Barry Rotman, MD

A Physician’s Thoughts on the Oura Ring: The Latest Health Trend

Gwyneth Paltrow. Jennifer Aniston. Prince Harry. Will Smith. Shaquille O’Neal. Mark Zuckerberg. Barry Rotman.

What do these people have in common? They’ve all publicly acknowledged wearing an Oura Ring — the new medical sensation.

Oura Health was founded in 2013 in Finland. Its product, the Oura Ring, was made commercially available as a sleep-tracking device in 2016. It began with Kickstarter funding in 2015 and expanded to a market capitalization of $2.55 billion by 2022.

The Oura Ring’s original goal — sleep tracking — has expanded to include many goals, including stress management, early disease detection, menstrual cycle tracking, and more.

In the growing field of consumer wearable health devices, the Oura Ring stands out as the most powerful. However, not all its functions are well-validated.

In this blog post, I’ll explore the hype surrounding the Oura Ring. What is it? How does it work? Which features are valuable, and which aren’t?

What Is an Oura Ring?

An Oura Ring is a five-gram, titanium-encased device designed to be worn on a finger. It communicates data to a smartphone app.

Despite its small size, it continuously measures:

• Motion
• Peripheral skin temperature
• Heart rate
• Heart rate variability
• Blood oxygen saturation

Two decades into the smartphone revolution, we’ve become accustomed to an astounding array of functions built into a small device. However, when I started medical school nearly forty years ago, a device like the Oura Ring was nothing but science fiction.

The Oura Ring includes:

• A 3D actigraphy device to record motion
• A thermometer to measure skin temperature
• A photoplethysmography device to measure pulse rate
• A pulse oximeter that records oxygen in the blood

In addition to direct sensor data, the smartphone app calculates various physiological parameters using user data (gender, age, height, and weight).

Some complex algorithms use large, international population-based measurements and AI analysis. For example, the Oura Ring’s sleep metrics are industry-leading. The ability to differentiate sleep stages (awake, light, deep, and REM) is about 80% accurate compared to overnight sleep studies.

For most applications, the Oura Ring combines four possible data sources:

1. Daily measured data
2. Individual data baseline
3. User-specific data
4. Population-based comparison metrics

For example, to detect the early onset of an infection, the Oura Ring notes a change in a person’s skin temperature, heart rate, breathing rate, and heart rate variability from his or her baseline. It compares that change to a predictive population-based model.

One study noted the Oura Ring’s ability to diagnose COVID infection an average of 2.75 days before the study subjects displayed enough symptoms to seek a COVID test.

On the other hand, building a function that incorporates many layers of data means that an inaccuracy at any point compromises the entire process’s accuracy.

For example, Oura Ring has a readiness function that combines your sleep, activity, and stress scores to reflect how prepared your body is for the day. The sleep score has good validation. However, both the literature and my experience suggest that the activity score isn’t accurate and that the magnitude of error increases as the intensity of exercise increases.

The more active you are, the more difficult it becomes for the Oura Ring to measure your heart rate and track the total amount of body motion. A similar challenge affects the stress score, which measures your sympathetic nervous system at rest. Physical activity normally increases sympathetic tone.

I’ve found that the Oura Ring doesn’t differentiate when I am truly at rest compared to a brief break in moving around, compromising the stress score’s accuracy. Therefore, I don’t trust the overall readiness score’s accuracy.

The Oura Ring continues to release new functions, such as menstrual cycle tracking, which appears to be at least as accurate as tracking daily oral temperature.

How Accurate Is an Oura Ring?

The Oura Ring provides exciting ways to learn about your body’s health status in real time. I’ve grouped many of the features into three categories depending on their current quality of clinical validation:

1. Accurate and valuable tool
2. Possibly accurate, use cautiously
3. Unproven, for entertainment purposes only

 

If using one of the functions motivates you to focus on a health aspect and improve your lifestyle choices, the feature is beneficial regardless of its proven accuracy level.

Does an Oura Ring Have Side Effects?

More knowledge isn’t always better.

Consumer wearables’ rising popularity has led to a new diagnosis: “orthosomnia,” an unhealthy obsession with achieving perfect sleep. Paradoxically, becoming overly focused on your quality of sleep leads to anxiety and frustration, which reduces your ability to sleep well. Knowing your sleep score upon arising can hurt your mood for the day.

Can an Oura Ring Help You Make Healthier Decisions?

I found the Oura Ring extremely helpful in my quest to become more “chill.”

I used it for several Metric-Driven Empowerment Cycles (MDECs), tracking sleep, HRV, and meditation. The measured outcome variable allowed me to make a series of adjustments to my life and observe the results. I followed only a few of the growing list of measurements my Oura Ring provided.

Depending on your interests, there are many compelling uses:

• Activity level
• Step count
• Active energy expenditure
• Total energy expenditure
• Body temperature
• Respiration rate
• Heart rate
• Heart rate variability
• Total sleep time
• Sleep stage time (awake, light, deep, and REM)
• Composite readiness score
• Composite stress score
• Composite resilience score
• Early infection detection
• Early pregnancy detection
• Menstrual cycle tracking

The list of functions continues to grow, as does the number of studies validating them.

Final Thoughts on the Oura Ring

There’s a wide array of consumer wearable health devices available. The Oura Ring is the best and will become the recommended device for Banner Peak Health’s patients.

The Oura Ring includes superb directions and educational materials. However, it becomes even more valuable when incorporated into an overall health plan.

Please let us know if you have an Oura Ring or are considering purchasing one. We want to help you derive the maximum health benefit from it.

---

by Barry Rotman, MD

Heart Rate Variability: A New Tool for Stress Management

Sometimes, you don’t realize you’re stuck in a rut until your life improves.

Life’s impediments can develop slowly, imperceptibly weighing you down. Your daily experience may be suboptimal, but since you’ve felt that way for many years, you feel normal. Only in retrospect do you realize, Wow! That wasn’t my best self. I can feel so much better!

Many sophisticated tests can measure health status.  How about a very simple one — the ability to wake up feeling great?

This blog will review my four-month quest to reach that goal and how I used heart rate variability (HRV) to do it.

How Stress and Heart Rate Variability Relate

I write a lot about stress and its health impacts.

For a risk factor as potent as stress, it’s surprising that we’ve lacked practical methods of measuring it until recently. The growing popularity of wearable devices has finally given us convenient access to this vital metric.

