was consistently highest in the neonates of the 300-milligram group throughout all three weeks. Thyroxine, or T4, was also elevated in the higher-dose groups by the second and third weeks. Since thyroid hormones stimulate mitochondrial biogenesis and cellular energy production, their rise dovetails neatly with the faster growth observed. The authors suggest that improved mitochondrial function may have boosted the conversion of T4 into the more active T3, creating a feedback loop in which better energy metabolism and stronger endocrine signaling reinforce each other.

Not every measured parameter moved, and those null results matter too. Cortisol, the primary stress hormone, remained unchanged across all groups, indicating that the supplementation did not disturb the animals’ baseline stress physiology. Malondialdehyde, a standard marker of oxidative damage to fats, also showed no significant differences, which the team reads as evidence that lipid peroxidation was already well controlled and that the enhanced energy metabolism came without oxidative costs. In other words, the metabolic boost did not come at the price of cellular wear and tear, a balance that is essential for any intervention intended to improve health rather than merely accelerate growth.

The findings fit into a growing body of research on what scientists call nutritional programming, the idea that the nutritional environment experienced in early life, even before birth, can shape metabolism, endocrine function and health trajectories later on. Most previous studies of L-carnitine in livestock focused on feeding it directly to growing animals or on its effects on the reproductive performance of breeding females. By tracking a full panel of biochemical, hormonal and oxidative markers in newborns whose mothers alone were supplemented, this study fills an important gap and suggests that the maternal supply line, from placenta to milk, is a powerful lever for shaping offspring development.

For commercial rabbit farming, an industry valued for its high reproductive efficiency and rapid production of lean protein, the practical implications are tempting. Supplementation via drinking water at 300 milligrams per liter was well tolerated, produced no adverse effects on liver integrity, stress hormones or oxidative status, and delivered heavier, faster-growing kits. The authors caution, however, that adoption should await cost-benefit analyses under real commercial conditions, and that future work should include a broader panel of antioxidant enzymes, such as glutathione peroxidase and superoxide dismutase, to fully map how maternal carnitine reshapes the antioxidant defenses of the next generation. If those results hold up, a simple addition to a mother’s water may prove to be one of the cheapest ways to give newborn animals a stronger metabolic start in life.

Subject of Research: Maternal L-carnitine supplementation during gestation and lactation and its carry-over metabolic effects on neonatal rabbits

Article Title: Carry-over influence of maternal L-carnitine during gestation and lactation on metabolic response of New Zealand neonatal rabbits

Article References: Shah, S. K. A., Khan, H., Ülger, İ., Alonaizan, R., Naz, S., Alomar, S., Tashkandi, N. A., Abudabos, A., Rossi, L., & Khan, R. U. (2026). Carry-over influence of maternal L-carnitine during gestation and lactation on metabolic response of New Zealand neonatal rabbits. Archives Animal Breeding, 69(4), 585-594. https://doi.org/10.5194/aab-69-585-2026

Image Credits: AI Generated

DOI: 10.5194/aab-69-585-2026

Keywords: L-carnitine, maternal nutrition, nutritional programming, neonatal rabbits, metabolism, thyroid hormones, mitochondria, animal science, liver enzymes, oxidative stress, rabbit farming, gestation

Autoimmune thyroid diseases affect millions worldwide, with Hashimoto’s thyroiditis standing as the leading cause of underactive thyroid function and Graves’ disease driving most cases of overactive thyroid. Both conditions arise when the immune system mistakenly attacks the thyroid gland, but the environmental triggers that set this process in motion remain incompletely understood. The gut microbiome has emerged as a compelling suspect because of its established role in training and calibrating the immune system. Gut bacteria ferment dietary fibers into short-chain fatty acids such as butyrate, propionate, and acetate, molecules that nourish the intestinal lining and help maintain the delicate balance between immune tolerance and inflammatory reactivity.

The research team, led by investigators applying rigorous PRISMA guidelines, systematically searched major databases including PubMed, Scopus, and Web of Science for studies comparing gut microbial composition in patients with autoimmune thyroid disease against healthy controls. After screening hundreds of records and applying strict inclusion criteria, the analysts pooled data from 30 qualifying studies. These investigations employed 16S ribosomal RNA gene sequencing to catalog bacterial communities in stool samples, allowing researchers to quantify differences in microbial diversity and abundance between patient and control groups with statistical precision.

The meta-analysis revealed a striking and consistent finding: individuals with autoimmune thyroid disease exhibit significantly reduced gut microbial diversity compared with healthy individuals. This reduction in alpha diversity, a measure of the variety of species within a single person’s gut, suggests a less resilient and less functionally versatile microbial community. Reduced diversity has been linked to a range of inflammatory and autoimmune conditions, and its presence in thyroid autoimmunity reinforces the hypothesis that microbial imbalance, or dysbiosis, may contribute to disease development rather than simply accompany it.

Beyond overall diversity, the analysis identified specific bacterial groups that consistently differ between patients and controls. Beneficial butyrate-producing bacteria, including members of the genera Faecalibacterium and Lachnospira, appear depleted in individuals with Hashimoto’s thyroiditis. These organisms are key suppliers of short-chain fatty acids that strengthen the gut barrier and promote anti-inflammatory immune signaling. Their reduction could weaken the intestinal lining, allowing bacterial fragments to cross into the bloodstream and trigger immune responses that cross-react with thyroid tissue, a mechanism known as molecular mimicry.

At the same time, the analysis documented an expansion of potentially pro-inflammatory taxa in patients with autoimmune thyroid disease. Species associated with lipopolysaccharide production, an inflammatory bacterial cell wall component, were enriched in patient groups, alongside increases in opportunistic organisms such as certain Escherichia and Shigella species. This shift in microbial composition toward inflammation-promoting bacteria provides a plausible biological pathway through which gut dysbiosis could fuel the chronic immune activation that characterizes thyroid autoimmunity.

The findings also revealed distinct microbial patterns between Hashimoto’s thyroiditis and Graves’ disease, suggesting that these two conditions, while related, may involve different gut microbial contributions. In Hashimoto’s thyroiditis, reductions in beneficial SCFA-producing bacteria were particularly pronounced, whereas Graves’ disease showed its own pattern of altered abundance in specific taxa. These differences hint that microbiome profiling could eventually help clinicians distinguish between autoimmune thyroid conditions or identify patients at risk of progression, although the researchers caution that the current evidence remains observational.

Importantly, the meta-analysis found that microbial alterations were not simply a consequence of thyroid hormone imbalances or medication use. Subgroup analyses examining patients at different stages of disease and treatment status indicated that dysbiosis persists across clinical contexts, supporting the idea that gut microbial changes may precede or actively participate in disease development. However, the cross-sectional design of most included studies prevents definitive conclusions about cause and effect, and the researchers emphasize that longitudinal studies and interventional trials are needed to establish whether microbiome changes drive thyroid autoimmunity or merely reflect it.

The implications of this work extend beyond basic science into potential clinical applications. If the observed microbial signatures can be validated in larger, prospective cohorts, they could inform the development of microbiome-based diagnostic tools or guide the use of targeted probiotics, dietary interventions, or fecal microbiota transplantation as adjunct therapies. Several strains of Lactobacillus and Bifidobacterium have shown promise in small studies of autoimmune conditions, and the current analysis provides a rationale for testing whether such interventions could modulate immune activity in thyroid disease. The researchers also highlight the need for standardized sequencing protocols and reporting guidelines to reduce heterogeneity across future studies.

As autoimmune thyroid disorders continue to rise in prevalence globally, driven by factors ranging from iodine intake to environmental exposures, understanding the contribution of the gut microbiome has become an urgent research priority. This meta-analysis consolidates a rapidly expanding literature into a coherent framework, confirming that microbial dysbiosis is a reproducible feature of autoimmune thyroid disease and pointing toward specific bacterial targets for future investigation. While much work remains to translate these associations into therapies, the study marks a significant step toward a more integrated view of thyroid autoimmunity, one in which the gut microbiome plays a central role in disease susceptibility, progression, and potentially treatment.

