Athletic Greens is one of the most successful supplement companies in the world, reportedly valued at over $1.2 billion and projected to grow to $1.83 billion by 2032.¹ A quick visit to their site is undeniably compelling—sleek design, confident claims, scientific-looking graphics, and an extensive list of studies. It promises improved health and well-being by filling nutrient gaps, boosting energy, supporting digestion and gut health, and enhancing brain function and mood. All for $79 per month with a subscription ($99 otherwise).

So, does it live up to the fanfare, or is there a faint whiff of “Show me great wealth, and I’ll show you a great scam”? As is often the case in the intersection of health and commerce, the truth likely lies somewhere in between. I’ll leave the final judgment to you.

Subscribe now

Part 1: The Founder

AG1 was founded by fitness entrepreneur Chris Ashenden. Before building a billion-dollar supplement company, Ashenden's earlier property businesses in New Zealand resulted in multiple convictions under the Fair Trading Act for misleading consumers in rent-to-own housing schemes.² Following the collapse of those companies, court-ordered fines and reparations went unpaid, and Ashenden eventually relocated to the United States, where he launched Athletic Greens.^{3, 4}

While this doesn’t make the supplement inherently bad, as investigative reporter Scott Carney points out, it does demonstrate Ashenden’s willingness to lie and exploit people for his own advantage.³

In October 2024, amid criticism following investigations into those past business dealings, Ashenden stepped down as CEO of AG1, though he has remained involved as an owner and board member.^{1, 4}

Part 2: The Marketing Machine

AG1 has executed one of the most effective marketing strategies in the supplement industry—leveraging podcasts, influencers, athletes, and celebrities at scale. According to the analytics platform Podscribe, AG1 has been promoted on over 700 podcasts in recent years, and the company has spent tens of millions on podcast advertising since 2022.¹ This does not make the product inherently questionable, but as Kerry Howley noted in a New York Magazine profile, “It is one thing to hear Athletic Greens promoted by Joe Rogan: it is another to hear someone who sells himself as a Stanford University scientist just back from the lab proclaim that this powder ‘covers all of your foundational nutritional needs’.”⁵ Ironically, to quote a piece in Fortune magazine:

Part 3: The Ingredients

AG1 contains a sweeping list of 75+ ingredients, including fruits and vegetables (e.g., bilberries, acerola cherries, broccoli), plant compounds (matcha, cocoa, spirulina), enzymes and extracts (bromelain, mushroom blends), added nutrients (vitamins A, B, C, E, K2, magnesium, zinc), and pro- and prebiotics. (Although given its name, I would have expected more leafy greens; alas, they are largely absent.) On paper, these are largely health-promoting compounds. However, the exact quantities of many of these ingredients are proprietary, raising a key question. Are the doses meaningful, or are they too minuscule to have an impact?

For example, meaningful cognitive benefits from blueberry consumption occur with intakes of 0.5 to 2 cups per day.⁶ Reduce that same amount to powder, and you are left with several tablespoons, which is more than a token sprinkle.

Some nutrients are provided in amounts far exceeding daily requirements. For example, vitamin C is 556% of the RDA, vitamin B12 is 16667% (yes, I had to double-check that number) of the RDA, and vitamin B6 is 294% of the RDA. While this is often dismissed as harmless (especially for water-soluble vitamins), that isn’t always the case.

For example, high doses of supplemental vitamin C may blunt exercise adaptations in certain contexts.⁷ Chronic high doses of vitamin B6 have been linked to peripheral neuropathy.⁸ (Although, to my knowledge, there have been no reported cases as a result of taking AG1.) And, although B12 supplementation is recommended (especially for vegetarians and those over the age of 50), several studies have linked long-term, high-dose supplementation and high circulating B12 concentrations to an increased risk of lung cancer, particularly among men who smoke.¹⁵ Thus, more is not always better, especially in supplemental form.

Part 4: The Studies vs. The Claims

AG1’s website highlights a range of studies supporting its claims. However, a closer look reveals that many references are conference abstracts (with lower evidentiary rigor) and only a small number of peer-reviewed human studies. All were funded by AG1. Industry funding does not necessarily invalidate the findings, but it does warrant careful interpretations.

In support of the gut-health claims, one of the cited peer-reviewed studies (the other was a conference abstract) used the SHIME model, a mechanical simulation, to test whether AG1 was fermentable.⁹ The findings showed that AG1 increased bacterial metabolite production (short-chain fatty acids). This is expected and relevant, but it has serious limitations because it does not replicate human physiology, including immune responses, nutrient absorption, and real-world dietary context. It simply showed that it was fermentable compared to a blank.

Several randomized controlled trials have been conducted comparing AG1 to a placebo (often maltodextrin) in humans. These found modest, but selective shifts in microbiome composition.^{10, 13} The question is whether these shifts are clinically meaningful. There were no reported changes in stool frequency or GI outcomes, nor were there improvements in clinical health or performance markers.

Notably, metabolite (or short-chain fatty acid) production, whereby healthy bacteria exert health benefits was either not reported or not measured.

One study did show that circulating markers of folate, vitamin C, and zinc were higher in the AG1 group (supporting its “fills nutrient gaps” claims).¹⁴ However, this is not surprising, given, as mentioned above, that the powder contains supplemental forms of these nutrients. It is also notable that this study used subjects who consumed a nutrient-poor standard Western diet.

Additional limitations include relatively small sample sizes, short durations (2 to 12 weeks), no comparisons with whole-food dietary patterns, and findings that were, at best, pilot-level.

In Conclusion

AG1 may offer a convenient vehicle for delivering vitamins and other bioactive compounds, but convenience should not be mistaken for necessity, and marketing, no matter how polished, is not a substitute for evidence. If individuals notice improvements in GI function, mood, or energy with its use—whether physiological or placebo—there’s value in that experience. Importantly, it appears to be safe, at least in the short term.

While future, longer-term studies on larger cohorts may yet demonstrate more tangible benefits, the current data remain limited. AG1 is more evidence-informed than many supplements, but the evidence to date supports underwhelming effects rather than the sweeping health claims implied by its marketing.

Ultimately, the most reliable and evidence-based approach to closing nutrient gaps, supporting gut health, improving recovery and physical performance, and enhancing cognitive function remains a plant-forward, fiber-rich diet, combined with consistent healthy lifestyle practices, as we outline in Staying in the Game.

Thanks for reading.

Share

Subscribe now

Leave a comment

References

1. Austin E. The battle over AG1-the influencer-famous, $100-a-month green supplement-is coming to a vending machine or grocery store near you. Fortune. Available at: https://fortune.com/2025/01/24/ag1-athletic-greens-supplements-green-powder-bryan-johnson/. Accessed April 10, 2026.

2. Milne J. AG1 Founder Chris Ashenden Resigns Amid Scrutiny of NZ Criminal History. The New Zealand Herald. Available at: https://www.nzherald.co.nz/business/billion-dollar-company-ag1-founder-chris-ashenden-resigns-amid-scrutiny-of-nz-criminal-history/SBBOE7BOCBDJNNBDRND3KCH2PA/?utm_source=chatgpt.com. Accessed July 5, 2026.

