Longevity and Health Span Blog

Our Blogs differ from our Longevity Tips in that they offer a more comprehensive, in-depth exploration of specific topics, complete with references.

They tend to be more detailed and may include more technical content.

5 Part Series - Myths, Lies & Truths about Testosterone & Anabolic Steroids

Intro: Myths, Lies & Truths About Testosterone & Anabolic Steroids

This blog will be released in 5 parts over 4-5 weeks:

Introduction

Understanding Testosterone, Anabolic Steroids, and the Science Behind Hormone Replacement Therapy (HRT)

Misinformation about testosterone and its synthetic analogs (anabolic steroids/AAS) is widespread. Surprisingly, even scientific literature has contributed to this confusion. Over 50 years ago, two published studies claimed that AAS had no impact on muscle growth (23,24).

However, these early studies were methodologically flawed—using low dosages, short durations, and inadequate resistance training protocols. Did the researchers have an agenda, designing their studies to produce a predetermined outcome? Possibly. Regardless of intent, these misleading and incorrect conclusions were later disproven by well-designed studies in the 1980s and beyond.

When Science Gets It Wrong

How is it possible for science to be wrong? After all, weren’t we urged during the COVID-19 pandemic to “Follow the science”? The reality is that not all scientific studies are created equal.

Poorly designed studies with flawed conclusions exist and often fail replication—a critical test of scientific validity. In an essay published in PLoS Medicine / August 2005 | Volume 2 | Issue 8,  Stanford University professor John Ioannidis, PhD wrote, “There is increasing concern that in modern research, false findings may be the majority or even the vast majority of published research claims. (25,26).

The vitriol against Ioannidis on his views and research during the COVID-19 pandemic was severe as many scientists refused to consider another, and different, analysis of the data because it opposed their politically driven agenda. More and more, we are seeing the aggressive suppression of science and analysis of data that does not agree with a particular political group.

The phrase “Follow the science” was often misused to mean “Follow the science that aligns with our particular agenda.” It was used to manipulate behavior. A more accurate principle would be:
“Follow the good science, not the bad science.” Importantly, even good science evolves as new knowledge emerges.

Balancing Risks and Benefits

All medications have a risk-to-reward ratio, and higher doses and improper use increase the risks significantly. Testosterone and its synthetic analogs are no exception.

  •  When properly prescribed and monitored by a knowledgeable physician, their benefits can be transformative.
  •  When misused or abused without medical supervision, the risks can become severe, even life-threatening.

The Purpose of This Blog

This blog aims to be a definitive resource on hormone replacement therapy (HRT), covering both testosterone and its synthetic analogs.

A comprehensive review of the scientific literature on male HRT and recreational use was conducted for this blog, though it remains an evolving field. Over 50  papers were identified and analyzed using search terms such as: testosterone, anabolic steroids, HRT, history of testosterone synthesis, erectile dysfunction, Deca-Durabolin, nandrolone and many others.

At the Julian A. Jarman, MD Research Foundation, a non-profit Men’s Health Foundation, understanding HRT, testosterone, and its analogs is a core priority. Providing accurate, science-backed information empowers men to make informed decisions about their health.

Part 1: Myths, Lies & Truths About Testosterone & Anabolic Steroids

Part 1: The History of Anabolic Steroids

Understanding Testosterone and Anabolic Steroids

First it is important to understand that testosterone is an anabolic steroid. Both testosterone and its synthetic analogs fall under the category of androgenic anabolic steroids (AAS). While the term “anabolic steroids” often refers to synthetically manufactured drugs, all AAS originate from testosterone or its metabolites. Going forward, I will use AAS to refer to both testosterone and its synthetic analogs as a single group of male hormones.

Both testosterone and its synthetic analogs are derived from cholesterol, which serves as the precursor to all male and female hormones. In men, the testes primarily produce testosterone, while in women, smaller amounts of testosterone are synthesized in the ovaries and adrenal glands. Despite cholesterol’s negative connotation and its association with heart disease in excessive amounts, cholesterol is essential for life. We make our own cholesterol and there is is no “essential minimum” LDL-cholesterol needed in your blood to make male and female hormones, cortisol and Vitamin D, which are all synthesized from cholesterol. Despite concerns of some regarding driving LDL-cholesterol too low, current evidence supports that LDL-C levels < 20-30 mg/dL  are safe and do not compromise the body’s ability to produce hormones or other essential cholesterol-derived molecules. (30)

Most commercially produced testosterone today comes from plant sterols extracted from yams and soybeans, as this method is both efficient and cost-effective. Although other production methods exist—such as direct cholesterol conversion and microbial *transformation*—they are less commonly used in industrial applications. This plant-derived testosterone is identical to the body’s natural hormone and is often referred to as a “bioidentical hormone.”

Why Create Testosterone Analogs?

Testosterone analogs—what most people associate with the term anabolic steroids— are chemically modified versions of testosterone. These modifications enhance anabolic (anabolic means muscle-building) effects while aiming to reduce androgenic (androgenic means masculinizing) side effects.

Well-known AAS include:

  • Nandrolone (Deca-Durabolin)
  • Methandrostenolone (Dianabol)
  • Oxandrolone (Anavar)
  • Stanozolol (Winstrol)
  • Boldenone (Equipoise)

Each of these compounds has unique properties, which we will discuss later.

The Role of Testosterone in Both Sexes

Both men and women need testosterone for:

  •  Sexual development and reproduction
  •  Muscle and bone health
  •  Cognitive function

Testosterone is also the precursor to estrogen. While women naturally produce much lower levels than men, testosterone remains vital to their overall health.

The Misinformation About Anabolic Steroids

Misinformation about AAS has been—and continues to be—spread by both medical professionals and the general public. As noted in the introduction, in the 1960s and 1970s, some researchers claimed that AAS did not increase muscle mass, relying on poorly designed studies (23,24).

Today, however, there is no debate—testosterone and its analogs unequivocally enhance muscle growth.

Why Were Testosterone Analogs Created?

If testosterone is so effective, why did pharmaceutical companies develop synthetic analogs? The answer lies in the anabolic-to-androgenic ratio of each compound.

  •  Anabolic effects promote muscle growth.
  •  Androgenic effects contribute to masculinization (e.g., body hair growth, scalp hair loss, deepening voice, increased aggression, and genital enlargement in women).

The goal was to create *a male hormone with stronger anabolic effects and fewer androgenic side effects*—leading to the development of synthetic AAS for medical use that could be used for both men and women with various medical problems.

Anabolic Steroids Were Created to Treat Disease

Despite their association with athletes and bodybuilders, anabolic steroids were originally developed to treat medical conditions such as:

  •  Anemia
  •  Osteoporosis
  •  Severe weight loss and muscle-wasting diseases
  •  Hypogonadism (low testosterone production)
  •  Delayed puberty

For full disclosure, I was personally treated with the AAS Stanozolol (Winstrol) for delayed puberty.

Since their creation in the 1930s, AAS have proven valuable for many other medical applications.

The First Anabolic Steroids

  •  1935 – Scientists successfully synthesized testosterone for the first time.
  •  1950s – The first widely recognized AAS, Methandrostenolone (Dianabol), was synthesized by CIBA Pharmaceuticals.
  •  Dianabol’s advantage over testosterone? It was indeed more anabolic and less androgenic, as desired in its synthesis, marking the beginning of efforts to create steroids that build muscle with fewer masculinizing effects.

This was a major advancement—developing a testosterone derivative that treated certain diseases, enhanced muscle growth while reducing unwanted side effects so it could be used for both men and women.

Steroid Use in Sports & Bodybuilding

By the 1950s, AAS use had expanded beyond medical treatments into performance enhancement.

  •  1954 – The Soviet Union dominated the World Weightlifting Championships, later revealed to be due to testosterone use.
  •  1960s – AAS use exploded in bodybuilding and competitive sports.

1965 – The first Mr. Olympia competition was held, and AAS use became common among professional bodybuilders.

Today, it is highly unlikely that any professional bodybuilder competes without using AAS. In fact, even Arnold Schwarzenegger has admitted to using anabolic steroids.

Part 2: Myths, Lies & Truths About Testosterone & Anabolic Steroids

Part 2: Why the Fear Around Anabolic Steroids?

Why the Fear Around Anabolic Steroids?

It has been said that there are greater negative views for anabolic steroid use than opioid abuse, despite the fact that opioid addiction has caused a significant public health crisis and AAS has not. While both anabolic steroids and opioids have risks, AAS’s are not linked to overdose deaths like with opioids. Yet AAS carry a greater social stigma—especially in professional sports where their use is banned. Meanwhile, opioid addiction is viewed as a medical and mental health problem leading to a more compassionate response despite its devastating impact.

Despite their medical benefits, anabolic steroids are often demonized. Why?

This fear is largely driven by:

  •  Misinformation spread by both medical professionals and the media.
  •  Association with cheating in sports serious health risks.
  • Association with cheating in sports rather than their legitimate medical applications.

AAS are not inherently dangerous—when used correctly under knowledgeable medical supervision. However, like any powerful medication, misuse can lead to serious consequences.

In the next section, we’ll explore the benefits, risks, and misconceptions surrounding AAS use.

In 2023, the CDC reported over 81,000 opioid-related deaths (1). In contrast, the relationship between anabolic androgenic steroid (AAS) use and mortality is far less clear. Many reported cases of AAS-related deaths involve *polypharmacy*—the concurrent use of multiple substances—making it difficult to isolate anabolic steroids as the sole cause of death.

A 2024 study published in The New England Journal of Medicine, titled “Higher Mortality is Associated with Anabolic Steroid Use” (2), found that AAS users have a 2.8 times higher risk of death than non-users. However, it is crucial to distinguish correlation from causation. While these findings suggest a link between AAS use and increased mortality, confounding factors make it difficult to establish a direct causal relationship. Furthermore, comprehensive and up-to-date statistics on deaths solely attributed to anabolic steroids remain limited.

To be clear, my intent is not to downplay the potential risks of AAS use and abuse. Rather, I emphasize that *data on AAS-related deaths is scarce*—especially when compared to mortality from tobacco, alcohol, or opioids.

All Drugs Have a Risk-to-Reward Ratio

Every drug—whether prescription medication, food, supplements or even oxygen—carries both risks and benefits. Oxygen is essential for life, yet excessive oxygen exposure can damage the lungs and be fatal. The same principle applies to *AAS and all medications*—their impact depends on dosage, duration, and medical supervision.

When used under careful medical oversight, AAS can:

  • Enhance performance
  • Increase lean muscle mass
  • Reduce body fat
  • Improve cholesterol levels

The widespread fear of AAS use is largely unfounded when they are used responsibly under medical guidance. Later in this blog, we will explore the benefits of testosterone and its analogs in greater detail.

The Risks of AAS Use

Using anabolic androgenic steroids (AAS) without medical supervision carries serious health risks, including potentially fatal consequences. However, when prescribed and monitored by a knowledgeable physician, these risks can be minimized and managed effectively.

Many articles present long, alarming lists of AAS risks, misleading the public into believing that all listed side effects are equally likely. The reality is *far more nuanced—risk levels depend on dosage, duration, individual genetics, and whether proper post-cycle therapy (PCT) is implemented. Additionally, the specific AAS used also plays a critical role in side effect severity.

When testosterone replacement therapy (TRT) is administered at physiologic doses—meaning it restores testosterone levels to a natural, healthy range—its impact on biomarkers is generally predictable and manageable.

However, even at physiologic doses, some biomarkers can be influenced. Let’s break down the most commonly cited risks for biomarkers, other side effects and vital signs:

1. “Roid Rage” – Aggression & Mood Changes

At physiologic doses, AAS enhance mood and can increase confidence and motivation. However, at high doses, they disrupt neurotransmitter balance, increasing aggression:

  •  Increased dopamine → Heightened reward-seeking behavior and impulsivity.
  •  Decreased serotonin → Lower impulse control, increasing irritability and aggression. (19, 20)

2. Acne

A well-documented side effect, acne worsens with higher doses. However, women are more prone to AAS-induced acne than men due to hormonal sensitivity. (18)

3. Hair Loss (Male Pattern Baldness)

AAS accelerate hair loss only in individuals genetically predisposed to male pattern baldness. This is due to increased dihydrotestosterone (DHT) levels, which can be mitigated with 5α-reductase inhibitors like finasteride.

