Protein Diet Longevity Risks: What the Evidence Actually Shows

Few nutritional debates generate more heat and less light than the question of how much protein a person should eat across a lifetime. On one side stand researchers pointing to rodent studies and epidemiological data suggesting that high-protein diets accelerate aging. On the other stand exercise physiologists and clinicians watching their patients lose muscle, fall, fracture bones, and age prematurely on protein-restricted diets. Both camps cite real data. Both are partially right. The truth, as the evidence increasingly reveals, is that the relationship between protein intake, longevity risks, and healthspan is not a straight line but a curve shaped by age, protein source, physical activity, and the molecular machinery that protein activates inside every cell.

Understanding those risks and benefits requires moving beyond headline numbers and into the biology. Protein is not simply building material. It is a signaling molecule, a regulator of some of the most consequential longevity pathways in human physiology. Getting the dose wrong in either direction carries real costs. This article examines what the peer-reviewed literature actually shows about protein diet longevity risks, where the evidence is strong, where it is genuinely contested, and what a science-informed approach to protein intake across the lifespan looks like in practice.

The mTOR Problem: Why Protein Is Never Just Food

The controversy over protein and longevity traces its molecular roots to a single enzyme complex: mTOR, mechanistic target of rapamycin. mTOR functions as a cellular nutrient sensor, a master switch that reads the availability of amino acids, particularly leucine and arginine, and uses that information to decide whether cells should grow and replicate or conserve resources and repair. When protein intake is high, mTOR is activated. When protein is restricted or cells are starved, mTOR is suppressed, and a competing process called autophagy, the cellular equivalent of a recycling program, ramps up instead.

The longevity implications of this switch are not subtle. In virtually every model organism studied, from yeast to worms to fruit flies to mice, reducing mTOR activity extends lifespan. Rapamycin, the pharmacological mTOR inhibitor, remains the most reproducible lifespan-extending drug ever tested in mammals. [1] The inference that followed was seemingly obvious: if mTOR drives aging and dietary protein activates mTOR, then high-protein diets must accelerate aging. This logic shaped a generation of nutritional recommendations and dozens of epidemiological studies.

The inference that dietary protein accelerates aging through mTOR is intellectually elegant. It is also incomplete. mTOR activation in skeletal muscle is not the same biological event as mTOR activation in a cancer cell, and conflating the two has generated more confusion than clarity.

The complication is that mTOR does not operate uniformly across all tissues, and its activation in skeletal muscle is not the same biological event as its activation in, say, a senescent immune cell or a rapidly dividing cancer progenitor. In muscle tissue, the brief, meal-stimulated pulse of mTOR activity triggered by protein ingestion drives muscle protein synthesis, the repair and reinforcement of contractile fibers. This is a fundamentally different signal than the chronic, nutrient-excess-driven mTOR hyperactivation associated with obesity and metabolic disease. The temporal pattern of the signal matters as much as its presence. [2]

This distinction is critical because it reframes the entire debate. The question is not whether to activate mTOR at all. The question is when, for how long, in which tissue, and at what baseline metabolic health. And that question has no single answer independent of a person's age, body composition, and activity level, all of which shift the risk-benefit calculation substantially.

What Epidemiology Shows, and Where It Breaks Down

The most-cited evidence linking high-protein diets to longevity risks comes from a 2014 paper by Levine and colleagues analyzing data from the NHANES III cohort. The study followed more than 6,000 American adults and found that respondents between 50 and 65 who reported high protein intake (greater than 20 percent of calories from protein) had a 74 percent increased risk of all-cause mortality and a fourfold increase in cancer mortality compared with those consuming low protein (under 10 percent of calories from protein). [3] These are striking numbers, and they were widely reported.

But the study contained a finding that most headlines omitted entirely. Among adults over 65, the association reversed. High protein intake in older adults was associated with a 28 percent reduction in all-cause mortality and a 60 percent reduction in cancer mortality. The relationship between protein intake and longevity risk was not a straight line. It was age-dependent, and profoundly so. The researchers hypothesized that IGF-1, a growth hormone whose levels are partially regulated by dietary protein, may mediate these opposing effects: elevated IGF-1 in midlife promotes cancer growth, while adequate IGF-1 in older age preserves muscle and immune function. [3]

Subsequent analyses have complicated the picture further. A large 2020 meta-analysis examining protein intake and all-cause mortality across multiple prospective cohort studies found no significant association between total protein intake and mortality risk when studies were pooled. [4] Animal protein showed a weak positive association with cardiovascular mortality; plant protein showed a modest protective association. But the effect sizes were small, the heterogeneity between studies was high, and residual confounding, the ever-present ghost in nutritional epidemiology, makes causal inference hazardous.