3. Carney S. AG1 Tried to Kill this Video…but it didn’t work. Available at: https://sgcarney.substack.com/p/ag1-tried-to-kill-this-video-but. Accessed April 10, 2026.

4. Carney S. The True Story of Athletic Greens (and the Real Estate Scam that Started it All). Scott Carney Investigates: YouTube; 2025.

5. Howley K. Andrew Huberman’s Mechanisms of Control. New Yorker Magazine. New York; 2024.

6. Tran PHL, Tran TTD. Blueberry supplementation in neuronal health and protective technologies for efficient delivery of blueberry anthocyanins. Biomolecules. Jan 14 2021;11(1).

7. Braakhuis AJ. Effect of vitamin C supplements on physical performance. Curr Sports Med Rep. Jul–Aug 2012;11(4):180–184.

8. Muhamad R, Akrivaki A, Papagiannopoulou G, Zavridis P, Zis P. The role of vitamin B6 in peripheral neuropathy: A systematic review. Nutrients. Jun 21 2023;15(13).

9. Kirby TO, Townsend JR, Sapp PA, et al. The novel synbiotic, AG1®, increases short-chained fatty acid production in the Simulator of Human Intestinal Microbial Ecosystem (SHIME) model®. Nutraceuticals. 2023;3(4):489–498.

10. La Monica MB, Raub B, Hartshorn S, et al. The effects of AG1® supplementation on the gut microbiome of healthy adults: a randomized, double-blind, placebo-controlled clinical trial. J Int Soc Sports Nutr. Dec 2024;21(1):2409682.

11. Townsend J, Gonzalez AM, Kirby T, et al. AG1® supplementation improves gut microbiome composition and function in highly active adults. Journal of the International Society of Sports Nutrition. 2025/09/30 2025;22(sup2):2550154.

12. Wood A, Sapp PA, Townsend JR, et al. AG1®, a multi-ingredient nutrition supplement, does not negatively impact blood safety biomarkers in healthy adults: a randomized controlled trial. Journal of the International Society of Sports Nutrition. 2025/09/30 2025;22(sup2):2550153.

13. Gonzalez AM, Townsend JR, Sapp PA, et al. Effect of AG1(®) supplementation on nutritional adequacy and gut microbial composition in trained adults. Front Nutr. 2026;13:1783951.

14. Sapp PA, Townsend JR, Edwards C, et al. AG1, a foundational nutrition supplement, closes nutrient gaps in healthy adults: A randomized controlled trial. Current Developments in Nutrition. 2025;9.

15. Fanidi A, Carreras-Torres R, Larose TL, et al. Is high vitamin B12 status a cause of lung cancer? Int J Cancer. Sep 15 2019;145(6):1499–1503.

Introduction: Junk Food by Any Other Name Is Still Junk Food

Imagine you are standing in a grocery store aisle, choosing between two identical products. One is labeled “high protein.” Which would you choose?

Chances are that many would reach for the protein-enhanced version. In 2025, some 44% of U.S. consumers, and 51% of Gen Z and millennials, are actively trying to boost their intake.¹

The food industry has happily obliged, and is cashing in. Protein chips. Protein cereal. Protein ice cream. Protein candy bars. The list seems endless. The protein market is now a massive business. Mintal, a market research firm, valued the U.S. protein market at $114.4 billion in 2024 and projected it would continue to grow 1.9% per year until 2028.²

But if you take a processed food and add processed protein powder to it, does it magically become healthier?

Alas, junk food by any other name is still junk food.

When it comes to preserving muscle mass, strength, and function as we age, the important question is not simply, “How much protein should I eat?” The better question is, “What dietary pattern best supports healthy aging muscle?”

As discussed in a previous post, sarcopenia is a multifaceted process involving neuromuscular junction degeneration, mitochondrial dysfunction, insulin resistance, hormonal alterations, fat infiltration, oxidative stress, and chronic inflammation.

In other words, this is not a single-nutrient problem.^{3, 4}

It requires a broader dietary approach and one that positively influences the many biological processes that contribute to muscle aging.

Subscribe now

Part 1: The Limits of Nutrient-by-Nutrient Thinking

Research on nutrition and sarcopenia generally falls into three categories:

1. Individual nutrients, such as protein, amino acids, or vitamin D

2. Specific foods or food groups

3. Overall dietary patterns

The first category receives most of the attention and is where most of the research is to be found. Yet foods and dietary patterns provide a more integrated and realistic framework for making recommendations.⁵

After all, few of us eat isolated nutrients. We eat meals.

Despite this obvious reality, nutrition science remains heavily influenced by reductionism: the tendency to focus on individual nutrients rather than the overall dietary pattern in which they are consumed.⁵

Part 2: How Much Protein Is Enough?

Longevity researcher Valter Longo, who has studied how protein intake interacts with long-term health outcomes, recommends protein intakes that seem remarkably low by today’s social media standards: approximately 0.8 g/kg/day before age 65 and around 1.0 g/kg/day thereafter. Research that he has published suggests that lower protein intake is associated with a reduction in cancer and overall mortality for those younger than 65.⁶

His recommendations are not far removed from those of several scientific organizations and expert panels.

The Nordic Nutrition Recommendations (NRR), which form the scientific basis for national dietary guidelines for all of the Nordic countries, set the protein target at 0.83g/kg/day, or 10-20% of total energy intake, for those under 65 and 1.2–1.5 g/kg/day for healthy adults over age 65. In fact, the NNR caps protein intake at 1.5 g/kg/day.⁷

Canada’s Dietary Reference Intakes set the adult protein RDA at 0.8 g/kg/day for adults 19 years and older. Unlike the Nordic Nutrition Recommendations, Canada does not currently provide a separate higher official protein RDA for adults over 65.⁸ However, several Canadian experts recommend 1.2–1.6 g/kg/day for physically active older adults.⁹

The World Health Organization and European Food Safety Authority recommend 0.83 g/kg/day, while the PROT-AGE study group recommends 1.0–1.2 g/kg/day for older adults.^{10, 11}

From: Calvani R. et. al. Diet for the prevention and management of sarcopenia. Metabolism. 2023.⁴

It is worth noting that, with sufficient calorie intake, it is surprisingly difficult to maintain protein intake at 0.83 g/kg/day. Most people—even those eating exclusively plant-based diets—tend to exceed it. True protein deficiency is relatively rare and generally occurs only in cases of severe malnutrition or chronic undernutrition, a condition known as protein-energy malnutrition.

Recent reviews of protein intakes for older adults align well with these recommendations.