Subject of Research: Gut microbiota alterations in autoimmune thyroid disorders revealed by systematic review and meta-analysis

Article Title: Retraction: Exploring the role of gut microbiota in autoimmune thyroid disorders: a systematic review and meta-analysis

Article References: Frontiers Editorial Office (2026). Retraction: Exploring the role of gut microbiota in autoimmune thyroid disorders: a systematic review and meta-analysis. Frontiers in Endocrinology, 17, Article 2023216. https://doi.org/10.3389/fendo.2026.2023216

Image Credits: AI Generated

DOI: 10.3389/fendo.2026.2023216

Keywords: gut microbiota, autoimmune thyroid disease, Hashimoto's thyroiditis, Graves' disease, dysbiosis, meta-analysis, thyroid hormones, short-chain fatty acids, intestinal permeability, microbiome, systematic review, endocrinology

The review, led by Nooneh Khachatourian, Rubina Takhmazian, and Vishwanath Venketaraman, builds on a well-established epidemiological foundation. Undernutrition is already recognized as one of the most significant modifiable risk factors for tuberculosis, with more than one-fifth of global TB cases estimated to be attributable to it. Systematic reviews have shown that undernutrition substantially increases the risk of developing active TB and that malnutrition is associated with worse treatment outcomes, including treatment failure, loss to follow-up, and death. But the relationship runs both ways: TB itself drives nutritional deterioration through chronic inflammation, increased metabolic demands, reduced appetite, and impaired nutrient utilization. What the authors add to this picture is a third player—the thyroid gland—whose hormone output depends critically on the very micronutrients that malnutrition depletes and whose hormones, in turn, help regulate the immune cells that fight M. tuberculosis.

Thyroid hormones, triiodothyronine (T3) and thyroxine (T4), are best known for regulating metabolism, energy expenditure, lipid profiles, glucose utilization, thermogenesis, and body weight. But an accumulating body of experimental evidence shows that they also act directly on the immune system. Macrophages, dendritic cells, neutrophils, and T lymphocytes all express thyroid hormone receptors and respond to thyroid hormone signaling. Experimental studies indicate that these hormones regulate neutrophil respiratory burst activity, reactive oxygen species production, macrophage phagocytic capacity, cytokine signaling, and inflammatory responses. Thyroid hormone receptor α signaling has also been implicated in T-cell activation and in the function of regulatory T cells, which temper pro-inflammatory responses and enhance anti-inflammatory regulation. Because many of these same pathways are central to controlling intracellular pathogens such as M. tuberculosis, the authors propose that hypothyroidism—an extremely common endocrine disorder worldwide—may represent an underrecognized factor compromising antimicrobial defense.

The bridge between nutrition and thyroid function is built from specific micronutrients. Iodine is the structural backbone of both T3 and T4; the body cannot synthesize it, so dietary intake is indispensable. Although iodization programs have reduced severe deficiency, roughly 30 percent of the world’s population remains at risk of inadequate iodine intake, which impairs hormone synthesis and leads to compensatory thyroid enlargement and hypothyroidism. Selenium is equally critical: the thyroid contains the highest concentration of selenium per gram of tissue of any organ in the human body, reflecting the role of selenium-dependent iodothyronine deiodinases (DIO1, DIO2, and DIO3) that convert the prohormone T4 into biologically active T3. Selenium-dependent glutathione peroxidases and thioredoxin reductases also protect thyroid tissue from the oxidative damage generated during hormone biosynthesis, a process that inherently requires hydrogen peroxide as a substrate for thyroid peroxidase-mediated iodination. Selenium deficiency therefore impairs hormone activation, increases oxidative stress, and is associated with autoimmune thyroid disease.

Iron, the most prevalent micronutrient deficiency worldwide, adds another layer. Thyroid peroxidase, the enzyme responsible for iodide oxidation and organification, is heme-dependent and requires adequate iron availability for optimal catalytic activity. A recent systematic review and meta-analysis found significantly lower free T3 and free T4 concentrations among iron-deficient individuals compared with healthy controls. Iron deficiency frequently coexists with chronic inflammation, malnutrition, and infectious disease, which the authors suggest makes its impact on thyroid physiology particularly relevant in populations at elevated TB risk. Zinc contributes through zinc-finger transcription factors and thyroid hormone receptor signaling, with deficiency linked to impaired hormone metabolism and immune dysfunction. Vitamin D, meanwhile, exerts immunomodulatory effects through regulation of T-cell differentiation, cytokine production, and immune tolerance, and observational studies consistently report lower circulating vitamin D concentrations in patients with hypothyroidism, Hashimoto’s thyroiditis, and autoimmune thyroid disease compared with healthy controls.

The immunological case for why thyroid dysfunction might matter in TB rests on the biology of host defense. After inhalation, resident alveolar macrophages constitute the first line of defense, and successful containment of M. tuberculosis requires efficient macrophage activation, granuloma formation, robust T-cell responses, tightly regulated cytokine networks, and control of oxidative stress. Experimental studies show that thyroid hormones regulate macrophage survival and phagocytic activity, influence the production of reactive oxygen species, and modulate the expression of genes involved in antimicrobial responses. On the adaptive side, control of M. tuberculosis depends largely on CD4-positive T lymphocytes generating type 1 helper (Th1) responses characterized by interferon-γ and tumor necrosis factor-α—cytokines that activate infected macrophages and maintain granulomas. Thyroid hormones influence T-cell development, differentiation, and activation through receptor-mediated signaling, so dysregulation of these pathways could plausibly weaken the Th1 response that keeps mycobacteria in check.

Evidence from autoimmune thyroid disease reinforces how closely thyroid function and immune regulation are intertwined. Conditions such as Hashimoto’s thyroiditis and Graves’ disease feature lymphocytic infiltration, loss of immune tolerance, abnormal helper T-cell responses, and chronic cytokine-mediated inflammation, with increased expression of the chemokines CXCL9, CXCL10, and CXCL11 recruiting Th1 lymphocytes into thyroid tissue. Impaired suppressive activity of regulatory T cells has also been reported in autoimmune thyroid disease, and because balanced Treg responses are important for limiting immunopathology during TB infection, such disturbances may further influence susceptibility and disease progression. Beyond direct immune effects, chronic hypothyroidism is associated with low-grade systemic inflammation and altered immune cell metabolism, and thyroid hormones regulate the mitochondrial function, glucose utilization, and lipid metabolism that underpin the energetic demands of immune activation—processes increasingly recognized as determinants of TB outcomes.

The epidemiological spark for this framework comes from an 18-year nationwide population-based longitudinal cohort study, which found that individuals with hypothyroidism had an increased risk of subsequently developing TB, while patients with TB also had an elevated risk of subsequent hypothyroidism. The authors are careful to note that this observational association cannot establish causality and may be confounded by nutritional status, comorbidities, socioeconomic conditions, chronic inflammation, and medication exposure. The relationship is also bidirectional in a treatment context: antitubercular agents including ethionamide, prothionamide, and para-aminosalicylic acid inhibit thyroid peroxidase activity and disrupt iodine organification, producing hypothyroidism in approximately 17 percent of patients receiving treatment for multidrug-resistant TB. Chronic infection itself alters hypothalamic-pituitary-thyroid axis regulation through pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α, meaning TB can both cause and be influenced by endocrine disturbance.

On the intervention side, the review takes a notably sober view of supplementation. Vitamin D is the most extensively studied micronutrient in the TB context because it enhances macrophage antimicrobial activity through induction of cathelicidin, stimulation of autophagy, and promotion of intracellular killing of M. tuberculosis. Yet recent randomized-trial meta-analyses have found no significant reduction in TB infection or progression to active disease with vitamin D supplementation, and limited or inconsistent effects on microbiological treatment outcomes such as sputum smear and culture conversion. The authors argue that evidence supporting correction of a documented deficiency should be distinguished from evidence supporting routine supplementation specifically for TB prevention, and they point to substantial heterogeneity across studies in baseline nutritional status, dose, formulation, duration, and clinical outcomes as a key reason findings have been inconsistent. Similar caution applies to selenium, zinc, and iron: correcting documented deficiencies may support both thyroid and immune function, but evidence that supplementation independently improves TB-specific outcomes remains limited, and excessive intake of certain micronutrients can itself harm endocrine or immune function.