The epidemiological literature on protein and longevity suffers from a fundamental methodological problem. Protein intake is almost never independent of other dietary and lifestyle variables. People who eat large quantities of animal protein often consume less fiber, more saturated fat, and more processed food. They may exercise differently, earn different incomes, and carry different baseline disease risk. Separating the effect of protein per se from the dietary pattern it accompanies is extraordinarily difficult, and most observational studies lack the granularity to do it well. This is not a reason to dismiss the epidemiology, but it is a reason to weight it carefully against mechanistic and interventional data.

Protein Source: The Variable That Changes Everything

When researchers began disaggregating protein by source rather than treating it as a single dietary variable, a clearer pattern emerged. The type of protein consumed appears to matter as much as the quantity, and possibly more. Multiple large cohort studies now consistently show that substituting plant protein for animal protein, particularly red and processed meat, is associated with reduced cardiovascular and all-cause mortality risk. [5]

The mechanistic explanations are plausible and multiple. Red meat, particularly processed red meat, delivers not just protein but also heme iron, N-glycolylneuraminic acid (Neu5Gc), trimethylamine N-oxide (TMAO) precursors, and advanced glycation end-products (AGEs). Each of these compounds has been independently associated with increased inflammatory burden, endothelial dysfunction, and accelerated vascular aging. [6] By contrast, plant-derived proteins arrive packaged with dietary fiber, polyphenols, and phytochemicals that support gut microbiome diversity and reduce systemic inflammation. The protein in a can of lentils is not the same biological package as the protein in a processed sausage, even if the gram count on paper looks similar.

The protein in a can of lentils is not the same biological package as the protein in a processed sausage, even if the gram count on paper looks similar. The container changes the content.

Animal proteins are not monolithic either. Dairy and fish proteins show neutral to favorable associations with longevity outcomes in most large cohort analyses, patterns that diverge sharply from red meat. Whey protein, derived from milk, contains high concentrations of leucine and cysteine, the latter being a precursor to glutathione, the body's primary endogenous antioxidant. Alpha-lactalbumin, a whey fraction, has a particularly favorable amino acid profile with evidence for supporting both muscle protein synthesis and metabolic health. [7] These distinctions matter for any practical recommendation about protein diet longevity risks.

Fish and seafood introduce another variable: omega-3 fatty acids, particularly EPA and DHA, which have independent anti-inflammatory and cardioprotective effects that complicate attribution. When a person eating salmon lives longer than a person eating processed red meat, attributing that difference to protein alone is methodologically indefensible. The observed benefits likely involve the entire dietary matrix.

The Sarcopenia Equation: Protein Restriction's Hidden Cost

Any honest analysis of protein diet longevity risks must account for the costs of insufficient protein, not just the potential costs of excess. Sarcopenia, the age-related loss of skeletal muscle mass and function, is one of the most consequential and underrecognized drivers of mortality and disability in older adults. Beginning around the fourth decade of life, adults lose roughly 3 to 8 percent of muscle mass per decade in the absence of deliberate countermeasures. After age 60, that rate accelerates. [2]

The clinical consequences of sarcopenia extend far beyond physical weakness. Skeletal muscle is the largest site of glucose disposal in the body, and its progressive loss drives insulin resistance, metabolic dysfunction, and eventually type 2 diabetes. Muscle also functions as a reservoir for amino acids that support immune function during illness. Frail, muscle-depleted older adults have higher rates of surgical complications, longer hospital stays, greater fall and fracture risk, and substantially higher all-cause mortality than their muscle-replete counterparts. Loss of muscle is not just a cosmetic problem. It is a life-threatening one. [8]

A fundamental biological problem compounds this risk in older adults: anabolic resistance. Aging muscle becomes progressively less sensitive to the protein synthesis stimulus triggered by dietary amino acids and exercise. Where a younger person's muscle responds robustly to 20 grams of leucine-rich protein per meal, an older person's muscle may require 35 to 40 grams to generate an equivalent anabolic response. [9] This means that protein recommendations calibrated for younger adults systematically under-serve older populations. The current RDA of 0.8 grams of protein per kilogram of body weight per day was set to prevent deficiency in healthy young adults. Growing evidence suggests it is inadequate for maintaining muscle mass and function in adults over 65. [8]

