Pip: Welcome to The Rolex Life — where the wristwatch is a metaphor and the CGM is very, very literal.
Mara: cnsnnts has been running a serious personal experiment this past month — glucose tracking, food strategy, training, and the mental architecture underneath all of it. That's the territory we're covering today.
Pip: Let's start with the glucose data, because the numbers are genuinely interesting.
CGM And Glucose Control
Mara: The core question here is whether a continuous glucose monitor can tell a non-diabetic person something meaningful about their metabolic health — not just flag disease, but reveal where on the spectrum they actually sit.
Pip: A study out of Yale frames this precisely. The setup: people with obesity, some with type 2 diabetes, some without, all wearing CGMs and running glucose tolerance tests. The finding on the anchor metric is stark — "CGM mean inversely correlated with insulin resistance indices when analyzing all participants together, GIR: r = -0.82, P less than 0.001."
Mara: That correlation coefficient is strong. What it means in practice is that a higher average glucose on your CGM tracks closely with lower insulin sensitivity — even before you have a diabetes diagnosis.
Pip: And the post draws out the practical implication: a CGM mean around 90 mg/dL is more consistent with better insulin sensitivity, while 105 to 110 may indicate greater compensatory insulin secretion. No diagnostic cutoffs, but a real signal.
Mara: The Attia Glucose post puts targets around that: fasting in the 80s, 24-hour average below 100, standard deviation below 15, and excursions above 140 kept rare or eliminated entirely. Peter Attia's own numbers — average around 90, standard deviation around 10 — are cited as a benchmark.
Pip: Holy Spikes CGM is where the rubber meets the road. An acai bowl sent the CGM beeping. Beer on an empty stomach spiked it above target. Cauliflower and potatoes at lunch: spike over 140. Gelato from Venchi: below 120. The data is genuinely surprising.
Mara: CGM is FASCINATING captures exactly that — real meals producing unexpected results, which is the whole point of wearing the device. And CGM as a feedback mechanism distills the response to one line: keep it under 110.
Pip: Some notes from the doctor adds clinical texture — elevated overnight glucose as a possible sign of sleep apnea, A1C a little high, CRP and insulin both elevated. The doctor's note that insulin raises blood pressure connects the CGM data to a broader picture.
Mara: The Update: Game of Hormones and Enzymes post is worth flagging here — it corrects earlier thinking on fat metabolism, clarifying that "calories determine the long-term scoreboard, hormones determine how the game is played." Insulin's role in suppressing fat mobilization is real, but it doesn't override energy balance.
Pip: And the first CGM post is where it all began — just getting used to the device, noting the numbers look better than five years ago, and committing to optimization. From there to a correlation coefficient of negative 0.82 is quite a month.
Mara: Which brings us to what you actually eat — and how you track it.
Weight Loss And Food Tracking
Mara: The practical challenge this segment addresses is how to actually manage food intake in real life — not in theory, but when you're busy, when the interface is annoying, and when one bad day feels like it undoes everything.
Pip: The post on measuring food opens the whole question with admirable honesty: "Need to figure out how to log food. MFP again? I hate that interface." Which is a more common starting point than most diet content admits.
Mara: That friction is real, and it matters — because the system only works if you actually use it. The glycemic understanding post and the Keto Carbs post are both attempts to build a framework that reduces the cognitive load of food decisions.
Pip: The Keto Carbs table is genuinely useful — non-starchy vegetables and berries at the top, naan and baguette at the bottom, with glycemic index and reasoning for each. Chickpea pasta cooled and reheated scores around 33 on the GI scale, which is lower than most people would guess.
Mara: Glycemic understanding goes deeper into the same territory — red lentil pasta in the low 30s, white durum pasta al dente surprisingly around 27 to 45, gluten-free rice and corn pasta up at 76. The takeaway is that gluten-free does not mean glucose-friendly.
Pip: Some weight numbers sets the map: 265 is low obesity, 240 is overweight, 220 is nice, 200 is optimal. Concrete, personal, no ambiguity about what the destination looks like.
Mara: Loosing weight in a busy city is the commitment stated plainly — one sentence, essentially: I will do this.
Pip: And Don't total your car because you scratch it is the psychological counterweight to all of it. The argument, drawn from a Reddit thread, is that a single bad day of overeating does not erase progress — "if you have a bad day and overeat, let's say an excess of 1200 cal or 2000, it doesn't matter. Forgive yourself. Continue on the same diet that you've been on and move on."