A 2026 review concluded:

“…however, current data indicate that a higher protein intake has no beneficial effect on muscle mass or muscle strength in healthy older adults. Yet, in patients with sarcopenia, a beneficial effect on muscle health can be assumed for an increase in protein intake when combined with resistance exercise.”¹²

The Belgian Society of Gerontology and Geriatrics reached a similar conclusion, finding low-quality evidence of a positive effect of protein supplementation on muscle mass, but no evidence of effects on muscle strength or physical performance.¹³

But things take a modest turn when higher protein intake is combined with resistance training. In that context, higher protein intakes can provide small additional gains in muscle mass. Across studies, the “sweet spot” appears to be approximately 1.2–1.6 g/kg/day; notably below the current influencer-driven recommendations of more than 2 g/kg/day.¹⁴

However, the gains are relatively small, typically about 0.4 to 0.7 kilograms of additional muscle mass compared with resistance training alone.¹⁴

Perhaps more importantly, higher protein intake tends to increase muscle mass without consistently improving strength or function. As discussed in my previous post, maintaining strength and function is ultimately the desired outcome.

Part 3: Protein Source Matters

However, the protein source may matter more than total protein intake. In adults aged 50–65, high protein intake has been associated with a 75% increase in overall mortality and a fourfold increase in cancer mortality over the following 18 years. Importantly, these associations were attenuated or abolished when the protein came primarily from plant sources.⁶

The NNR also advises that protein come predominantly from plant sources, and Canada’s dietary guidance encourages greater consumption of beans, tofu, lentils, and other protein-rich plant foods. Notably, these recommendations were developed by scientific panels and were not industry- or influencer-driven.

In fact, diets high in red and processed meat have been linked, in some studies (but not all), to adverse effects on muscle mass. A 2022 review found that plant-based protein intake was associated with a lower risk of sarcopenia, whereas a high-fat, meat-heavy U.S. dietary pattern was linked to a higher risk.¹⁵ The traditional British diet—high in animal protein, butter, sweets, and desserts—has also been strongly associated with an increased risk of sarcopenia.⁵

A 2022 study that followed nurses for 22 years found that animal protein intake was associated with a higher risk of frailty, whereas higher plant protein intake was associated with a lower risk, even after adjustment for other lifestyle factors.¹⁶

Part 4: Chicken is Protein. Beans Are the Package Deal

One consequence of a highly reductionist view of nutrition is that foods get compartmentalized by their dominant macronutrient. Chicken becomes “protein.” Potatoes become “carbs.”

But one of the great virtues of plant foods is that they are rarely so one-dimensional. High-carbohydrate plant foods, like rice and potatoes, contain some protein (and yes, all whole plant foods contain all nine essential amino acids, though in varying amounts). Likewise, higher-protein plant foods like beans also provide carbohydrate, fiber, resistant starch, antioxidants, phytochemicals, and other health-promoting nutrients.¹⁷

Chicken is, well, mostly protein and fat.

Part 5: Dietary Patterns that Protect Muscle

Fruits and vegetables are the two food groups most consistently associated with a reduced risk of sarcopenia.¹⁸ These foods are considered myoprotective, likely because they are rich in antioxidants, have anti-inflammatory properties, and are less acid-producing (see below).⁵

Higher intake of fruits and vegetables is also a marker of a healthier overall dietary pattern and, often, a healthier lifestyle.¹⁴ While studies do attempt to account for this, it is important to acknowledge that the evidence is not perfect. We are awash in studies on protein intake, but relatively few studies have examined whole-food intake, and even fewer are interventional trials. The role of specific foods therefore deserves more research.¹⁸

Still, the pattern is consistent.

A healthy Mediterranean dietary pattern—rich in fruits, vegetables, legumes, whole grains, nuts, seeds, and other plant foods—has been most consistently associated with improved skeletal muscle outcomes, including a lower risk of sarcopenia and frailty.¹⁴

As a 2021 review concluded, “The current evidence suggests that the RDA may be sufficient to maintain LBM [lean body mass] in healthy postmenopausal women; it could be associated, at least in part, with healthy dietary patterns, such as the Mediterranean diet.”¹⁹

This dietary pattern provides a favorable combination of macronutrients, micronutrients, fiber, and phytochemicals within the food matrix.⁵

A study of European adults found that higher dietary fiber intake—essentially, greater intake of less-processed plant foods—was associated with a lower risk of sarcopenia, even after adjusting for protein intake and physical activity.²⁰

A low Dietary Inflammatory Index score is also considered muscle-protective.^21-23 This dietary pattern is rich in whole grains, fruits, and green vegetables, may include fish, and is low in red meat, butter, fatty foods, and processed grains.

Most of these conclusions are based on prospective and cross-sectional epidemiological studies. However, the strength of causal inference is supported by the consistency of the findings, their biological plausibility, and their reproducibility across studies.

Part 6: Why Plant-Forward Patterns Make Biological Sense

One possible reason is that foods such as meat, fish, eggs, and dairy are more acid-producing and may contribute to a more catabolic internal environment.²⁴ Evidence suggests that blood pH becomes slightly more acidic with age, which may further amplify this concern.²⁵

Byproducts of meat consumption, including ammonia, indole compounds, and phenols, may exacerbate inflammatory responses. Inflammation can activate pathways such as FOXO, which contributes to muscle wasting.²⁶ Higher inflammation also decreases insulin sensitivity, which in turn promotes anabolic resistance, or the impaired ability of insulin and amino acids to stimulate muscle protein synthesis.²⁷

Diets higher in saturated fat may also be problematic, as fat infiltration into muscle tissue and cells can interfere with energy production and muscle fiber contraction.^{28, 29}

A healthy plant-forward diet may therefore help mitigate several processes involved in sarcopenia.⁵ Such a diet is also higher in fiber, which supports a healthier gut microbiome. The microbiome, in turn, influences inflammation, muscle protein synthesis, and anabolic resistance, a topic we dive into in Chapter 6 of Staying in the Game.

Part 7: The mTOR-AMPK Balancing Act

Protein enthusiasts often hang their hats on the nutrient-sensing pathway of mTOR. mTOR stimulates muscle protein synthesis in response to nutrients, particularly the amino acid leucine. This relationship underpins the “leucine trigger hypothesis” and helps explain why protein-rich foods can stimulate muscle growth.³⁰

AMPK works differently. It is generally activated during energy stress, including exercise and periods of low energy availability such as fasting. It functions as a cellular fuel gauge, promoting energy production, mitochondrial maintenance, autophagy, and metabolic repair, while dampening energy-intensive growth signals such as mTOR.

In simplified terms, mTOR promotes growth, while AMPK promotes repair and metabolic housekeeping.³¹

With aging, this balance becomes more complex. Overactivation of mTOR may impair muscle protein synthesis and contribute to muscle protein degradation, whereas AMPK activation appears to improve mitochondrial health, reduce inflammation, and preserve muscle quality.³²

mTOR has also been described as a “master determinant” of lifespan and aging.^{33, 34, 35} One proposed strategy for slowing aspects of the aging process is to inhibit excessive mTOR activity. One of the safest ways to do this is to limit animal protein intake.

Part 8: The Bottom Line: Build a Pattern

The question of protein adequacy must be considered within the broader context of diet and lifestyle.

Yes, older adults may benefit from somewhat higher protein intakes, particularly when they are engaged in progressive resistance training. But more is not always better, and protein alone is not the solution.