I’ve written about how heart rate variability (HRV) reflects the balance between our sympathetic and parasympathetic nervous systems. More stress increases the sympathetic tone, reducing the variability in timing between each heartbeat. Less stress allows for a greater parasympathetic tone, increasing the timing variability between each heartbeat.

Basically, the higher your heart rate variability, the more “chill” you are.

Recent blogs have illustrated the value of MDECs (Metric-Derived Empowerment Cycles), techniques for generating actionable health data to help people improve their health. Heart rate variability, as measured by wearable devices, is a helpful metric-derived empowerment cycle.

Heart rate variability reflects the sum of physiological and psychological stress sources. Worried about a final exam? Bad night of sleep? Too much (or any) alcohol? Hard workout? Sore back? Laid off from a job? Your heart rate variability will reflect it.

Technically, heart rate variability doesn’t measure the total amount of stress we are exposed to. Rather, it measures how our body reacts to stress — a subtle but important distinction.

Stress is an inevitable part of the human condition. In manageable amounts, it propels us forward, but if its intensity and duration exceed our ability to cope, we suffer adverse consequences. Heart rate variability as a metric-derived empowerment cycle quantifies how our body reacts to our total stress burden. It can also track the results of our stress-management efforts.

Heart Rate Variability’s Role in Fitness

The current abundance of products that measure heart rate variability (Apple Watch, Garmin, Whoop, Oura Ring, etc.) reflects heart rate variability’s popularity in the fitness community. Analyzing daily heart rate variability provides a valuable tool to assist athletes in monitoring their response to training.

A hard workout doesn’t make you stronger, per se; rather, a successful recovery makes you stronger. Knowing your heart rate variability can help you adjust your workouts’ intensity and timing.

For instance, an athlete who wakes up feeling “off” and notices an unusually low heart rate variability score might be better served by scaling back or eliminating a hard workout that day rather than risk overtraining and slowing overall improvement.

While using heart rate variability for sports training may be the primary use case driving its popularity, measuring variation over longer periods of time can guide decisions that affect a wider range of health outcomes.

Short-term stress is adaptive. It helped our ancestors outrun predators. It’s the chronic, elevated stress of modern life that raises our risk for obesity, heart disease, diabetes, cancer, sleep disorders, and mental health conditions. Heart rate variability informs how a person can better cope with stress and reduce the risk of these types of illnesses.

My Stress-Reduction Journey

Over the last year, I’ve experimented with different methods for measuring heart rate variability, including wearables such as Whoop or the Oura Ring and smartphone apps that use a chest strap or the phone camera. How heart rate variability is measured affects its utility.

Heart rate variability varies every second of the day and night in response to variables such as emotional state, exercise, medications, diet, and sleep. For heart rate variability to assess individual variables such as less sugar intake or more exercise, other factors need to be standardized.

A common approach is to measure heart rate variability while asleep, which reduces factors that might interfere with the result. For example, Whoop uses a proprietary algorithm to average the response throughout the night, preferentially calculating heart rate variability during slow-wave sleep, and the Oura Ring records the heart rate variability level every five minutes and presents an average for the night.

I use the Oura Ring because I appreciate its straightforwardness, and I like tracking my heart rate variability throughout the night. My Oura Ring has taught me that chocolate, sugary desserts, and alcoholic beverages impair my sleep and lower my heart rate variability when I consume them close to bedtime. In fact, I can correlate how many hours the effect lasts with how much I consume.¹

In general, measuring heart rate variability at night eliminates many influences that occur while we’re awake. However, issues that arise at night, like a sleep disorder, can affect it. As I described in a prior blog, a SleepImage device taught me that I had a mild case of obstructive sleep apnea, which contributed to my reduced heart rate variability.

I also use the app HRV4Training to monitor my heart rate variability daily. Its protocol relies on a one-minute pulse reading through the smartphone camera, done while sitting immediately after waking up. It eliminates the effects of sleep disorders and other factors that come into play once you begin your day.

The Oura Ring has a great feature labeled “unguided session” that monitors your heart rate variability for a predetermined amount of time, allowing you to run experiments and determine their effect on your heart rate variability. I use it to track my physiological response to my 20-minute meditation sessions. My heart rate variability rises two or four times higher than my nighttime values (even after treating my obstructive sleep apnea), confirming my meditation’s efficacy.²

In addition to providing daily feedback, heart rate variability monitoring tracks changes over weeks and months.

In January 2024, I began addressing many years of deferred maintenance in my life. I embarked on an extensive process of physician appointments, lab studies, sleep monitoring, diet modification, therapy, and dietary supplements.

Many of these interventions would be expected to raise my heart rate variability:

1. I began taking a fish oil supplement to reduce my cardiovascular risk. Fish oil has been found to have anti-depressant benefits. I hadn’t been suffering from depression, but any mood improvement may raise heart rate variability.
2. I included more Zone 2 training in my exercise regime.
3. I improved my sleep/wake cycle synchronization using a TUO lightbulb. I now get more sleep and don’t need an alarm.
4. I began treating my mild obstructive sleep apnea.
5. I reduced my alcohol and sugar consumption.
6. I began B12 replacement for borderline low levels.
7. I reshaped my work responsibilities as a physician.
8. I began adhering more consistently to 20-minute meditation sessions each morning.
9. I adopted a “no news after nine” rule to reduce my news consumption.

My monthly average heart rate variability rose a remarkable 25%, from 19 ms in January 2024 to 25 ms in April 2024. This very significant improvement correlates with how much better I feel.

Heart Rate Variability: Final Thoughts

This blog is not a precise prescription for how to feel better. Rather, it’s an example of how HRV monitoring can guide decisions to improve one’s life. For the first time in years, I wake up feeling great.

I want to bring heart rate variability monitoring’s benefits to patients at Banner Peak Health. Reach out to learn how it can help you achieve your health goals.

Footnotes:

1. Before my April 6 nocturnal Oura Ring recording, I consumed one glass of wine with dinner. Both my heart rate and heart rate variability were elevated until around 3 a.m., reflecting the increased sympathetic tone associated with processing even a small amount of alcohol. Most nights, I drink no alcohol. For example, the April 11 tracing illustrates a comparably low HRV score from other factors distributed more evenly throughout the night.