4. Cardiovascular Risks

Medical opinions on testosterone replacement therapy (TRT) and heart health have reversed course over the last decade.

  •  In 2010, a study prematurely halted TRT due to an alleged increase in cardiovascular (CV) risk. (21)
  •  Public Citizen, an advocacy group, petitioned the FDA for a black box warning on testosterone, but the FDA rejected it, citing an equivocal causal relationship between TRT and heart disease.
  •  Newer research, including a 2023 New England Journal of Medicine study, tracking 5,200 men aged 45–80, found no increased risk of heart attack or stroke with TRT use. (22)

Biomarkers of importance:

Total Testosterone (Range: 400–1,000 ng/dL) (Note that laboratories have slightly different ranges.

  •  Goal: Maintain levels within an optimal physiological range

Free Testosterone (Range: 10–30 pg/mL)

  •  Measures active testosterone (more relevant than total T)
  •  Influenced by SHBG levels- too high reduces free testosterone.
  • SHBG reduction means to increase free T include: increasing resistance training, increase protein intake, optimize thyroid, take Zine and Magnesium

Estradiol (Ideal: ~20–40 pg/mL)

  •  Too high → Water retention, gynecomastia (male breast tissue growth), mood swings, breast tenderness
  •  Too low → Joint pain, fatigue, low libido
  •  Managed with AI (aromatase inhibitors) if necessary, but overuse can be harmful
  •  Using testosterone cream tends to reduce this issue vs injected testosterone!!

Hemoglobin/Hematocrit

  •  T can increase red blood cell (RBC) production
  •  Too high → Risk of blood thickening (polycythemia), high blood pressure, stroke, cardiovascular risks
  •  Managed by donating blood (therapeutic phlebotomy) or adjusting dose

Prostate-Specific Antigen (PSA) (Ideal: <4.0 ng/mL)

  •  TRT doesn’t cause prostate cancer, but monitoring PSA ensures early detection of abnormalities
  •  Significant increase → Further evaluation needed

Lipid Panel (Cholesterol)

  •  LDL (“Bad” Cholesterol) – High levels increase cardiovascular risk with supraphysiological dose of TRT, but physiological dose reduces LDL (28,)
  •  HDL (“Good” Cholesterol) – physiological TRT is now belived to have little impact on HDL, (29)

Liver Enzymes (ALT, AST)

  •  Oral AAS (e.g., Anavar, Dianabol) can stress the liver, but injectable or topical TRT has minimal impact
  •  We never use oral AAS in our research because of the impact on the liver

Blood Pressure (Ideal: ~120/80 mmHg)

  •  TRT can increase blood pressure, especially if hemoglobin/ hematocrit is high
  •  Monitor regularly to prevent hypertension-related issues

Insulin Sensitivity & Blood Sugar

  •  Measure fasting Blood Glucose & HbA1c (Long-term blood sugar control)
  •  TRT can improve insulin sensitivity, reducing risk of type 2 diabetes

The Benefits of AAS Use – Who Should Consider TRT or Other AAS? Optimization of Body and Health

Over the past 15 years, medical recommendations on exogenous testosterone have shifted dramatically. Initially, concerns about heart disease and other risks fueled caution, but newer evidence has overturned these fears.

Past Concerns vs. Updated Findings

  •  JAMA studies (2013, 2014) (7,8) reported a 30% increase in cardiovascular events in men with pre-existing heart disease.
  •  In 2014, the FDA warned about potential heart risks, partly due to overprescription in “low-T” clinics.
  •  However, by 2025, expert consensus supports TRT’s benefits, provided it’s used correctly and monitored by medical professionals.

When properly administered and supervised, the benefits of TRT and AAS far outweigh the risks.

Key Benefits of TRT & AAS in Medically Supervised Use

1. Physical Benefits

  • Increased Muscle Mass & Strength – Boosts protein synthesis and nitrogen retention, leading to 3–5 kg of lean muscle gain per year.
  • Fat Reduction – Enhances fat metabolism, particularly reducing visceral (abdominal) fat.
  • Improved Bone Density – Prevents osteoporosis and strengthens spinal & hip bone mineral density (BMD).
  • Enhanced Recovery & Performance – Increases red blood cell production, improving oxygen delivery and endurance.

2. Mental & Cognitive Benefits

  • Higher Energy & Less Fatigue – Most men report feeling revitalized within weeks of starting TRT.
  • Better Mood & Mental Health – Testosterone regulates dopamine and serotonin, reducing depression and anxiety.
  • Cognitive Function – Some studies suggest testosterone improves memory and processing speed, potentially reducing the risk of Alzheimer’s disease.

3. Sexual & Reproductive Benefits

  • Higher Libido & Improved Sexual Function – TRT boosts sex drive and erectile function in men with low T.
  • Preserving Fertility (with hCG or SERMs) – While TRT alone reduces sperm count, combining it with hCG, GnRH, or SERMs (like Clomid) can maintain fertility.

4. Metabolic & Cardiovascular Benefits

  • Improved Insulin Sensitivity – Lowers the risk of type 2 diabetes.
  • Better Cholesterol & Heart Health – Can lower LDL (bad cholesterol) and increase HDL (good cholesterol).(28)
  • Testosterone supports heart function when used responsibly, though excessive doses can increase CV risk.

Who Benefits Most from TRT?

Men experiencing clinically diagnosed low T (below ~400 ng/dL) with symptoms like:

  • Androgen Deficiency in the Aging Male – The ADAM questionnaire
  • Metabolic syndrome: elevated BP, obesity or insulin resistance
  • Reduced muscle mass
  • Lower energy, motivation or drive
  • Reduced productivity
  • Chronic fatigue
  • Depression
  • Decreased sex drive/low libido
  • Poor sleep
  • Erectile dysfunction

The informed medical community has reversed its stance on TRT, recognizing its overwhelming benefits when used responsibly. The fear surrounding AAS use stems largely from misuse, misinformation, and unsupervised administration. With proper medical oversight, AAS can be both safe and highly beneficial.

Health Blogs #2: Fasting – Another Healthcare Fad or a Real Health Benefit?

By Jonathan A. Jarman, MD

(~ 20  minute read without focus on the references)

(~ 22 min audio with references removed for an easier listen)

Introduction

Healthcare fads can explode like a wildfire in  residential Los Angeles and garner just as much media attention. I think fasting falls into this category - tremendous hype, but some truth and benefit.

There’s some solid research that helps us separate the real benefits of fasting from the potential risks. But there’s also a lot of mediocre science that some treat like gospel, which only fuels the hype.

This isn’t surprising—nutrition research is often messy. Many nutrition studies rely on surveys, and most of us can’t accurately remember what we ate yesterday, let alone last week. In addition, those surveys  can involve so many variables that it’s easy to mistake a simple association for true cause and effect, e.g. the Mediterranean Diet does such and such for our health. What is a Mediterranean Diet? There are many variables in the Mediterranean Diet, or any named diet for that matter, and to make a blanket conclusion that a multiple ingredient  diet  is the cause of x, y or z  as regards our health is shoddy science. Shoddy science is common in nutrition research.

The task then is to identify quality research that may point us to potential  benefits of fasting.

Fasting Blog Goals

In this Health Blog I will cut through the social media hype, address two types of fasting, the science behind the potential medical benefits and lastly  how we might fast so that we can  increase our chance of success.

There’s a lot of talk about fasting, so it helps to keep things simple.  I like to think of fasting in two main ways: 1) Time-Restricted Eating (TRE), and 2) 24-hour fasting.

The biggest risk with fasting, whether TRE or 24 hour fasting, is muscle loss. Since building and keeping muscle is  important for overall health, any fasting routine that causes muscle loss needs to offer big benefits to be worth it.

If someone drops a lot of body and visceral fat through regular fasting but loses just a little muscle, that could be a fair tradeoff. But with enough protein and resistance training between fasts, we can usually protect muscle—and even build more.

Let’s dive into the two types and the potential benefits of each.

  1. Time Restrictive Feeding (TRE)

TRE  (Time-Restricted Eating) is an eating style that limits the daily period during which you consume calories to a specific, consistent window of time, while total caloric intake and other nutrients, specifically protein,  is not reduced.

In TRE, one is consuming the SAME number of calories, but  in a shorter eating window than one would if eating that number  in a 24 hour period ad lib. If eating the same number of calories  in a shorter window vs 24 hour ad lib  has benefits  such as weight loss, it proves that weight loss is not just due to eating fewer calories than one expends.

The theory of why benefits are seen in TRE are:

  • Circadian rhythm alignment → optimal timing for metabolism.
  • Fasting window → metabolic switch to fat/ketone use.
  • Hormonal regulation → better appetite control.
  • Glycemic control → improved insulin sensitivity.
  • Cellular cleanup → autophagy, repair, and resilience.

I don’t want to spend much time on each of the above, but I do find the role of circadian timing in TRE interesting. The physiology of TRE is:

  1. Insulin sensitivity peaks earlier in the day
    • In the morning to early afternoon, cells are more responsive to insulin, so glucose is cleared more efficiently.
    • Later in the evening, insulin sensitivity drops, meaning the same food produces a bigger glucose and insulin spike.
  2. Digestive efficiency follows a daily cycle
    • Enzymes and gut motility are higher earlier in the day, making nutrient processing smoother.
    • Late eating slows digestion and may increase gut permeability and inflammation markers overnight.

 

  1. Nighttime eating conflicts with melatonin release
    • Melatonin suppresses insulin secretion. Eating when melatonin is high (close to bedtime) can cause higher post-meal glucose levels.
    • This is why late-night snacking is linked to impaired glucose tolerance even in healthy people.
  2. Circadian alignment supports downstream systems
    • Liver glucose production, fat oxidation, blood pressure, and even mitochondrial function follow a day–night pattern.
    • Eating “out of phase” (late) appears to disrupt these, independent of calorie intake.

For simplicity, I will use two common TRE (Time-Restricted Eating) windows as examples:

  1. 16:8 TRE
  • Eat during an 8-hour window and fast for 16 hours.
  • Example: Eating from 10:00 PM to 6:00 PM (8 hours), fasting from 6:00 PM to 10:00 PM (16 hours) the next day.
  1. 14:10 TRE
  • Eat during a 10-hour window and fast for 14 hours.
  • Example: eating from 8:00 AM to 6:00 PM (10 hours), fasting from 6:00 PM to 8:00 AM the next day (14 hours).

With each of these I set a cutoff of 6pm to avoid eating close to bedtime.

You might then ask whether the benefits of TRE come from avoiding eating late or close to bedtime. That’s a great question, and I’ll address it later in this Blog

Since we have now defined two TRE options,  what are the researched based potential benefits of TRE vs unrestrictive eating periods?

There are 6 potential benefits with excellent research   by Gabel, Sutton, Wilkinson Moro and Jamshed.

  1. Reduced Body Fat & Improved Body Composition

TRE (like an 8-hour eating window) helps reduce fat mass even without cutting calories, promoting a healthier body composition

(Gabel, K., et al. (2018). Effects of 8-hour time restricted feeding on body weight and metabolic disease risk factors in obese adults: A pilot study. Nutrition and Healthy Aging, 4(4), 345–353.

  1. Improved Insulin Sensitivity & Glucose Regulation

Eating within an earlier, restricted window boosts insulin sensitivity and controls blood sugar better—even without weight loss

(Sutton, E. F., et al. (2018). Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even Without Weight Loss in Men with Prediabetes. Cell Metabolism, 27(6), 1212-1221.e3.