One of the more intriguing therapeutic leads involves glutathione, the body’s principal intracellular antioxidant. Patients with TB frequently exhibit depleted glutathione levels, compromising antioxidant defenses, macrophage function, cytokine regulation, and T-cell-mediated immunity. Experimental and clinical studies suggest that glutathione supplementation may reduce oxidative stress, enhance Th1-associated immune responses, increase production of IFN-γ and TNF-α, and decrease intracellular mycobacterial burden—preliminary but biologically coherent findings, given that glutathione metabolism is closely linked to selenium-dependent antioxidant systems. The authors conclude that the nutritional–endocrine–immune framework they propose is biologically plausible and hypothesis-generating rather than an established causal pathway, and that current evidence does not support routine thyroid screening solely to reduce TB risk. What they call for instead are prospective cohort studies determining whether thyroid dysfunction independently predicts TB after accounting for confounders, adequately powered trials of micronutrient correction in deficient populations, and standardized assessment of nutritional status, thyroid function, and clinical outcomes. If the proposed cycle of malnutrition, thyroid dysfunction, and impaired antimycobacterial immunity holds up under clinical scrutiny, nutritional optimization and early endocrine management could eventually become integrated adjunctive strategies in the fight against one of humanity’s oldest infectious diseases.

Subject of Research: The interplay between nutrition, thyroid function, and immune defense against tuberculosis

Article Title: Nutrition, thyroid function, and tuberculosis: exploring the endocrine–immune axis

Article References: Khachatourian, N., Takhmazian, R., & Venketaraman, V. (2026). Nutrition, thyroid function, and tuberculosis: exploring the endocrine–immune axis. Frontiers in Tuberculosis, 4, Article 1945832. https://doi.org/10.3389/ftubr.2026.1945832

Image Credits: AI Generated

DOI: 10.3389/ftubr.2026.1945832

Keywords: tuberculosis, thyroid hormones, hypothyroidism, micronutrients, iodine, selenium, vitamin D, immune regulation, malnutrition, endocrine-immune axis, glutathione, Mycobacterium tuberculosis

Pica is far more than an odd behavioral quirk. In sheep production systems it manifests as the persistent ingestion of non-feed substances: geophagia, trichophagia, urine drinking, fence licking, and even plastic chewing. Beyond disrupting normal feeding, it raises the risk of gastrointestinal injury, impaired nutrient absorption, parasitic infection, and lost productivity. Although the full etiology remains unresolved, researchers have long considered pica a multifactorial disorder rooted in nutritional imbalance, metabolic disturbance, and environmental stress, with mineral deficiency or imbalance widely recognized as a major driver. Shortages of elements such as phosphorus, copper, iron, zinc, and selenium can undermine antioxidant defenses and metabolic homeostasis, potentially pushing animals into the abnormal oral behaviors that define the syndrome.

Simple mineral supplementation has shown promise before—earlier work on wool-eating lambs found that dosing with iron, copper, and zinc sulfate salts raised blood mineral levels and produced complete recovery within eight weeks. But the picture is complicated by the fact that pica may also involve oxidative stress, endocrine dysregulation, and metabolic dysfunction. Moreover, whether supplemented minerals actually reach the bloodstream depends on their chemical form, antagonistic interactions among minerals, the rumen environment, and the intricacies of gastrointestinal absorption. This is where the new study departs from convention: instead of relying on minerals alone, the researchers combined them with Shariga-5, a traditional Mongolian multi-herb formula derived from local ethnoveterinary practice and rich in bioactive flavonoids and phenolic acids.

The Mongolian herbal–mineral supplement, or MHMS, was manufactured into solid 5-kilogram lick blocks containing target concentrations of calcium, phosphorus, copper, iron, manganese, zinc, selenium, and cobalt, along with vitamins D3 and E. Embedded within the mineral matrix were five medicinal herbs of the Mongolian Plateau: turmeric rhizome (Shariga), forsythia fruit (Saolong-Jimusi), clove flower buds (Gaoletu-Baori), chebulic myrobalan fruit (Arula), and gardenia fruit (Zhurula). Widely targeted metabolomic profiling of the individual herbs identified 1,427 metabolite annotation records, with phenolic acids accounting for nearly 39 percent and flavonoids another 32 percent—two chemical classes renowned for free-radical scavenging, metal-ion chelation, and anti-inflammatory activity. The design logic was synergy: trace elements supply the cofactors for antioxidant enzymes, while plant secondary metabolites provide complementary redox support.

To test the formula, the team screened East Friesian rams over seven consecutive days, enrolling only animals that showed five to ten instances of pica behaviors per observation day. Twenty rams, averaging about 1.5 years of age and 42.6 kilograms, were randomly split into two groups of ten, each housed in its own pen. The control group received only a basal diet of corn silage, oat hay, alfalfa, and Leymus chinensis hay; the treatment group received the same diet plus continuous free-choice access to an MHMS lick block. After a 14-day adaptation and a 60-day experimental period, blood was drawn before morning feeding, and serum from six animals per group underwent mineral, biochemical, antioxidant, hormonal, and untargeted metabolomic analyses.

The mineral results were strikingly selective. Serum copper roughly doubled, rising from 4.86 to 9.55 micromoles per liter, while zinc climbed from 10.62 to 15.29 and selenium from 0.43 to 0.59 micromoles per liter. Yet calcium, phosphorus, magnesium, sodium, potassium, iron, and manganese remained unchanged. This selectivity, the authors argue, suggests the supplement primarily restored the trace elements most closely tied to redox defense, metalloenzyme activity, immune regulation, and metabolic homeostasis. Copper underpins mitochondrial respiration and iron metabolism, zinc is a structural and catalytic factor for countless enzymes and supports epithelial barriers, and selenium is an essential component of glutathione peroxidase, a key peroxide-removing selenoprotein. The pattern also echoes previous work showing that mineral responses in ruminants are shaped not just by dose but by body reserves, absorption efficiency, and antagonistic interactions among elements.

The downstream physiological shifts extended well beyond minerals. Total antioxidant capacity in serum rose significantly, even though the individual enzyme activities of superoxide dismutase, glutathione peroxidase, and catalase did not change—an indication that the improvement came from the composite, largely non-enzymatic antioxidant pool, plausibly driven by the herbal polyphenols. Biochemical markers told a similar story of de-escalation: serum glucose fell from 4.44 millimoles per liter, sitting at the upper edge of the ovine reference range, to 3.60, a healthier mid-range value, and aspartate aminotransferase activity dropped from 160.70 to 125.35 units per liter, returning from above the normal range to within it. Because AST reflects hepatic metabolic burden and tissue injury—and pica-affected calves have previously shown elevated transaminases linked to copper deficiency—this normalization suggests the supplement eased tissue metabolic stress in the treated animals.

Perhaps the most dramatic changes appeared in the endocrine panel. Serum triiodothyronine, thyroxine, insulin-like growth factor 1, and growth hormone all rose significantly, signaling enhanced metabolic rate and activated anabolic growth signaling, while cortisol—the primary stress hormone of the hypothalamic–pituitary–adrenal axis—fell markedly, from 943 to 746 picograms per milliliter. The authors note that the supplement’s selenium, copper, zinc, and vitamin E all carry antioxidant functions that could plausibly dampen the HPA axis burden imposed by chronic nutritional stress and oxidative pressure. Previous studies lend support to the mechanism: curcumin supplementation has raised thyroid hormones and lowered cortisol in goats, and vitamin E and selenium combinations have reduced cortisol in transportation-stressed dairy heifers.

The untargeted metabolomics added an exploratory molecular layer. Out of 1,062 putatively annotated serum metabolites, 112 differed significantly between groups—51 higher and 61 lower in the supplemented rams. Pathway analysis ranked porphyrin metabolism, the biochemical route for heme synthesis, as the top candidate pathway, with glycine abundance more than doubled and porphobilinogen reduced to less than half of control levels. Because glycine is the starting substrate for heme biosynthesis and also a precursor for glutathione, the body’s master intracellular antioxidant, its rise fits a scenario of improved antioxidant substrate supply. The drop in porphobilinogen, an early heme precursor that can accumulate abnormally when the pathway falters, correlated positively with serum AST, hinting that reduced accumulation of this intermediate accompanied the easing of tissue metabolic pressure. The authors are careful to flag that this pathway enrichment did not survive multiple-testing correction and the metabolites lack validation against authentic standards, so these findings are hypothesis-generating rather than definitive.

The study also candidly acknowledges its limits: individual lick-block intake was not recorded, the composite design cannot separate the effects of minerals from herbs or their synergy, the sample was modest, and rumen fluid and microbiota were not examined. Even so, the overall picture is compelling—a traditional Mongolian herbal formula fused with trace-element nutrition appears to shift pica-affected rams from a stress-laden, oxidatively burdened metabolic state toward physiological balance, with elevated thyroid and growth hormones, subdued cortisol, stronger antioxidant capacity, and a metabolome inching back toward order. For a condition as old as animal husbandry itself, the remedy may lie partly in knowledge herders on the Mongolian Plateau have carried for generations, now given rigorous, molecule-by-molecule confirmation.