2. My Oura Ring functions as a biofeedback mechanism, demonstrating my meditation’s physiological impact. This is a tracing of an abbreviated 10-minute meditation session. The average heart rate variability of 84 ms reflects a value fourfold higher than my average nocturnal value for the year. Compared to being asleep, I reach a state four times more chill during meditation, quantitative evidence of its powerful impact!Peripheral skin temperature correlates with heart rate variability. This tracing demonstrates meditation’s impact on peripheral skin temperature, which progressively warms during the session. When we’re nervous (increased sympathetic tone), our hands become cold and clammy. As we calm down, they warm up, reflecting an increased parasympathetic tone. My finger became warmer during the meditation session.

---

by Barry Rotman, MD

The Benefits of Continuous Glucose Monitoring

In earlier blog posts, I’ve discussed the concept of Metric-Derived Empowerment Cycles (MDECs).

Measurement devices now provide actionable data that incentivize and track the results of healthy behaviors. It can be a long journey from thinking about behavior change to initiating change to sustaining it. That’s human nature. We need all the help we can get.

Generating a metric, or “putting a number on it,” can be a very powerful tool to motivate behavioral change by quantitating a baseline and providing a measurable path to improvement. Continuous glucose monitors enable one of the most valuable MDECs we use at Banner Peak Health.

Chronically elevated blood glucose levels are associated with the development of diabetes, which elevates the risk for a wide range of illnesses, including heart disease, stroke, cancer, and kidney disease. The root causes of elevated glucose are multifactorial and include diet, stress, exercise, and sleep. The physiology of blood glucose is very complex.

What Is a Continuous Glucose Monitor?

The ability to measure glucose levels has come a long way since the days when practitioners would taste urine to detect sweetness, indicating excess sugar excretion. (The term diabetes mellitus is derived from Greek diabetes, meaning to pass through, and from Latin mellitus, meaning honey or sweet.)

By the 1840s, tests using chemical reagents could detect sugar in urine. By 1913, blood glucose levels could be measured in a lab. By the 1960s, blood glucose could be semi-quantitatively measured using a chemical test strip reacting with a drop of blood, though the process was cumbersome and not available for home use.

The true revolution in blood glucose monitoring came in the 1980s with the advent of handheld glucometers and reagents on test strips, allowing convenient self-monitoring. There were still significant constraints, however. One-time-use test strips were expensive, and the process of poking and testing was painful and time-consuming. Only the most dedicated of patients could comply with a two- to four-times-a-day testing regimen.

The technology in continuous glucose monitors, such as the current models, the Dexcom G7 and Freestyle Libre, has progressively improved over the last 15 years. The monitors have a very small tube, or cannula, that inserts into the subcutaneous region under the skin. The probe contains enzymes that generate an electrical signal proportional to the concentration of glucose in the interstitial fluid. Strictly speaking, blood glucose is not being measured directly. However, in most circumstances, the interstitial fluid is very close to the blood glucose level, with current models accurate to less than 10% deviation from blood levels.

The sensor remains attached to the skin for 10–14 days, depending on the model, and sends the results to a smartphone for patient viewing and subsequent transmission to a healthcare provider.

Modern Continuous Glucose Monitoring

The cost and complexity of early continuous glucose monitors relegated their use to the most complicated diabetic patients — those requiring insulin therapy and at greater risk for dangerously high and low levels of blood glucose. Today, the devices are also used for less complicated diabetic patients. They still require a prescription, however.

Just this year, Dexcom released a model, Stelo, that will be approved for sale without a prescription. It offers the same accuracy as their prescription model, the G7, but won’t be approved for those requiring insulin treatment.

The less expensive and more widely available Stelo model opens the way for continuous glucose monitoring to move from treatment of diabetes to prevention of diabetes.

Diabetes represents an unfortunate culmination of many years of progressive metabolic dysfunction. This lengthy process presents ample opportunity to modify behavior and prevent the onset of diabetes.

In medicine 2.0 (disease treatment), medications are the dominant treatment modality. In contrast, medicine 3.0 (disease prevention) relies predominantly on lifestyle choices — how you eat, sleep, exercise, and manage stress. Continuous glucose monitors, once relegated to the realm of medicine 2.0, are now poised to realize their full potential as a powerful tool for medicine 3.0!

Who Should Use a Continuous Glucose Monitor?

As part of screening blood tests, you’ve most likely had your fasting blood glucose level and possibly hemoglobin A1c (HgbA1c) measured. A fasting (12 hours without eating) blood glucose level can indicate your risk of diabetes:

Your HgbA1c level reflects your average glucose level over the past three months (see footnote 1) and is expressed as a percentage:

An elevated fasting blood glucose or HgbA1c indicates that you are at increased risk of developing diabetes or that you have diabetes. And these aren’t rare findings. An estimated 40 million adults in the U.S. have diabetes, and close to 100 million have prediabetes.

Several classes of medications can reduce the risk of progressing from prediabetes to diabetes as well as treat existing diabetes. However, the underlying causes of diabetes — insulin resistance, excess caloric intake, reduced exercise, and fat deposition — are best treated by reversing the lifestyle choices that created them in the first place. Medication can provide a backup safety net if lifestyle modifications don’t create enough benefit.

Continuous glucose monitoring offers a vital monitoring tool for anyone with borderline or elevated fasting blood glucose and HgbA1c levels to better understand their body’s unique physiology and guide lifestyle modifications.

How to Use Data From Continuous Glucose Monitoring

People often have an overly simplified understanding of blood glucose, envisioning a straightforward pipeline from the gut to the blood. Sugar goes in one side and comes out the other. The reality is much more complex.

I envision blood glucose as analogous to a beach ball, surrounded by multiple foam pellet guns bombarding the beach ball with shots of varying intensity from different directions. The movement of the beach ball is determined by the net effect of all the pellet guns. Some of these “pellet guns” are:

• Physical activity — Increased muscle cell usage consumes more glucose.
• Stress — Increased hormone levels of adrenaline and cortisol raise glucose.
• Illness — Infections increase adrenaline and cortisol, which raise glucose.
• Sleep deprivation — Lack of sleep increases adrenaline and cortisol, which raise glucose.
• Meal timing — Longer duration between eating reduces glucose levels.
• Medications — Some medications, such as glucocorticoids, can markedly raise glucose; others, such as thiazide diuretics and statins, can subtly raise glucose.
• Food intake — Certain foods raise glucose more rapidly; individual responses to different foods can vary considerably.

By wearing a continuous glucose monitor, you can learn about the unique effect of all these variables and more on your personal glucose levels.