Mara: The bodybuilder analogy makes it concrete: one day of 10,000 calories doesn't stop someone from being a bodybuilder. Months of it does. The damage is in the pattern, not the incident.
Pip: That framing matters because perfectionism is often what breaks consistency — and consistency is what the training section is entirely about.
Training, Health, And Recovery
Pip: The training posts aren't about programming or periodization — they're about showing up when it counts and recognizing that the ability to do so isn't guaranteed.
Mara: The anchor post puts it directly: "It is a privilege to be able to run. To be able to build my body. I have feet, arms, legs. I am healthy enough to do it. I will lift weights until I cannot. I will do cardio until I cannot."
Pip: That's a different frame than optimization. It's closer to gratitude as a training philosophy.
Mara: Strength was not scary documents the first return to a real gym after a long gap — full squats, overhead press, light weight, but done. Iron supplementation seems to be working adds a clinical note: iron numbers improving marginally, the doctor watching it, a possible explanation for recent stamina issues.
Pip: Foundations are daily is the operating system underneath all of it — sleep, food, gym, cardio, and settling the mind, all listed as non-negotiable dailies rather than aspirational goals.
Mara: Visualizing Strength is the most forward-looking post — a projection to December 30th, 2026, after four months of consistent lifting. Back over two plates on squat, deadlift feeling strong, a marathon on the horizon. "Calmness in the gym, strength, good blood work" as the measure of a year well spent.
Pip: The physical work and the mental work turn out to be the same project — which is exactly what the next segment is about.
Mindset And Personal Discipline
Mara: The question running through these posts is how someone with an intense, ambitious life actually builds and sustains the internal structure to follow through — not just on good days, but as a baseline.
Pip: Proof of devotion reframes the whole thing: "Addiction is proof that you are capable of intense devotion. You just serve a false God." The argument is that an addictive personality isn't a liability — it's a redirectable asset.
Mara: Stanford Stagnation is a practical tool for getting unstuck: what am I avoiding, where do I start, how do I win today, what habits are working against me. Four questions, no filler.
Pip: How to empty the mind goes into the neuroscience of mental silence — Ajahn Brahm's technique of attending to the gaps between words, which quiets the internal narrator as a side effect rather than a goal. The point being that trying to stop thinking activates the very machinery you're trying to silence.
Mara: Foundations, Maintenance and Growth introduces a personal framework for managing a high-stakes finance career alongside a writing ambition — the stated principle being "nothing important should die unintentionally."
Pip: And Foundational thinking — Confidence in yourself is where the whole architecture lands: the run and the strength session need to become as automatic as brushing your teeth. Not motivation. Habit.
Mara: What connects all of it is the same underlying logic — measure accurately, respond to the data, and build systems that don't depend on willpower alone.
Pip: The CGM is just the most literal version of that. Everything else — the food tables, the training log, the mindset frameworks — is the same feedback loop running in parallel.
Oxidative stress occurs when the body produces more reactive molecules (free radicals and other oxidants) than it can effectively manage. Excessive oxidative stress can damage cells, impair blood vessels, contribute to insulin resistance, and accelerate certain age-related processes.
But some oxidative activity is essential. The goal is balance, not elimination.
1. What Causes Oxidative Stress?
Your body naturally produces reactive oxygen species (ROS), especially during energy production and immune activity.
Increases oxidative stress
Helps reduce or regulate it
Chronic high blood sugar
Better glucose control
Visceral fat and insulin resistance
Fat loss and improved metabolic health
Smoking and air pollution
Avoiding smoke and pollutants
Chronic inflammation
Addressing underlying inflammation
Poor sleep and sleep apnea
Adequate sleep and apnea treatment
Heavy alcohol consumption
Limiting alcohol
Excessive exercise without recovery
Regular exercise with recovery
Poor nutrient intake
Vegetables, fruit, nuts, and other nutrient-rich foods
2. What Does Oxidative Stress Do?
Body system
Potential impact
Heart and blood vessels
Reduces nitric oxide availability, impairing vessel relaxation and contributing to hypertension
Metabolism
Can worsen insulin resistance and glucose regulation
Mitochondria
Can damage cellular components involved in energy production
Brain
Associated with neurodegenerative diseases
DNA and cells
Damages proteins, lipids, and DNA
Aging
Contributes to some processes associated with cellular aging
Inflammation
Can amplify inflammatory responses, creating a feedback loop
These relationships are complex. Oxidative stress may be both a cause and a consequence of disease.