Hopefully, this relieves some of the pressure to chase protein goals that can be difficult, unnecessary, and sometimes anxiety-producing to reach.

Additionally, as with so many conditions, an ounce of prevention is worth a pound of cure. Early healthy dietary, exercise, and other lifestyle practices also play a key role in preventing or delaying sarcopenia and its associated outcomes.

The message, then, is not simply to eat more protein. It is to build—and sustain—a dietary pattern and lifestyle that support muscle strength and function, metabolism, and long-term health across the lifespan.

Share

Subscribe now

Leave a comment

Thanks for reading, subscribing, and sharing.

References

1. Stambor Z. Gen Z and millennials fuel the rising demand for protein. Available at: https://www.emarketer.com/content/protein-product-trend-2025-consumer-demand-growth?utm_source=chatgpt.com. Accessed June 22, 2026.

2. From Steaks to Shakes: Understanding the US Protein market. Mintel. Available at: https://www.mintel.com/insights/food-and-drink/from-steaks-to-shakes-understanding-the-us-protein-market/?utm_source=chatgpt.com. Accessed June 22, 2026.

3. Khaksarian M, Sharafi MH, Souri F. Musculoskeletal degeneration and cardiovascular aging: a narrative review of shared mechanobiological pathways. Mol Biol Rep. May 30 2026;53(1).

4. Calvani R, Picca A, Coelho-Júnior HJ, Tosato M, Marzetti E, Landi F. Diet for the prevention and management of sarcopenia. Metabolism - Clinical and Experimental. 2023;146.

5. Ruiz-Valenzuela RE, Artacho R, Ruiz-López MD, Molina-Montes E. Healthy dietary patterns and risk of sarcopenia in adults Aged > 50 years: A systematic review and meta-analysis considering EWGSOP1 and EWGSOP2 criteria. Nutrients. Aug 26 2025;17(17).

6. Levine ME, Suarez JA, Brandhorst S, et al. Low protein intake is associated with a major reduction in IGF-1, cancer, and overall mortality in the 65 and younger but not older population. Cell Metab. Mar 4 2014;19(3):407–417.

7. Blomhoff R, Andersen, R., Arnesen, E. K., Christensen, J. J., Eneroth, H., Erkkola, M., Gudanaviciene, I., Halldorsson, T. I., Høyer-Lund, A., Lemming, E. W., Meltzer, H. M., Pitsi, T., Schwab, U., Siksna, I., Thorsdottir, I., & Trolle, E. Nordic Nutrition Recommendations 2023. Nordic Council of Ministers. Available at: https://pub.norden.org/nord2023-003/protein.

8. Dietary reference intakes tables: Reference values for macronutrients. Health Canada. Available at: https://www.canada.ca/en/health-canada/services/food-nutrition/healthy-eating/dietary-reference-intakes/tables/reference-values-macronutrients.html. Accessed June 23, 2026.

9. Traylor DA, Gorissen SHM, Phillips SM. Perspective: Protein Requirements and Optimal Intakes in Aging: Are We Ready to Recommend More Than the Recommended Daily Allowance? Adv Nutr. May 1 2018;9(3):171–182.

10. Bauer J, Biolo G, Cederholm T, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. Aug 2013;14(8):542–559.

11. Panel E. EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA); Scientific Opinion on Dietary Reference Values for protein released for public consultation. EFSA Journal. 20xx:63.

12. Eidam A, Benzinger P, Bauer JM. [Protein intake and preservation of function in old age : Current evidence and present research gaps]. Z Gerontol Geriatr. May 28 2026.

13. Gielen E, Beckwée D, Delaere A, De Breucker S, Vandewoude M, Bautmans I. Nutritional interventions to improve muscle mass, muscle strength, and physical performance in older people: an umbrella review of systematic reviews and meta-analyses. Nutr Rev. Jan 9 2021;79(2):121–147.

14. Granic A, Sayer AA, Cooper R, Robinson SM. Nutrition in the prevention and treatment of skeletal muscle ageing and sarcopenia: a single nutrient, a whole food and a whole diet approach. Proc Nutr Soc. Dec 2025;84(4):340–355.

15. Coelho-Junior HJ, Calvani R, Azzolino D, et al. Protein intake and sarcopenia in older adults: A systematic review and meta-analysis. Int J Environ Res Public Health. Jul 18 2022;19(14).

16. Struijk EA, Fung TT, Rodríguez-Artalejo F, et al. Protein intake and risk of frailty among older women in the Nurses’ Health Study. J Cachexia Sarcopenia Muscle. Jun 2022;13(3):1752–1761.

17. Gardner CD, Hartle JC, Garrett RD, Offringa LC, Wasserman AS. Maximizing the intersection of human health and the health of the environment with regard to the amount and type of protein produced and consumed in the United States. Nutr Rev. Apr 1 2019;77(4):197–215.

18. Hong S-H, Bae Y-J. Association of dietary vegetable and fruit consumption with sarcopenia: A systematic review and meta-analysis. Nutrients. 2024;16(11):1707.

19. Silva TR, Oppermann K, Reis FM, Spritzer PM. Nutrition in menopausal women: A narrative review. Nutrients. Jun 23 2021;13(7).

20. Montiel-Rojas D, Nilsson A, Santoro A, et al. Dietary fibre may mitigate sarcopenia risk: Findings from the NU-AGE cohort of older European adults. Nutrients. Apr 13 2020;12(4).

21. Diao H, Yan F, He Q, et al. Association between Dietary Inflammatory Index and sarcopenia: A meta-analysis. Nutrients. 2023;15(1):219.

22. Itsiopoulos C, Mayr HL, Thomas CJ. The anti-inflammatory effects of a Mediterranean diet: a review. Curr Opin Clin Nutr Metab Care. Nov 1 2022;25(6):415–422.

23. Pu R, Man Q, Song S, et al. The Dietary Inflammatory Index and Sarcopenia in Older Adults in Four Chinese Provinces: A Cross-Sectional Study. Nutrients. 2025;17(3):478.

24. Correia EML, de Andrade ESA, Oliveira Dos Santos AC. Assessment of the acidifying potential of diet and sarcopenia in individuals 50 years of age or older: a cross-sectional study. BMC Nutr. Jan 8 2026;12(1):24.

25. Wieërs MLAJ, Beynon-Cobb B, Visser WJ, Attaye I. Dietary acid load in health and disease. Pflügers Archiv - European Journal of Physiology. 2024/04/01 2024;476(4):427–443.

26. Pohl A, Schünemann F, Bersiner K, Gehlert S. The Impact of Vegan and Vegetarian Diets on Physical Performance and Molecular Signaling in Skeletal Muscle. Nutrients. Oct 29 2021;13(11).

27. Dardevet D, Rémond D, Peyron MA, Papet I, Savary-Auzeloux I, Mosoni L. Muscle wasting and resistance of muscle anabolism: the “anabolic threshold concept” for adapted nutritional strategies during sarcopenia. ScientificWorldJournal. 2012;2012:269531.