Those using continuous glucose monitors to reverse prediabetes most commonly use them for several months.

The first step involves understanding the magnitude of the problem. Knowing your blood glucose level every five minutes, 24/7, provides a much more nuanced understanding of your metabolism than a one-time fasting level or an average level over 90 days.

The second step involves identifying the unique variables that influence your blood glucose levels. What happens after a fight with a family member, a poor night’s sleep, a head cold, a long hike, or a particular type of meal?

A big part of this learning process involves your response to different foods. Yes, a sugary soda will generate a rapid blood sugar spike in most people. However, we’re learning that there exists much greater variation in individual responses to different foods than previously thought. You may process a sweet potato very differently than someone else.

The third step involves using the continuous glucose monitor to track the progress of your behavior modifications. Basically, you run a set of experiments on yourself. What happens if you go to bed an hour earlier, meditate, eliminate a bedtime snack, eat brown rice instead of white, cut out soda and juice, or vary the carbohydrate content of your meals? Once you learn how you respond, you can change your habits and see the benefits.

Often after a month or two, the law of diminishing returns kicks in and the rate of new knowledge declines. If successful, you reach a new equilibrium of behaviors and maintain your blood glucose at a healthier level. You won’t need continuous glucose monitoring in the long term.

Some people may require more time or another round of usage. However, for those without medication-treated diabetes, the process should be relatively brief.

Final Thoughts

We’re living amid a silent epidemic of metabolic dysfunction. Many diabetics, and the vast majority of those with prediabetes, are unaware of their status.

At Banner Peak Health, we’re careful to identify risk factors like prediabetes and diabetes and are very aggressive in working with patients to mitigate their risks. Continuous glucose monitoring provides patients with a powerful tool to learn about their unique glucose metabolism and guide them to better health.

Footnote:

1. HgbA1c measurement relies on an interplay between red blood cells and glucose in the blood. Hemoglobin is a large, complex protein that binds iron and carries oxygen in the blood. Red blood cells are packed with hemoglobin, allowing them to transport oxygen throughout the body.

Red blood cells last about three months before they’re degraded, and their hemoglobin is broken down and recycled. Glucose sticks to hemoglobin molecules in a dose-dependent fashion. The higher the concentration of glucose, the more of it will stick to hemoglobin.

HgbA1c reflects the percentage of hemoglobin molecules with glucose stuck to them. Because red blood cells and the hemoglobin within them only last around 90 days, HgbA1c reflects an average level of glucose in the blood during that time.

---

by Barry Rotman, MD

The Magic of Zone 2

It’s common knowledge that exercise is good for you, but the exact mechanisms of action are less known.

Which stimuli influence what physiological systems? What’s the correct exercise “dose”? How can we measure the effects?

The study of sports physiology has grown rapidly, generating fascinating insights. I’m excited to discuss them today.

The intensity of cardiovascular exertion can be divided into zones, ranging from no exertion to complete exhaustion. While there are various systems, I’ll describe only one — Zone 2 (my favorite!) — defining its unique physiology and explaining its magical properties.

Spoiler: It’s all about the mitochondria.

What Contributes to Cardiovascular Exertion?

I’m a huge fan of the Tour de France bike race. Two hundred of the world’s best bike riders pedal over 2,000 miles in three weeks. The competition is so intense that after scores of hours of racing, the top three finishers may be only minutes, or even seconds, apart.

As a recreational bicyclist, I’m fascinated by the bike handling skills and tactics of racing. As a physician, I’m awestruck observing the best endurance athletes on the planet.

Even among the world’s best riders, there are once-in-a-generation athletes. Tadej Pogacar, a Slovenian, won his first Tour de France at 21, the youngest champion since 1904. He won the Tour in 2020 and 2021.

Watching Tadej take off up a mountain, leaving behind the world’s best riders, is awe-inspiring. In addition to winning the one-in-a-billion genetic lottery, Tadej trains with Dr. Inigo San Millan, a top sports physiologist and coach.

Dr. San Millan raced as an amateur cyclist in the Basque region of Spain before earning a medical degree. He is now a research scientist at the University of Colorado in Boulder.

In addition to sports physiology, Dr. San Millan’s research focuses on metabolic disorders. Much of his work focuses on mitochondrial function, which is prominent in metabolic disorders and sports physiology.

In “Outlive,” Peter Attia cites a 2017 study by Dr. San Millan and George Brooks, which describes the foundational ideas behind Zone 2 training. The authors examined the mitochondrial function of three groups: world-class cyclists, recreational cyclists, and inactive people with pre-diabetes or diabetes.

By comparing how mitochondria function in the world’s best endurance athletes as opposed to diabetics, the study sheds light on metabolic flexibility — what fuel sources the mitochondria can “burn” for energy.

How Your Body Metabolizes Energy

A brief discussion of energy metabolism biochemistry will help us understand Dr. San Millan’s study.

The mitochondria consume either fatty acids or glucose to produce energy. Fatty acids are the preferred fuel source. They have twice the energy density of glucose, 9 kcal/gram, compared to 4 kcal/gram.

Thus, a kilogram of fat (2.2 lbs) provides approximately 9,000 kcal of energy. The average person has many kilograms of fat, which can be mobilized for energy, providing a vast “gas tank.”

In contrast, the body’s storage of glucose in the form of glycogen is limited to around 600 grams, or approximately 2,400 kcal of energy — less than the energy from a quarter of a kilogram of fat. Food sources provide additional glucose, but the digestive system can’t effectively absorb many nutrients during intense exercise.

The liver produces glucose through a process known as gluconeogenesis, but it has a limited capacity and isn’t as energy-efficient as other fuel sources. Gluconeogenesis doesn’t contribute much energy for exercise but prevents low blood sugar during low food intake.

Not only are fatty acids a more plentiful and efficient fuel source for exercise, but their combustion byproducts are also “cleaner” than glucose ones.

Glucose metabolism generates lactic acid, which contains a lactate molecule and a hydrogen ion. Lactic acid has been described as the “bad” waste product from exercise. For example, we used to think that after an intense workout, your thighs burned because of lactic acid buildup.

This is only partially true.

The lactate molecule is beneficial, functioning as an energy source that adjacent muscle cells can consume. The associated hydrogen ion remains a bad factor, lowering the pH in the region and impairing further muscle functioning. The hydrogen ions from glucose metabolism generate a ceiling on muscular energy production’s quantity and duration. In contrast, fatty acids burn cleaner, generating only carbon dioxide and water.