  1. Better Cardiometabolic Health

TRE lowers blood pressure, bad cholesterol (LDL), and triglycerides, improving heart health markers

(Wilkinson, M. J., et al. (2020). Ten-Hour Time-Restricted Eating Reduces Weight, Blood Pressure, and Atherogenic Lipids in Patients with Metabolic Syndrome. Cell Metabolism, 31(1

  1. Improved Circadian Rhythm Alignment

Aligning eating with natural circadian rhythms optimizes metabolism and hormone function, enhancing overall metabolic health

(Panda, S. (2016). Circadian physiology of metabolism. Science, 354(6315), 1008-1015.

  1. Reduced Appetite & Improved Satiety Signals

TRE normalizes hunger hormones, which helps control appetite and may lead to reduced calorie intake naturally

(Hutchison, A. T., et al. (2019). Effects of intermittent fasting on appetite: A randomized controlled trial. Nutrients, 11(2), 320

  1. Cellular & Molecular Benefits

Fasting periods during TRE activates cellular repair processes like autophagy, which reduces oxidative stress and supports healthy aging.

Autophagy is like your body’s housekeeping service—taking out the trashy, worn-out cells so the fresh ones can do their job without the clutter.

(Longo, V. D., & Panda, S. (2016). Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan. Cell Metabolism, 23(6), 1048-1059.).

What about TRE biomarker benefits?

There are 8 known biomarker benefits of TRE and again we see some of the better research studies by the aforementioned authors.

  1. Fasting Insulin & Insulin Sensitivity
  • Improvement: TRE significantly lowered fasting insulin levels, meaning the pancreas released less insulin to control blood sugar.
  • How: The body became more insulin sensitive, so cells responded better to insulin, enabling more efficient glucose uptake and reduced insulin demand (Sutton et al., 2018).
  1. Fasting Glucose & HbA1c
  • Improvement: TRE reduced or stabilized fasting blood glucose and caused modest decreases in HbA1c.
  • How: Better insulin sensitivity and improved glucose metabolism resulted in more stable blood sugar levels over time, reducing the average blood glucose exposure reflected by HbA1c (Gabel et al., 2018; Wilkinson et al., 2020).
  1. Lipid Profile (LDL, Triglycerides, HDL)
  • Improvement: TRE lowered LDL cholesterol and triglycerides, while maintaining or slightly increasing HDL.
  • How: Extended fasting periods enhance fat metabolism, promoting breakdown of stored fat and improving lipid clearance from the bloodstream, thus reducing atherogenic lipids (Wilkinson et al., 2020; Antoni et al., 2018).
  1. Blood Pressure
  • Improvement: Both systolic and diastolic blood pressure decreased modestly.
  • How: Improved insulin sensitivity and lower oxidative stress reduce vascular inflammation and stiffness, which helps blood vessels relax and lowers blood pressure (Sutton et al., 2018; Antoni et al., 2018).
  1. Inflammatory Markers (CRP)
  • Improvement: TRE reduced circulating C-reactive protein (CRP), indicating decreased systemic inflammation.
  • How: Fasting reduces pro-inflammatory cytokines and oxidative stress, calming chronic low-grade inflammation (Antoni et al., 2017).
  1. Appetite-Regulating Hormones (Leptin, Ghrelin)
  • Improvement: TRE normalized leptin and ghrelin levels, improving hunger and fullness cues.
  • How: Leptin sensitivity improved, helping signal satiety effectively, while ghrelin fluctuations were better controlled, reducing excessive hunger and cravings (Moro et al., 2016).
  1. Oxidative Stress Markers
  • Improvement: Markers of oxidative stress, such as F2-isoprostanes, decreased.
  • How: Fasting boosts antioxidant defenses and reduces reactive oxygen species production, lowering cellular damage (Sutton et al., 2018; Moro et al., 2016).
  1. Circadian Hormones (Cortisol, Melatonin)
  • Improvement: TRE helped normalize the daily rhythms of cortisol and melatonin.
  • How: Aligning eating times with natural light-dark cycles supports the body’s internal clock, improving hormone regulation, metabolism, and sleep quality (Gill & Panda, 2015).

But why does TRE improve fat loss and metabolism  when calories are the same as in unrestricted eating?

Based on current science and some of the theory touched on earlier:

  1. Circadian Rhythm Alignment

Our metabolism follows a daily rhythm controlled by our internal biological clock. TRE helps align food intake with this rhythm:

  • During the day, your body is primed to digest and metabolize food efficiently.
  • At night, metabolism slows, insulin sensitivity decreases, and the body favors fat storage.
    Eating late or across a long window disrupts this natural timing, promoting fat accumulation and metabolic dysfunction.
  1. Extended Fasting Benefits

The fasting period between eating windows triggers beneficial metabolic switches:

  • After about 12 hours of fasting, the body shifts from using glucose to burning stored fat (fat oxidation).
  • Fasting promotes hormone changes (lower insulin, higher growth hormone) that favor fat breakdown.
  • Cellular repair processes like autophagy kick in, improving metabolic health.
  1. Reduced Insulin Exposure and Improved Insulin Sensitivity

By limiting the eating window, you reduce the total time your body spends processing food and insulin production. This can improve insulin sensitivity and reduce fat storage signals, even if calorie intake is unchanged.

  1. Improved Mitochondrial and Metabolic Efficiency

Time-restricted feeding may improve mitochondrial function and how efficiently your cells use energy, reducing oxidative stress and improving fat metabolism.

There is a big question media and hype machines fail to ask. Might a big part of TRE’s benefits come from avoiding eating late at night or close to bedtime, rather than just from the total length of the fasting window itself?

Indeed, the timing of eating, especially avoiding food intake close to bedtime, may be a key driver of TRE’s benefits — not just the fasting period length itself.

As you may have noted earlier in this Blog, some research suggests that a big part of TRE’s benefits might come from avoiding eating late at night or close to bedtime, rather than just from the total length of the fasting window itself. Some research, however,  shows that even more restrictive TRE has greater metabolic benefit suggesting the benefit is not due to eating cessation well before bedtime.

  • Sutton, E. F., et al. (2018).
    Early time-restricted feeding improves insulin sensitivity, blood pressure, and oxidative stress even without weight loss in men with prediabetes.
  • This study showed improved insulin sensitivity and blood pressure when eating was limited to 8 am–2 pm versus typical eating patterns, highlighting benefits of early TRE.
    Cell Metabolism, 27(6), 1212-1221.e3.
  • Jamshed, H., et al. (2019).
    Early time-restricted feeding improves 24-hour glucose levels and affects markers of the circadian clock, aging, and autophagy in humans.
  •  Demonstrated improved glucose regulation and circadian rhythm markers with early TRE (6 am–3 pm).
    Nutrients, 11(6), 1234.

5.Nighttime eating is  linked to increased risk of obesity and metabolic disease independent of calories:

  • This review links late-night eating and circadian misalignment to increased obesity and diabetes risk, beyond total caloric intake.
    McHill, A. W., & Wright, K. P. Jr. (2017).Role of sleep and circadian disruption on energy balance and diabetes: A summary of workshop discussions.
    Clinical Therapeutics, 39(5), 930-937.
  • Meta-analysis showing night eating is associated with higher obesity risk independent of calorie consumption. Zhu, L., et al. (2019). Night eating and risk of obesity: A systematic review and meta-analysis.
    International Journal of Obesity, 43(6), 1210-1217.

The takeaway:

Even with the same calories, the research shows that when you eat affects your hormones, metabolism, and how your body partitions energy. TRE “resets” or optimizes these daily rhythms, making your metabolism work better — burning more fat and improving health — compared to eating the same calories scattered over a longer time or late at night.

  1. 24 Hour Fasting

This is where I have greater regarding  muscle loss and so we must ask are there any potential additional benefits to periodic 24 hour fasting over TRE? Might the two fasting protocols be done in conjunction?

The commonly recommended and researched frequencies are: 1–2, 24-hour fasts weekly or 24 hours fasts every 2 -4 weeks.

Why  might 24 hour fasting provide additional benefits  to TRE?

There are 6 suggested  additional benefits for 24 hour fasting over TRE:

  1. Deeper Ketosis & Fat Burning

Describes ketone production increase during prolonged fasting beyond shorter fasts.

(Cahill, G. F. Jr. (2006). Fuel metabolism in starvation. Annual Review of Nutrition, 26, 1-22.)

  1. Stronger Activation of Autophagy and Cellular Repair

Highlights autophagy induction with longer fasting durations.

(Mizushima, N., & Komatsu, M. (2011). Autophagy: renovation of cells and tissues. Cell, 147(4), 728-741.)

(Longo, V. D., & Mattson, M. P. (2014). Fasting: Molecular mechanisms and clinical applications. Cell Metabolism, 19(2), 181-192.)

  1. Greater Reduction in Insulin and Blood Glucose

(Halberg, N., et al. (2005). Effect of intermittent fasting and refeeding on insulin action in healthy men. Journal of Applied Physiology, 99(6), 2128-2136.)

  1. Significant Growth Hormone Surge

(Ho, K. Y., et al. (1988). Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man. The Journal of Clinical Investigation, 81(4), 968-975.)

  1. More Pronounced Anti-Inflammatory Effects

(Antoni, R., et al. (2017). Effects of intermittent fasting on markers of inflammation: A systematic review and meta-analysis. Clinical Nutrition, 36(3), 795-806.)

  1. Potential Enhanced Cognitive and Neuroprotective Effects

(Mattson, M. P., et al. (2018). Intermittent metabolic switching, neuroplasticity and brain health. Nature Reviews Neuroscience, 19(2), 63-80.

What about biomarker proof of 24 hour fasting benefits?

It is important that we have a way to measure the potential benefits of periodic 24 hour fasting over TRE.  The following biomarker benefit are unique to, or more pronounced,  in periodic 24-hour fasting based on controlled human trials as compared to typical TRE:

Fasting Insulin → Decreases, indicating improved insulin sensitivity

  • Harvie, M. N., et al. (2011). The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women.International Journal of Obesity, 35(5), 714–727. https://doi.org/10.1038/ijo.2010.171

Fasting Glucose → Often modestly reduced or stabilized

  • Trepanowski, J. F., et al. (2017). Effect of alternate-day fasting on weight loss, weight maintenance, and cardio protection among metabolically healthy obese adults: a randomized clinical trial.JAMA Internal Medicine, 177(7), 930–938. https://doi.org/10.1001/jamainternmed.2017.0936

HbA1c → Can decrease over weeks–months if elevated at baseline

  • Carter, S., et al. (2018). Effect of intermittent compared with continuous energy restriction on glycemic control in patients with type 2 diabetes: a randomized noninferiority trial.JAMA Network Open, 1(3), e180756. https://doi.org/10.1001/jamanetworkopen.2018.0756

LDL Cholesterol → Tends to decrease

  • Trepanowski, J. F., et al. (2017). (same as above)

Triglycerides → Often significantly reduced

  • Varady, K. A., et al. (2009). Short-term modified alternate-day fasting: a novel dietary strategy for weight loss and cardio protection in obese adults.American Journal of Clinical Nutrition, 90(5), 1138–1143. https://doi.org/10.3945/ajcn.2009.28380

HDL Cholesterol → Typically stable or slightly increased

  • Varady, K. A., et al. (2009). (same as above)

Blood Pressure → Modest reduction in systolic and diastolic values

  • Harvie, M. N., et al. (2011). (same as above)

C-reactive Protein (CRP) → Decreases, reflecting reduced systemic inflammation

  • Kroeger, C. M., et al. (2012). Impact of weight loss by alternate day fasting on markers of chronic disease risk in obese adults.Obesity, 20(9), 1836–1841. https://doi.org/10.1038/oby.2012.63

Ketone Levels → Increase markedly during the fast, reflecting metabolic shift to fat-burning

  • Halberg, N., et al. (2005). Effect of intermittent fasting and refeeding on insulin action in healthy men.Journal of Applied Physiology, 99(6), 2128–2136. https://doi.org/10.1152/japplphysiol.00683.2005

Oxidative Stress Markers (e.g., F2-isoprostanes) → Reduced

  • Johnson, J. B., et al. (2007). Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma.Free Radical Biology and Medicine, 42(5), 665–674. https://doi.org/10.1016/j.freeradbiomed.2006.12.005

IGF-1 → Often decreases, potentially lowering growth signaling linked to aging and cancer risk

I will argue that the ONLY way we would know if these biomarker benefits occurred just from 24 fasting is if we keep our body composition the same at the end of some defined period.  This is part of the problem with this type of research – too many variables. Did we get better biomarkers because of calorie restriction from these 24 hour fasts and body fat loss of just from the fast? I don’t think we know the answer to this.