28. Abbatecola AM, Paolisso G, Fattoretti P, et al. Discovering pathways of sarcopenia in older adults: a role for insulin resistance on mitochondria dysfunction. J Nutr Health Aging. Dec 2011;15(10):890–895.

29. Jang SY, Choi KM. Impact of adipose tissue and lipids on skeletal muscle in sarcopenia. J Cachexia Sarcopenia Muscle.2025;16(4):e70000.

30. Glynn EL, Fry CS, Drummond MJ, et al. Excess leucine intake enhances muscle anabolic signaling but not net protein anabolism in young men and women. J Nutr. Nov 2010;140(11):1970–1976.

31. Sirago G, Picca A, Calvani R, Coelho-Júnior HJ, Marzetti E. Mammalian target of rapamycin (mTOR) signaling at the crossroad of muscle fiber fate in sarcopenia. Int J Mol Sci. Nov 10 2022;23(22).

32. Chen CN, Liao YH, Tsai SC, Thompson LV. Age-dependent effects of caloric restriction on mTOR and ubiquitin-proteasome pathways in skeletal muscles. Geroscience. Dec 2019;41(6):871–880.

33. Stallone G, Infante B, Prisciandaro C, Grandaliano G. mTOR and aging: An old fashioned dress. Int J Mol Sci. Jun 6 2019;20(11).

34. Johnson SC, Rabinovitch PS, Kaeberlein M. mTOR is a key modulator of ageing and age-related disease. Nature. Jan 17 2013;493(7432):338–345.

35. Blagosklonny MV. TOR-driven aging: speeding car without brakes. Cell Cycle. Dec 15 2009;8(24):4055–4059.

Sarcopenia is a generally recognized term for the loss of muscle mass. A more nuanced definition, however, is from a 2025 paper:¹

• Probable sarcopenia: low muscle mass only

• Confirmed sarcopenia: low muscle mass + low muscle strength

• Severe sarcopenia: low muscle mass + low strength + impaired physical performance (everyday movement and daily tasks become compromised).

Sarcopenia is strongly associated with a host of adverse health outcomes, including frailty, mortality, and hospitalization. Hence, loss of muscle mass is a legitimate concern. However, when it comes to predicting falls, loss of independence, and premature death, declines in strength and power appear to matter more than loss of muscle mass alone.¹

This highlights an important distinction: muscle size and muscle quality*. These are not necessarily the same. The ability to generate force (strength) and to do so quickly (power) matters more for climbing stairs, preventing falls, and staying independent.² Unfortunately, we lose power and strength faster than we lose mass.³ Thus, the primary goal is not simply to preserve muscle mass but to preserve strength and power.⁴

In younger individuals, mass is correlated with strength. Among older individuals at the highest risk, however, muscle quality is more strongly associated with strength than with mass.⁵

Alas, a myopic focus on ever-higher protein intakes is not the best defense. If the problem is multifaceted, the solution must be too.

It is worth noting that no medications enhance fitness or functional capacity, and none that reduce frailty. Rather, as I will discuss, exercise does the job rather well.⁷

“Physical fitness can neither be achieved by wishful thinking nor outright purchase.” ~ Joseph Pilates

Exercise Modalities

A 2025 paper published in The Journal of Nutrition, Health and Aging, titled Global Consensus on Optimal Exercise Recommendation for Enhancing Healthy Longevity in Older Adults, concluded that, “Overall, the choice, or ability to engage in PA [physical activity] significantly impacts the trajectory of decline with aging.” ⁸

Salient Point #1: Move more.

While obvious, it is worth stating: being physically active matters.

While walking, cycling, running, or swimming are encouraged, they alone are not enough to fully address the risk of sarcopenia. The body requires a reason to maintain strength, power, and resilience. Resistance training provides that reason.

Salient Point #2: Train Across Multiple Fitness Modalities

The cornerstone of preserving muscle function with age is progressive resistance training (PRT). As we grow older, relatively high-intensity resistance training, combined with power, balance, and agility work, becomes increasingly important. Collectively, these approaches are known as multicomponent exercise training.⁸

From: Izquierdo, M et. al. Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR). J. Nutr. Health and Aging. 2025

Aerobic capacity and muscle strength are also closely intertwined and are bidirectional.⁶ One supports the other.⁹ In fact, reduced skeletal muscle capillarization has been linked to anabolic resistance, potentially impairing the muscle-building response to strength training.¹⁰ Thus, cardiovascular exercise still matters.

For resistance training, the recommendation is to perform 8-10 lifts targeting major muscle groups, 2-3 times per week.

But if you want the greatest return on your training investment, power training deserves special attention.

Salient Point #3: Don’t Forget Power Training

Power training targets both strength and the speed of force production. In practical terms, this means moving a load as quickly as possible during the lifting phase while maintaining control during the lowering phase.

A typical power-training repetition involves:

• A controlled eccentric (lowering) phase.

• A rapid concentric (lifting) phase.

This approach can be safely integrated into a traditional resistance-training program.

Depending on the exercise and individual capabilities, training loads typically range from 40–80% of one-repetition maximum (1RM).

Research suggests that peak muscle power can improve similarly across light (20%), moderate (50%), and heavy (80%) resistance loads. However, heavier loads tend to produce greater strength gains, while moderate loads (50%) may yield superior improvements in functional capacity.^{8, 11}

Low-load, high-velocity training should be approached cautiously, particularly in individuals with underlying joint issues, as very rapid movements may increase the risk of injury.

The benefits extend well beyond muscle. Studies indicate that power training can improve not only strength and power, but also neuromuscular function, physical performance, bone health, and even aspects of cognitive function.¹²

Salient Point #4: Prioritize Power for the Big Movers.

In practical terms, exercises such as squats, leg presses, bench presses, and similar machine- and free-weight movements can be performed with an emphasis on moving the weight quickly during the lifting phase and slowly and under control during the lowering phase.⁸

Traditional strength training can then complement this work for smaller muscle groups.

In this case, variety is more than the spice of life—it is an evidence-based strategy for maintaining function, independence, and resilience with age.

This type of training also helps preserve bone density, a topic I discussed in an earlier post. And for the runners out there, maximal strength training may improve running economy by up to 5%.¹³

Salient Point #5: If Needed, Get Help.

If you are unsure of the correct lifting technique or training progression, hire someone with experience to work with you. It is worth the investment.

In a subsequent post, I will examine dietary strategies to reduce the risk of sarcopenia. [Spoiler alert: it has less to do with piling on protein and far more to do with types of foods and dietary patterns. I began this discussion in my previous post on Muscle and Protein.]

* Muscle quality is a broad term that encompasses both the structural and functional characteristics of muscle. It is often associated with high muscle density, which reflects a lower degree of fat infiltration within and around muscle tissue (myosteatosis) and a greater capacity for force production. Muscle quality is commonly assessed as strength relative to muscle mass, i.e., how much force a muscle can generate for its size.⁵ In other words, it is not merely the amount of muscle that we carry that matters, but how well the muscle works.