A 2018 meta-analysis and systematic review across 49 randomized controlled trials found that protein supplementation significantly increased muscle mass and strength gains in adults engaged in resistance training, with larger effects observed at protein intakes above 1.62 grams per kilogram per day. [10] The PROT-AGE Study Group, a consortium of international experts in aging and nutrition, has recommended that healthy older adults consume 1.0 to 1.2 grams per kilogram of body weight daily, with higher targets of 1.2 to 1.5 grams per kilogram for those who are physically active or recovering from illness. [11]

These numbers sit well above the conventional RDA, and they illustrate a genuine tension in the protein longevity debate. The epidemiological signals suggesting longevity risks from high protein, derived largely from middle-aged cohorts, must be weighed against the mechanistic and clinical evidence showing that protein restriction in older adults accelerates the very processes, muscle loss, frailty, immune decline, that shorten healthspan most directly. A policy that may be protective at 50 may be harmful at 75.

IGF-1, Cancer, and the Growth Signal Paradox

Insulin-like growth factor 1 (IGF-1) sits at the center of the protein-cancer-longevity debate. IGF-1 is a peptide hormone produced primarily in the liver in response to growth hormone signaling, and its levels are partially responsive to dietary protein intake, particularly animal protein. IGF-1 promotes cellular growth, proliferation, and survival. In a healthy, young organism with intact surveillance mechanisms, these are desirable properties. In an older organism with accumulated genomic damage and a higher burden of pre-cancerous cells, they become double-edged.

Epidemiological data linking higher IGF-1 levels to increased risk of breast, prostate, and colorectal cancers have generated legitimate concern. [12] The growth signal that protein intake amplifies could, in theory, accelerate the progression of occult tumors that would otherwise remain dormant. This is the mechanistic basis for the midlife protein restriction hypothesis, and it is not frivolous. Centenarian studies have found that long-lived individuals tend to have lower circulating IGF-1 than age-matched controls, a pattern also observed in genetic models of extended longevity. [13]

The practical difficulty is that IGF-1 is not a purely malevolent hormone. It plays critical roles in neuronal survival, cardiovascular health, and immune function. In older adults, lower IGF-1 is associated with frailty, cognitive decline, and cardiovascular mortality, creating a clinical dilemma where the optimal level is not zero and not maximal but context-dependent. [14] The cancer risk associated with high IGF-1 appears most pronounced in middle age, when the reservoir of accumulated cellular damage is growing but cancer surveillance mechanisms are still functional enough to be overwhelmed rather than simply inoperative. After 70, the risk calculus appears to shift.

Additionally, resistance exercise, which is strongly associated with reduced cancer risk and extended healthspan, also transiently elevates IGF-1 in muscle tissue. The context of IGF-1 elevation matters. Exercise-driven IGF-1 signaling in muscle is associated with beneficial adaptations, not cancer promotion. The tissue specificity and temporal pattern of growth factor signaling cannot be captured by a single serum measurement, which is part of why the epidemiology of IGF-1 and longevity remains difficult to interpret. [15]

Autophagy, Protein Intake, and the Cleansing Window

One of the most compelling arguments for periodic protein restriction involves autophagy, the cellular self-cleaning process that degrades damaged proteins, dysfunctional organelles including mitochondria, and intracellular pathogens. Autophagy is suppressed by mTOR activation and therefore suppressed by protein feeding. When mTOR is quiescent, during fasting, protein restriction, or sleep, autophagy ramps up and the cell clears its metabolic debris. Think of it as the overnight cleaning crew that can only work when the office is empty.

Impaired autophagy is implicated in nearly every age-related disease of significance: neurodegeneration in Alzheimer's and Parkinson's disease, cardiac dysfunction, cancer, and metabolic syndrome. [16] Promoting autophagy through dietary strategies, including intermittent fasting, time-restricted eating, and strategic protein cycling, has become an active area of longevity research. The theoretical framework is sound. The clinical evidence in humans, however, is substantially thinner than the mechanistic story suggests.