However, the body’s ability to metabolize fatty acids has a finite capacity. With increased energy demand, the systems available to metabolize fatty acids become saturated. Less efficient glucose metabolism is recruited and added to fatty acid consumption to increase energy production further.

Back to the Groundbreaking Study...

Inigo San Millan and George Brooks wanted to explore how efficiently each group of people used fatty acids, the preferred fuel source, before using glucose.

Each participant rode an exercise bike with a step-up protocol requiring progressively more power output every 10 minutes. At each step, each participant’s oxygen consumption, carbon dioxide production, power production, and serum lactate level were recorded.

By analyzing this data, the researchers could calculate the composition of fuel sources used at each power level. For example, because lactic acid is a metabolite of glucose but not fatty acids, it would remain in the low range at lower power levels when fatty acids were the predominant fuel and climb at higher levels as more glucose was used.

Each participant started with more fatty acids burned than glucose. As power increased, additional glucose was consumed, and the percentage of fatty acids burned became smaller.

However, the key finding was the vast differences between the study groups.

The world-class cyclists produced staggering amounts of power while maintaining a stable serum lactate level, meaning they were extremely efficient at burning fatty acids and processing any lactate generated from the glucose they burned. They possessed the best mitochondria on the planet, derived from fortunate genetics and effective training regimens. (More on that topic later.)

In contrast, the deconditioned participants with pre-diabetes or diabetes had the opposite response. These participants had higher lactate levels at rest than the world-class cyclists had while producing large amounts of power. Even before exercising, these participants couldn’t readily access fatty acids and had to rely on glucose, which produced lactic acid.

With minimal exercise, the hydrogen ions from the lactic acid began rapidly building up and limiting exercise duration. This process drastically limited their power — a small fraction of the world-class cyclists. The recreational cyclists had outcomes between these two extremes.

The Surprising Results

So, what explains the pre-diabetic and diabetic participants’ results?

Metabolic syndrome — the process of insulin resistance and other hormonal dysfunction that leads to pre-diabetes and potentially diabetes — degrades mitochondrial function through various mechanisms, such as fewer mitochondria and fewer proteins within each mitochondria. These processes limit the ability to metabolize fatty acids and effectively generate power for exercise.

Fortunately, these changes are reversible.

Zone 2

How does the study relate to Zone 2?

Dr. Inigo San Millan defines zones based on the body’s fuel source:

• Zone 1: An intensity that allows mitochondria to utilize fatty acids but doesn’t exceed their capacity.
• Zone 2: The intensity that maximizes mitochondrial fatty acid utilization for power.
• Zone 3: Occurs when the power requirements exceed the mitochondrial capacity for fatty acid utilization and progressively more glucose utilization is required.
• Zone 4–6: The mitochondria no longer use fatty acids and are defined by other energy sources.

The study has profound implications for athletic training and improving the metabolic health of pre-diabetics and diabetics.

Dr. Inigo San Millan’s training regimen for Tadej Pogacar involved more time in Zone 2 than in any other zone. For Tadej Pogacar to become one of the world’s fastest endurance athletes, he had to spend lots of time biking relatively slowly.

What Is Zone 2?

Zone 2 is a level of exertion at which you can converse. It involves riding at an “all-day” pace.

Zone 2 training intensity improves mitochondrial function by increasing the number and efficiency of mitochondria in muscle cells. In particular, it enhances metabolic flexibility, which maximizes the mitochondria’s consumption of fatty acids for fuel.

As we discussed, fatty acids are the preferred fuel because:

1. The body has tremendous fatty acid storage.
2. Fatty acid consumption burns cleanly, with no negative feedback loop blocking its metabolism.
3. Fatty acid provides a foundation for further levels of metabolism.

Zone 2-enhanced mitochondrial ability allows athletes to go farther more efficiently and reach a higher peak output. Once the power requirement exceeds the mitochondria’s ability to metabolize fatty acids, the body relies on less efficient and more time-limited substrates, such as glucose.

I think of Zone 2 as the booster stage of a multistage rocket ship. The faster and farther it moves the rocket, the less the rocket relies on smaller subsequent stages.

In prior blogs, I’ve discussed the value of measuring VO2 max at peak output, noting that it measures the ability of the entire cardiopulmonary system to function. Zone 2 training at lower intensity provides the foundation that supports other energy systems that allow the body to reach peak output. A massive booster rocket gets you into the sky faster and farther.

Paradoxically, you must go slow to get fast. This is Dr. San Millan’s message and the secret to Tadej Pogacar’s success.

This message has been lost on recreational athletes, who, like me, have limited time for training and assume they should “go hard” whenever possible. Workout apps like Garmin and Strava reinforce this ethos with features to set new personal records, measure peak power outputs, and compete against your friends.

In contrast, effective Zone 2 training requires a relatively slow and deliberate training regimen.

How to Create a Personalized Zone 2 Training Program

The first step to creating a Zone 2 training program is identifying your Zone 2 parameters.

This process is more nuanced than reading the workout equipment at the gym, which identifies your “fat-burning” zone as 50–70% of your maximum heart rate. This approximation overlooks many individual characteristics.

Two more accurate techniques for identifying one’s Zone 2 include:

1. Replicate the protocol Inigo San Millan and George Brooks used. Measure fingerstick lactate levels or exhaled carbon dioxide and oxygen levels to calculate how intensely you can exercise before you leave the Zone 2 region of fatty acid metabolism. This level of intensity can be expressed in terms of heart rate or power output and can serve as a guide for further workout intensity.
2. Use your rate of perceived exertion (RPE), a 10-point scale from absolute rest to complete exhaustion. RPE scores your intensity assessment based largely on your breathing rate, which correlates with exertion. (Carbon dioxide and serum acidity rise with activity level, leading to more rapid breathing.) Zone 2 corresponds to an RPE of 5–6 out of 10 and has a breathing rate that allows you to speak in full sentences.

How much Zone 2 training you need depends on your goals. Professional and elite endurance athletes may spend 80% of their training time in Zone 2, which can be tens of hours a week. The minimum effective dose for us “time-crunched” athletes would be three hours a week, providing noticeable benefits without hurting professional or personal commitments. It may take several months for the maximum benefit to accrue.