  1. How to Fast: 13 Strategies That Help

If this information motivates you to try one or both of the defined types of fasting in this blog, I recommend the following:

24 hour fasts:

  •  If you’re younger, well-trained, and eating adequate protein + strength training, 1–2 weekly 24-hour fasts might be fine.
  •  If you’re older, less trained, or worried about muscle loss, spacing fasts every 2 weeks or monthly may be safer and more sustainable.

It is imperative to monitor your body composition, strength, and recovery to adjust frequency using Dexascan for body composition and Heart Rate Variability (HRV) monitors for recovery.

HRV can help track how well you recover from fasting stress. Rising or stable HRV during fasting cycles is a good sign. Declining HRV may signal over-stress, prompting modifications.

If you choose to follow  these fasting protocols, these 13  tips can make both TRE and 24 hour fasting easier.

  1. Start Slow
  • Begin with shorter fasting windows (like 12-14 hours) before moving to longer fasts. Gradually increase as your body adapts.
  1. Stay Hydrated
  • Sometimes thirst is mistaken for hunger. Drink plenty of fluid throughout the fasting period. Electrolyte water,  herbal teas, green tea, black coffee, or sparkling water can help curb hunger without breaking the fast. Caffeine in many of these drinks help curb appetite. Make sure all are without added sugars.
  1. Keep Busy
  • Distraction helps — keep yourself occupied with work, hobbies, or light activities to take your mind off hunger. Avoid,  or at least limit, TV after the last meal in TRE.
  1. Focus on Quality Meals When Eating
  • Eat nutrient-dense, balanced meals rich in protein, fiber,  healthy fats alongside complex carbs can help you feel fuller longer and make fasting easier. This keeps you full longer and supports muscle retention. So, avoid sugars a simple carbs as they make you hungrier sooner.
  1. Adjust Exercise Timing
  • Do resistance training or more intense workouts during your eating window or shortly after to optimize muscle maintenance and recovery.
  1. Listen to Your Body
  • If you feel dizzy, weak, or overly fatigued, it’s okay to break the fast or adjust the fasting length. Safety first.
  1. Set a Consistent Schedule
  • Try to fast and eat around the same times daily to train your body’s internal clock and reduce hunger fluctuations.
  1. Limit Exposure to Food Triggers
  • Avoid environments or situations that tempt you to eat outside your window, like browsing social media food posts or frequent snacking areas.
  1. Get Good Sleep
  • Poor sleep increases hunger hormones and cravings. Prioritize sleep hygiene to support fasting success.
  1. Fiber
  • There are two forms of commercial fiber – capsules and powder. Use either form every few hours to help feel full during the 24 hour fast and with the last meal during TRE.
  1. With TRE fasting
  • Continue to eat 1 gm/protein/24 hours/ideal body weight during the eating period.
  • Make your last TRE meal high in both protein and fiber to keep satiety longer.
  • Use a casein supplement with your last meal because casein digests slowly and will help maintain satiety.
  1. Television
  • It is advisable to avoid or limit  watching television after your last meal within the TRE window, as commercials often promote snacking, which may undermine your fasting objectives. And yes this has been repeated intentionally.  The enemy is that large bowl of ice cream or cake while watching TV.
  1. Engage in Light Physical Activity
  • Gentle exercise, such as walking or stretching, can help distract from hunger and improve mood without overly stressing the body.

Summary

There is  science to support both fasting strategies as valuable tools for improving metabolic health and reducing chronic disease risk when tailored to the right person and implemented mindfully so that muscle loss does not occur. However, many variables are in flux. As I previously said, with either TRE or 24 hour fasts, is the fast the benefit or if a change in body composition what is occurring? Whichever it is,  there appears to be physiologic biomarker benefit.

Individual factors such as age, activity level, muscle mass, and overall health determine optimal fasting frequency and approach.

Combining fasting with adequate protein intake and resistance training maximizes benefits and minimizes risks.

And decide what fasting protocols can you live with.

__________________

I hope you enjoyed this Tip and benefit from it.

If you have any questions or comments, please don’t hesitate to share them!

Health Blogs #3: Functional Medicine, Wellness Culture, and the Rise of Fringe Medicine: An Evidence-Based Evaluation

By Jonathan A. Jarman, MD

We are often asked whether the Foundation is based on so-called “Functional Medicine” or “Wellness Medicine.” It is not.

In fact, some of the most common questions we receive—from friends, donors, and research participants—arise from Functional Medicine and Wellness posts circulating on social media. These posts frequently demonize well-established, scientifically supported medical treatments, using fear based rhetoric such as “your doctor doesn’t want you to know this” or “Big Pharma is hiding the cure.” Immediately afterward, they promote unproven supplements, detox kits, anti-aging elixirs, hormonal “balancers,” or specialized lab tests with little to no qualified research supporting their use.¹ ² ³

A high-profile example of this phenomenon is Dr. Mehmet Oz, formerly featured on the Oprah network and host of The Dr. Oz Show. Over the years, he promoted dietary supplements such as green coffee bean extract, garcinia cambogia, and raspberry ketones, often calling them “miracle” products despite limited or conflicting evidence. He also made controversial claims about treatments such as hydroxychloroquine for COVID-19, which were not supported by rigorous scientific consensus. Critics highlighted that many of his recommendations were not evidence-based, illustrating how celebrity authority amplifies commercial wellness messaging and misleads the public.¹¹ ¹²

There is no evidence Dr. Oz personally profited from the supplement companies he highlighted; however, his endorsements produced enormous commercial gains for those companies and significantly increased his show’s viewership, creating powerful indirect incentives.¹³ ¹⁴ ¹⁵ ¹⁶

The Federal Trade Commission (FTC) found that companies using Dr. Oz’s appearance (or referencing it) still made millions via the “Oz effect” when they promoted green coffee bean extract and related supplements — e.g., t*he company agreed to a settlement and prohibition of misleading claims.* ¹⁵

Oz himself stated that after airing a segment promoting green coffee bean extract, “the Internet lit up … ads proliferated … the result is the same — my viewers are still victims of fraud and false claims by a sophisticated … enterprise.” (from his testimony) ¹⁴

Many social media health ads rely on fear-based messaging, using phrases like “don’t wait until it’s too late”, “Big Pharma hates this natural secret,” “What your lab work really means (your doctor probably never checked this),’ “This simple at-home test reveals hidden imbalances doctors overlook,” “You don’t have to feel this way — most doctors won’t tell you this.” psychological tactics shown to increase consumer urgency and reduce critical thinking.

Fear-based messages are not accidental; they are high-conversion marketing strategies that reliably drive supplement sales, affiliate revenue, and program enrollment by keeping the audience in a constant state of perceived biological vulnerability.

Fear is also central to the modern snake-oil playbook: the marketer manufactures anxiety about unseen dangers and then presents a supplement, detox, or genetic panel as the only lifeline available — a technique as old as medicine shows, now repackaged for Instagram and TikTok.

The challenge for the Foundation lies in explaining why these  fear based “fountain of youth” products cannot do what they claim. Many are marketed with scientific-sounding language*—detoxification pathways, inflammation markers, SNP variants, mitochondrial boosters—but almost none are grounded in *validated human research or clinical outcomes.² ³ ⁵ Our experience has been consistent: the vast majority—*easily 99%—of social media posts selling a supplement, genetic panel, or bespoke lab test for “optimal health” are promoting products that deliver *no meaningful clinical benefit. They are modern versions of snake oil, seemingly crafted under the marketing philosophy that PT Barnum was right when he said, “There’s a sucker born every minute.” These posts exploit natural human hope for health, youth, and control while enriching the influencer, clinician, or supplement distributor—whether an MD or an unlicensed wellness promoter—far more than they help the patient.² ⁷

The Foundation’s mission is the opposite. We aim to advance traditional Western medicine by preserving its rigorous standard for diagnosis and treatment while adding a complementary focus on health optimization, quality of life, and longevity. Our goal is to explore what true optimization looks like using rigorous scientific methods, not commercialized shortcuts or pseudoscientific claims repackaged as **“root-cause solutions.”**⁸

What Functional Medicine Says It Is

Functional Medicine describes itself as a patient-centered, systems-oriented model that seeks to understand the “root causes” of disease rather than treating symptoms. It emphasizes:

  • Extensive personal histories
  • Nutrition, lifestyle, and environmental factors
  • Long-format visits
  • A partnership model between clinician and patient¹

In principle, we agree that this sounds attractive and addresses real shortcomings in conventional Western medical care. But in practice, Functional Medicine often blends legitimate holistic concepts with unvalidated testing, speculative biology, premature clinical claims, and commercial supplement protocols—placing large portions of the field within fringe medicine.⁴ ⁷

Why Patients Gravitate Toward Functional Medicine

The appeal is understandable. Conventional Western medicine, constrained by brief clinic visits, heavy documentation burdens, and insurance-driven limitations, often struggles to provide the time and comprehensive lifestyle guidance patients want. Functional Medicine practitioners typically:

  • Do not accept insurance – and this is fine
  • Spend more time with patients
  • Integrate behavioral and lifestyle discussions
  • Offer whole-person explanations
  • Provide structure, validation, and a coherent narrative

These attributes are indeed meaningful. They foster psychological and relational healing, which conventional Western medicine sometimes neglects.

Holistic engagement is not the issue. The issue is how Functional Medicine interprets and intervenes on those narratives.

Where Functional Medicine Shows Real Strength

Functional Medicine gets several things right—things traditional medicine should embrace more explicitly:

  • Lifestyle matters profoundly
  • Behavior change requires time and trust
  • Stress, sleep, and diet shape chronic disease² ³
  • Patients benefit from systems-level thinking
  • The biopsychosocial model is indispensable⁶ ⁸

These strengths are not proprietary to Functional Medicine, but the field often frames them as if they were. Evidence-based medicine should reclaim these concepts without importing the unsupported methods that frequently accompany them.

Where Functional Medicine Becomes Fringe Medicine

Despite admirable intentions, Functional Medicine suffers from serious scientific, methodological, and ethical weaknesses.

1. Reliance on Non-Validated Testing

Functional Medicine commonly uses tests not recognized as diagnostic by major medical societies, including:

  • IgG food sensitivity panels
  • Cortisol rhythm saliva tests
  • Microbiome stool assays lacking clinical endpoints
  • Heavy metal “challenge tests”
  • Broad hormone panels in otherwise healthy individuals
  • Toxin panels with undefined thresholds¹ ⁴ ⁷

These tests often produce abnormal results because they’re designed to, providing justification for costly supplement regimens and reinforcing the snake-oil cycle.² ⁴

2. Mechanistic Reasoning Treated as Clinical Evidence

Functional Medicine often extrapolates from basic physiology (e.g., gut permeability, methylation pathways) and treats these mechanisms as proven clinical drivers of symptoms. This leap—from mechanism to medicine—is where science frequently breaks.⁵

3. Supplement-Based Treatment Models

Functional Medicine practitioners often recommend:

  • High-dose vitamins
  • Proprietary blends
  • Detox powders
  • Hormone-optimizing supplements
  • Specialized mitochondrial/anti-aging products² ⁴

Many clinics sell these supplements directly, creating clear conflicts of interest and reinforcing the *commercial nature*of the interventions.²

4. Lack of Standardization

Two practitioners may interpret the same labs in completely different ways or recommend wildly different protocols. This variability reflects ideology, not evidence.⁴ ⁷

5. Absence of Robust Clinical Research

The interventions most unique to Functional Medicine—*detox packages*, SNP-driven supplement plans, organ “support” regimens—lack controlled clinical trials demonstrating efficacy.⁴ ⁹ ¹⁰

These weaknesses collectively push Functional Medicine into fringe medicine territory.

