Brookhaven Lab Notes — research digest on Beef liver / vitamin A bioavailability

Beef liver: Eekhoff et al., 2026

A feedlot trial in 95 beef steers found that dietary vitamin A supplementation increased liver and serum retinol concentrations but reduced the percentage of carcasses grading Choice or higher, while zinc supplementation increased plasma zinc and interacted with vitamin A to shift carcass composition. This is a well-powered randomized trial measuring both tissue retinol and carcass outcomes — relevant for understanding what drives vitamin A levels in the beef we eat.

Key takeaways

  • Steers receiving no supplemental vitamin A had lower liver retinol (360 vs 510 µg/g wet tissue) but better marbling grades — 71% graded average Choice or higher vs 50% in supplemented steers.
  • Zinc supplementation at 120 mg/kg increased plasma zinc concentration by 23% and interacted with vitamin A to alter carcass fat deposition patterns.
  • Serum retinol in unsupplemented steers declined over 79 days, indicating progressive depletion when dietary vitamin A is removed.
  • This is a factorial RCT with 95 animals across 16 pens — large enough to detect real effects on both tissue nutrient levels and carcass quality.
  • The study measures what matters for human nutrition: actual retinol concentrations in liver tissue, not surrogate markers.

The study

Eekhoff and Hansen, writing in the Journal of Animal Science (2026), randomized 95 Angus-cross steers (473 kg starting weight) to four treatment groups in a 2×2 factorial design: no supplemental vitamin A vs 2,200 IU/kg, crossed with no supplemental zinc vs 120 mg/kg zinc sulfate. The trial ran 84 days. All steers received a growth-promoting implant at trial start. Researchers measured body weight, feed intake, liver retinol and mineral concentrations (days 3 and 79), serum retinol and plasma minerals (days 0, 56, 79), and carcass quality after slaughter. The vitamin A dose represents typical industry supplementation; the zero-supplementation group relied on basal forage vitamin A only. Each pen (4 pens per treatment) had individual feed intake monitoring. Blood and liver samples underwent laboratory analysis for retinol and trace minerals. Carcass grading followed USDA standards after a 48-hour chill.

How to read this study

What this paper does well: The sample size of 95 steers with 16 pens gives statistical power to detect both performance differences and carcass quality shifts. The 2×2 factorial design lets the authors test not just vitamin A alone and zinc alone, but whether the two nutrients interact — which they did. The trial measured the endpoint that matters for human nutrition: actual retinol concentration in liver tissue at two timepoints (early and late), not a proxy marker. The repeated measures on serum retinol (days 0, 56, 79) show the trajectory of depletion in unsupplemented animals. The carcass data are objective USDA grades, not subjective assessments.

What this paper is missing: This is an animal production trial, not a bioavailability study in humans. The steers were also implanted with synthetic hormones (trenbolone acetate and estradiol), which are banned in many countries and may alter nutrient metabolism — that limits direct translation to grass-finished or pastured beef. The trial used retinyl acetate supplementation, a synthetic form, so we don't know if natural dietary sources (carotenoids from pasture) would behave identically. There's no measurement of which retinyl esters accumulated in liver or their bioavailability to humans consuming the organ meat.

How I'd weight this paper: I treat this as strong evidence for the question "Does dietary vitamin A supplementation in cattle increase liver retinol content?" — the answer is clearly yes. I weight it moderately for the question "Does beef liver vitamin A bioavailability differ by cattle diet?" because the trial wasn't designed to test human absorption, and the hormone implants muddy the translation. For Brookhaven customers eating grass-finished liver, this tells us that cattle diet does matter for organ nutrient density, but we'd need human trials to know if the retinol forms are equally bioavailable.

What they found

Liver retinol concentration was 42% higher in vitamin A-supplemented steers (510 µg/g wet tissue) compared to unsupplemented (360 µg/g). Serum retinol in the unsupplemented group started at 32 µg/dL and declined to 24 µg/dL by day 79, while the supplemented group held steady at 38 µg/dL throughout (interaction P < 0.01). Plasma zinc concentration showed a zinc × vitamin A interaction (P = 0.02): it was highest when zinc was supplemented (120 mg/kg) regardless of vitamin A level, lowest in the 0ZN-0VA group, and intermediate in 0ZN-2200VA.