Most human autophagy data comes from short-term fasting studies measuring autophagy markers in peripheral blood cells, not the tissues where autophagy most matters: neurons, cardiomyocytes, and hepatocytes. Whether the autophagy induction observed during a 24-hour fast translates into meaningful long-term cellular rejuvenation in humans remains an open question. [17] What is clearer is that chronic protein restriction sufficient to suppress mTOR continuously would also suppress muscle protein synthesis continuously, a trade-off that in older adults is likely harmful on balance.

A more nuanced approach, one supported by emerging evidence, involves cycling between periods of protein-stimulated mTOR activation (particularly around resistance exercise) and periods of lower protein intake that permit autophagy. This is not a strict protocol but a biological logic: eat enough protein at the right times to build and repair muscle, and allow sufficient windows of lower protein availability for cellular housekeeping. For older adults focused on preserving muscle while supporting longevity pathways, this represents a more sophisticated target than either chronic high-protein or chronic protein restriction. [2]

Kidney Health: A Genuine Risk in Specific Populations

Perhaps the most evidence-backed concern about high-protein diets involves renal function, and it illustrates the importance of individualizing protein recommendations rather than applying population-wide targets. The kidneys filter protein metabolic waste products, primarily urea and creatinine, and high protein intake increases the glomerular filtration rate (GFR), the volume of blood filtered per minute. In healthy kidneys, this increased workload appears to be well-tolerated. Multiple systematic reviews have found no evidence that high protein intake accelerates renal function decline in people with normal kidney function. [18]

The picture changes dramatically in people with existing chronic kidney disease (CKD). In compromised kidneys where nephrons, the microscopic filtering units, have already been lost, the increased hydraulic pressure associated with high-protein diets can accelerate the progressive loss of remaining functional tissue. Protein restriction to 0.6 to 0.8 grams per kilogram per day is a standard therapeutic intervention in CKD to slow disease progression. [19] For individuals with undiagnosed CKD, which affects approximately 37 million Americans and often produces no symptoms until significant damage has occurred, high-protein diets could be inadvertently harmful.

This underscores a principle that runs through every aspect of protein diet longevity risk assessment: baseline health status and individual biology mediate outcomes. A recommendation appropriate for a healthy 35-year-old athlete is not necessarily appropriate for a 60-year-old with hypertension, and applying population-level protein advice without screening for renal function is clinically imprecise. Baseline laboratory testing, including serum creatinine, estimated GFR, and urine albumin-to-creatinine ratio, is essential context for any personalized protein recommendation.

The Gut Microbiome Connection

An often-overlooked dimension of protein diet longevity risks involves the gut microbiome. The trillions of bacteria residing in the human colon do not simply process dietary residues passively. They are metabolically active communities that produce signaling molecules influencing inflammation, immune regulation, and even brain function. The composition and metabolic output of that community is shaped substantially by what a person eats, including how much protein and what kind.

High animal protein diets, particularly those rich in red meat, alter microbiome composition in ways that generally reduce microbial diversity and increase the abundance of bacteria that produce pro-inflammatory metabolites. TMAO, mentioned earlier as a cardiovascular risk factor, is not produced by the human body directly. It is produced by gut bacteria from dietary precursors abundant in red meat, particularly carnitine and choline, and then absorbed into circulation. [20] Individuals with microbiome compositions favoring TMAO-producing bacteria generate more TMAO from the same dietary load, which may partly explain why cardiovascular risk from red meat consumption varies considerably between individuals.

Plant-based protein sources, packaged as they are with prebiotic fiber, generally support a more diverse and anti-inflammatory microbiome. Whether this microbiome benefit is a primary driver of the plant protein longevity associations or a secondary passenger effect remains an open question, but it represents a plausible mechanistic path that does not require invoking mTOR or IGF-1. The diversity of the gut ecosystem may itself be a longevity asset, and the type of protein consumed is one lever that influences it. [21]

Exercise: The Variable That Rewrites the Equation

No analysis of protein intake and longevity can be complete without addressing the variable that most consistently modifies the risk-benefit calculation: physical activity, and specifically resistance training. The evidence that regular resistance exercise, even initiated in the seventh or eighth decade of life, attenuates sarcopenia, improves metabolic health, reduces all-cause mortality, and extends functional healthspan is among the most robust in all of medicine. [22]

Resistance training fundamentally changes what dietary protein does in the body. In an sedentary individual, dietary amino acids above maintenance requirements are oxidized or converted to glucose and stored as fat. mTOR activation without mechanical stimulus produces limited muscle protein synthesis. In an individual engaged in regular resistance training, the same dietary protein drives meaningful muscle hypertrophy, strength, and metabolic adaptation. The protein is being directed, purposefully, into tissue that extends life. [10]

Resistance training fundamentally changes what dietary protein does in the body. The same gram count that accumulates as metabolic waste in a sedentary person becomes structural reinforcement in someone who trains.