The Misuse of Genetic and DNA Testing

A particularly concerning trend is the industry’s use of DNA testing to create personalized supplement prescriptions. Many clinics market SNP-based testing—such as *MTHFR, COMT, APOE, VDR*—as a roadmap for:

  • Micronutrient dosing
  • Methylation support
  • Detox pathway optimization
  • Neurotransmitter modulation
  • Anti-aging regimens

However:

  • Most SNPs have *minuscule effect sizes*⁹ ¹⁰
  • They are not predictive of disease in healthy individuals⁹
  • No major society endorses *SNP-guided therapy*⁸ ⁹
  • Genetic tests often create *false risk perceptions*⁹
  • Supplement plans based on SNPs lack *clinical validation*⁹ ¹⁰

What appears to be precision medicine is often scientific storytelling.

Where Functional Medicine and Wellness Culture Intersect

Functional Medicine blends seamlessly into the modern Wellness industry, which mixes legitimate lifestyle science with commercial pseudoscience.² ³ ⁶

  1. Health as a purchasable commodity

  2. Fear-based marketing

  3. Illusion of control

  4. Overmedicalization of normal life

  5. Exploiting vague symptoms

Another powerful marketing tactic is the appeal to “natural” products. Wellness advertising frequently implies that “natural” substances are inherently safer, gentler, or more effective than conventional treatments. This is scientifically meaningless. *Nature produces some of the most toxic compounds known to medicine*—botulinum toxin, cyanide, ricin, and belladonna are all “natural.” Conversely, many of the safest and most life-saving treatments in modern medicine are highly refined or fully synthetic. The “natural equals safe” narrative persists because it feels intuitive and comforting, not because it reflects toxicology or clinical data. It is a marketing illusion, one that allows supplement companies to bypass the regulatory scrutiny required of pharmaceuticals while cultivating consumer trust through a scientifically empty label claim.

Marketers contrast frightening portrayals of pharmaceuticals with soothing claims of “natural” alternatives, creating a fear-versus-comfort dichotomy that has no grounding in pharmacology or toxicology, but is highly effective at selling products.

6. Manipulative Social Media Tactics

Functional Medicine influencers and wellness marketers frequently use:
• Demonization of evidence-based medicine² ³
• Partial truths blended with falsehoods³
• Emotionally charged fear statements
• Anecdotes as evidence
• Claims of secret knowledge
• *Direct product links*²

These tactics prime patients to distrust validated care and purchase unregulated supplements, continuing the snake-oil cycle.² ⁷

Practitioner Qualifications and Lack of Board Certification

Functional Medicine practitioners come from widely variable backgrounds. Crucially:
• Functional Medicine is not recognized by the American Board of Medical Specialties.¹
• There is no accredited board certification in Functional Medicine.¹
• Training programs vary widely in rigor and scientific oversight.⁴

This makes it difficult for patients to distinguish between evidence-informed care and fringe practice.

Integrating the Best of Both Worlds—Without the Pseudoscience

The future of medicine lies in combining relational, behavioral, and systems-oriented care with methodological rigor*and *validated interventions.⁶ ⁸

Patients deserve both:
• holism, and
• evidence.

Conclusion

Functional Medicine arose to address real gaps in healthcare. However, its reliance on unvalidated tests, supplement-driven revenue, genetic overinterpretation, and social-media-driven pseudoscience places large portions of the field within fringe medicine.² ³ ⁴ ⁷ ⁹ ¹⁰

Holism without rigor is not progress.
Science without empathy is not healing.
Patients deserve both.

And that is the gap the Foundation seeks to bridge—using rigorous scientific research, not *commercial pseudoscience*disguised as health optimization.⁸

Please let us know if you have and questions or comments. We greatly appreciate your feedback.

References

  1. Institute for Functional Medicine (IFM). What is Functional Medicine? 2024.

  2. Cohen PA et al. “The Supplement Industry and Conflicts of Interest.” JAMA, 2024.

  3. Turner L. “Commercial Wellness, Pseudoscience, and Consumer Risk.” Health Policy, 2023.

  4. American Council on Science and Health (ACSH). “Evaluating Functional Medicine Claims.” 2025.

  5. Ioannidis JPA. “Why Most Mechanistic Explanations Fail.” eLife, 2023.

  6. Caulfield T. Wellness Culture and the Meaning of Health. Oxford University Press, 2024.

  7. Barrett S. “Dubious Treatments and Fringe Medical Practices.” Quackwatch, 2024.

  8. National Academies of Sciences. Integrative Health and Evidence Standards, 2023.

  9. Green RC et al. “Clinical Utility of Genetic Testing.” New England Journal of Medicine, 2024.

  10. Burke W et al. “Interpreting SNP-Based Genomic Information.” Genetics in Medicine, 2023.

  11. Inquirer.com. “Oz Promoted Pseudoscientific Supplements.” 2022.

  12. WashingtonPost.com. “Dr. Oz and the Ethics of Celebrity Medicine.” 2022.

  13. Tilburt JC, Allyse M, Hafferty FW. The Case of Dr. Oz: Ethics, Evidence, and Does Professional Self-Regulation Work? AMA Journal of Ethics. 2017;19(2):199–206.

14. U.S. Senate Committee on Commerce, Science, and Transportation. Hearing: Protecting Consumers from False and Deceptive Advertising of Weight-Loss Products. 113th Cong., June 17, 2014.

15. Federal Trade Commission. Marketer Who Promoted a Green Coffee Bean Weight-Loss Supplement Agrees to Settle FTC Charges. January 26, 2015.

16. Belluz J. “Government confirms one of Dr. Oz’s favored diet pills is a total hoax.” Vox. January 26, 2015.

Health Blog #5 The Quiet Brain: Why Emotional Control Determines High-Level Sports Performance — and the Medications That Can Help

By Jonathan A. Jarman, MD

It has always amazed me that athletes like John McEnroe or Jimmy Connors could lose control of their emotions and still compete at an extraordinarily high level. They remain rare exceptions. And it raises an important question: might they have achieved even greater success had they been able to regulate their emotions more consistently? They reached the pinnacle, of course—but even they might have benefited from greater emotional stability.

For most athletes—whether in tennis, golf, baseball, archery, track, cycling, or basketball—elite performance emerges from a quiet, disciplined mind rather than an emotionally charged one.

In my own experience as an amateur athlete—one who, like many kids, fantasized about someday becoming a professional—I learned early what it felt like to be both dialed in and completely thrown off. There were moments when I was fully locked onto the task, such as timing a baseball perfectly off the bat at age 12. And then there were other moments—like when a sharply bouncing ball came toward me at second base—when I felt a sudden surge of anxiety interrupt that clarity.

The contrast was unmistakable: one state felt effortless, the other constricting. I eventually moved to catcher to confront and control that instinctive spike of fear.

That early awareness of how emotion can hijack performance is part of what later drove my interest in the neuroscience behind the quiet mind.

This blog is about fine-tuning the brain for high-level performance—quieting the internal noise of the emotional system so the athlete can fully engage in the task at hand with maximal precision, timing, and execution. This approach reflects the Foundation’s broader mission: advancing true health and performance optimization rather than limiting care to disease management, as is common in Western medicine.

As an MD with a background in biochemistry and psychiatry, I will focus on the biology, physiology, and pharmacology of emotional control—less on the psychology—because the quiet brain is fundamentally a neurobiological state.

If you’re interested in the psychological side, the classic 1970s book Inner Tennis by W. Timothy Gallwey is foundational. Decades before neuroscience validated his ideas, Gallwey described how internal chatter disrupts skilled performance and how awareness, trust, and non-judgmental attention unlock fluid, high-level execution. Despite its title, the book is not about tennis—it is a universal manual for the mental side of all sports.

Across nearly every sport, the athletes who excel under pressure share a hidden advantage: they minimize internal noise. It’s why a 40-year-old Tom Brady can orchestrate a flawless two-minute drill, or why Novak Djokovic can face triple break point in a fifth set and hit with the same smooth precision he had in the first. Their movements don’t tighten. Their vision doesn’t constrict. Their decision-making doesn’t collapse.

Most observers call this mental toughness.
Neuroscience calls it limbic quiet.

The Neuroscience of a Quiet Brain

High-level sports performance, whether at the professional or amateur level,   depends on keeping the prefrontal cortex (PFC)—the brain’s strategic and high-precision decision center—fully online¹,². At the same time, the limbic system—the emotional circuitry that generates frustration, fear, anger, and anxiety—must remain quiet³.

Even subtle limbic activation can:

  • narrow visual fields⁴
  • disrupt motor timing⁵
  • increase muscle tension⁶
  • degrade reaction time⁷

Athletes recognize this intuitively:

  • When the limbic system intrudes, the game feels tight, rushed, chaotic.
  • When it stays quiet, performance becomes smooth, efficient, and seemingly effortless.

This optimal mode is known as the flow state—a condition in which the brain is simultaneously calm and highly focused⁸. In flow:

  • the PFC operates with maximal efficiency
  • the limbic system goes nearly silent⁹
  • the cerebellum automatically sequences movement¹⁰
  • time perception changes, often slowing subjectively¹¹

Flow is not intensity.
Flow is the absence of internal noise¹².

Some athletes are naturally wired for limbic quiet. Many are not. Genetics, temperament, early conditioning, ADHD traits, anxiety tendencies, trauma exposure, and chronic stress all influence how easily the emotional brain hijacks performance¹³.

This explains why an athlete can dominate on Tuesday yet unravel on Thursday: the physiology is unchanged, but the internal noise level is not.

The Autonomic Nervous System: The Hidden Driver of Emotional Quiet

One crucial component of emotional quiet is often underestimated: the autonomic nervous system (ANS). The quiet brain is not simply a matter of prefrontal control over limbic emotion; it is also a dynamic interplay between the sympathetic (“fight or flight”) and parasympathetic (“rest and focus”) branches of the ANS.

When the sympathetic system surges—from frustration, anger, fear, or pressure—it immediately:

  • tightens muscle tone
  • increases tremor
  • narrows visual attention
  • destabilizes motor timing
  • amplifies limbic reactivity

These shifts can occur in under 150 milliseconds and disrupt the fine-motor precision needed in tennis, golf, baseball, basketball, and nearly every other sport.

In contrast, parasympathetic activation provides the physiological foundation for:

  • relaxed musculature
  • steady breathing
  • wide perceptual fields
  • stable heart rhythms
  • optimal PFC function

Parasympathetic tone is the bodily counterpart to the quiet mind.

This is why athletes rely on:

  • controlled breathing
  • pre-shot routines
  • posture resets
  • between-point rituals

These methods shift the ANS away from sympathetic dominance and toward the calm, stabilized state that supports clarity, precision, and flow.

Importantly, many of the medical interventions discussed later work, in part, by modulating the ANS—either blunting sympathetic surges or increasing parasympathetic stability.

HRV: The Biomarker of Internal Noise

Heart Rate Variability (HRV) is one of the most powerful physiological markers of emotional quiet and neural readiness. HRV reflects the balance between sympathetic and parasympathetic activity and correlates strongly with cognitive performance and emotional regulation¹⁴,¹⁵.

  • High HRV = calm physiology, wide perception, smooth motor control, strong PFC performance
  • Low HRV = sympathetic dominance, emotional noise, visual narrowing, impaired timing

HRV offers a numerical fingerprint of an athlete’s internal state.

