Chemiluminescent Immunoassay Analyzer

Angelika Bogusz et al. (2026) · Nutrients

This randomized controlled trial of 46 women with endometriosis explored whether a fish-derived lipid supplement (a mixture of marine omega-3 fats such as EPA and DHA, plus compounds called squalene and alkylglycerols) adds anything to a Healthy Eating Plate diet. Endometriosis is a long-term, estrogen-dependent condition in which tissue similar to the uterine lining grows outside the uterus. Researchers increasingly describe it as an inflammatory condition, in which signaling proteins called cytokines (messengers that coordinate immune cells) help drive pelvic pain. Omega-3 fats are known to influence these immune pathways, but evidence in endometriosis has been limited, so the team treated the work as exploratory. Women aged 22 to 48 with confirmed endometriosis were randomly assigned to one of two groups for 12 weeks. Both groups followed an individualized Healthy Eating Plate diet with meal plans from a dietitian. One group also took the fish-derived lipid product, dosed by body weight (0.5 mL per kilogram daily). Blood and stool samples were collected before and after to measure five cytokines and fecal calprotectin (a marker of gut inflammation). Pain was rated on a 0 to 10 visual analog scale, and quality of life was scored with the 30-item Endometriosis Health Profile. The clearest signal was in IL-10, a cytokine that restrains immune activation: levels rose in the supplement group and the adjusted difference between groups was significant (about 5-fold higher; 95% CI 1.32 to 19.48; p = 0.019). Other cytokines gave mixed results, with IL-1β, TNF-α, and IL-6 landing right at the edge of significance (p = 0.050 to 0.057) and fecal calprotectin unchanged. Average pain scores dropped within the supplement group (5.0 to 4.3; p = 0.011), yet the difference between groups was not significant. A pain drop of at least 1 point was more common with the supplement (73.9% versus 34.8%; adjusted risk ratio 2.11, meaning roughly twice the likelihood). Quality-of-life scores did not differ between groups, and the paper did not report safety outcomes. The authors describe the pain and IL-10 findings as hints worth testing rather than proof of benefit, since most outcomes showed no consistent advantage over diet alone. The study was small, lasted only 12 weeks, had no placebo, relied on self-reported food records, and ran many secondary analyses without statistical correction. The supplement was also a complex mixture, so the effects cannot be pinned on omega-3 fats alone. The authors call for larger, longer trials that measure fatty acid levels in blood and examine immune cells directly.

Zahra Najdgholami et al. (2025) · Frontiers in endocrinology

This 12-week open-label randomized controlled trial with 70 women explored whether daily flaxseed intake could shift reproductive hormone patterns in polycystic ovary syndrome (PCOS), a common endocrine condition affecting 6 to 15 percent of women of reproductive age. PCOS involves hyperandrogenism (elevated androgen hormones) and disrupted ovulation, often accompanied by a low or borderline follicle-stimulating hormone (FSH) that limits egg follicles from fully maturing. Flaxseed is a plant-based food rich in phytoestrogenic lignans (plant compounds structurally similar to estrogen) and omega-3 fatty acids, both proposed to influence the hormone pathways governing follicle development and gonadotropin balance. Seventy women diagnosed with PCOS at a clinic in Ahvaz, Iran were randomly assigned to 12 weeks of either 30 grams of daily milled flaxseed added to salads, yogurt, or cold drinks, combined with standard diet and exercise guidance, or the same lifestyle guidance without flaxseed. Blood tests measuring FSH, luteinizing hormone (LH), anti-Mullerian hormone, estradiol, DHEAS, and androstenedione were drawn at baseline and after 12 weeks using enzyme immunoassays and chemiluminescent assays, timed to each participant's menstrual cycle phase where applicable. FSH rose significantly more in the flaxseed group than in controls (treatment effect 0.87, 95% CI 0.086-1.75, p=0.027), meaning flaxseed users saw a measurably larger increase in this follicle-stimulating hormone than those on lifestyle changes alone. The ratio of LH to FSH also dropped significantly with flaxseed (treatment effect -0.341, 95% CI -0.63 to -0.08, p=0.031), a lower ratio pointing toward more balanced gonadotropin secretion, since an elevated LH/FSH ratio is a hallmark of PCOS. No significant between-group changes appeared for AMH, LH alone, estradiol, DHEAS, or androstenedione, indicating flaxseed's measured effect was specific to FSH and its ratio to LH rather than the broader hormone panel. Weight, BMI, lipids, and blood sugar stayed similar between groups, and no adverse events were reported, suggesting the 30-gram daily dose was well tolerated over the 12 weeks. The authors propose that flaxseed's omega-3 fatty acids and lignans may support follicle-stimulating hormone receptor activity and gonadotropin regulation, though this mechanism was not directly tested in the trial. The open-label design, unavoidable for a dietary intervention, the single-center setting, and the absence of testosterone and insulin measurements limit how broadly the results extend. The authors identify larger, longer randomized trials incorporating androgen and insulin outcomes as the needed next step for confirming flaxseed's role in PCOS management.

Imran Amjad et al. (2025) · PloS one

This pragmatic randomized controlled trial with 106 adults explored whether chiropractic spinal adjustments change measurable biological markers, not just how patients feel. Researchers tracked three systems: neuroplasticity (the nervous system's capacity to adapt, measured via brain-derived neurotrophic factor or BDNF — a protein that supports brain and nerve health), stress response (measured through cortisol, the body's primary stress hormone, sampled from blood, saliva, and hair), and inflammation (tracked via cytokines like IL-6 and TNF-α, signaling proteins immune cells use to coordinate the body's inflammatory response). The goal was to see whether chiropractic care's known benefits for pain and function might trace back to changes at this biological level. Pain-free adults aged 20-60 with a history of recurrent (subclinical) spinal discomfort were randomly assigned to 12 weeks of chiropractic spinal manipulation — delivered about three times weekly by a registered chiropractor — or a closely matched sham procedure with no actual spinal thrust. Eighty-eight of the 106 enrolled completed the 12-week assessment. Blood, saliva, and hair samples were analyzed via laboratory immunoassay at baseline, 12 weeks, and a 16-week follow-up. Blinding worked well: 94% of participants in both groups believed they had received real chiropractic care. After 12 weeks, the chiropractic group showed meaningfully higher blood BDNF (up 150 units, p=0.009 — a strong statistical signal this wasn't due to chance) and higher IL-6 (p<0.001) than the sham group, alongside lower TNF-α at both 12 and 16 weeks (p=0.023 and p=0.028). The researchers interpret the IL-6 rise not as harmful inflammation but as a "myokine" effect — the same kind of signal muscles release after exercise — since it appeared alongside lower TNF-α and IFN-γ, the markers more classically tied to harmful inflammation. By 16 weeks, blood cortisol and IFN-γ were lower in the chiropractic group than sham, though this reflected the sham group's levels rising over that period more than a further chiropractic effect. Markers like CRP and several immune cell counts (CD4, CD8, CD56) showed no clear group differences. Only five participants reported mild, short-lived muscle soreness; no other adverse events occurred. This is among the first studies to track chiropractic's biological effects over months rather than single sessions, offering a possible mechanism — neuroplasticity, stress-hormone, and inflammation changes — behind chiropractic's reported clinical benefits. But the effects were modest, confidence intervals were wide, and the single-site Pakistani sample of 88 completers, with over 30% dropout by 16 weeks, limits how far these findings generalize. Larger trials that connect these biomarker shifts to actual pain relief and function are the next step.