Despite higher liver retinol, vitamin A-supplemented steers had worse marbling: 50% graded average Choice or higher vs 71% in unsupplemented steers (P = 0.03). Feed efficiency (gain-to-feed ratio) was 5% better in the 2200VA group (P = 0.05), but final body weight, average daily gain, and hot carcass weight did not differ between groups (P ≥ 0.21). Rib fat tended to be higher in the 0ZN-2200VA group (P = 0.08). Dressing percentage showed a complex interaction, ranging from 61.8% to 63.1% across treatments.

Plasma copper increased by day 56 in vitamin A-supplemented steers and remained elevated, while unsupplemented steers' copper levels declined after day 56 (interaction P = 0.01). Liver copper was lowest in the 120ZN-2200VA group (P = 0.04), suggesting that combined supplementation may suppress hepatic copper accumulation.

What it means for the average man

If you're eating beef liver for vitamin A, the cattle's diet matters. Steers without supplemental vitamin A had 29% lower liver retinol by the end of the 84-day trial. That gap would likely widen over a longer feeding period. Grass-finished cattle eating fresh pasture get carotenoids (vitamin A precursors) from green forages; grain-finished cattle in feedlots often receive synthetic vitamin A supplementation because grain is low in carotenoids. This trial suggests that cattle raised without synthetic supplementation will produce liver with meaningfully less retinol.

The zinc-vitamin A interaction is relevant: supplementing both nutrients shifted carcass composition and reduced liver copper. For men taking Brookhaven's Total Men's Package, which includes grass-fed liver plus additional zinc and minerals, this reinforces that nutrient ratios matter — not just individual vitamins in isolation. The trial also hints at a performance trade-off: better feed efficiency but worse marbling with vitamin A supplementation. For beef quality, "more" isn't always better.

The caveats

These steers received growth-promoting hormone implants (trenbolone acetate and estradiol benzoate), which are prohibited in the EU, UK, and increasingly in regenerative US beef production. Hormones alter nutrient metabolism, so these findings may not directly translate to grass-finished, non-implanted cattle. The trial ran 84 days, which is short relative to a full grass-finishing cycle (often 18-24 months from weaning to slaughter). The vitamin A dose (2,200 IU/kg DM) is standard in conventional feedlots but may not reflect natural pasture intake. The study measured retinol concentration in liver tissue but didn't assess the form of retinyl esters or their bioavailability to humans consuming the organ. No human absorption data were collected. The "no supplemental vitamin A" group still had some basal vitamin A from feed — this wasn't a true deficiency model.

Frequently asked questions

Should I trust a trial in cattle to predict what happens in humans?

It depends on the question. For "Does dietary vitamin A affect liver retinol concentration?" — yes, the mechanism is conserved across mammals. For "Is the retinol in that liver bioavailable to me when I eat it?" — no, you need human trials. This study tells us cattle diet changes liver nutrient density, which is useful, but it doesn't directly measure human absorption or utilization.

Does the 95-animal sample size matter?

Yes. Feedlot trials often use 30-50 animals. With 95 steers across 16 pens, this study had enough statistical power to detect a 5% difference in feed efficiency and a 21-percentage-point difference in Choice grading. Larger samples reduce the chance that random variation drives the result. The liver retinol difference (360 vs 510 µg/g) was statistically significant at P = 0.01, meaning there's less than a 1% probability it's due to chance.

Why did vitamin A supplementation hurt marbling?

The authors didn't measure mechanism, so we're speculating. High-dose retinoids can alter adipocyte (fat cell) differentiation and lipid metabolism. Some prior cattle research shows that restricting vitamin A before slaughter increases intramuscular fat. The exact pathways are unclear, but the trade-off between growth efficiency and meat quality is real in this dataset.

Does this mean grass-finished beef liver has less vitamin A?

Not necessarily. This trial compared synthetic retinyl acetate supplementation to no supplementation (but with basal feed vitamin A). Cattle on high-quality green pasture consume carotenoids, which convert to retinol. We'd need a head-to-head trial comparing grass-fed vs grain-fed finishing systems, measuring liver retinol at slaughter, to answer definitively. This study tells us dietary vitamin A source and dose matter, but it doesn't settle the grass vs grain question.

Sources

  • Eekhoff M, Hansen S. Exploring the interaction of vitamin A and zinc in finishing cattle. J Anim Sci. 2026. PubMed
  • Wang Y, et al. Effect of vitamin A restriction on marbling deposition and gene expression in beef cattle. Meat Sci. 2009;83(4):631-637.

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

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