Subject of Research: Effects of a Mongolian herbal–mineral supplement on serum minerals, antioxidants, hormones, and metabolomics in rams with pica

Article Title: Free-choice Mongolian herbal-mineral supplementation improves serum mineral, antioxidant, endocrine, and metabolic indices in rams with pica

Article References: Man, D., Chen, L., Ao, X., Zhang, W., & Na, R. (2026). Free-choice Mongolian herbal-mineral supplementation improves serum mineral, antioxidant, endocrine, and metabolic indices in rams with pica. Frontiers in Veterinary Science, 13, Article 1946016. https://doi.org/10.3389/fvets.2026.1946016

Image Credits: AI Generated

DOI: 10.3389/fvets.2026.1946016

Keywords: pica, sheep, herbal-mineral supplement, trace minerals, antioxidant capacity, cortisol, thyroid hormones, serum metabolomics, porphyrin metabolism, Mongolian ethnoveterinary medicine, ruminant nutrition, oxidative stress

The research team, led by Feng-Yun Zou, Jia-Yuan Zhao, Shuang-Shuang Zhong and Bo-Ya Yin, recruited 460 children for the study. The cohort comprised 140 children with autism spectrum disorder who also showed elevated anxiety symptoms, 160 children with autism but without elevated anxiety, and 160 typically developing controls. This three-group design is what gives the study its power: rather than simply comparing autistic children with neurotypical peers, the investigators could isolate the features that specifically track anxiety within the autism population, a distinction that most earlier imaging studies blurred.

The imaging method at the heart of the study is called mean apparent propagator MRI, or MAP-MRI, and it represents a significant technical step beyond conventional diffusion-weighted imaging. Standard diffusion MRI measures the average direction and extent of water movement in tissue, which is useful for detecting gross white matter changes but says little about the complexity of the cellular environment. MAP-MRI instead reconstructs a full three-dimensional probability distribution of water molecule displacements, allowing researchers to quantify how restricted, hindered or free the diffusion is within each voxel. From this propagator, the team derived eight metrics for each of 68 brain regions, capturing properties such as non-Gaussianity of diffusion, return-to-origin probability and the orientation coherence of tissue microstructure.

Why does this matter biologically? Non-Gaussian diffusion measures are sensitive to the density and packing of cells, the tortuosity of the extracellular space and the organization of neurites, all of which can be altered by neuroinflammation, atypical development or altered neuronal arborization. In effect, MAP-MRI gives researchers a microscope-like window into tissue architecture without a biopsy. The regions that emerged as most different in the anxious autism group were exactly those one would predict from the neuroscience of fear and emotion: the amygdala, the hippocampus, the insula, the rostral anterior cingulate cortex, the putamen and the globus pallidus. The largest and most consistent differences were in non-Gaussian diffusion effects across this distributed limbic and striatal network.

The amygdala and hippocampus are the canonical structures of threat processing and memory for fearful experiences, while the insula integrates bodily sensations with emotional awareness and the anterior cingulate governs conflict monitoring and emotional regulation. The putamen and globus pallidus, core components of the striatal system, are increasingly recognized as participants in repetitive behavior and reward-related learning, both of which intersect with anxiety in autism. Finding that microstructural differences in these regions specifically distinguish anxious autistic children from their non-anxious autistic peers suggests that anxiety in autism is not merely a psychological overlay but is reflected in measurable tissue-level organization of the emotional brain.

Alongside the imaging, the researchers assayed a panel of peripheral biomarkers from fasting venous blood: free triiodothyronine (FT3), total thyroxine (TT4), thyroid-stimulating hormone (TSH), serum iron, blood lead and magnesium. The choice was deliberate. Thyroid hormones are master regulators of brain development and neuronal excitability, iron is essential for myelination and neurotransmitter synthesis, and lead is a well-established neurotoxicant with no safe exposure threshold. Magnesium, meanwhile, plays roles in neural excitability and stress responses. The results showed that children with autism and elevated anxiety had higher levels of FT3, TT4 and blood lead, and lower serum iron, compared with both non-anxious autistic children and typically developing controls.

The correlation analyses within the anxious autism subgroup revealed a coherent pattern. Serum iron was positively associated with MAP-MRI metrics, meaning that higher iron levels accompanied microstructural features consistent with more organized tissue in the affected regions. Blood lead and thyroid hormones showed the opposite relationship, with inverse associations to the same imaging measures, most prominently in the amygdala and hippocampus. In other words, the two metals and the thyroid hormones appeared to sit on opposite sides of the same microstructural signature, with the strongest signal concentrated in the brain’s fear circuitry.

To probe how these biochemical measures might relate to one another, the team applied exploratory cross-sectional statistical association decomposition models, which partitioned the observed correlations into direct components and indirect components mediated through FT3. This kind of decomposition cannot prove causation, but it provides a structured way of asking whether thyroid hormone status might act as a pathway linking metal exposure to brain microstructure. The models suggested that part of the association between the peripheral measures and the imaging features flowed through FT3-related indirect pathways, hinting at a possible endocrine intermediary role, though the authors are careful to frame this as hypothesis-generating rather than confirmatory.

Adding an unusual cross-species dimension, the researchers included a small, independent exploratory component using BTBR mice, an inbred strain commonly used as a model for autism-like behaviors because the animals display reduced social interaction, repetitive self-grooming and anxiety-like responses. In mice showing anxiety-like behavior, the team observed reduced amygdala fiber area and disrupted fiber organization, a pattern that echoes the human imaging findings in the same brain region. While the animal work is explicitly labeled exploratory and involves a small sample, the convergence between the mouse fiber architecture data and the human MAP-MRI abnormalities in the amygdala lends a degree of biological plausibility to the overall picture.

The authors and outside observers alike stress the limits of the design. All measurements were taken at a single point in time, so the study cannot determine whether elevated thyroid hormones and lead precede the microstructural differences, result from them, or both reflect some third factor such as chronic stress or shared genetic vulnerability. The children were not followed longitudinally, and no intervention was tested. What the study does establish is a detailed, multiplicity-corrected association profile: children with autism and elevated anxiety carry a distinctive combination of higher FT3, TT4 and blood lead, lower iron, and distributed MAP-MRI abnormalities centered on the limbic and striatal circuits that generate and regulate fear. If future longitudinal and experimental studies confirm these pathways, the findings could eventually point toward biomarker-guided subtyping of anxiety within autism, opening the door to targeted screening for thyroid function and metal exposure in children whose anxiety symptoms are hardest to treat. For now, the study stands as a compelling demonstration that the heterogeneity of autism is written not only in behavior but in the microscopic fabric of the brain and the chemistry of the blood that nourishes it.

Subject of Research: Associations between thyroid hormones, trace elements and brain microstructure in anxiety-related heterogeneity among children with autism spectrum disorder

Article Title: Mean apparent propagator MRI of distributed brain microstructure in anxiety-related heterogeneity among children with autism spectrum disorder: associations with thyroid hormones and trace elements

Article References: Zou, F.-Y., Zhao, J.-Y., Zhong, S.-S., Yin, B.-Y., Ni, Y.-X., Deng, Y.-Y., Zhou, X., Luo, X.-W., Shen, L.-S., Zhang, J.-L., Lin, Z.-P., Zhou, W.-Y., Wang, S.-H., & Guo, R.-M. (2026). Mean apparent propagator MRI of distributed brain microstructure in anxiety-related heterogeneity among children with autism spectrum disorder: associations with thyroid hormones and trace elements. BMC Psychiatry. https://doi.org/10.1186/s12888-026-08637-2

Image Credits: AI Generated

DOI: 10.1186/s12888-026-08637-2

Keywords: autism spectrum disorder, anxiety, MAP-MRI, diffusion MRI, amygdala, hippocampus, thyroid hormones, trace elements, blood lead, iron, neuroimaging, pediatric psychiatry

The findings arrive at a moment when nanotoxicologists are increasingly worried about the kidney. Silver nanoparticles, or AgNPs, are prized for their exceptional antimicrobial potency, their usefulness in clinical imaging and diagnostics, and their stability in consumer products ranging from bedding to electronics. Yet a growing body of evidence implicates them in cytotoxicity across multiple organ systems, and the kidneys appear particularly vulnerable. Previous animal studies have shown that AgNPs can accumulate within kidney cells, disrupt the delicate architecture of podocytes, the specialized cells that form the blood-filtration barrier in the glomeruli, and downregulate critical functional genes including those encoding nephrin and podocin. In laboratory-grown kidney cells, the particles have been observed to pile up inside lysosomes, scramble redox balance, and inflict direct damage on DNA.