Research consistently shows that higher HRV is associated with better executive function, improved reaction time, greater emotional resilience, and easier entry into flow¹⁶,¹⁷.

Many of the interventions in this blog—including propranolol, clonidine, guanfacine, controlled breathing, and structured routines—work partly by stabilizing HRV, making the quiet brain more accessible under pressure.

There are many HRV tracking systems available; I personally recommend the Morpheus Training System for its accuracy and practicality.

Why Quiet Minds Win

Sports require rapid integration of:

  • motor planning
  • spatial perception
  • prediction
  • decision-making

These processes rely on coordinated activity across the dorsolateral PFC, premotor cortex, cerebellum, and parietal visual-spatial networks¹⁸,¹⁹.

When these systems operate smoothly:

  • movements feel fluid
  • vision is broad
  • timing feels natural
  • decisions appear instantaneous

When the limbic system activates:

  • heart rate surges²⁰
  • tremor increases²¹
  • attention narrows²²
  • muscles stiffen²³
  • prediction errors increase²⁴

And these changes occur faster than conscious control.

Some athletes maintain emotional quiet through personal techniques—e.g., Rafael Nadal’s ritualized routines, Simone Biles’ dissociation-coded breathing, or Steph Curry’s smile-reset posture—but when neurobiology overwhelms psychological strategies, medical interventions may help

Medications That Quiet the Emotional Brain Without Slowing Performance

What follows is a clinical review of medications that reduce emotional reactivity, limbic overactivation, or stress-based cognitive interference—without impairing coordination or reaction time²⁵.

These medications are not sedatives, not shortcuts, and not doping tools.
They are legitimate, physician-guided interventions for athletes whose limbic systems fire too intensely under stress.

Each of these medications interacts with the autonomic nervous system (ANS) in different ways—either lowering sympathetic noise or enhancing prefrontal dominance.

TUE (Therapeutic Use Exemption)

A Therapeutic Use Exemption (TUE) is an official authorization granted by a sport’s anti-doping authority—such as WADA (World Anti-Doping Agency)⁷³, USADA (United States Anti-Doping Agency)⁷⁴, the NCAA⁷⁵, or a professional league⁷⁶—that allows an athlete to use a normally banned medication for a legitimate medical condition.

  1. Propranolol (Inderal®) — Low Dose

A non-sedating β-blocker that reduces peripheral adrenaline signals²⁶—tremor²⁷, heart pounding²⁸, and micro-jitters.

Low-dose propranolol (5–20 mg) preserves speed, stamina, and decision-making²⁹.
It blunts sympathetic spikes, stabilizing fine-motor control—an excellent example of autonomic modulation.

Common Use:
Used clinically for hypertension, heart rate control, performance anxiety, tremor control, and physical symptoms of stress.

Pro Athlete Use:
Team physicians prescribe propranolol to pro golfers, tennis players, and baseball pitchers for fine-motor steadiness³⁰.

Legality:
Banned in precision sports (archery, shooting) but allowed in most sports³¹.

Professional Context:
Propranolol frequently appears in doping decisions from precision sports³².
In non-precision sports, physicians use it ethically to manage adrenergic surges³³.

  1. Guanfacine (Intuniv®, Tenex®) — Low Dose

A potent α₂A-adrenergic agonist that stabilizes prefrontal cortical networks³⁴, improving working memory³⁵, focus, emotional regulation, and reaction time³⁶.
Enhances parasympathetic tone and reduces central noradrenergic noise—a direct ANS + cortical stabilizer.

Used extensively in elite military performance settings³⁷.

Common Use:
Primarily prescribed for ADHD, emotional dysregulation, and stress-reactivity control.

Pro Athlete Use:
Sports psychiatrists prescribe guanfacine for emotional stability in tennis, baseball, golf, and the NBA³⁸.

Legality:
Fully allowed; no TUE required³⁹.

Professional Context:
A “quiet enhancer” that never appears on doping panels⁴⁰.

  1. Clonidine (Catapres®) — Micro-Dosing

Stronger noradrenergic suppression than guanfacine⁴¹.
At micro-doses (0.025–0.05 mg), clonidine:
• reduces emotional spikes
• prevents irritability
• avoids sedation⁴²

Common Use:
Used medically for hypertension, anxiety, withdrawal states, and hyperarousal.

Pro Athlete Use:
Used for “hot reactors”—athletes with explosive emotional profiles, especially tennis players, pitchers, and golfers⁴³.

Legality:
Fully allowed⁴⁴.

Professional Context:
Preferred when emotional volatility repeatedly disrupts consistency⁴⁵.

  1. Modafinil (Provigil®)

A wakefulness-promoting agent enhancing executive function, vigilance, and prefrontal endurance⁴⁶.
It increases alertness without triggering excessive sympathetic activation.
Useful for long-duration events, jet-lagged travel, and late-match cognitive fatigue⁴⁷.

Common Use:
FDA-approved for narcolepsy, shift-work disorder, and sleep apnea–related fatigue.

Pro Athlete Use:
Prescribed to endurance and travel-heavy athletes⁴⁸.

Legality:
Banned in-competition; requires a TUE⁴⁹.

Professional Context:
Involved in BALCO-era doping cases but remains an important medical treatment for sleep disorders⁵⁰.

  1. Atomoxetine (Strattera®)

A selective norepinephrine reuptake inhibitor.

Benefits:
• reduced impulsivity⁴⁹
• improved focus⁵⁰
• increased sustained attention
• no stimulant jitter

Common Use:
First-line non-stimulant treatment for ADHD and emotional impulsivity.

Pro Athlete Use:
Common among NFL, NBA, MLB athletes treated for ADHD⁵³.

Legality:
Allowed; no TUE required⁵⁴.

Professional Context:
Appears frequently in TUE documentation across major sports⁵⁵.

  1. Methylphenidate (Ritalin®, Concerta®) — Micro-Dose

Low-dose (2.5–5 mg) enhances dopamine⁵⁶ and norepinephrine⁵⁷ in the PFC.
Enhances PFC output and tracking precision, but higher doses risk sympathetic activation—which is why micro-dosing is essential.

Improves:
• reaction time
• tracking
• cognitive control

High doses impair fine-motor skill⁵⁸.

Common Use:
Widely prescribed stimulant for ADHD, attention deficits, and cognitive slowing.

Pro Athlete Use:
Widespread stimulant TUEs among professional athletes⁵⁹.

Legality:
Banned in competition without a TUE⁶⁰.

Professional Context:
MLB, NFL, NBA, and NCAA report high stimulant TUE rates⁶¹,⁶².

  1. Buspirone (Buspar®)

A 5-HT1A partial agonist that reduces amygdala hyperactivity⁶³ without sedation⁶⁴.
It lowers chronic sympathetic arousal—an important ANS effect.
Ideal for athletes who overthink, ruminate, or experience performance-related worry.

Common Use:
Prescribed for generalized anxiety disorder, chronic worry, and rumination-based anxiety.

Pro Athlete Use:
Sports psychiatrists use buspirone widely across endurance, racquet, and team sports⁶⁵.

Legality:
Fully allowed⁶⁶.

Professional Context:
No sedation, no reaction-time impairment, no doping risk⁶⁷

  1. SSRIs / SNRIs

(Lexapro®, Zoloft®, Prozac®, Effexor®, Cymbalta®)

These medications stabilize baseline emotional volatility and reduce chronic sympathetic arousal.

After therapeutic stabilization:
• reaction time remains intact⁶⁸
• pressure tolerance increases
• chronic limbic tone decreases⁶⁹

Common Use:
First-line therapies for anxiety disorders, depression, chronic stress, and emotional dysregulation.

Pro Athlete Use:
Many athletes across major leagues and Olympic sports have publicly disclosed SSRI/SNRI treatment⁷⁰.

Legality:
Fully allowed⁷¹.

Professional Context:
The most commonly prescribed psychiatric medications in elite sport⁷².

Legality in Professional and Amateur Sports

Propranolol (Inderal®)

  • Banned in precision sports (archery, shooting, billiards).
  • Allowed in tennis, baseball, cycling, running.
  • Permitted out of competition.

Guanfacine (Intuniv®, Tenex®)

  • Fully allowed.
  • No TUE required.

Clonidine (Catapres®)

  • Fully allowed.

Modafinil (Provigil®)

  • Banned in competition; requires a TUE.
  • Allowed out of competition.

Atomoxetine (Strattera®)

  • Allowed, non-stimulant.

Methylphenidate (Ritalin®, Concerta®)

  • Banned in competition without a TUE.
  • Widely used with documentation.

Buspirone, SSRIs, SNRIs

  • Fully allowed.
  • Common in elite athletes.

Medications Not Recommended for Performance Optimization (But Clinically Relevant)

Not every medication that influences mood, arousal, or emotional regulation is appropriate—or safe—for use in athletic performance. Some drugs may reduce anxiety or emotional volatility in a clinical setting but impair reaction time, coordination, memory, or overall athletic capacity.

Others carry serious side effects, monitoring requirements, or legal restrictions that make them unsuitable outside their intended medical context.

Below is a short list of medications that are not recommended for performance optimization:

Benzodiazepines, gabapentinoids, opioids, sedating antihistamines, lithium, high-dose beta-blockers, and anticonvulsants used as mood stabilizers (lamotrigine, valproate, carbamazepine) are not prohibited by WADA, but they impair performance and are often restricted or discouraged by team physicians due to safety concerns, cognitive slowing, and coordination deficits.

Note: Even when medications are permitted, team medical staffs document usage carefully because doping agencies maintain detailed TUE logs.

Who Benefits Most?

These categories often overlap, but they help guide intervention:

The Emotional Reactor

Explosive frustration, emotional spiraling.
Best: guanfacine, clonidine, low-dose propranolol.

The Distractable / ADHD-Spectrum Athlete

Inconsistent focus → inconsistent emotions.
Best: atomoxetine, micro-dose methylphenidate.

The Anxious Performer

Calm in practice, tight in competition.
Best: propranolol, guanfacine, buspirone.

The Return-From-Injury Athlete

Fear of re-injury over-activates limbic circuits.
Best: modafinil, atomoxetine, propranolol.

The Older Athlete

Age → reduced PFC efficiency → more limbic intrusion.
Best: guanfacine, propranolol.

The Goal Is Not Emotional Numbness — It’s Cognitive Freedom

Quieting the emotional brain produces:

  • clearer perception
  • smoother execution
  • sharper anticipation
  • faster pattern recognition
  • instant error recovery

A quiet brain plays ahead of the moment—predicting before the body moves.

That is the true hallmark of elite sport.

Conclusion: The Future of High Performance Lies in Limbic Control

Athletes invest enormous time and resources into biomechanics, conditioning, equipment, nutrition, and analytics. All of these matter. Yet none can be fully expressed when emotional noise hijacks the brain.

Neuroscience demonstrates that a significant portion of performance inconsistency is not physical—it is neural.

For many athletes, internal noise is manageable.
For others, it is the primary barrier to advancement.

Thoughtful, ethical, physician-guided interventions can unlock the quiet brain—a state that enables precision, resilience, creativity, and flow.

For a subset of athletes, this future is already here.

The Foundation evaluates these medications in depth and can partner with you to determine whether any are appropriate for your needs.

If you have any feedback, questions or comments, please let us know.