Share

Leave a comment

References

1. Ruiz-Valenzuela RE, Artacho R, Ruiz-López MD, Molina-Montes E. Healthy dietary patterns and risk of sarcopenia in adults Aged > 50 years: A systematic review and meta-analysis considering EWGSOP1 and EWGSOP2 criteria. Nutrients. Aug 26 2025;17(17).

2. Menant JC, Weber F, Lo J, et al. Strength measures are better than muscle mass measures in predicting health-related outcomes in older people: time to abandon the term sarcopenia? Osteoporos Int. Jan 2017;28(1):59-70.

3. Bahat G, Kilic C, Eris S, Karan MA. Power versus sarcopenia: Associations with functionality and physical performance measures. The Journal of Nutrition, Health and Aging. 2021/01/01/ 2021;25(1):13-17.

4. Bolte J, Smelter AA, Norton L. Are we giving too much weight to lean mass loss? Mol Metab. Nov 2025;101:102253.

5. Goodpaster BH, Carlson CL, Visser M, et al. Attenuation of skeletal muscle and strength in the elderly: The Health ABC Study. Journal of Applied Physiology. 2001;90(6):2157-2165.

6. Khaksarian M, Sharafi MH, Souri F. Musculoskeletal degeneration and cardiovascular aging: a narrative review of shared mechanobiological pathways. Mol Biol Rep. May 30 2026;53(1).

7. Gustafsson T, Ulfhake B. Aging skeletal muscles: What are the mechanisms of age-related loss of strength and muscle mass, and can we impede its development and progression? Int J Mol Sci. Oct 11 2024;25(20).

8. Izquierdo M, de Souto Barreto P, Arai H, et al. Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR). J Nutr Health Aging. Jan 2025;29(1):100401.

9. Ferguson C, Furrer R, Murach KA, Hepple RT, Rossiter HB. Power and endurance: Polar opposites or willing partners? Med Sci Sports Exerc. Nov 1 2025;57(11):2480-2495.

10. Moro T, Brightwell CR, Phalen DE, et al. Low skeletal muscle capillarization limits muscle adaptation to resistance exercise training in older adults. Exp Gerontol. Nov 2019;127:110723.

11. de Vos NJ, Singh NA, Ross DA, Stavrinos TM, Orr R, Fiatarone Singh MA. Effect of power-training intensity on the contribution of force and velocity to peak power in older adults. J Aging Phys Act. Oct 2008;16(4):393-407.

12. Martins AD, Fernandes O, Pereira A, et al. The effects of high-speed resistance training on health outcomes in independent older adults: A systematic review and meta-analysis. Int J Environ Res Public Health. Apr 28 2022;19(9).

13. Støren O, Helgerud J, Støa EM, Hoff J. Maximal strength training improves running economy in distance runners. Med Sci Sports Exerc. Jun 2008;40(6):1087-1092.

Protein has long occupied a pedestal in the world of nutrition. Unlike its macronutrient siblings, fat and carbs, it has largely escaped demonization. In fact, thanks in large part to a confluence of influencers and industry marketing, we are now routinely admonished to consume more of it: more than double, or even triple, the recommended daily allowance (RDA) of 0.8 grams/kilogram.

The message especially resonates with an aging population increasingly fearful of sarcopenia, the age-related loss of muscle mass. To be fair, this is a legitimate concern and not entirely misplaced. But loss of muscle function and power may matter even more than loss of muscle itself, a topic for another day.

At first glance, the argument seems intuitive: muscle is made of protein; therefore, it follows that consuming ever more protein should preserve or build more muscle. But intuition is not evidence. The real question is this: Does consuming large amounts of protein solve the problem (or problems)?

The evidence suggests a far more nuanced and complex answer. As we explore in our book, Staying in the Game, protein adequacy and skeletal health are influenced by exercise load and intensity, other nutritional factors (such as carbohydrate intake, total calories, and fiber), inflammation, gut health, and insulin sensitivity.^{1, 2}

But for context, let’s briefly explore some protein history.

A Short History of Protein

In 1842, Justus von Liebig, a German organic chemist, classified food components into two categories: plastic (protein) and respiratory (fat and carbohydrate).³ Plastic food, or protein, was regarded as the “substance for growth and repair and the source of all energy.” In Liebig’s words, it was the “only true nutrient.”³

Liebig also believed that exercise literally burned muscle tissue. The implication was, therefore, that physical activity required continual protein replacement.

His beliefs were entirely speculative, lacking any grounding in scientific experimentation. Yet they were accepted without review by other scientists for many years. As a result, by the 1890s, the US Department of Agriculture was recommending extraordinarily high protein intakes, well over 100 grams daily, for working men. (Given the recent guidelines, it appears that history can and does repeat itself.)

Liebig’s ideas also helped turn public opinion against carbohydrate-rich, plant-forward diets. Protein became nutritionally exalted, and, by extension, animal flesh assumed nutritional supremacy. Liebig even marketed his own beef extract supplement: Liebig’s Extract of Meat.

In many ways, Liebig became the influencer of his era.

Putting it To the Test

Fast-forward to the early 1900s. Russell Chittenden, professor of physiological chemistry at Yale University, decided to put Liebig’s theory to the test.⁴

Chittenden recruited thirteen elite Yale athletes who, in his words, were “accustomed to living a vigorous life under varying conditions, and who naturally had a great liking for the pleasures of eating.” He persuaded them to dramatically reduce their protein intake, from more than 100 grams daily to less than 50 grams.

Exactly how he convinced young men who enjoyed “the pleasures of eating” to voluntarily decrease their protein (but not calorie) intake was, unfortunately, not divulged. Nevertheless, in the name of science, they complied.

Their food was weighed and recorded, and nitrogen balance and uric acid levels were meticulously monitored. Strength and performance tests were conducted before and after the dietary intervention. These were not novices; they were already highly trained men who had spent years refining their athletic skills and physical capacities.

(Picture from: Physiological economy in nutrition, with special reference to the minimal protein requirement of the healthy man. An experimental study. By R. Chittenden)

Six months later, the athletes were retested under identical conditions. The results were astounding and ran counter to the conventional wisdom of the time.

Chittenden reported that “Every man, without exception, showed a decided improvement in his muscular power.” Overall, average gains approached 30%.⁴

Now, without a control group, we cannot know with certainty whether the improvements resulted from the dietary change itself or from continued training. But these men were already highly trained athletes; thus, dramatic improvements from training alone are highly improbable.

One likely explanation is that by lowering protein intake, they increased carbohydrate intake, an ergogenic shift that endurance and strength athletes alike often underestimate even today. Yet more than a century later, the dominant narrative remains largely unchanged: ever-higher protein intake is essential for building muscle, supporting strength training, preventing loss of muscle mass, and optimizing body composition.

Since Liebig’s time, thousands of studies on protein metabolism, muscle physiology, aging, and performance have been conducted. The cumulative evidence paints a far more nuanced, complex, and less conclusive picture than the simplistic “more protein equals more muscle” narrative that dominates social media.

But the notion that most people are chronically deficient, and that ever-escalating intake is the answer to aging, strength, or weight loss, deserves more scrutiny.

