Growing up, many of us remember dutifully taking a few more bites of protein (and, of course, vegetables) to appease our moms before we were allowed to progress to the sweet, carb-heavy goodness of dessert. Lately, it seems hard to say whether our moms would be delighted or horrified to see what has happened to protein since.

Just walk into any grocery store right now, and protein is everywhere. Protein water. Protein chips. You can even request protein foam on your favorite fancy latte. Somewhere, a bodybuilder is chugging a protein shake the size of a fire extinguisher as you read this. It’s safe to say this is not your mother’s protein.

To be fair, protein deserves at least some of its mom-and-jock-endorsed reputation. It helps build muscles, keeps you feeling full, and is an essential nutrient we truly can’t live without. Older adults, especially, have been told to eat more of it as they age. 

So, is more protein always better? According to a large review of several recent studies, the answer may be no.

“We think of protein as beneficial,” Dr. Dudley Lamming, a professor at the University of Wisconsin-Madison and lead researcher of the review, told Popular Science, “but a number of studies have started to come out showing that when you look at large populations over the course of decades, people who were eating more protein over the course of these decades were having higher rates of age-related diseases.”

A pattern in the data sparked new questions 

Lamming didn’t set out looking for a problem with protein. If anything, he was surprised by a contradiction he was noticing between population data and the conventional wisdom about protein—people who ate more protein over time were showing higher rates of cancer, diabetes, and cardiovascular disease. 

“The question is, how can this be?” he remembers wondering.

Lamming’s review looked at more than 350 studies in total, most of which were conducted in mice and other lab models, examining things like lifespan, metabolic health, and cellular aging. 

But a smaller slice, about five or six randomized trials, tested protein restriction directly in people. Those human trials showed consistent short-term benefits: People lost weight, their fat mass declined, and in one study of people with type 2 diabetes, insulin sensitivity improved.

Lamming adds that these results do not appear to be associated with mere calorie reduction.

“In fact, because dietary protein is satiating, people in our studies and others actually ate more calories when they were on a protein-restricted diet,” he says. “But they lost weight, and that’s because energy expenditure increases.”

One hormone may explain what’s happening

To understand the potential connection between protein restriction and increased energy expenditure, Lamming’s review explored existing mouse studies on the topic. Findings from these studies indicate that when protein intake drops, the liver releases a hormone called FGF21. That hormone signals the brain, which in turn triggers what researchers call “beiging.”

“This is a process that essentially tells your fat tissue to stop simply storing fat, but actually to start metabolizing it and burning it for energy,” says Lamming. 

In practice, protein restriction doesn’t mean cutting protein out altogether. Most people get about 16 to 17 percent of their calories from protein; in the studies Lamming and his team reviewed, that’s typically cut by around half, down to roughly seven to nine percent.

“We’re not talking about restricting to an unhealthy level where you’re protein insufficient,” he says. “What we’re really talking about, in most cases, is restricting down to the recommended daily allowance as reported by the World Health Organization, which is about 0.8 grams per kilogram [of body weight].” 

So the average man (weighing an average of about 200 pounds) would need about 73 grams of protein a day. The average woman, on the other hand, (weighing about 170 pounds) would need 62 grams of protein a day. For reference, a small three ounce filet of salmon contains about 24 grams of protein.

You don’t necessarily have to restrict protein as a whole to achieve these benefits, either; mouse studies found that cutting back on specific amino acids, including methionine, isoleucine, and valine, may provide some of the same benefits in terms of fat mass, blood sugar control, and longevity. 

Exercise may change the equation

This doesn’t necessarily mean everyone should be in a hurry to throw away their protein waffles. Lamming is careful to note that people who exercise routinely may be an exception.

“We actually think that dietary protein has negative metabolic health outcomes for sedentary people, like the general population, since most of the population is fairly sedentary,” he says. “But maybe people who are exercising need more protein to help build muscle, and maybe it wouldn’t have these negative metabolic outcomes.”

Although these findings are based only on mouse studies so far, they may suggest that working out might protect against the downsides of higher protein intake, Lamming says. 

“Fortunately,” he says, “a lot of the people who are very pro-protein are also people who are exercising.”

Lamming says his team plans to test these ideas—specifically, whether protein supplementation genuinely benefits those who exercise, and whether restriction benefits those who don’t—more directly in both mice and people over the next few years.

“For your typical person who’s not engaged in exercise, we would suspect, based on our research, that eating more calories in the form of protein would be detrimental,” he says. 

