top of page
Search

The Protein Panic That Wasn't: When Bad Science Goes Viral

How one flawed study terrified millions about eating protein, and why the new evidence changes everything


In 2014, a bombshell study hit the headlines: "High protein diet as bad as smoking for middle-aged people." The research, published in the prestigious journal Cell Metabolism, claimed that eating animal protein increased your risk of dying from cancer by a staggering 400% if you were between ages 50-65.

The findings were so dramatic that they made international news. People panicked. Protein became the new villain.

There was just one problem: The study was fundamentally flawed.

Now, a new analysis using the exact same dataset has revealed what many scientists suspected all along, i.e. the original conclusions were wrong. Not just a little wrong. Spectacularly, methodology-destroyingly wrong.

Let me show you what really happened, and what this teaches us about how nutrition science can go so catastrophically off the rails.


The Original Claim: A Four-Fold Increase in Cancer Risk

The 2014 study by Levine and colleagues analysed data from NHANES III, a large US health survey from 1988-1994. Here's what they reported for people aged 50-65:

  • High protein intake (≥20% of calories): 74% increased risk of death from any cause

  • High protein intake: 400% increased risk of cancer death (HR=4.33)

  • Moderate protein intake (10-19% of calories): Still a 3x increased cancer risk

  • The culprit? Animal protein specifically, working through IGF-1 (a growth hormone)

The implication was clear: Eat animal protein in middle age, and you're basically smoking cigarettes.


Why People Believed It

The study had several things going for it:

  • Published in a high-impact journal (Cell Metabolism)

  • Used a large dataset (NHANES III)

  • Had a plausible biological mechanism (IGF-1)

  • Fit perfectly with the growing "plant-based is best" narrative

But as we'll see, none of that mattered when the methodology was broken.


Enter the Rebuttal: Same Data, Completely Different Results

A new study published in Applied Physiology, Nutrition, and Metabolism (2025) went back to the same NHANES III dataset. Same people. Same time period. Same mortality outcomes.

But they used proper statistical methods.


The New Findings:

For ALL adults (15,937 people, 3,843 deaths):

Outcome

Animal Protein

Plant Protein

All-cause mortality

No association (HR=0.99)

No association (HR=1.02)

CVD mortality

No association (HR=1.02)

No association (HR=1.01)

Cancer mortality

Protective (HR=0.95)

No association (HR=1.08)

IGF-1 levels

No association with any mortality

No association with any mortality

Translation: Animal protein didn't increase mortality risk. In fact, it was slightly protective against cancer death.

For ages 50-65 specifically (the group that supposedly had 400% increased cancer risk):

  • No association with all-cause mortality

  • No association with CVD mortality

  • Animal protein was protective for cancer (HR=0.87, meaning 13% lower risk)

  • IGF-1 had zero relationship with mortality

The 400% increased cancer risk? It disappeared entirely.


What Went Wrong: A Masterclass in Bad Methodology

So how did the same dataset produce such wildly different results? The answer reveals fundamental problems with how the original study was conducted.


Problem #1: Using "Actual Intake" Instead of "Usual Intake"

What the original study did:

  • Used single-day dietary recalls

  • Assumed what people ate on one random day represented their typical diet

Why this is a problem: Think about your own eating. Did yesterday's diet perfectly represent what you usually eat? What if they happened to catch you on the day you ate a steak, or the day you had a salad?

Single-day recalls are notoriously unreliable. This is Nutrition Science 101.

What the new study did:

  • Used sophisticated statistical modeling (Markov Chain Monte Carlo method)

  • Estimated "usual intake" by accounting for day-to-day variability

  • Co-modeled multiple nutrients simultaneously to reduce measurement error

This is standard practice in modern nutritional epidemiology. The original study simply didn't use it.


Problem #2: Arbitrary, Unequal Groups

What the original study did: Created three protein intake groups with wildly different sizes:

  • Low protein (<10% of calories): n=437 people (tiny group)

  • Moderate protein (10-19%): n=4,798 people (huge group)

  • High protein (≥20%): n=1,146 people (medium group)

Why this is a problem: When you compare a tiny group (437 people) to much larger groups, and you have relatively few mortality events in the small group, the statistical estimates become extremely unstable. Small random fluctuations get magnified into huge apparent risks.