In the next installments, I will take a deeper look at what the evidence actually says about protein requirements in older adults—and, more importantly, what fitness strategies genuinely help preserve muscle mass, function, and power as we age.

Share

Subscribe now

Leave a comment

References

1. Tipton KD, Witard OC. Protein requirements and recommendations for athletes: relevance of ivory tower arguments for practical recommendations. Clin Sports Med. Jan 2007;26(1):17-36.

2. Przewłócka K, Folwarski M, Kaźmierczak-Siedlecka K, Skonieczna-Żydecka K, Kaczor JJ. Gut-muscle axis exists and may affect skeletal muscle adapation to training. Nutrients. May 18 2020;12(5).

3. Whorton JC. Muscular vegetarianism: the debate over diet and athletic performance in the progressive era. J Sport Hist. 1981;8(2):58-75.

4. Chittenden R. Physiological economy in nutrition, with special reference to the minimal protein requirement of the healthy man. An experimental study: Frederick A Stokes Company; 1905.

For years, I resisted resistance training, convinced that my decades of pounding trails and pavement would be enough to preserve my bones. After all, I have completed multiple IRONMAN races. With iron in the name, surely that should count for something.

Weight training, in my mind, was for people chasing ego-enhancing biceps and six-pack abs. That, plus the gym felt like foreign territory: intimidating machines, clanging steel, recycled air, and mirrors everywhere. No blue skies. No mountain vistas. No alpine breezes. Give me heavy breathing over heavy metal any day.

But I also follow the science. The uncomfortable truth is that being a slightly built, postmenopausal woman is not particularly good for one’s bones.

As we discuss in Staying in the Game, menopause (and the resulting decline in estrogen) is described as “a catastrophic event for the female skeleton.” Men have certain advantages: they are generally heavier and more muscular, both of which are protective for bone health. But they are hardly immune. Worldwide, osteoporosis affects roughly one in five women and one in twenty men over age 50.¹

Even endurance male athletes are not exempt.

One study of highly trained male master cyclists, who had trained and raced for an average of 20 years, reported lower bone mineral density (BMD) than in healthy, age- and weight-matched controls.² Surprisingly, even a history of earlier weight-bearing activity did not appear to confer lasting protection. The likely explanation is a combination of insufficient ongoing skeletal loading after midlife and an age-related acceleration of bone density decline. Running, by contrast, appears considerably more osteogenic; cyclists are approximately seven times more likely than runners to exhibit osteopenia of the lumbar spine (although runners are not immune either).³

Herein lies a disturbing paradox for athletes and fitness-focused adults: extraordinary VO₂max, superb cardiovascular fitness, and pristine metabolic health do not necessarily guarantee healthy bones.

It is well established that resistance training is critical for slowing both muscle and bone loss. But the research has become more nuanced in recent years. Simply “moving more” or “lifting weights” is not enough if the goal is to preserve—or even rebuild—bone.

Bone responds to heavy loading. It does not need pampering. Specifically, it responds to high mechanical strain, progressive overload, novel loading patterns, and rapid force generation.⁴

In practical terms, the preponderance of evidence suggests that effective bone-building programs include:⁴

• Loads exceeding ~70-80% of one-repetition maximum (with some studies suggesting >80%). This translates to adding enough weight to reach fatigue after 4-5 reps.

• Resistance training two to three times weekly

• Sessions lasting approximately 35–40 minutes

• Multi-joint exercises such as squats, overhead presses, rows, pulldowns, calf raises, and loaded carries

• Power training or rapid force production

Additionally, patience and consistency matter enormously.

Bone remodeling is not rapid. Skeletal adaptation occurs slowly and quietly over months. Meaningful changes often require 6–9 months of sustained mechanical loading. This is also why progressive overload matters: bones adapt only when they continue to receive a reason to do so.

High Velocity Resistance Training (HVRT)

More recently, researchers have become interested in high-velocity resistance training (HVRT), which also offers skeletal benefits—perhaps even surpassing those of traditional resistance training in some contexts.⁵

HVRT involves performing the concentric (lifting) phase of a movement with maximal speed and force, followed by a slower eccentric (lowering) phase. Imagine slowly lowering into a squat, then explosively driving upward.⁵

Interestingly, even relatively light-load power training has been shown to improve pelvic BMD in older women.⁶ Another study found that power training preserved bone density more effectively over two years than traditional, albeit lower intensity, progressive resistance training.⁷

This matters because lighter, faster movements may feel less intimidating—and therefore more approachable—for many older adults than heavy lifting (especially if machines are used). Other examples include jumping, hopping, medicine ball throws, and certain plyometric exercises.

The LIFTMOR Trial

The landmark study that helped transform thinking in this area was the 2018 LIFTMOR trial.⁸

The investigators boldly went where others had feared to go. They enrolled women with low to very low bone mass in a high-intensity lifting program: squats, deadlifts, and overhead presses performed at 80–85% of one-repetition maximum, along with impact-loading exercises (pulling up on a bar, then letting go and landing as forcefully as possible). Conventional wisdom had long warned against such training in women with osteoporosis.

Instead, the opposite happened.

Not only did these women tolerate the program safely under supervision, but their bones became stronger. The study fundamentally challenged the long-standing notion that fragile bones must always be treated with care. A subsequent study on men showed similar promising results.⁹

Ultimately, however, the best approach is likely not either/or, but both/and.

Resistance Training + Aerobic Training

A 2025 meta-analysis reported greater improvements in bone density among individuals who combined resistance and aerobic exercise than among those who engaged in either modality alone.⁴ One possible explanation is that appropriately dosed aerobic exercise improves insulin sensitivity and reduces inflammation.

Of course, there are no guarantees that what has been lost can be fully restored. The nature of aging is that systems erode over time. Brain volume declines. Muscle mass diminishes. Cardiovascular capacity wanes. Bones thin. Alas, I cannot run a mile as fast or jump as high as I could in my twenties.

But aging does not have to be catastrophic. The tide can be slowed.

And perhaps that is the real promise of lifestyle medicine—not immortality, but compression of frailty. More years of strength. More years of independence. More years of doing what we love with the people we love.

Regular high-intensity resistance and power training, especially when combined with aerobic exercise, balance work, agility training, and sound nutrition, can preserve and even improve physical and cognitive function well into the later years of life. Better function means better quality of life. And less fragility means less dependence on others for care.

As I often tell my clients,

“The most unselfish thing you can do is take care of yourself.”

So, if you will excuse me, I am off to the gym. It is still not my favorite place, but I am learning to embrace it. (Darn that science).

Share

Subscribe now

Leave a comment

References

1. Bone Biology. International Osteoporosis Foundation. Available at: https://www.osteoporosis.foundation/health-professionals/about-osteoporosis/epidemiology?utm_source=chatgpt.com. Accessed May 12, 2026.

2. Nichols J, Palmer J, Levy S. Low bone mineral density in highly trained male master cyclists. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. 08/01 2003;14:644-649.