Lamming’s own suggestion for sedentary people: Consider skipping the protein-added version of a product when a regular option is available.

He was quick to add, however, that those who can safely exercise certainly should.

“No one’s going to argue that more exercise would be bad,” he says.

In Ask Us Anything, Popular Science answers your most outlandish, mind-burning questions, from the everyday things you’ve always wondered to the bizarre things you never thought to ask. Have something you’ve always wanted to know? Ask us.

The post You might be eating too much protein appeared first on Popular Science.

Researchers in Brazil have demonstrated that a hybrid advanced oxidation process can transform pharmaceutical-laden wastewater into an effluent that is dramatically safer for plants, earthworms, onion root cells, and beneficial microorganisms, offering a rigorous ecotoxicological case for reusing treated sewage in agriculture. The study, published in Environmental Science and Pollution Research, addresses a long-standing blind spot in water treatment: proving that a chemically “clean” effluent is also biologically compatible.

Conventional wastewater treatment plants were never designed to strip out recalcitrant organic micropollutants such as pharmaceuticals, and trace amounts routinely slip through into receiving waters. Advanced oxidation processes (AOPs) attack these stubborn compounds by generating highly reactive free radicals that fragment contaminant molecules. But chemical degradation alone does not guarantee safety. As contaminants break down, they spawn transformation products (TPs) that can, in some cases, be as toxic as—or more toxic than—the parent compounds. The research team, led by Lucas Gustavo da Costa and Alam Gustavo Trovó of the Federal University of Uberlândia, together with collaborators at the Oswaldo Cruz Institute, set out to answer a deceptively simple question: does measurable chemical removal of micropollutants actually translate into reduced biological harm?

The centerpiece of their work is the H₂O₂/S₂O₈²⁻/UVC process, a hybrid system that combines hydrogen peroxide and persulfate with short-wave ultraviolet C radiation. UVC photons cleave both oxidants simultaneously, generating hydroxyl radicals (HO•) and sulfate radicals (SO₄•⁻) in the same reaction volume. This dual-radical strategy outperforms systems relying on either oxidant alone, or on peroxymonosulfate (HSO₅⁻), which is costlier and demands more energy for activation. The hybrid route also resists interference from inorganic species commonly found in real effluents, making it an economically attractive candidate for deployment at full-scale treatment plants. The process had already been chemically optimized in the team’s earlier work using multivariate mixture design and rotatable central composite design experiments; the new study is its first integrated biological stress test.

The experiments used real municipal effluent from a wastewater treatment plant in Uberlândia, Minas Gerais, sampled after the plant’s final tertiary treatment stage of coagulation-flocculation with ferric chloride and flotation. The effluent was enriched with three pharmaceuticals representing different therapeutic classes: colchicine (COL, an antimitotic agent), nitazoxanide (NTZ, an antiparasitic), and sulfamethoxazole (SMX, a widely detected antibiotic), each at 325 nmol L⁻¹—equivalent to 130, 100, and 82 micrograms per liter, respectively. That concentration was deliberately chosen as high enough for direct HPLC–DAD analysis without preconcentration, yet low enough to be environmentally representative. Treatment was carried out in an amber glass reactor irradiated by two 8-watt UVC mercury lamps emitting at 254 nm, with a measured irradiance of 4.9 W m⁻². Residual oxidants were neutralized with sodium thiosulfate before any biological testing, ensuring that observed effects could not be attributed to leftover peroxide chemistry.

The ecotoxicological battery spanned multiple trophic levels and levels of biological organization. Oxidative stress was assessed in the earthworm Eisenia andrei by measuring malondialdehyde (MDA), a marker of lipid peroxidation, and protein carbonylation, an irreversible oxidative modification of proteins. Phytotoxicity was evaluated using lettuce (Lactuca sativa) seeds and a growth index combining germination rate and root elongation. Cytotoxicity and genotoxicity were quantified in onion (Allium cepa) root meristems through the mitotic index and the frequency of chromosomal and nuclear aberrations—micronuclei, chromosome breaks, stickiness, bridges, and nuclear buds—across 5,000 cells per sample. Finally, growth inhibition was tested in two environmentally relevant microbes: Azospirillum brasilense, a plant growth-promoting bacterium used in soybean cultivation, and Saccharomyces cerevisiae, a yeast that persists in soils and fermentative niches.