The Practical Benefits of Zone 2 Training

Zone 2 training has become vital to elite athletes’ competitiveness. It can also provide a welcome boost for recreational athletes.

For decades, I’ve biked five to seven hours a week. Given the hilly terrain where I ride, most of that time has been spent above Zone 2 going uphill or below Zone 2 going downhill. I’ll ride in Zone 2 for three hours a week and observe its effects.

In addition to allowing athletes to enhance performance, I suspect the greatest potential benefit of Zone 2 training is improving the metabolic health of those with pre-diabetes and diabetes. We’re amid an unprecedented epidemic of pre-diabetes and diabetes, which correlates with an elevated body mass index. Over 120 million adults in the U.S. are estimated to be affected!

Mitochondria are the key to understanding insulin resistance and metabolic dysfunction, which leads to pre-diabetes and diabetes. Skeletal muscle cells metabolize up to 90% of the body’s glucose. These cells’ metabolic health, including their mitochondrial function, impacts how the body uses glucose.

Whenever we consume more calories than we burn, we’re in caloric excess. Excess calories are converted to fat and distributed throughout the body. Some locations, such as the thighs and buttocks, have minimal health effects. In contrast, other locations, such as the liver and abdomen, create problems.

Fat deposited within muscle cells impairs mitochondrial function by inhibiting fatty acid use and glucose uptake into the cell, reducing mitochondrial density and efficiency and creating localized inflammation. When muscle cells can no longer adequately metabolize glucose and fatty acids, glucose levels rise, creating a vicious cycle leading to pre-diabetes and, ultimately, diabetes.

This frightening process has a silver lining: the most effective treatment involves rehabilitating the mitochondria within muscle cells through Zone 2 exercise! No pill, injection, or drug effectively prevents diabetes as much as diet and exercise.

Diet modification is crucial to reverse caloric excess, which deposits fat into cells such as muscle cells and impairs their function. Zone 2 exercise is the most potent tool for improving muscle cell mitochondrial function and can reverse the metabolic effects of pre-diabetes and diabetes.

Final Thoughts

Three hours a week of Zone 2 training appears to be a good minimum dosage for improving metabolic health and athletic performance. More would be better, but even three hours can be a significant commitment.

Zone 2 training “magically” provides a performance boost to recreational athletes who’ve plateaued within a busy schedule. More importantly, Zone 2 training “magically” corrects the metabolic dysfunction that causes pre-diabetes and diabetes.

At Banner Peak Health, we’re excited to explore Zone 2 training. We help patients determine their Zone 2 parameters, advise on Zone 2 training programs, and monitor their progress. Give us a call and be part of the magic!

---

by Barry Rotman, MD

Fish Oil: To Take or Not to Take

For me, 2024 is a year of introspection and growth.

I’m redefining my professional role and optimizing my own health. The two are intertwined under the umbrella of “me-search,” which involves using myself as a subject in a series of N=1 trials to better understand the latest healthcare techniques.

Being on the “cutting edge” of medicine requires a critical approach to evaluating and selecting medical options. Unfortunately, the metaphor of a sharp instrument doesn’t accurately describe the current landscape. It’s the opposite — an amorphous blob better represents the rapidly growing pool of heavily hyped, minimally evaluated medical treatments. Strolling down the supplement aisle or googling “weight loss” unleashes an avalanche of options.

Separating the wheat from the chaff isn’t easy.

For example, my new primary care doctor recommended I take a fish oil supplement to protect my heart. I trust her advice, but I also wanted to review the current medical evidence for fish oil supplements. Like many dietary supplements, the general consensus has swung back and forth.

Our story begins on a frigid ice floe in the North Atlantic…

Early Fish Oil Studies

In the 1970s, researchers noted that the native population of Greenland had lower rates of cardiac disease than those in Denmark or the United States, despite a diet much higher in saturated fats. These epidemiological findings led to the idea that people in Greenland who ate more marine vertebrates (whale, seal, and fish) had higher levels of n-3 fatty acids, which made them less likely to get heart disease.

In 1985, a new study demonstrated the cardioprotective effects of n-3 fatty acids in fish. A randomized cohort of heart attack survivors either ate two meals of oily fish a week or not. After two years, the group that ate oily fish had a 29% lower all-cause mortality rate than the group that didn’t.

Researchers then attempted to assess the benefit of n-3 fatty acids as a dietary supplement rather than through fish consumption.

Before exploring more recent fish oil studies, I want to describe some methodological challenges in conducting high-quality nutritional research.

The Challenges of Medical Research

The preponderance of poor-quality research has made nutritional advice the laughingstock of Western medicine. The frequent back-and-forth of conflicting advice makes the average politician appear steadfast:

Eggs are good for you. Eggs are bad for you. Don’t eat butter; eat margarine. Don’t eat margarine — it’s loaded with trans-saturated fat that will kill you. Calcium supplements make your bones strong. Calcium supplements are bad for your heart.

Flawed research methodologies generate conflicting advice.

Most nutritional research relies on epidemiological studies, observing who consumes what and the outcomes. This type of research has advantages: You can study many people, and more people will volunteer to fill out a questionnaire every year than eat prepackaged food for every meal for six weeks.

Epidemiological studies are also easier and less expensive, allowing them to run for many years. The study subjects represent the general population instead of the few people willing to volunteer for an interventional study.

However, dietary epidemiological studies have significant shortcomings. Can you remember everything you ate yesterday? Six weeks ago? Six months ago? Self-reported dietary questionnaires are a notorious source of error.

Also, individuals who may have suffered a bad outcome, such as cancer, can remember in much greater detail what they may have eaten in the past, introducing another form of bias.

However, the largest source of error stems from the principle that association does not equal causation. A study might find that ice cream consumption is associated with a higher risk of drowning, but this doesn’t mean ice cream consumption causes drowning. Rather, both are more likely to occur during hot weather.

There can be confounders: variables associated with both the possible risk factor and the clinical outcome being studied.

Epidemiological literature is replete with examples of supplements such as vitamin E and folate that purportedly reduce the risk of heart disease and antioxidant supplements that reduce the risk of cancer. They frequently overlook the potential “healthy lifestyle” confounder.

An individual who chooses to take a vitamin E or antioxidant supplement is often very different from someone who doesn’t take either supplement. The decision to take any supplement can be a marker for a whole host of other choices associated with better health outcomes — more sleep, less alcohol intake, more exercise, and an overall interest in maximizing one’s health.