This reframes the mTOR concern substantially. If the longevity risks of mTOR activation are mediated by indiscriminate cellular growth, the solution is not necessarily to suppress mTOR chronically but to direct its activation toward skeletal muscle through mechanical stimulus. Exercise makes protein a more targeted tool. The concern about high protein diets in sedentary middle-aged individuals is more defensible than the same concern applied to physically active adults of any age. Separating protein intake from physical activity in any longevity risk analysis produces conclusions that are likely to mislead.

Protein Timing, Distribution, and Practical Considerations

The science of protein timing adds a further layer of practical nuance. Most research on muscle protein synthesis suggests that the anabolic response to protein feeding is maximized by distributing intake across three to four meals providing 30 to 40 grams of high-quality protein each, rather than concentrating intake in a single large meal. The so-called muscle full effect means that flooding the system with 80 grams of protein at dinner produces a similar acute anabolic response to consuming 40 grams, with the excess substrate oxidized rather than utilized for synthesis. [23]

For older adults with anabolic resistance, evening emphasis of protein intake, particularly a leucine-rich protein source before sleep, has shown promise in some studies for augmenting overnight muscle protein synthesis. Casein protein, digested slowly, provides a sustained amino acid release during the overnight fast. For athletes and aging adults alike, the distribution of protein across the day may be as consequential as the total daily intake. [23]

Protein quality, measured by the Digestible Indispensable Amino Acid Score (DIAAS), also matters in ways that pure gram counting conceals. Animal proteins and certain plant proteins, such as soy and quinoa, provide complete essential amino acid profiles. Most other plant proteins are limited in one or more essential amino acids, requiring complementary combinations to achieve equivalent biological value. For plant-dominant eaters targeting higher protein intakes for muscle preservation, strategic food combining or supplementation with complete protein sources becomes a practical necessity rather than an optional refinement.

For those seeking a high-quality, complete protein source that supports muscle protein synthesis without the cardiovascular concerns associated with red meat, Alpha-Lactalbumin Protein provides a leucine-rich, rapidly absorbed whey fraction with a favorable amino acid profile and emerging evidence for metabolic benefits. Pairing quality protein with resistance training and monitoring metabolic markers through programs like Longevity Optimization represents the kind of individualized, data-driven approach that translates population-level evidence into actionable personal strategy.

Synthesizing the Evidence: A Framework for Different Life Stages

Drawing together what the evidence shows, a coherent age-stratified picture emerges that is more nuanced than either "protein is dangerous" or "eat as much protein as possible." In early and middle adulthood, roughly ages 18 to 60, the evidence for moderating animal protein intake, particularly red and processed meat, is reasonable and largely consistent across study designs. Replacing animal protein with plant protein sources appears protective for cardiovascular health and possibly for cancer risk, likely through multiple mechanisms including microbiome effects, reduced inflammatory mediators, and differences in the accompanying dietary matrix. The absolute magnitude of these effects is modest in most studies, but across a lifetime, modest differences compound.

After 60, the priorities shift. Sarcopenia, frailty, and metabolic dysfunction become the dominant threats to healthspan and survival. The evidence for higher protein intake in this population, targeting 1.2 to 1.6 grams per kilogram of body weight per day, is supported by multiple randomized trials and expert consensus. For older adults engaged in resistance training, even higher intakes may be beneficial. The concern about mTOR-driven cancer promotion in this age group is not absent, but it is substantially outweighed by the evidence linking muscle preservation to survival. The IGF-1 story also appears to reverse in older age, with adequate levels associated with protection rather than risk. [14]

Across all ages, individual clinical context matters enormously. Kidney function should be assessed before high protein targets are set. Dietary protein source should favor a mix of lean animal proteins, fish, dairy, and diverse plant proteins over a pattern dominated by processed red meat. Physical activity, particularly resistance training, is not optional context but a core determinant of what protein intake achieves biologically. And for those pursuing comprehensive longevity optimization, programs that integrate metabolic monitoring with personalized nutrition and lifestyle guidance, such as Longevity Optimization, represent the clinical infrastructure that makes population-level research personally actionable.