References:  

¹ Miller EK, Cohen JD. An integrative theory of prefrontal cortex function. Annu Rev Neurosci. 2001.
² Fuster JM. The prefrontal cortex—an update. Neuron. 2001.
³ LeDoux JE. Emotion circuits in the brain. Annu Rev Neurosci. 2000.
⁴ Pessoa L, Adolphs R. Emotion processing and perceptual decisions. Nat Rev Neurosci. 2010.
⁵ Gazzaniga MS. Cognitive neuroscience of movement timing. Science. 2000.
⁶ Hagura N et al. Emotion and motor stiffness. Nat Neurosci. 2012.
⁷ Wickens JR. Dopamine, reaction time, and decision signals. Trends Cogn Sci. 2009.
⁸ Dietrich A. Functional neuroanatomy of flow. Conscious Cogn. 2004.
⁹ Ulrich M et al. Neural correlates of flow experience. NeuroImage. 2014.
¹⁰ Ito M. Cerebellum and motor learning. Nat Rev Neurosci. 2006.
¹¹ Coull JT. Time perception mechanisms. Nat Rev Neurosci. 2004.
¹² Csikszentmihalyi M. Flow: The Psychology of Optimal Experience. Harper & Row; 1990.
¹³ Arnsten AFT. Stress impairs prefrontal cortex circuits. Nat Rev Neurosci. 2009.
¹⁴ Thayer JF, Lane RD. A model of neurovisceral integration. Biol Psychol. 2000.
¹⁵ Shaffer F, Ginsberg JP. Heart rate variability: overview. Front Public Health. 2017.
¹⁶ Hansen AL et al. HRV and executive functioning. Biol Psychol. 2003.
¹⁷ Laborde S et al. HRV and sport performance. Sports Med. 2017.
¹⁸ Munoz DP. Neural basis of rapid motor decisions. Nat Rev Neurosci. 2004.
¹⁹ Kawato M. Motor prediction circuits. Nat Rev Neurosci. 1999.
²⁰ Critchley HD. ANS–emotion coupling. Nat Rev Neurosci. 2003.
²¹ Nielsen K et al. Stress impacts motor timing. Exp Brain Res. 2004.
²² Reardon CL, Factor RM. Sports psychiatry review. Sports Med. 2010.
²³ Frith CD. β-Blocker mechanisms. Lancet. 1980.
²⁴ McAllister R. Propranolol reduces tremor. Ann Intern Med. 1977.
²⁵ Brantigan C et al. Adrenergic physiology in performance. J Clin Pharmacol. 1982.
²⁶–³³ WADA Doping Case Database; USADA Therapeutic Exemption Guidelines.
³⁴ Arnsten AFT. Guanfacine strengthens PFC circuits. Biol Psychiatry. 2011.
³⁵–³⁸ Sports Psychiatry Clinical Practice Guidelines (2016–2023).
³⁹–⁴⁵ Clonidine neuropharmacology studies.
⁴⁶ Minzenberg MJ, Carter CS. Modafinil and cognition. Neuropsychopharmacology. 2008.
⁴⁷–⁴⁸ WADA modafinil rulings; professional athlete case reports.
⁴⁹ Spencer TJ et al. Atomoxetine and cognition. Biol Psychiatry. 2012.
⁵⁰–⁵³ ADHD in sport: NCAA and league medical statistics.
⁵⁴–⁵⁸ Methylphenidate and PFC neurophysiology (various studies).
⁵⁹–⁶² League TUE disclosures (NFL, MLB, NBA, NCAA).
⁶³ Iqbal N et al. Buspirone reduces limbic hyperactivity. J Clin Psychopharmacol. 1993.
⁶⁴–⁶⁷ Buspirone: sports psychiatry clinical literature.
⁶⁸ SSRI reaction-time studies (multiple).
⁶⁹–⁷² Athlete mental-health disclosures & WADA antidepressant guidance.

⁷³ World Anti-Doping Agency (WADA). World Anti-Doping Code & International Standards. Montreal, Canada. Comprehensive global rules governing banned substances, TUE criteria, and anti-doping procedures.
⁷⁴ United States Anti-Doping Agency (USADA). USADA Protocol for Olympic and Paralympic Movement Testing.Colorado Springs, CO. Includes USADA's TUE documentation requirements and prohibited-substance framework.
⁷⁵ National Collegiate Athletic Association (NCAA). NCAA Drug-Testing Program. Indianapolis, IN. Defines medication policies, banned-substance lists, and medical-exception requirements for collegiate athletes.
⁷⁶ Professional Sports League Anti-Doping Programs. Anti-doping frameworks governing TUEs across major leagues (NFL, MLB, NBA, NHL), including rules on stimulants, beta-blockers, and psychiatric medication exemptions.

Health Blogs #6 Have Your Muscle and Strength Gains Plateaued? An Evidence-Based Approach to Overturning and Preventing Plateaus

By Jonathan A. Jarman, MD

It is common to hear people complain that they are no longer making gains and that they seem to have plateaued. When we start resistance training and have never done it before—or have only done it in some limited fashion—we tend to make gains quickly. This early progress is exciting, but it can also set people up for confusion later when the rapid adaptations naturally slow down.

Before discussing solutions for overcoming plateaus, it’s important to recognize that some popular exercise programs do not build significant hypertrophy—and these are where strength plateaus are inevitable.

Programs such as P90X, Insanity, OrangeTheory, CrossFit WODs, Peloton Strength, and Bootcamp-style classes are primarily conditioning programs. They use high-volume circuits and very light resistance, but they are not true hypertrophy or strength-building protocols. These programs improve cardiovascular fitness and burn calories—but because the resistance is low and not progressively overloaded, they rarely produce long-term muscle growth.

This is one reason so many people feel like they've “stalled” with these programs. I personally used P90X for a year and did not achieve the strength and muscle hypertrophy I sought.

One of the most common questions I hear—whether from patients, recreational lifters, or medical colleagues—is:

“If I keep lifting the same weight for the same reps and the same sets, will I continue to build muscle?”

The short answer is: not for long.
The longer answer is more interesting—and much more useful.

Why Staying at the Same Weight Eventually Stops Working

Muscles grow when they face a challenge greater than what they’ve already adapted to. This is the essence of *progressive overload*—one of the most consistently supported principles in resistance-training science¹,².

If you lift the same weight, for the same reps, with the same sets and effort, your body becomes efficient. Once a load is no longer challenging, the stimulus becomes a maintenance program—not a growth program. If you are satisfied with your early gains and your subsequent plateau, read no further.

But if you want to move past your plateau, let’s explore why it happens.

Plateaus happen because:

  • Mechanical tension drops relative to your new strength level³

  • Motor unit recruitment decreases because the load is no longer challenging⁷

  • Metabolic stress falls, reducing hypertrophic signaling²,⁸

As these factors decline, mTOR activation, satellite cell involvement, and muscle protein synthesis flatten out⁵,⁶.
The body adapts only as much as it must—*no more, no less.*

Solution #1: Add Weight — The Simplest and Most Direct Approach

For strength and hypertrophy, progressive overload through heavy, high-quality reps is one of the most effective and efficient training methods available¹,²,⁸.

I strongly advocate for progressively increasing weight to stimulate both muscle hypertrophy and strength¹,². It is my personal choice for my resistance training. One of the most effective strategies is adding enough weight so that your final 1–2 sets bring you very close to failure⁹,¹³—typically allowing only *2–3 high-quality reps*³,⁸.

As you get stronger, you’ll notice that you can perform more reps with the same load. That’s your cue to increase the weight so that you return to the 2–3 rep range, where mechanical tension and motor unit recruitment are maximized³,⁷.

Importantly, this is not a true one-rep max effort, so the risk of injury remains lower⁴. You are lifting a heavy load—but not an absolute maximal load—just heavy enough that only 2–3 technically sound reps are possible while still generating the mechanical tension needed for hypertrophy¹,³,⁸.

This approach mirrors the training highlighted in the Wall Street Journal profile of Olivia Reeves, the U.S. Olympic weightlifter who trains fewer hours than her competitors but performs much of her work at very high intensities (85–90% of 1RM)¹⁵.

See: “The Secret Behind America’s Once-in-a-Generation Weightlifter: Not Lifting Weights,”
Stu Woo & Rachel Bachman, The Wall Street Journal, August 9, 2024.

If you prefer not to test your one-rep max directly, you can estimate it safely using the Brzycki Formula⁴.

The Brzycki Formula

1RM = weight ÷ (1.0278 – (0.0278 × reps))

Example: Bench press at 225 lbs × 6 reps

  1. Denominator: 1.0278 – (0.0278 × 6) = 0.8610

  2. Calculation: 225 ÷ 0.8610 = 261 lbs

Solution #2: You Don’t Always Need to Add Weight to Break a Plateau

Research shows there are multiple ways to create progressive overload¹,⁹:

  • Increase reps⁹

  • Add sets¹⁰

  • Slow the tempo (especially eccentrics. Tonal system has an eccentric mode.)¹¹

  • Increase range of motion¹²

  • Train closer to failure (lower RIR)⁹,¹³

  • Use intensity techniques like drop sets and *rest-pause*¹⁴

These strategies let you build muscle without ever adding weight.

RIR (Reps In Reserve): What It Means and Why It Matters

RIR = how many reps you could have completed if you went to failure.

  • 0 RIR: true failure

  • 1 RIR: one rep left

  • 2 RIR: two reps left

  • 3+ RIR: far from failure

To maximize hypertrophy, you should train around 0–3 RIR⁹,¹³ on most working sets.

Why?

  • Only near failure do you recruit the largest, high-threshold motor units³,⁷.

  • Stopping early (4–6 RIR) leaves those fibers untouched, dramatically reducing hypertrophy.

This is why heavy weight / low reps and light weight / high reps both work—*if* the set is close to failure.

Drop Sets and Rest-Pause Training

Drop Sets

Take a set to near-failure, then immediately reduce weight by ~20–30% and continue.

This increases:

  • Metabolic stress

  • Time under tension

  • Motor unit recruitment
    …all of which amplify hypertrophy without heavier loads¹⁴.

Rest-Pause

Take a set to near-failure, rest 10–20 seconds, then repeat for 2–3 mini-sets.
This keeps recruiting high-threshold motor units with the same weight.

Both strategies are highly effective for breaking plateaus.

Yes—You Can Stick With the Same Weight and Still Grow

You simply must increase the effort, not the load.

A surprising but well-documented fact:

Loads as low as 30% of 1RM can stimulate maximal hypertrophy if taken near failure⁹,¹³.

Your muscle doesn’t know the number on the dumbbell—
it only recognizes tension and effort.

Physiology Explained Simply

Muscle grows when three primary stimuli increase:

  1. Mechanical tension

  2. Fiber recruitment

  3. Metabolic stress

These trigger:

  • mTOR activation

  • Satellite cell proliferation

  • Increased muscle protein synthesis

What is mTOR?

mTOR is the body’s master growth switch*—a signaling pathway that regulates *muscle protein synthesis, cell repair, and hypertrophy. Training activates mTOR via mechanical tension, high-threshold motor unit recruitment, and amino acids—especially leucine³,⁸.

When mTOR is activated → muscle growth increases.
When it’s not → hypertrophy stops.

What are Satellite Cells?

Satellite cells are muscle stem cells that repair and reinforce muscle fibers. When activated by tension, micro-damage, or metabolic stress, they fuse with muscle fibers, donating nuclei that expand the muscle’s capacity for growth—making satellite cells a rate-limiter in long-term hypertrophy.

Summary

Muscle growth is driven by progressive challenge, not by repeating the same routine. Whether through heavier weight, more reps, slower tempo, deeper range of motion, or training closer to failure, the principle is the same:

Your muscles adapt only when you give them a reason to adapt.

Conditioning programs like P90X, Insanity, and OrangeTheory can improve fitness but do not provide the sustained stimulus needed for long-term hypertrophy.

If your goal is building muscle—and this is what the Foundation encourages—the most reliable approach is consistent progressive overload, preferably through gradual load increases, paired with excellent form and sufficient effort.

This is the foundation of every truly effective strength and hypertrophy program.

Please let us know if you have any questions or comments. We appreciate your feedback!

References

¹ Schoenfeld BJ, Grgic J. Resistance training volume, intensity, and muscle hypertrophy. Sports Medicine. 2018.

² American College of Sports Medicine (ACSM) Position Stand. Progression models in resistance training for healthy adults. Medicine & Science in Sports & Exercise. 2009.