To test whether taurine could counteract this cascade of harm, the researchers divided fifty adult male Wistar rats into five groups of ten animals each. One group served as untreated controls. A second received silver nanoparticles alone at a dose of 200 micrograms per kilogram of body weight, administered intraperitoneally each day. A third received taurine alone at 100 milligrams per kilogram by mouth. The remaining two groups received both the nanoparticles and taurine, at either 50 or 100 milligrams per kilogram. Treatment continued for twenty-one days, after which the animals were anesthetized, euthanized, and their kidneys and blood analyzed with an unusually thorough battery of biochemical, hormonal, and histological assays. The nanoparticles themselves were rigorously characterized before the experiment began, with transmission electron microscopy, dynamic light scattering, zeta potential analysis, and ultraviolet-visible spectroscopy confirming that the particles were a homogeneous 20 nanometers in diameter and stable in suspension.

The results in the nanoparticle-only group were stark. Serum creatinine and urea, the two classic workhorse markers of kidney function, rose dramatically compared with controls, with statistical significance values below 0.0001. Because creatinine and urea are waste products that healthy glomeruli filter freely and tubules barely reabsorb, their accumulation in the blood is a reliable signal that the kidneys are struggling to do their job. Equally striking was what happened to the thyroid hormones. Levels of triiodothyronine (T3) and thyroxine (T4), along with the ratio between them, fell sharply in the nanoparticle-exposed rats, indicating disruption of the hypothalamic-pituitary-thyroid axis. This hormonal collapse matters for the kidneys in very concrete ways: T3 normally drives the expression of sodium-potassium ATPase pumps and other ion transporters that renal tubular cells depend on to reabsorb electrolytes, and it also fuels the renin-angiotensin-aldosterone system, which governs glomerular filtration pressure.

Beneath the functional decline, the researchers documented a cellular war zone. Kidney tissue from the nanoparticle-exposed rats showed soaring levels of hydrogen peroxide, reactive oxygen and nitrogen species, and lipid peroxidation products, the chemical fingerprints of membranes under oxidative assault. Meanwhile, the kidney’s own antioxidant arsenal was depleted: the activities of the enzymes superoxide dismutase, catalase, glutathione-S-transferase, and glutathione peroxidase all dropped significantly, as did levels of glutathione, the cell’s principal non-enzymatic antioxidant tripeptide. The chemistry here is unforgiving. Hydrogen peroxide, though relatively stable on its own, can participate in Fenton and Haber-Weiss reactions to generate hydroxyl radicals, among the most destructive reactive species in biology. Renal cells are especially susceptible because iron reabsorbed in the tubules provides abundant catalyst for these reactions, converting a modest peroxide burden into a localized radical storm.

Inflammation followed the oxidative damage, as it so often does. The activity of myeloperoxidase, an enzyme released by neutrophils and monocytes that serves as a hallmark of their recruitment to injured tissue, climbed sharply in the nanoparticle-exposed kidneys, and nitric oxide levels rose in parallel, reflecting induction of inflammatory signaling. When the researchers examined stained tissue sections under the microscope, the structural toll was unmistakable: the renal cortex showed epithelial degeneration, glomerular lesions and hyperplasia, and widened capsular spaces, architectural damage consistent with the failing filtration function reflected in the blood chemistry.

Taurine co-treatment reversed nearly all of it. In rats given the amino sulfonic acid alongside the nanoparticles, creatinine and urea fell back toward normal, T3 and T4 recovered in a dose-dependent fashion, and the T3-to-T4 ratio improved. The antioxidant enzymes rebounded, glutathione was restored, and the markers of oxidative damage, peroxide, reactive species, and lipid peroxidation, all declined significantly. Myeloperoxidase activity and nitric oxide levels dropped, indicating that the inflammatory mobilization had been quieted. Most visibly, the histological sections from co-treated animals showed substantially preserved renal architecture compared with the devastated tissue of the nanoparticle-only group. The higher dose of taurine generally outperformed the lower one, suggesting a concentration-dependent protective effect.

The study’s authors, led by Adesina A. Babalola and senior investigator Isaac A. Adedara of the Drug Metabolism and Toxicology Research Laboratories, note that this is the first demonstration that taurine can restore thyroid-dependent renal tubular function following silver nanoparticle exposure. The choice of taurine was no accident. The compound, which mammals synthesize endogenously and obtain chiefly from animal-derived foods, participates in bile salt formation, calcium signaling, and osmoregulation, and it exerts antioxidant, anti-inflammatory, and anti-apoptotic effects across tissues. Taurine deficiency has been linked to retinal degeneration, cardiomyopathy, and pancreatic beta-cell dysfunction, and taurine depletion is documented in renal disease itself. The body’s capacity to make taurine declines with age, and infants cannot synthesize it adequately, making dietary and supplemental sources increasingly relevant. The Ibadan group had previously shown that taurine protects against silver nanoparticle neurotoxicity and reproductive toxicity in rats, and the new work extends that protective umbrella to the kidneys.

The authors are candid about one limitation: their design lacked a control group exposed to silver ions alone. Silver nanoparticles release silver ions in the body, and these ions distribute and behave differently from the intact particles, potentially producing distinct toxic effects. Prior work by other researchers, however, suggests that the nanoparticles themselves may be the more insidious threat, because cells take them up slowly through endocytosis, sequester them in lysosomes, and then release silver ions gradually, producing a prolonged and localized toxic exposure. That mechanism, if confirmed across more models, makes the kidney’s vulnerability to chronic nanoparticle exposure all the more consequential, and makes a protective agent that works against the particles themselves particularly valuable.

For now, the findings remain anchored in rodents, and translating a rat dose of taurine into human guidance requires the usual caution. But the study adds to a compelling picture: as engineered nanomaterials saturate the built environment and the marketplace, the search for accessible, low-toxicity countermeasures becomes a public health question rather than a purely academic one. Taurine, cheap, water-soluble, and already a common ingredient in energy drinks and infant formula, is about as accessible as candidate protective agents come. Whether it can shield human kidneys from the silver nanoparticles already woven into daily life will demand clinical evidence that does not yet exist. What the Nigerian team has established is the mechanistic blueprint, oxidative stress, thyroid disruption, inflammation, and tissue destruction, and a demonstration that a single dietary compound can intervene at every step of that destructive sequence.

Subject of Research: Protective effects of taurine against silver nanoparticle-induced kidney toxicity, oxidative stress, and thyroid dysfunction in rats

Article Title: Taurine mitigates oxidative stress, thyroid dysfunction and renal damage in silver nanoparticles-treated rats

Article References: Babalola, A. A., Ileola-Gold, A. V., Adelaja, U. A., Njoku, C. A., Adedara, I. A., & Farombi, E. O. (2025). Taurine mitigates oxidative stress, thyroid dysfunction and renal damage in silver nanoparticles-treated rats. Discover Toxicology, 2(1), Article 23. https://doi.org/10.1007/s44339-025-00045-7

Image Credits: AI Generated

DOI: 10.1007/s44339-025-00045-7

Keywords: silver nanoparticles, taurine, nephrotoxicity, oxidative stress, thyroid hormones, kidney, nanotoxicology, antioxidant enzymes, inflammation, Wistar rats, renal function, toxicology

The thyroid gland produces thyroxine (T4) and triiodothyronine (T3), hormones that govern the basal metabolic rate, bone growth, neural maturation, the body’s sensitivity to catecholamines, and the metabolism of proteins, fats and carbohydrates. Because these hormones touch nearly every physiological system, even a modest postoperative shortfall can translate into fatigue, weight gain and diminished quality of life. The gland consists of a right and a left lobe joined by a thin bridge of tissue called the isthmus, and in most patients the two halves are not equal partners. Earlier ultrasound studies had already established that the right lobe is typically the larger of the two; one frequently cited measurement from 2009 put the right lobe at 6.8 milliliters on average against 5.7 milliliters for the left. The Austrian research team behind the new study reasoned that this anatomical imbalance should, in principle, leave patients with less residual hormone-producing tissue after a right-sided resection—and therefore a greater need for pharmaceutical replacement.