It's like flipping a coin 10 times vs. 1,000 times. With only 10 flips, you might get 7 heads and conclude coins are biased. With 1,000 flips, the true probability emerges.

What the new study did:

  • Used equal-sized tertiles (thirds) of protein intake

  • Each group had similar numbers of participants

  • This provides stable, reliable estimates

Problem #3: The IGF-1 Red Herring

The original study's proposed mechanism was that protein → IGF-1 → cancer. But they never actually tested whether IGF-1 levels predicted mortality in their dataset.

The new study measured this directly:

  • IGF-1 levels: Zero association with all-cause mortality (HR=1.00)

  • IGF-1 levels: Zero association with CVD mortality (HR=0.99)

  • IGF-1 levels: Zero association with cancer mortality (HR=1.00)

The proposed mechanism? It didn't exist in the data.


The Bigger Picture: Why This Matters Beyond Protein

This isn't just about protein. It's about how:

1. Single Studies Can Be Dangerously Misleading

Even in prestigious journals. Even with large datasets. Even with plausible mechanisms. If the methodology is flawed, the conclusions are worthless, or even worse, harmful (damn now most people fear red meat).

The original study likely caused:

  • Millions of people to unnecessarily restrict protein

  • Older adults to under-consume protein (particularly problematic for muscle maintenance)

  • Confusion about basic nutrition advice

  • Erosion of trust in nutrition science

2. Extraordinary Claims Require Extraordinary Evidence

A 400% increase in cancer risk? That's extraordinary. For context:

  • Smoking increases lung cancer risk by ~2,000%

  • Heavy drinking increases liver cancer risk by ~300-600%

The claim that eating chicken could be remotely comparable to smoking should have raised immediate red flags.

3. Replication and Re-analysis Are Essential

Science is supposed to be self-correcting, but only if we:

  • Re-examine controversial findings

  • Use proper methods

  • Publish contradictory results (not just confirming studies)

This study did exactly that. It took 11 years.

4. Biological Plausibility Isn't Proof

Yes, IGF-1 is a growth factor. Yes, growth factors can theoretically promote cancer. But:

  • The dose-response relationship matters

  • Other protective mechanisms exist

  • Real-world outcomes trump theoretical mechanisms

The IGF-1 story sounded plausible, but the data didn't support it.

What the Evidence Actually Shows About Protein

Let me be clear about what we can conclude from the current body of evidence:

✅ Well-Supported:

  • Adequate protein is essential for muscle maintenance, especially in older adults

  • Both animal and plant proteins can be part of healthy diets

  • Very high protein intakes (within normal dietary ranges) do not increase mortality risk

  • Protein source matters less than overall diet quality

❓ Still Uncertain:

  • Whether there's an optimal protein level for longevity (vs. just adequacy)

  • Whether protein timing matters for outcomes beyond muscle

  • Long-term effects of very high protein intakes (>2.0 g/kg/day)

❌ Not Supported:

  • That animal protein in normal amounts increases mortality

  • That we should fear protein intake in middle age

  • That IGF-1 from dietary protein meaningfully affects mortality

  • That plant protein is necessarily superior for longevity

Practical Takeaways

If you're under 65 and sedentary/lightly active:

  • Minimum: 0.8 g/kg body weight (the RDA - bare minimum to avoid deficiency)

  • Optimal: 1.2-1.6 g/kg for better body composition and satiety

  • Don't fear animal protein sources

  • Focus on overall diet quality, not single nutrients

If you're under 65 and physically active/strength training:

  • Target: 1.6-2.2 g/kg body weight

  • Higher end (2.0-2.2 g/kg) supported for muscle building and maintenance

  • Distribute across meals (20-40g per meal) for optimal muscle protein synthesis

  • Both animal and plant sources work, but animal proteins are more efficient per gram

If you're over 65 (sarcopenia risk increases):

  • Minimum: 1.0-1.2 g/kg body weight

  • Optimal: 1.2-1.6 g/kg (potentially higher with resistance training)

  • Consider 1.6-2.0 g/kg if strength training - older adults may have "anabolic resistance"

  • Protein timing matters more: aim for 25-40g per meal (higher threshold than younger adults)

  • Animal proteins particularly valuable for leucine content and amino acid completeness

  • Resistance training + adequate protein critical for maintaining muscle mass and independence

If you're trying to lose weight (any age):

  • Target: 1.6-2.4 g/kg (of goal body weight, not current weight if obese)

