Scientific reports · 2026

This double-blind randomised trial with 72 people who have moderate to severe chronic kidney disease explored whether a daily Lactobacillus plantarum probiotic could slow the decline of kidney function. Chronic kidney disease affects about 10% of people worldwide, and in moderate stages (3 and 4) there are few ways to slow it. The gut-kidney axis is the idea that waste molecules produced by gut bacteria, such as indoxyl sulfate, can burden the kidneys, so changing the gut bacteria with a probiotic might help. The main yardstick was eGFR (estimated glomerular filtration rate), a blood-test estimate of how much blood the kidneys filter each minute. The study ran at a nephrology centre in Mansoura, Egypt, between May and November 2025. Participants were adults with eGFR between 15 and 59, mostly men around 60 years old, and many also had hypertension or diabetes. They were randomly assigned to a daily capsule of 10 billion L. plantarum bacteria (37 people) or an identical dummy capsule (35 people) for six months, while all continued standard kidney care. Neither patients nor staff knew who received which capsule. Kidney function moved in opposite directions. eGFR rose by a median of 4.85 in the probiotic group (30.8 to 36.1) and fell by 1.5 in the placebo group (31.7 to 29.7); after adjusting for starting values the probiotic group's eGFR was 7.72 higher (95% CI 5.63 to 9.82, p < 0.001). Serum creatinine fell by 0.3 mg/dL with the probiotic and rose by 0.1 with placebo, and measured creatinine clearance rose by 7.8 mL/min versus a 4.9 fall. The result held in stage 3 and 4 and in people with and without diabetes. Urine indoxyl sulfate did not differ between groups, and protein in the urine rose in both. Nobody in the probiotic group had disease progression versus three people on placebo (8.6%, p = 0.11), and no side effects were reported. The authors conclude that the probiotic may improve eGFR and that its effect did not appear to work by lowering indoxyl sulfate. Limits include a single centre, only six months, no measurement of gut bacteria or inflammation, a urine rather than blood toxin test, kidney function estimated from creatinine rather than measured directly, and several analyses done after the fact, so the results are preliminary and need confirmation in larger, multi-centre trials with longer follow-up.

Clinical and translational science · 2021

This randomised, open-label trial with 90 people who have Hashimoto's thyroiditis explored whether six months of selenium supplements changes the immune and thyroid markers of the disease. Hashimoto's thyroiditis is an autoimmune condition in which the immune system attacks the thyroid gland, measured through antibodies to thyroid peroxidase (TPOAb) and thyroglobulin (TGAb). Selenium is a trace mineral built into antioxidant proteins that the thyroid relies on, and regulatory T cells (Tregs) are immune cells that keep overactive immune responses in check, so the researchers also tracked these cells to see whether selenium acts through them. Conducted at a hospital endocrinology department in Nanjing, China, the study enrolled 90 adults with Hashimoto's who were not taking levothyroxine, about a third of them with mildly raised TSH (subclinical hypothyroidism). Forty-three took a 200 μg selenium-enriched yeast tablet daily for six months and 47 received no treatment, with both groups advised to keep iodine intake adequate. Blood and urine tests at baseline, three months and six months measured thyroid antibodies, thyroid hormones, selenium levels and Treg cells by flow cytometry. Selenium blood levels roughly doubled with the supplement (median 73.6 to 187.2 μg/L). By six months, TPOAb fell by 28.4 IU/ml in the selenium group while staying unchanged in controls (p = 0.001), TGAb fell by 48.8 IU/ml while rising by 18.3 in controls (p = 0.001), and TSH edged down (−0.16 mIU/L) while rising in controls (+0.48, p = 0.001). The largest TSH effect appeared in the 29 people with subclinical hypothyroidism (a fall of 2.5 mIU/L versus a rise of 1.91 in controls, p = 0.002). Activated Tregs were higher with selenium (13.19% vs 11.49%, p = 0.012), but the overall Treg percentage was not significantly different (p = 0.214). Free T3 and free T4 did not differ, and no adverse effects were reported. The authors suggest selenium may lower thyroid antibodies by raising antioxidant capacity and activated Tregs, with the greatest TSH benefit in subclinical cases. The evidence is limited: no placebo, open-label allocation, one hospital, a small sample, exploratory subgroup findings (interaction tests for selenium level were not significant), and only blood markers over six months, so symptoms, disease course and levothyroxine need were not assessed. The results apply only to people not taking levothyroxine, and the authors call for pre-specified trials.

Nutrients · 2025

This single-blind randomised pilot study with 45 people who have Hashimoto's thyroiditis explored whether a Mediterranean diet or a gluten-free diet changes the body's balance between damaging molecules and antioxidants. Hashimoto's thyroiditis is an autoimmune condition in which the immune system attacks the thyroid gland, and patients tend to show higher oxidative stress, meaning an excess of reactive molecules that injure tissue. The Mediterranean diet is a plant-based pattern built on vegetables, legumes, fruit, nuts, whole grains and olive oil, while the gluten-free diet removes wheat, rye, barley and related grains, and the researchers compared both with simply eating as usual. The study ran at a university hospital in Messina, Italy. Participants were adults aged 18 to 65 with newly diagnosed Hashimoto's, normal thyroid function and no thyroid medication, split evenly into three groups of 15: Mediterranean diet, gluten-free diet or free diet. A dietitian explained each regimen individually, and a three-day food record checked adherence. Blood tests at the start and after 12 weeks measured thyroid hormones, thyroid antibodies and four oxidative-stress markers (AGEs, GPx, TRxR and TEAA). Thyroid hormone and antibody levels did not change significantly in any group, including TPO-Ab and Tg-Ab (the antibodies that mark the immune attack on the thyroid). The Mediterranean diet group, however, showed significantly lower AGEs (advanced glycation end products, damaged proteins linked to oxidative stress) and significantly higher GPx, TRxR and TEAA, which are antioxidant enzymes or overall measures of antioxidant defence (p < 0.001 versus baseline and versus the other two groups). The gluten-free and free-diet groups showed no significant change in these markers (p > 0.05). TPO-Ab fell numerically with the gluten-free diet but not significantly, which the authors read as no relevant effect of gluten restriction on thyroid autoimmunity or function after 12 weeks. In other words, the antioxidant signal appeared only with the Mediterranean pattern. The authors conclude that the Mediterranean diet had a strong antioxidant effect and that a gluten-free diet did not improve redox balance in people with Hashimoto's who do not have coeliac disease. The study has clear limits: only 15 people per group, 12 weeks of follow-up, laboratory markers rather than symptoms or quality of life, and no change in thyroid antibodies, so the findings are preliminary and cannot be generalised to all autoimmune thyroid disorders.