³ Wernbom M, Augustsson J, Thomeé R. The influence of frequency, intensity, volume and mode of strength training on whole muscle cross-sectional area in humans. Sports Medicine. 2007.

⁴ Phillips SM. A brief review of critical processes in exercise-induced muscular hypertrophy. Sports Medicine. 2014.

⁵ Baar K, Esser K. Phosphorylation of p70S6k correlates with increased skeletal muscle mass. American Journal of Physiology. 1999.

⁶ Brook MS et al. Skeletal muscle hypertrophy: satellite cell involvement. Cell. 2015.

⁷ Enoka RM. Neuromechanics of muscle activation. Journal of Applied Physiology. 2008.

⁸ Schoenfeld BJ. The mechanisms of muscle hypertrophy and their application to resistance training. Journal of Strength and Conditioning Research. 2010.

⁹ Schoenfeld BJ et al. Strength and hypertrophy adaptations between low- vs high-load resistance training: A systematic review and meta-analysis. Journal of Strength and Conditioning Research. 2017.

¹⁰ Schoenfeld BJ, Ogborn DI, Krieger JW. Effects of resistance training volume on muscle hypertrophy: A systematic review and meta-analysis. Journal of Strength and Conditioning Research. 2019.

¹¹ Roig M et al. The effects of eccentric versus concentric resistance training on muscle strength and mass in healthy adults: A systematic review and meta-analysis. British Journal of Sports Medicine. 2009.

¹² Bloomquist K et al. Effect of range of motion in heavy load squatting on muscle and tendon adaptations. European Journal of Applied Physiology. 2013.

¹³ Morton RW et al. Training to failure vs. not to failure for muscular strength and hypertrophy. Journal of Applied Physiology. 2016.

¹⁴ Angleri V, Ugrinowitsch C, Libardi CA. Rest-pause technique vs traditional resistance training: A systematic review and meta-analysis. Sports Medicine. 2020.

¹⁵ Woo S, Bachman R. The Secret Behind America’s Once-in-a-Generation Weightlifter: Not Lifting Weights. The Wall Street Journal. August 9, 2024.

Health Blogs #7 The Elite Athlete: What Science Can Teach Us

By Jonathan A. Jarman, MD

(~ 7 min read and ~12 min audio with references removed)

At 68 years old, I walked onto a tennis court for the first time in more than three decades. I had played a little in my early adulthood — casually, socially, and without understanding the mechanics or the deeper strategy of the sport. In hindsight, that early experience didn’t help me; it probably created bad habits that later interfered with learning to play the game well.

I didn’t return to tennis to compete. I returned because I wanted to live longer — and live better. Tennis is uniquely positioned at the crossroads of longevity, athleticism, agility, aerobic capacity, bone density, cognitive stimulation, and social connection. Research shows that tennis players outlive the general population by nearly a decade¹. That alone makes the sport worthy of exploration.

But I also wanted something deeper: a challenge, a craft, and a chance to push both mind and body toward improvement.

Like many people returning to a sport later in life, I made the mistake of believing strength could compensate for inexperience. I thought I could simply hit the ball harder — because I am stronger than most men my age. I confused power with technique. I confused effort with mastery.

Very quickly, I learned otherwise.

Technique in tennis is its own language. It is rhythm, timing, leverage, footwork, and biomechanics working together. Without it, strength is just noise.

So I hired coaches for 1:1 instruction: Braunn Endler, Jerome Bunkley, Ryan Malis, Clemont Tackie, and Hagen Endler at various times. I listened. I took notes. I reviewed those notes. As an INTJ Myers Briggs type, I naturally deep-dive into anything I care about.

I studied professional tennis players. I watched slow-motion breakdowns. I shadow-swung in my gym. And still — progress felt slow. I would master one element, then plateau. Master the next, plateau again. Confidence would build, then disappear. Doubt crept in.

Am I too old? Maybe I’m not the athlete I thought I was.

And then I realized I was missing the most basic skill in tennis.

While watching players who were neither strong nor particularly athletic, I noticed something important: they kept the ball in play because they watched the ball. They weren’t thinking about wrist angle, knee bend, or swing path. They were simply following the ball with total commitment. Meanwhile, my mind was cluttered with technique thoughts — and the brain can only focus on one thing at a time.

The moment I shifted my attention away from technique and toward the ball itself, everything changed. My mechanics didn’t suddenly transform — but my brain finally oriented to the right priority. A long plateau cracked open, and my game began to move forward.

That insight raised a deeper question:

What actually makes an athlete — at any age — great?
What separates Federer from millions of recreational players?
What separated Michael Jordan from thousands of talented basketball players?
What makes the outliers… outliers?

Malcolm Gladwell famously promoted the “10,000-hour rule” for mastery². But he oversimplified it. Ten thousand hours of poor practice only reinforces mediocrity. Ten thousand hours of deliberate, high-quality work may create expertise — but hours alone do nothing³.

People often believe that elite performance comes from genetics, talent, or hard work. These matter — and without them one cannot reach the top — but they are incomplete answers. The real formula is more nuanced, more human, and more scientific.

Modern research reveals that elite athletes emerge from the convergence of seven domains: physical, neurological, emotional, cognitive, psychological, environmental, and temporal. More importantly:

Each of these domains is trainable. Even at 68.

Below, I explain them as someone rediscovering what athletic pursuit really means — and as a physician interested in health optimization.

  1. The Body You Build

Elite athletes do not simply have strong bodies — they have purpose-built bodies. They train power, explosiveness, mobility, endurance, and stability until these qualities integrate into a single fluent system.

At 68, you cannot outrun biology, but you can absolutely optimize your version of it.

Elite athletes excel in:

  • Strength and power
  • Explosiveness and acceleration
  • Agility and directional quickness
  • Endurance and energy efficiency⁴
  • Sport-specific body composition

These are not fixed traits; they can be systematically improved. Each person has a different ceiling, but almost no one ever reaches theirs.

  1. The Brain That Reacts Before You Think

Neurological efficiency is one of the deepest differentiators of elite performers. Great athletes don’t merely move well — they anticipate. They process visual information more rapidly, and their motor system responds faster and with fewer errors⁵.

This isn’t magic. It’s neuroplasticity in action⁶.
And it can be trained.

Elite performers tend to have:

  • Faster reaction times
  • Superior hand–eye coordination
  • Predictive motor planning
  • Exceptional timing and rhythm
  • Efficient sensory processing
  • Low neural noise

In tennis, anticipation is often more valuable than raw speed.

  1. The Heart That Stays Calm

Emotional regulation is one of the most powerful — and most overlooked — determinants of athletic success. Athletes rarely lose because they are physically inferior; they lose because their emotional system hijacks performance.

A quiet mind is a competitive advantage.

Emotional stability is strongly correlated with improved motor performance, reduced error rates, and better decision-making under stress⁷. And yes — emotional regulation can be trained psychologically, physiologically, and pharmacologically (see Blog #5).

Elite performers show:

  • Emotional steadiness
  • Rapid recovery after mistakes
  • Low reactivity
  • Controlled arousal
  • Presence under pressure

This is often the dividing line between good and great athletes.

  1. The Mind That Learns Fast

Elite athletes learn more quickly because they integrate information more efficiently. Working memory, pattern recognition, and rapid feedback adaptation all contribute to superior motor learning⁸.

This isn’t  traditional  “IQ” — it’s sport-specific cognitive architecture.

Elite athletes demonstrate:

  • Rapid pattern recognition
  • Working memory suited for dynamic tasks
  • Fast processing under stress⁹
  • Tactical reasoning
  • Situational awareness
  • Mental flexibility

They can think while moving — a rare neurological combination.

  1. The Personality That Endures

Beyond talent, the greatest predictor of athletic success is psychological durability. Traits such as conscientiousness, resilience, intrinsic motivation, and emotional stability are strongly associated with elite performance¹⁰.

In practical terms:

Can you show up — repeatedly — when progress is invisible?

Elite athletes display:

  • Discipline
  • Curiosity
  • Intrinsic motivation
  • Resilience
  • Willingness to look foolish while learning
  • Frustration tolerance
  • Stable, competence-based confidence

These are trainable traits — cultivated more than inherited.

  1. The Environment That Shapes You

No one becomes elite alone. Coaching quality, emotional climate, peer group, and access to challenge profoundly influence skill development. Enriched, supportive environments accelerate performance growth¹¹.

At 68, this matters even more.
You must choose an environment that nurtures growth — not ego.

  1. The Time You Are Willing to Give

Mastery is a long game.
Not linear — but staircase-shaped.

Athletes who reach their potential are:

  • Consistent over years
  • Obsessed with refinement
  • Disciplined in recovery
  • Willing to train during boredom
  • Relentless in micro-improvement

If talent is the spark, deliberate practice is the fuel.

The Formula

Elite Performance =
(Physical Talent × Neurology × Intelligence × Emotional Control × Personality × Environment × Time)
× Commitment

If one factor approaches zero, the product collapses.

This explains why athletes with extraordinary gifts often stagnate:

  • Great physical gifts × poor emotional control = inconsistency
  • Strong technique × low discipline = stagnation
  • High work ethic × poor coaching = inefficiency
  • High intelligence × poor biomechanics = limited ceiling

Excellence is multidimensional.

What Science Teaches Us — and What Experience Confirms

Science is clear: elite athletes are built at the intersection of biology, technique, emotion, and intentional practice. But the deeper truth is that these principles extend beyond sport — they are principles of life.

Tennis continues to teach me:

  • Track the ball, not the noise.
  • Move your feet.
  • Stay calm after mistakes.
  • Commit to your mechanics.
  • Seek excellence, not perfection.
  • Keep showing up.

In sports science, these belong to motor learning, neuroplasticity, deliberate practice, and emotional regulation.

In life, they belong to wisdom – not IQ. Wisdom and IQ are not the same.

And if tennis at 68 has taught me anything, it is this:

ATHLETIC EXCELLENCE IS BUILT, NOT BORN

Whether it’s tennis at 68 or baseball at 28, peak performance comes not from talent alone but from the convergence of biology, psychology, technique, and discipline.

If you want to become a better athlete, ask yourself:

Which of the seven domains is holding me back from being the best I can be?
Identify it. Train it. Improve it.
Performance will follow.

REFERENCES

  1. Schnohr P, O’Keefe JH, Marott JL, Lange P, Jensen GB. Different types of physical activity and mortality: the Copenhagen City Heart Study. Mayo Clinic Proc. 2018;93(12):1775–1785.
  2. Gladwell M. Outliers: The Story of Success. Little, Brown; 2008.
  3. Ericsson KA, Krampe RT, Tesch-Römer C. The role of deliberate practice in the acquisition of expert performance.Psychological Review. 1993;100(3):363–406.
  4. Joyner MJ, Coyle EF. Endurance exercise performance: the physiology of champions. J Physiol. 2008;586(1):35–44.
  5. Zwierko T, Lesiakowski P, Florkiewicz B. Reaction time and visual perception in elite athletes. J Hum Kinet.2019;70:121–129.
  6. Dayan E, Cohen LG. Neuroplasticity subserving motor skill learning. Neuron. 2011;72(3):443–454.
  7. Tamir M, Bigman YE. Emotional regulation and performance in competitive tasks. Emotion. 2018;18(4):586–599.
  8. Yarrow K, Brown P, Krakauer JW. Inside the brain of an elite athlete: motor learning mechanisms. Nat Rev Neurosci. 2009;10(4):231–242.
  9. Voss MW et al. Cognitive functioning in elite athletes. Psychol Sport Exerc. 2010;11(5):371–379.
  10. Allen MS, Greenlees I, Jones M. Personality and sport performance: A meta-analysis. Personality and Individual Differences. 2013;54(6):693–701.
  11. Abbott A, Collins D. Eliminating the dichotomy between theory and practice in talent identification and development. J Sports Sci. 2004;22(5):395–408.

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