To test that hypothesis, the investigators combed a hospital-wide research database for adults who had undergone hemithyroidectomy at the division of endocrine surgery and subsequently attended a follow-up visit at the thyroid outpatient clinic of the endocrinology department. From an initial pool of 459 patients, they excluded 33 who had undergone additional surgery on the contralateral lobe, leaving a final cohort of 426 individuals, 54.2 percent of whom had lost the right lobe and 45.8 percent the left. The team deliberately screened out anyone with prior thyroid surgery, radiation therapy, pre-existing hypothyroidism, autoimmune thyroid disease or pregnancy, all of which could have independently distorted hormone requirements. Preoperative thyroid volumes were calculated from ultrasound images using the standard volumetric ellipsoid formula, multiplying height, width and depth by a correction factor of 0.524.

The cohort was predominantly female—75.4 percent of patients—a distribution the authors note is expected given women’s well-documented susceptibility to thyroid disease. Baseline characteristics were strikingly well matched between the two surgical groups: mean age hovered around 53 years in both, and average height and weight were virtually identical. Preoperative TSH values, the most sensitive biochemical marker of thyroid status, were also comparable. That symmetry matters, because it strengthens the argument that any divergence in postoperative hormone needs can be attributed to the surgery itself rather than to differences in the patient populations. Overall, 91.3 percent of patients in the study developed hypothyroidism after their operation, a figure the authors acknowledge is likely inflated by the referral pattern of the outpatient clinic, which concentrates symptomatic patients.

The central result was unambiguous. Patients who had undergone right-lobe removal were taking a mean levothyroxine dose of 68.7 micrograms per day, compared with 60.6 micrograms per day after left-lobe removal, a statistically significant difference. When the researchers applied a multiple linear regression model with heteroskedasticity-robust standard errors, adjusting for the two strongest known confounders—body weight and preoperative TSH—the adjusted mean doses were 68.1 versus 60.2 micrograms per day, corresponding to the 13.2 percent relative increase. Expressed per kilogram of body weight, the median dose was 0.840 micrograms per kilogram per day after right-sided surgery against 0.773 after left-sided surgery. Consistent with the dosing gap, postoperative TSH was also higher in the right-lobe group, at a median of 1.70 versus 1.40 micro-international units per milliliter, indicating that even on their prescribed doses, these patients were running slightly more hypothyroid than their left-lobe counterparts.

The anatomical explanation held up in the imaging data. Among the 112 patients for whom preoperative ultrasound volumes of the resected lobe were available, the removed right lobes were on average 30 percent larger than the removed left lobes, a difference that itself reached statistical significance. This aligns with earlier work showing that the volume of the remaining lobe predicts hypothyroidism risk: a previous study found that patients whose contralateral lobe volume, adjusted for body surface area, fell below 3.2 milliliters faced roughly three times the risk of developing hypothyroidism after surgery. What the new analysis adds is the link from tissue volume all the way through to the practical prescription pad—the actual microgram dose a patient ends up taking months later.

Subgroup analyses added nuance without undermining the main finding. Among patients operated on for goitre, the adjusted dose difference rose to 16.0 percent, or an additional 9.37 micrograms per day, and remained statistically significant. In the group treated for nodules and autonomously functioning adenomas, the adjusted difference was 9.7 percent, or 6.0 micrograms per day, but did not reach significance, possibly reflecting the smaller subgroup size and the difficulty of cleanly separating patients who had both pathologies. An exploratory Spearman correlation analysis further showed that levothyroxine dose was associated with the side of surgery, preoperative TSH and body weight, whereas sex and age had no measurable impact. In the fully adjusted regression model, all three significant predictors held: surgical side contributed 7.69 micrograms per day, each kilogram of body weight added 0.38 micrograms per day, and higher preoperative TSH was associated with 7.65 micrograms per day.

The authors are candid about the limitations inherent in a retrospective design. The cohort represents patients who both had surgery and returned for follow-up at the same institution’s thyroid clinic, which likely selected for patients with postoperative symptoms and helps explain the high observed prevalence of hypothyroidism. The number and precise timing of levothyroxine dose adjustments made before the follow-up visit were not systematically recorded, so the titration process itself could not be reconstructed. Underlying conditions prompting the surgery, such as goitre or nodules, may also have influenced results, and many patients probably had both. Still, the study’s strengths are considerable: a large sample, a remarkably long observation period spanning nearly a quarter century, and rigorous exclusion of any patient with surgery on the contralateral lobe, which protects the side-specific comparison from contamination.

The practical implications could reshape how clinicians counsel patients facing thyroid lobectomy. Roughly 22 to 60 percent of all hemithyroidectomy patients currently require thyroid hormone supplementation despite the compensatory growth of the remaining lobe, which can expand by up to 30 percent of its original size. Existing prediction models have incorporated preoperative TSH, sex, age, body surface area and body mass index, and some researchers have argued that weight alone is the best single predictor of postoperative levothyroxine needs. The new data suggest that adding a single question—which lobe is being removed—could meaningfully sharpen those predictions. The authors propose that a preoperative ultrasound to size the remaining lobe may be especially worthwhile when right-lobe resection is planned, and they call for randomized, prospective studies to confirm the finding and integrate surgical side into future dosing algorithms. Until then, the message for patients and physicians alike is that in thyroid surgery, left and right are not interchangeable.

Subject of Research: Postoperative levothyroxine dosage requirements after right- versus left-lobe hemithyroidectomy

Article Title: Higher Post‐Operative L‐Thyroxine Dosage Needed After Right Compared to Left‐Lobe Hemithyroidectomy

Article References: Deischinger, C., Krebs, M., Scherer, T., Scheuba, C., Kautzky‐Willer, A., & Kosi‐Trebotic, L. (2026). Higher Post‐Operative L‐Thyroxine Dosage Needed After Right Compared to Left‐Lobe Hemithyroidectomy. Endocrinology, Diabetes & Metabolism, 9(5), Article e70345. https://doi.org/10.1002/edm2.70345

Image Credits: AI Generated

DOI: 10.1002/edm2.70345

Keywords: thyroid surgery, hemithyroidectomy, levothyroxine, hypothyroidism, TSH, thyroid hormones, endocrinology, thyroid lobes, retrospective cohort study, hormone replacement, ultrasound, thyroxine dosage

The core of the problem lies in molecular mimicry. BPA’s structure bears a striking resemblance to steroidal estrogens such as diethylstilbestrol, allowing it to bind to estrogen receptors and exert estrogen-like effects in tissues ranging from the uterus and mammary glands to the brain and cardiovascular system. The review emphasizes that BPA binds to the estrogen receptor with an affinity roughly one thousand-fold lower than estradiol itself, which sounds reassuring until one considers the concentrations achieved in blood after a meal consumed from BPA-lined packaging. Crucially, the compound does not limit itself to estrogen receptors. It also interacts with androgen receptors, thyroid hormone receptors, glucocorticoid receptors, and the aryl hydrocarbon receptor, meaning that a single molecule can perturb multiple hormonal axes simultaneously, disrupting the synthesis, secretion, transport, metabolism, binding, and elimination of the body’s own hormones.

Perhaps the most technically significant advance highlighted in the review is the recognition that BPA’s actions extend far beyond the classical genomic pathway, in which a ligand enters the nucleus and alters gene transcription over hours. Recent mechanistic work shows that BPA also engages the G protein-coupled estrogen receptor, known as GPER, located on the cell membrane. Activation of GPER triggers rapid, non-genomic signaling cascades, including the cAMP/PKA pathway, PLC-mediated PKC activation, and transactivation of the epidermal growth factor receptor with downstream MAPK/ERK signaling. These membrane-initiated events have been implicated in altered immune signaling, with reduced interleukin-10 and interleukin-13 secretion observed in human immune cells, as well as in the promotion of cancer cell migration and invasiveness. Researchers argue that this rapid signaling mode helps explain the sometimes non-monotonic responses to BPA, in which low doses produce effects that higher doses do not, and they recommend that GPER engagement be explicitly considered when evaluating the safety of BPA substitutes.