What Remains Genuinely Uncertain

Scientific honesty requires naming what is not yet known. The human evidence on protein intake and longevity comes overwhelmingly from observational studies, which can demonstrate association but cannot establish causation. The randomized controlled trial evidence on protein and mortality is essentially nonexistent. No trial has randomized thousands of middle-aged adults to high versus low protein diets and followed them for decades, and such a trial is unlikely to be conducted. The mechanistic animal data, though compelling, extrapolates across species whose biology differs meaningfully from humans.

The optimal protein intake for longevity in a physically active 50-year-old with no metabolic disease remains genuinely uncertain. The claim that any specific gram-per-kilogram target is the "right" number for healthspan is currently unsupportable by the evidence. What is supportable is a framework: prioritize protein source quality alongside quantity, calibrate intake to age and muscle preservation needs, contextualize recommendations within physical activity patterns, screen for kidney disease before setting high targets, and treat the current evidence as a basis for individualized assessment rather than universal prescription. The science is good enough to guide intelligent decisions. It is not yet good enough to replace them with algorithms.

Conclusion: The Real Risk Is a False Dichotomy

The question posed at the outset of this article was whether high-protein diets carry longevity risks. The answer is: it depends, and the precision of that dependency matters enormously for the quality of the advice that follows. The longevity risk of a 52-year-old sedentary man eating 200 grams of protein daily from processed meat looks very different from the longevity risk of a 72-year-old woman eating 90 grams of protein daily from fish, legumes, and dairy while engaging in three resistance training sessions per week. Both are "high protein" relative to the RDA. Their biological contexts are not remotely similar.

The real risk in the protein and longevity debate is not any specific gram count. It is the flattening of a complex, context-dependent biological relationship into a simple prescription. Protein is one of the most important dietary variables in human healthspan, but it operates through a web of interacting factors: age, protein source, physical activity, kidney function, microbiome composition, hormonal status, and the temporal pattern of intake. Each of those factors carries its own weight in the outcome. Attending to all of them simultaneously is the work of precision medicine, not population-level nutrition advice. The evidence points clearly in that direction, even if it does not yet tell us exactly how far to walk.

FAQ

Is a high-protein diet bad for longevity?

The relationship is age-dependent. Epidemiological data suggests that high animal protein intake in middle age (50 to 65) is associated with increased mortality risk, potentially through IGF-1 and mTOR pathways. In adults over 65, higher protein intake is associated with reduced mortality risk, likely by protecting against sarcopenia and frailty. Protein source and physical activity level significantly modify these associations.

How much protein should I eat for longevity?

There is no single optimal number, but current evidence suggests adults under 60 should aim for at least 1.0 gram per kilogram of body weight daily, with emphasis on plant and lean animal sources. Adults over 60 benefit from 1.2 to 1.6 grams per kilogram daily to counter anabolic resistance and sarcopenia. Those with chronic kidney disease require individualized, clinically supervised protein targets.

Does plant protein increase longevity more than animal protein?

Multiple large cohort studies associate replacing animal protein, particularly red and processed meat, with plant protein with reduced cardiovascular and all-cause mortality. The benefit likely reflects the full dietary matrix (fiber, polyphenols, reduced inflammatory metabolites) rather than protein per se. Fish and dairy proteins show more neutral to favorable associations and should not be conflated with red meat.

Does protein intake affect autophagy?

Yes. Dietary protein activates mTOR, which suppresses autophagy, the cellular recycling process associated with longevity. Periods of lower protein availability (during fasting, sleep, or time-restricted eating) allow autophagy to increase. Evidence suggests strategic protein cycling, timed around exercise, may support both muscle maintenance and autophagy induction, though robust long-term human trial data remain limited.

Can too much protein damage kidneys?

In people with normal kidney function, high protein intake does not appear to accelerate renal decline. In people with existing chronic kidney disease (CKD), higher protein intake can accelerate loss of nephron function. Approximately 37 million Americans have CKD, often asymptomatically. Screening for renal function before setting high protein targets is recommended, particularly in middle-aged and older adults.