3. Rector RS, Rogers R, Ruebel M, Hinton PS. Participation in road cycling vs running is associated with lower bone mineral density in men. Metabolism. Feb 2008;57(2):226-232.

4. Xiaoya L, Junpeng Z, Li X, Haoyang Z, Xueying F, Yu W. Effect of different types of exercise on bone mineral density in postmenopausal women: a systematic review and network meta-analysis. Scientific Reports. 2025/04/05 2025;15(1):11740.

5. Haque I, Schlacht TZ, Skelton DA. The effects of high velocity resistance training on bone mineral density in older adults: A systematic review. Bone. Feb 2024;179:116986.

6. Hamaguchi K, Kurihara T, Fujimoto M, et al. The effects of low-repetition and light-load power training on bone mineral density in postmenopausal women with sarcopenia: a pilot study. BMC Geriatrics. 2017/05/02 2017;17(1):102.

7. von Stengel S, Kemmler W, Kalender WA, Engelke K, Lauber D. Differential effects of strength versus power training on bone mineral density in postmenopausal women: a 2-year longitudinal study. Br J Sports Med. Oct 2007;41(10):649-655; discussion 655.

8. Watson SL, Weeks BK, Weis LJ, Harding AT, Horan SA, Beck BR. High-intensity resistance and impact training improves bone mineral density and physical function in postmenopausal women with osteopenia and osteoporosis: The LIFTMOR randomized controlled trial. J Bone Miner Res. Feb 2018;33(2):211-220.

9. Harding AT, Weeks BK, Lambert C, Watson SL, Weis LJ, Beck BR. A comparison of bone-targeted exercise strategies to reduce fracture risk in middle-aged and older men with osteopenia and osteoporosis: LIFTMOR-M semi-randomized controlled trial. J Bone Miner Res. Aug 2020;35(8):1404-1414.

• “You need more protein.”

• “Animal protein is superior.”

• “Plant protein is incomplete.”

These aren’t the most useful statements.

A better question, and one that reflects how we actually eat, is:

What happens when we replace one source of protein with another?

A recent systematic review and meta-analysis in Clinical Nutrition (Barrantes-Espinola et al., 2026) examined the effects of isocaloric substitution—replacing animal protein with plant protein while keeping total calories constant.

This matters because it isolates choice, not just intake.

What They Found

Across multiple large prospective cohorts, substitution of plant for animal protein was associated with lower all-cause mortality, with strong reductions in cardiovascular mortality. The findings for cancer were less consistent (it depended on the type of cancer). The most pronounced benefits occurred when plant protein replaced red and processed meats.

The Signal

This is a consistent pattern across studies. Shifting protein intake toward plant sources is associated with better long-term health outcomes. This aligns with prior work (e.g., JAMA Internal Medicine, Song et al., 2016) and broader dietary pattern research (e.g., PREDIMED trial). Indeed, one of the recommendations of the Scientific Advisory Committee Report of the 2025 Dietary Guidelines is to “substitute processed or unprocessed red meat with plant sources of protein (such as beans, peas, lentils, nuts, seeds, or soy) for adults and older adults, which is associated with a lower risk of cardiovascular disease morbidity.”

The Noise

Yes, these are observational data—and the familiar refrain follows: correlation does not equal causation. Fair enough. It is entirely possible that those who consume less meat also differ in other meaningful ways—smoking less, drinking less, and engaging more consistently in health-promoting behaviors.

But this is not a naïve comparison. The studies included in this meta-analysis adjusted for a comprehensive range of lifestyle and demographic factors, including diet quality, physical activity, smoking, and alcohol intake.

Moreover, the strength of inference is supported by several factors: consistent findings across multiple cohorts, biological plausibility of the observed associations, and reproducibility across diverse populations and time periods.

Biological Plausibility

Protein doesn’t act in isolation; the food complex matters.

Plant protein sources are embedded within a broader nutritional matrix aligned with favorable health outcomes. They are typically accompanied by dietary fiber (including microbiota-accessible carbohydrates), polyphenols, unsaturated fats, and a range of vitamins and minerals. These components support gut microbial diversity, enhance short-chain fatty acid production, and improve lipid and vascular health.

Animal protein sources—particularly red and processed meats—are accompanied by less favorable nutritional and biochemical profiles. These include saturated fat, heme iron (a pro-oxidant), nitrates and nitrites, and compounds such as choline and carnitine, which can be metabolized by the gut microbiota into trimethylamine N-oxide (TMAO), a biomarker associated with cardiovascular risk. High-temperature cooking can also generate heterocyclic amines, which are known carcinogens. Other products contain bacterial endotoxins.

Collectively, these factors have been linked to less favorable lipid profiles, impaired vascular function, increased oxidative stress and inflammation, and the production of adverse gut-derived metabolites.

Thus, the health effects of protein reflect not only its amino acid composition but also the broader dietary context in which it is consumed.

What This Means for Performance Longevity

There is a persistent belief that one must “eat muscle to make muscle.” This has intuitive appeal—but physiology is not so literal. The body breaks down protein into amino acids and reallocates them according to need, not source.

A plant-protein-forward approach can more than meet protein requirements, support physical output and recovery, and promote muscle protein synthesis. Indeed, when embedded within a high-quality dietary pattern, it offers advantages for preserving muscle and metabolic health across the lifespan.

Practical Takeaway

You do not need to overhaul your diet overnight. Consider swapping meat for lentils, beans, edamame, tofu, nuts, and seeds. Even partial substitution carries benefit.

The Bottom Line

It’s not just how much protein you eat; it’s where it comes from that matters.

Planetary health is also a key consideration. To quote the paper at hand, “Shifting dietary patterns toward plant-protein offers a dual opportunity to improve population health while reducing environmental impact.”

In the long game of human health, planetary health, and performance, our choices compound.

Share

Subscribe now

Leave a comment

References

1. Barrantes-Espinola G, Alberti P, Jaramillo-Morales E, et al. Isocaloric substitution of animal protein with plant protein and its impact on all-cause, cardiovascular, and cancer mortality: A systematic review and meta-analysis. Clin Nutr. 2026;61.

2. Song M, Fung TT, Hu FB, et al. Association of animal and plant protein intake with mortality. JAMA Intern Med. 2016;176(10):1453–1463.

3. Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. New Eng. J. Med. 2013;368:1279–1290.

4. https://www.dietaryguidelines.gov/2025-advisory-committee-report.

5. Gardner CD, Hartle JC, Garrett RD, Offering LC, Wasserman AS. Maximizing the intersection of human health and the health of the environment with regard to the amount and type of protein produced and consumed in the United States. Nutr Rev 2019: 77(4):197-215.

6. Nelson ME, Hamm MW, Hu FB, Barns SA, Griffin TS. Alignment of health dietary patterns and environmental sustainability: A systematic review. Adv Nutr. 2016;7(6):1005-1025.

7. Gazzani D, Zamboni F, Spelta F, et. al. Vegetable but not animal protein intake is associated to a better physical performance: a study of a general population sample of adults. Food Nutr Res. 2019;63.