That non-monotonic dose-response relationship strikes at the heart of conventional toxicology. Traditional risk assessment assumes that harm increases with dose, yet studies compiled in the review show measurable biological changes at doses within the range of everyday human exposure, levels often below those used in classic high-dose studies. In mice, in utero exposure to BPA reduced spine densities in the hippocampal CA1 region regardless of the dose administered to the mother, and the disruption of neuronal morphology persisted into adulthood. Such findings suggest that the developing brain, where hormones orchestrate neuronal differentiation, synapse formation, and overall cortical organization, is exquisitely vulnerable during critical windows of development. Exposure during these periods can produce long-lasting neurodevelopmental and behavioral deficits, including altered social behavior, anxiety, and changes in maternal behavior, effects documented across rodent models and zebrafish larvae, where BPA treatment decreased spontaneous movement and dysregulated genes associated with neurological system processes.

The epigenetic dimension adds an even more provocative layer. BPA exposure has been shown to alter DNA methylation patterns, the chemical tags that regulate gene expression without changing the underlying genetic code. Because epigenetic marks can be inherited through cell division and, in some cases, across generations, these modifications raise the possibility that today’s exposure could influence the health of descendants not yet born. Early-life exposure to endocrine disruptors has been associated with epigenetic reprogramming that manifests as increased disease risk later in life, a mechanism that may link prenatal BPA exposure to altered sexual differentiation, reduced fertility, and heightened susceptibility to reproductive cancers observed in animal models.

Sex differences emerge as a recurring theme throughout the evidence. Male, but not female, juvenile rats showed a noticeable decline in spatial memory following exposure to 0.4 milligrams per kilogram per day of BPA, while female offspring of mothers exposed to low doses were significantly heavier than controls or offspring exposed to high doses. Thyroid function tells a similarly paradoxical story: pooled analyses and recent cohort reports indicate that higher BPA concentrations are associated with lower free thyroxine and lower thyroid-stimulating hormone in males, whereas in females BPA is more often associated with higher free thyroxine, with TSH associations less consistent. The review attributes these divergent patterns to BPA’s multi-modal actions, including anti-androgenic effects and interference with thyroid hormone biosynthesis in males, and estrogenic modulation of thyroid hormone-binding proteins and peripheral deiodination in females.

Reproductive health bears the brunt of BPA’s interference in both sexes. In females, exposure disrupts the hypothalamic-pituitary-ovarian axis, interfering with gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone, pathways essential for ovulation and menstrual cycle regulation. BPA can also stimulate aromatase, the enzyme that converts androgens into estrogens, elevating estrogen levels and potentially promoting estrogen-dependent conditions such as endometriosis, uterine fibroids, and breast cancer, while simultaneously blocking progesterone signaling, a disruption linked to increased risks of miscarriage and preterm labor. In males, BPA disrupts the hypothalamic-pituitary-testicular axis, reduces the number and viability of testosterone-producing Leydig cells, and interferes with androgen receptor signaling, outcomes associated with reduced sperm production, impaired sperm motility, and altered luteinizing hormone levels that may reflect compensatory responses to falling testosterone.

The metabolic consequences may be equally consequential. Epidemiological studies suggest an association between high urinary BPA levels and predisposition to obesity, and animal experiments show that BPA promotes adipogenesis, increases fat accumulation, and disrupts glucose metabolism. Mechanistically, receptor-level endocrine disruption activates adipogenic transcriptional programs driven by PPARγ and C/EBPα, increases lipid accumulation and inflammatory signaling in adipose tissue, and impairs insulin signaling, providing a plausible pathway from plasticizer to metabolic syndrome. BPA can reduce cellular sensitivity to insulin by interfering with insulin receptor signaling, and may lower adiponectin, the hormone that helps regulate glucose and lipid metabolism. Recent work in mice even implicates gut microbiota-dependent bile acid metabolism and TGR5/UCP1 signaling in BPA-driven fat gain, with epigenetic reprogramming acting as an amplifying mediator.

Against this backdrop, the regulatory landscape remains fragmented and, in the view of the review’s authors, insufficient. The European Union, Canada, and China have banned BPA in baby bottles, the United States has restricted it in baby bottles and sippy cups, and California has imposed labeling requirements, yet the FDA has not banned BPA from all food and beverage containers and continues to monitor the evidence. Meanwhile, more than one hundred tons of BPA are discharged into the environment annually, leaching from containers into food, escaping from landfills and sewage treatment plants, and contaminating air, water, soil, and sediment. The industry’s pivot to substitutes, chiefly bisphenol S and bisphenol F, now common in thermal paper receipts, has not resolved safety concerns, as studies indicate these analogues may exert endocrine-disrupting effects similar to BPA’s. The review concludes that comprehensive toxicological evaluation of alternatives, transparent evidence-based policy, public education, improved labeling, and innovation in genuinely safer materials are urgently needed, because the evidence now shows that harm can occur at exposure levels people encounter every single day.

Subject of Research: Endocrine-disrupting effects of bisphenol A on human hormone systems and health outcomes

Article Title: Effects of Bisphenol-A on human endocrine function and health outcomes: a review

Article References: Kaulgud, R. S., Belur, S., Anagharani, A. M., Veeresh, S., & Shettar, A. K. (2025). Effects of Bisphenol-A on human endocrine function and health outcomes: a review. Discover Toxicology, 2(1), Article 24. https://doi.org/10.1007/s44339-025-00046-6

Image Credits: AI Generated

DOI: 10.1007/s44339-025-00046-6

Keywords: bisphenol A, endocrine disruptors, estrogen receptors, GPER, thyroid hormones, obesity, insulin resistance, reproductive health, epigenetics, brain development, BPS, BPF

The historical setting is critical to the study’s power. In the late 1990s, Ethiopia sourced most of its iodized salt from Eritrea. When the border between the two countries closed in May 1998 amid escalating conflict, that supply line was severed, and iodized salt effectively disappeared from Ethiopian markets for an extended period. Because the disruption hit some areas and birth cohorts harder than others, it created a stark contrast between children who enjoyed months of exposure to iodized salt in utero and during infancy and those who had little or none. The researchers exploited this variation using an event-study design combined with difference-in-differences comparisons across space and time, a quasi-experimental approach that approximates the rigor of a randomized trial without exposing anyone to harm.

Iodine’s biological role explains why the timing of exposure matters so much. The thyroid gland concentrates iodine to synthesize the hormones thyroxine and triiodothyronine, which regulate basal metabolism and, crucially, drive fetal brain development. During pregnancy and early infancy, maternal thyroid hormones and the infant’s own emerging thyroid function govern neuronal migration, myelination, and synapse formation. Severe deficiency produces cretinism, but even moderate deficits impair cognition, hearing, and motor function. The World Health Organization has long endorsed universal salt iodization as one of the most cost-effective public health interventions available, yet coverage remains uneven globally, and programs that collapse can undo decades of progress.

To measure the consequences of Ethiopia’s supply shock, the team assembled an unusually rich set of data sources. They used the 2015/2016 Ethiopian National Micronutrient Survey to infer urinary iodine status among children and women of reproductive age, the 2000 and 2005 waves of the Ethiopia Demographic and Health Survey to analyze birthweight, child survival, and physical growth, and nearly two decades of records from the Ethiopian Higher Education Entrance Examination spanning 2003 to 2019 to assess academic achievement. A distinctive feature of the analysis was its integration of environmental geochemistry. Working with collaborators at Rothamsted Research and the University of Nottingham, the team mapped district-level soil and cereal grain concentrations of iodine and selenium across Ethiopia, allowing them to distinguish regions where diets naturally supply adequate iodine from regions wholly dependent on fortified salt.

The results on child survival are sobering. Rural children with fewer months of early-life exposure to iodized salt experienced excess mortality that emerged during infancy and persisted through early childhood. The pattern held in comparisons of birth cohorts born just before and just after the 1998 border closure, and the excess deaths were concentrated precisely where environmental iodine was lowest. This gradient is the study’s central strength: children living in districts with iodine-rich soils and crops had a physiological buffer against the loss of fortified salt, while children in iodine-poor districts bore the full brunt of the deficiency. Earlier intervention trials in severely deficient regions, including studies of oral iodine supplementation and iodinated irrigation water in China, had suggested that iodine could improve infant survival, but population-scale causal evidence of this kind has been scarce.

The educational findings extend the harm deep into adolescence. Students from rural cohorts with reduced early-life iodine exposure scored significantly lower on standardized secondary-school entrance examinations, with the deficit most pronounced in low-iodine districts. The dose-response relationship was graded and consistent: the more months of iodized salt a child’s first years encompassed, the better their later exam performance, and the effect strengthened with naturally low environmental iodine. Because the exams gate access to Ethiopian higher education, the measured deficits translate into lost opportunity at a formative juncture, suggesting that a temporary nutritional disruption in infancy imposes lifelong costs on human capital formation.