Thus, the supplement didn’t cause a better health outcome per se. Rather, taking the supplement was a marker for variables associated with a better health outcome.

To create better nutritional studies, researchers have turned to the gold standard for interventional trials: the placebo-controlled, double-blind, randomized controlled trial.

What Is a Randomized Controlled Trial?

In a randomized controlled trial, half the participants are randomly assigned to receive the intervention and the other half to receive a placebo. Neither the study subject nor the researchers are aware of the treatment allocations.

The confounder problem is eliminated because, with a large enough study population, the randomization process should create two equivalent groups. Any confounders would be evenly distributed between the two groups and not contribute to a net difference in effect. This methodology forms the foundation of our assessment of drug therapies.

However, there is one tremendous difference between a randomized controlled drug trial and a nutritional supplement: Before starting a drug trial for a cholesterol-lowering medication such as rosuvastatin, none of the study participants would have rosuvastatin in their bodies.

That is not the case in many nutritional intervention studies, where study subjects have a range of baseline values. (Please see the appendix below for a more detailed discussion.)

For example, a study of vitamin D supplementation, a hormone the body makes in response to sunshine, may have a very different result when conducted in Norway, near the Arctic Circle, than in Costa Rica, near the equator. One could argue that the variability in baseline values shouldn’t be a factor because they’re the same in the intervention and control groups. However, this phenomenon can still critically weaken the studies and, I believe, heavily contribute to the uncertainty in interpreting fish oil supplementation studies.

In statistics, “power” refers to the likelihood of detecting a difference between study groups, should one exist. In practical terms, when designing a study, the smaller the effect size you hope to detect, the more study subjects you need to demonstrate a statistically significant result. The opposite is true for larger effect sizes.

Intuitively, this makes sense. If a hypothetical antibiotic cured 90% of everyone who received it compared to only 20% of those receiving a placebo, not as many study subjects would be needed.

However, a blood pressure medication that only reduced systolic blood pressure by a few points would require many study subjects to demonstrate a difference with statistical significance.

Whenever a study concludes that there was no treatment effect, was there actually no treatment effect, or was the study “underpowered” (that is, there weren’t enough study subjects for the magnitude of clinical benefit to demonstrate statistical significance)?

Let’s return to a hypothetical cohort of individuals enrolled in a nutritional supplement study, such as for fish oil. The study subjects are divided into three subsets based on their starting baseline level of n-3 fatty acids, the active ingredient in fish oil:

1. Those with a deficiency of n-3 fatty acids are expected to have the greatest benefit from supplementation.
2. Those with a normal level of n-3 fatty acids may receive little or no benefit from supplementation.
3. Those with an excess of n-3 fatty acids may suffer side effects from further supplementation.

Ideally, you would measure each participant’s baseline level, categorize them into a subset, and study each group’s physiological responses separately.

Fish oil studies haven’t followed such protocols, but some offer interesting clues.

The VITAL Study

The VITAL study, published in the prestigious New England Journal of Medicine in 2019, became the definitive study for evaluating fish oil supplementation’s effect on cardiovascular disease and mortality.

With careful methodology and over 25,000 study participants, the study concluded that “omega-3 fatty acid supplementation did not reduce major cardiovascular events,” which became the prevailing wisdom.

Based on that study, I stopped taking fish oil supplements. However, that much-publicized conclusion masked a very different story.

First, the study demonstrated no significant difference in treatment groups for major cardiovascular events (the cumulative total of myocardial infarction, stroke, or death from cardiovascular causes). Yet, some outcomes showed benefits of fish oil supplementation: a 28% reduction in myocardial infarction (MI) and a 50% reduction in death from an MI.

The analysis I was most interested in was hidden in the supplemental material (available separately online but not included in the published document): The study participants weren’t stratified according to their n-3 fatty acid baseline levels.

However, they were analyzed according to whether they consumed more or less than an average of 1.5 fish meals per week, which would be expected to correlate with baseline levels. Out of 25,435 study participants, 13,514 reported eating less than an average of 1.5 fish meals per week.

The less frequent fish eaters showed a statistically significant 19% reduction in major cardiovascular events — the opposite conclusion of analyzing the entire cohort. By analyzing the subgroup of the population with a probable deficiency, the study demonstrated a statistically significant improvement with supplementation. This proves my point that the key to conducting a meaningful supplement study is to analyze those who actually have a deficiency.

When assessing whether to implement findings from a research study, “generalizability” becomes important — that is, are the participants and treatments evaluated in a particular study comparable to the patient sitting in front of you in the clinic? For example, a treatment that works great for young military recruits may not be the best choice for a frail 90-pound woman.

The VITAL study results are generalizable: if you have a suspected or documented low level of n-3 fatty acid, fish oil supplements are proven to reduce your risk of major cardiac events. Unfortunately, the press popularized the opposite conclusion.

Since the VITAL study’s publication, several large meta-analyses of fish oil supplementation for cardiac health have been published that support fish oil’s benefits. (A meta-analysis combines the data from multiple studies to create a much larger cohort to analyze.) This increases the study’s power and the ability to find statistically significant treatment effects.

Again, this supports my contention that early fish oil studies were effectively “too small” because only a subset of the participants were deficient in n-3 fatty acids and could be expected to benefit from supplementation.

My primary care doctor felt my n-3 fatty acid levels were borderline. In the context of my elevated blood pressure and borderline cholesterol levels, she believes fish oil supplementation will safely and effectively reduce my risk for adverse cardiac outcomes (in addition to other prescribed medications).

Fish oil supplements are very safe. Side effects are usually limited to gastrointestinal events such as indigestion and “fishy-tasting” belches. Fish oil has a very mild anticoagulant effect, which is one of the mechanisms for its beneficial effects. However, if you’re already on a prescribed blood thinner such as Plavix, Eliquis, or Xarelto, please ask your doctor about the risks and benefits of adding fish oil.

Some fish oil preparations contain mercury, a toxic metal. Unfortunately, our oceans are so polluted with mercury that it’s become part of the marine food chain.

Even the smallest creatures, such as plankton, can accumulate mercury. The fish that eat the plankton concentrate the mercury, and the bigger fish that eat the smaller fish continue to concentrate the mercury. Thus, larger fish, such as tuna and swordfish, have higher mercury levels than smaller fish, such as anchovies and sardines.

Higher-quality fish oil manufacturers use exclusively smaller fish and don’t have problems with mercury contamination.