The untreated enriched effluent told a worrying story. It exhibited substantial genotoxicity in onion cells—21%, approaching the 24% seen with the positive control, methyl methanesulfonate—and severe phytotoxicity, with lettuce growth indices far below the 80% threshold that signals absence of toxicity. Even the unspiked effluent itself suppressed lettuce growth, achieving a growth index of only 47%, evidence that bioactive compounds survive conventional treatment. In earthworms, individual aqueous solutions of NTZ and SMX raised MDA levels by 37.2% and 23.5% respectively, while the three-compound mixture increased lipid peroxidation by 38.0%, pointing to additive or synergistic oxidative stress mechanisms involving reactive oxygen species and Fenton-type chemistry within cells.

The picture changed decisively after oxidation. Following 10 minutes of UVC-driven treatment—the point at which 80% chemical degradation had been achieved, matching the minimum removal target proposed in the European Union’s COM(2022)541 directive—genotoxicity fell to 10%, and after 20 minutes, corresponding to the limit of quantification for the parent compounds, it dropped further to 6%, a statistically significant reduction. The plant growth index climbed above 80%, crossing from toxic territory into biocompatibility. The mitotic index in onion cells remained statistically indistinguishable from the deionized-water control (around 39–40% versus 40%), demonstrating that the process generated no cytotoxic byproducts capable of arresting cell division. And crucially for agricultural applications, neither the treated effluent nor its transformation products inhibited growth of A. brasilense or S. cerevisiae.

The mechanistic details are instructive. In the untreated enriched effluent, micronuclei—membrane-bound DNA fragments expelled from the nucleus during flawed cell division—were among the most frequent aberrations, indicating clastogenic and aneugenic damage. Colchicine exposure predictably produced C-metaphase accumulation, a signature of its tubulin-binding, spindle-disrupting mechanism first described in Allium nearly a century ago. SMX depressed the mitotic index and induced chromosomal damage, consistent with prior findings in Vicia faba. NTZ, whose genotoxicity had never before been reported, produced chromosome breaks, stickiness, and nuclear buds. After oxidation, the overall aberration burden fell sharply, particularly micronuclei and stickiness, although a few bridges and polyploid cells persisted even at 20 minutes—a reminder that some transformation products or resistant residuals may linger.

The microbial results came with a subtlety. Reduced A. brasilense growth after treatment initially looked like a red flag, but the team attributes it to depletion of assimilable organic matter, which serves as radical scavenger during oxidation and as a nutrient source afterward—not to toxicity. The negative control likewise grew slowly. This distinction matters because AOPs are designed to mineralize organic carbon, and a nutrient-poorer medium should not be misread as a more toxic one. For S. cerevisiae, no inhibition occurred at any stage of treatment, although NTZ alone significantly depressed yeast optical density, reinforcing the compound’s cell-cycle interference potential even at nanomolar-scale exposures.

The study’s broader significance lies in its methodological stance. By adopting an “effect-driven approach,” the team evaluated the toxicity of whole reaction mixtures without needing to isolate and identify individual transformation products—an impractical task given that many degradation byproducts are not commercially available. Their findings align with a growing consensus that treatment efficacy must be judged not merely by parent-compound removal but by the nature and reactivity of the resulting transformation products. Biochemical biomarkers such as MDA and protein carbonylation detected sublethal disturbances that mortality-based endpoints would have missed entirely, providing early warnings of cellular distress at environmentally relevant concentrations.

One caveat deserves attention: while lipid peroxidation declined after treatment, protein carbonylation rose slightly—1.05-fold above control—suggesting some transformation products may still provoke protein oxidation even as lipid damage subsides. The authors flag this discrepancy and call for future identification of the specific TPs responsible, alongside expanded organism panels, longer-term exposure studies, and pilot-scale validation across different environmental matrices.

The regulatory context sharpens the urgency. The EU’s proposed urban wastewater treatment directive mandates at least 80% removal of specified organic micropollutants and microbiological control for agricultural reuse, yet it conspicuously omits eco-compatibility assessment of the treated water itself. This study supplies exactly that missing dimension, showing that a process satisfying the chemical benchmark also delivers measurable biological benefit—lower genotoxicity, restored plant growth, intact cell division, and unharmed beneficial microbes. As water scarcity intensifies globally and reuse becomes less optional, the Brazilian team’s integrated bioassay framework offers a template for ensuring that the water farmers irrigate with is not merely chemically compliant, but genuinely ecologically safe.