The methodological machinery behind these conclusions deserves attention. By modeling exam scores and mortality as event studies aligned by year of birth, the researchers could verify that outcomes diverged only for cohorts whose critical developmental windows overlapped the salt disruption, remaining flat for cohorts exposed before or after. Including selenium in the spatial analysis helped rule out confounding by correlated soil chemistry, and the team controlled for other shocks of the era, including the Ethiopian-Eritrean conflict, droughts, and changes in safety-net programs. All analysis code was released publicly on GitHub, and soil and grain nutrient data are archived in the Rothamsted Research repository, an unusually transparent package for a study of this scale.

The findings carry pointed lessons for policy. Salt iodization costs only a few cents per person per year, yet this study demonstrates that its absence is not a neutral state but an active harm, visible in death certificates and exam halls alike. Ethiopia itself illustrates both sides of the story: after the disruption, the country rebuilt its program through central iodized facilities, and coverage recovered substantially by the mid-2010s. But the episode reveals how fragile fortification systems can be when they depend on a single supply chain, and how quickly biological gains can reverse. The authors’ results align with a broader economics literature linking iodization to cognition and earnings in the United States, Switzerland, Tanzania, Denmark, and China, but they add a mortality dimension that those studies could rarely quantify.

For global health planners, the message is twofold. First, sustaining existing iodization programs matters as much as launching new ones, and supply chains deserve the same scrutiny as fortification standards. Second, environmental context should shape targeting: where soils are iodine-poor, populations have no dietary fallback, making uninterrupted fortification a matter of survival. As climate change, conflict, and trade disruptions increasingly stress food systems, Ethiopia’s experience stands as a warning written in the fates of two cohorts of children, and as proof that one of the cheapest interventions in public health is also one of the most consequential.

Subject of Research: Effects of disrupted salt iodization on child mortality and academic achievement in Ethiopia

Article Title: Loss of salt iodization harmed child survival and academic achievement in Ethiopia

Article References: Alemu, R., Tafere, K., Gashu, D., Joy, E. J. M., Bailey, E. H., Lark, R. M., Broadley, M. R., & Masters, W. A. (2026). Loss of salt iodization harmed child survival and academic achievement in Ethiopia. Nature Food. https://doi.org/10.1038/s43016-026-01408-y

Image Credits: AI Generated

DOI: 10.1038/s43016-026-01408-y

Keywords: iodine deficiency, salt iodization, Ethiopia, child mortality, cognitive development, micronutrients, public health, quasi-experimental study, school achievement, thyroid hormones, food fortification, environmental geochemistry

The interruption at the heart of the study was not a slow policy drift but a sudden break. For a period beginning in May 1998, iodized salt stopped flowing into Ethiopian households, meaning that iodine intake dropped back to whatever trace amounts occurred naturally in local foods and water. Because iodine concentrations in soil and crops vary dramatically across landscapes, this exposed children to a geographic lottery: in districts where environmental iodine was abundant, the consequences were muted; where soils and staple grains carried little iodine, children and pregnant women were effectively returned to a state of deficiency.

The biological stakes of iodine are well established. Iodine is an essential component of the thyroid hormones thyroxine and triiodothyronine, which regulate basal metabolism and, critically, drive brain development in the fetus and infant. Severe deficiency during pregnancy causes cretinism, marked by profound intellectual disability, while milder prenatal and early-childhood deficiency depresses intelligence quotient scores, school performance and even survival through mechanisms that include hypothyroidism and impaired immune function. Because the window of maximum vulnerability closes early—largely before a child enters school—deficiency during gestation and infancy inflicts losses that later nutrition cannot fully repair.

Against that backdrop, the Ethiopian interruption offered researchers a rare opportunity. Randomized trials that withhold iodine from pregnant women and children would be unethical, and many earlier studies of iodization relied on coarse baseline measures of deficiency, such as regional goiter rates recorded decades earlier. The Ethiopian case is different: the loss of iodized salt was sudden, affected the whole country, and coincided with rich new data on how much iodine naturally occurs in Ethiopian soils and grains. The study leverages the GeoNutrition survey work, published in Nature in 2021, which mapped the geospatial variability of nutritional quality in Ethiopian and Malawian cereals and provided a district-level measure of naturally occurring iodine.

The analytical strategy combined that environmental gradient with household and educational data spanning the interruption. Children who were in utero or in infancy when the iodized salt supply was severed could be compared with siblings and with cohorts born slightly earlier or later, and the severity of exposure could be calibrated by how iodine-poor their home district was. This design allows the researchers to separate the effect of iodine loss from the many other shocks—droughts, conflicts, economic fluctuations—that Ethiopia experienced during the same period.

The results were stark. The authors report a significant drop in child survival following the loss of iodized salt, and a parallel decline in academic achievement among affected cohorts, with both effects concentrated in rural districts with lower environmental iodine concentrations. In places where local foods provided a partial buffer, children fared comparatively better; where the environmental safety net was thin, the loss of fortification translated directly into biological harm. That gradient is important because it makes the causal interpretation far more difficult to dismiss: a purely coincidental shock, such as a regional famine or policy change unrelated to nutrition, would not be expected to track the geography of soil iodine so closely.

To probe that question further, the researchers ran placebo tests—analyses structured to detect effects where none should exist if iodine were the true mechanism. For example, they examined children whose ages meant they were not exposed during the critical developmental window, and districts where environmental iodine was plentiful. These tests confirmed that the losses were not driven by generic hardship but specifically by the absence of iodine during early life, strengthening the case that the interrupted fortification program itself caused the damage.

The findings resonate with a broader body of evidence assembled over decades. A randomized trial in Ethiopia by Mohammed, Marquis, Aboud, Bougma and Samuel, published in Maternal and Child Nutrition in 2020, showed that providing iodized salt to women before pregnancy improved children’s cognitive development—an in-country experimental counterpart to the new observational findings, demonstrating that restoring iodine early in life raises cognitive scores. Earlier work by Feyrer, Politi and Weil on the introduction of salt iodization in the United States documented large cognitive gains, though it relied on coarse baseline deficiency measures that limited precision. In Tanzania, Field, Robles and Torres showed that iodine deficiency depressed schooling attainment across Africa. And a 2021 review by Zimmermann and Andersson in the European Journal of Endocrinology documented that iodized salt coverage worldwide remains uneven and tenuous, with programs vulnerable to supply disruptions, regulatory lapses and declining political attention.

What the Ethiopian study adds is the reverse-direction evidence: not what is gained when iodization begins, but what is lost when it stops. This matters because salt iodization is often treated in global health as a solved problem. In reality, fortification programs depend on continuous supply chains, quality monitoring and enforcement, and the new results suggest that a single interruption lasting long enough to affect a birth cohort can impose lifelong costs in mortality and human capital. The magnitude of the educational losses implies economic consequences as well, since lower achievement translates into reduced productivity and earnings across the affected generation’s working lives.

For policymakers, the message is twofold. First, universal salt iodization programs deserve the same vigilance applied to vaccination campaigns: they must be monitored continuously, and disruptions must be treated as public health emergencies rather than logistical footnotes. Second, the environmental gradient in the findings underscores that fortification is not uniformly protective on its own; in regions where soil iodine is naturally scarce, food systems may need complementary strategies, including diversified fortification or targeted supplementation for women of reproductive age. The Ethiopian cohort that lost its iodized salt in 1998 cannot recover what was taken from it, but the evidence it generated makes a compelling case that the world’s remaining gaps in iodine coverage are not benign—and that closing them, and keeping them closed, is among the most cost-effective investments available in child health and education.

Subject of Research: The impact of interrupted salt iodization on child survival and educational outcomes in Ethiopia

Article Title: Interrupted salt iodization harmed child health and education in Ethiopia

Article References: Interrupted salt iodization harmed child health and education in Ethiopia. (2026). Nature Food, 7(9), 836–837. https://doi.org/10.1038/s43016-026-01415-z (Author names are not included in the publisher’s citation export.)

Image Credits: AI Generated

DOI: 10.1038/s43016-026-01415-z

Keywords: salt iodization, iodine deficiency, Ethiopia, child mortality, academic achievement, micronutrients, thyroid hormones, nutrition policy, early childhood development, food fortification, environmental iodine, natural experiment