I’ve begun taking fish oil from Nordic Naturals. They use only small fish and manufacture high-quality products, and their capsules don’t need to be refrigerated until after opening the bottle.

Fish oil can degrade if stored too long in a warehouse or exposed to extreme heat during shipping. I recommend ordering directly from Nordic Naturals — they’re careful about how they store and ship their products.

At Banner Peak Health, we strive to be at the forefront of healthcare, particularly prevention. We’re always looking for aspects of cardiovascular risk to identify and mitigate. Low levels of n-3 fatty acids are an important risk factor that can be safely treated with fish oil supplementation.

Appendix:

Many randomized controlled trials of dietary supplements suffer from the design flaw of aggregating all study participants regardless of their baseline levels.

This population can more accurately be considered as composed of three sub-groups: those with deficient, normal, or excess levels before any supplementation.

Those who are deficient at baseline are the ones who can benefit from supplementation.

Those with normal baseline levels would NOT be expected to benefit from supplementation.

Those with excess levels at baseline are at risk of a worse outcome with additional supplementation.

Therefore, an analysis of the entire cohort may not have the statistical power to detect a treatment benefit because the number of participants with the possibility of improvement may be too small to reach statistical significance.

---

by Barry Rotman, MD

Exercise — The Real Fountain of Youth

In my last blog post, I introduced the Metric-Driven Empowerment Cycle (MDEC, pronounced “em-deck”), in which new health-monitoring technologies provide actionable data that informs behavior modification, which improves the patient’s health. MDEC-based healthcare focuses on preventing illness rather than simply treating it.

Most of the time, that data-informed behavior modification includes some form of exercise.

Exercise’s Impact on Heart Disease

Physicians have been prescribing exercise as medicine since Hippocrates’ day, but exercise benefits weren’t researched until 1953, when British epidemiologist Dr. Jeremy Morris studied transit workers on double-decker buses.

Dr. Morris compared the rate of coronary heart disease (CHD) among bus drivers, who sat for 90% of their shift, with conductors, who climbed over 600 steps a day. The sedentary drivers’ CHD rate was 42% higher than the conductors’.

Dr. Morris confirmed these findings in another study. He compared the rate of CHD among postal workers with desk jobs against that of workers who walked to deliver the mail. The former group had a 33% higher CHD rate.

Dr. Jeremy Morris died in 2009 at age 99. He swam, jogged, and cycled well into his old age.

We now have many decades of literature documenting the staggering health benefits of exercise. It reduces the risk of dementia, mitigates the effects of menopausal hot flashes, minimizes depression, prevents diabetes... I could go on.

Despite the billions of dollars spent on anti-aging drug research, exercise remains the best route we have to the mythical “Fountain of Youth.”

How Exercise Has Helped Me

I’m an avid cyclist. I’ve pedaled thousands of miles in my life, and I’m convinced that my many decades of commitment to fitness have reduced the impact of my genetic predisposition to cardiometabolic disease.

Obesity and diabetes run down both sides of my family tree. Both my parents were physically active, not overweight, and didn’t have diabetes or coronary heart disease. However, all their siblings were overweight and had manifestations of cardiometabolic disease such as high blood pressure, diabetes, and coronary heart disease.

In attempting to practice what I preach, I devote considerable effort to cardiovascular and strength training, working to maintain a normal weight with healthy levels of muscle and fat mass. Nonetheless, my parameters, such as blood pressure, cholesterol levels, and glucose levels, are still borderline — not the levels one would expect given my level of fitness and body composition.

I’m working hard against my genes. For both personal and professional reasons, I’m passionate about exercise’s role in maximizing health and longevity.

I look forward to helping all my patients set personal records and achieve athletic goals. Of course, the greatest gains will accrue to those who are currently the least fit.

The Exercise Dose-Response Curve

The human body is a machine that has evolved for movement. An inactive machine will rapidly break down, i.e., our bodies will devolve into a diseased state if we don’t keep moving.

None of our vital structures will operate appropriately. The heart won’t pump as efficiently. The joints will become stiff and more susceptible to injury. The body can go into caloric excess with surplus energy stored as fat, which gets distributed into abnormal locations such as the liver and muscle cells, creating inflammation and insulin resistance. And so on.

Fortunately, just as physical inactivity can trigger a negative cascade of events, physical activity can reverse the process.

There is an exercise dose-response curve that describes how health benefits change with increasing quantities of both cardiovascular and strength training exercise:

• The first section of the curve has a steep upward slope, reflecting a region that is the “best deal,” or the most improvement in health for even a minimal increase in exercise.
• The next region has a wide range of quantities of exercise in which “more is better” in terms of benefit.
• A small section of the maximum amount of exercise reflects a region in which “more is worse.”

Exercise is the most valuable for the least fit. For these people, exercise corrects a diseased, malfunctioning body. Those with higher levels of fitness can still improve their health but don’t have the same magnitude of dysfunction that needs to be addressed.

Once you advance beyond the steep upslope that rescues the physically inactive, the curve climbs appreciably before flattening. In this region of the curve, incrementally more fitness brings additional health benefits.

Large epidemiological studies illustrate this association by examining the link between longevity and VO2 max, the maximum volume of oxygen your body can use during peak exertion. VO2 max represents the fitness of your entire cardiopulmonary system, which is improved through exercise.

These studies demonstrate a consistent, stepwise improvement in longevity, beginning with the lowest rung of fitness and continuing to the top tier. In fact, the magnitude of benefit from moving from least fit to moderately fit (not even the top tier!) exceeds the reduction in mortality risk of quitting cigarettes or overcoming diabetes. Strength training and muscle mass maintenance also benefit the preservation of function and longevity.

Eventually, the graph slopes downward, which applies to extreme athletes (who compete and train for intense long-distance events, such as running an ultramarathon). They can train so hard that they overwhelm the stress/recovery cycle, creating a chronic inflammatory state with deleterious health effects.

This group comprises a minute fraction of the population but illustrates the concept that “too much of a good thing may no longer be a good thing.”

Final Thoughts

My goal is to see everyone reap the benefits of increased exercise. I also want to keep an eye out for those who may be overtraining.

Of course, the devil is in the details. Creating appropriate training regimens and motivating everyone will be an exciting professional challenge. Exercise will become the foundation of Medicine 3.0 at Banner Peak Health!

---

by Barry Rotman, MD