  • Higher protein improves satiety, preserves muscle during caloric deficit

  • Even higher intakes (2.4-3.0 g/kg) may be beneficial during aggressive cuts

For everyone:

  • The RDA (0.8 g/kg) is NOT optimal - it's the minimum to prevent deficiency

  • Variety matters - both animal and plant proteins offer benefits

  • Context matters - protein within a healthy dietary pattern

  • Individual needs vary - activity level, health status, age all matter

  • No evidence of harm from protein intakes up to 2.0-2.2 g/kg in healthy individuals

The Meta-Lesson: How to Read Nutrition Headlines

Next time you see a dramatic nutrition headline, ask:

  1. Is this a single study? (Wait for replication)

  2. How was intake measured? (Single recall? Food frequency questionnaire? Biomarkers?)

  3. How were groups defined? (Equal sizes? Arbitrary cutoffs?)

  4. Is there a dose-response? (More exposure = more effect?)

  5. Is the effect size plausible? (400% increase should make you suspicious)

  6. Did they test their proposed mechanism? (Or just assume it?)

  7. What do other studies show? (Consistency matters)


The Bottom Line

The protein panic of 2014 was built on methodological quicksand. When proper statistical methods were applied to the exact same data, the terrifying findings evaporated.

Animal protein doesn't increase your mortality risk.

It might even be slightly protective against cancer.

IGF-1 levels aren't the longevity boogeyman we were told they were.

This doesn't mean you should eat only animal protein, or that plant proteins aren't valuable. It means the story is much more nuanced than "animal protein will kill you."

Adequate protein intake—from whatever sources you prefer—supports healthy aging. The RDA of 0.8 g/kg/day is a minimum, not an optimal target. For most people, somewhat higher intakes (1.0-1.2 g/kg/day) appear safe and may be beneficial, especially for maintaining muscle mass as we age. Most people would benefit from intakes HIGHER than the RDA, especially:

  • Older adults (to combat sarcopenia)

  • Active individuals (to support training adaptations)

  • People trying to lose weight (to preserve muscle and increase satiety)

The real sweet spot for most people: 1.6-2.0 g/kg/day, not the outdated 0.8 g/kg RDA.


The real lesson? Be skeptical of nutrition sensationalism. Even when it's published in prestigious journals. Even when it has a plausible mechanism. Even when it confirms your existing beliefs.

Good science requires good methods. And good methods, as this study shows, can completely overturn bad conclusions.


Technical Details (For the Nerds)

Study Design:

  • Population: 15,937 US adults from NHANES III (1988-1994)

  • Follow-up: Through 2006 (median 174 months)

  • Mortality events: 3,843 total (1,742 CVD, 862 cancer)

  • Statistical method: Hazard ratio models with bootstrap variance estimation (1,000 replications)

Key Methodological Improvements:

  • Multivariate MCMC method for usual intake estimation

  • Simultaneous modeling of energy, total protein, animal protein, plant protein, fats, and carbohydrates

  • Adjustment for age, sex, physical activity, smoking, and energy intake

  • Equal-sized tertiles rather than arbitrary groupings

  • Direct testing of IGF-1 associations (n=5,753 subsample)

Conflict of Interest Disclosure: This study was funded by the National Cattlemen's Beef Association (sponsor had no role in design, analysis, or interpretation). Authors have consulting relationships with food industry. This is important context, though the use of proper statistical methodology and transparent data reporting allows independent verification.

Want to dive deeper?

The full study: Papanikolaou Y, Phillips SM, Fulgoni VL. Animal and plant protein usual intakes are not adversely associated with all-cause, cardiovascular disease-, or cancer-related mortality risk: an NHANES III analysis. Appl Physiol Nutr Metab. 2025;50:1-8.

The original controversial study: Levine ME, 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. 2014;19(3):407-417.


What do you think? Were you influenced by the 2014 protein scare? Let me know in the comments.

 
 
 

Comments


Join the Club

Join my health and fitness newsletter, delivered every two weeks.

Practical nutrition breakthroughs, smart training tactics, zero hype.

Thanks for submitting!

RACHA HYDE

FITNESS COACH

& NUTRITIONIST

United Kingdom
Online Worldwide



info@rachahyde.com

  • Facebook
  • Twitter
  • Instagram
  • White YouTube Icon

Get in touch

bottom of page