3. The Nitric Oxide Connection
Nitric oxide (NO) is a beneficial molecule that helps blood vessels relax.
But a reactive molecule called superoxide can destroy it:
Nitric oxide + Superoxide → Peroxynitrite
This means:
Less nitric oxide is available.
Blood vessels may become less able to relax.
Blood pressure and cardiovascular risk may increase.
Antioxidant defenses help preserve normal nitric oxide signaling.
The temporary stress signals your cells to strengthen mitochondria, improve antioxidant defenses, and adapt to physical demands.
Short-term, controlled oxidative stress can be beneficial. Chronic, excessive oxidative stress can be harmful.
This adaptive response is an example of hormesis.
5. What About Antioxidant Supplements?
Antioxidants help control oxidative reactions, but taking more is not necessarily better.
CoQ10: Supports mitochondrial electron transport and antioxidant defenses.
Vitamin C: A water-soluble antioxidant.
Vitamin E: Protects cellular lipids against oxidation.
Glutathione: A major intracellular antioxidant involved in maintaining redox balance.
The body also produces its own powerful antioxidant enzymes.
High-dose supplements have generally not demonstrated consistent improvements in longevity or cardiovascular outcomes. Some can interfere with beneficial exercise adaptations.
6. How Do You Minimize Harmful Oxidative Stress?
The most practical interventions are:
Exercise regularly, with adequate recovery.
Maintain healthy blood glucose and insulin sensitivity.
Reduce excess visceral fat.
Get sufficient sleep and address sleep apnea.
Eat a nutrient-rich diet with vegetables, fruit, and other whole foods.
Avoid smoking and excessive alcohol.
Manage blood pressure and chronic medical conditions.
Bottom Line
Oxidative stress is not inherently bad. It is part of normal metabolism, immunity, and cellular adaptation.
The real problem is chronic oxidative imbalance that overwhelms the body’s defenses.
Rather than trying to eliminate free radicals with supplements, the best-supported approach is to improve metabolic health, exercise consistently, sleep adequately, and maintain the body’s natural antioxidant systems.
How Coenzyme Q10 powers mitochondria, protects cells from oxidative stress, preserves nitric oxide, and may influence cardiovascular and metabolic health.
TL;DR
Coenzyme Q10 (CoQ10) is an essential molecule that helps cells produce energy and defend themselves against oxidative damage. It is particularly important in energy-intensive organs such as the heart, brain, kidneys, and muscles.
CoQ10 has two primary biological functions:
Energy production: CoQ10 transports electrons within mitochondria, enabling the production of ATP, the body’s principal cellular energy currency.
Antioxidant protection: CoQ10 helps protect cellular membranes against oxidative damage and may preserve nitric oxide (NO), a molecule essential for healthy blood-vessel relaxation and circulation.
This second function is particularly interesting. Excessive oxidative stress can destroy nitric oxide, contributing to endothelial dysfunction, elevated blood pressure, and cardiovascular disease. CoQ10 may help preserve nitric oxide availability by supporting antioxidant defenses.
Research suggests potential benefits for certain patients with heart failure and possibly migraine prevention. Evidence for lowering blood pressure, improving athletic performance, treating statin-related muscle symptoms, and improving metabolic health is less consistent.
The important distinction: CoQ10 is essential for human biology, but taking more CoQ10 does not necessarily improve health. Its benefits depend on whether supplementation actually addresses a limiting factor in the body.
1. What Exactly Is CoQ10?
Coenzyme Q10, also called ubiquinone, is a fat-soluble molecule present in nearly every human cell.
The name ubiquinone comes from its ubiquitous presence throughout the body. The Q10 refers to a chemical structure containing ten isoprenoid units.
Unlike vitamins, which generally must be obtained from the diet, the human body can manufacture CoQ10. We also obtain small quantities from foods, particularly meat, fish, and certain nuts.
CoQ10 exists primarily in two interconvertible forms:
Ubiquinone: The oxidized form, which can accept electrons.
Ubiquinol: The reduced form, which can donate electrons and function as an antioxidant.
The molecule continuously cycles between oxidation states as it performs its functions.
This dual identity—as both an electron carrier and an antioxidant—is what makes CoQ10 biologically interesting.
2. CoQ10’s First Major Function: Producing Cellular Energy
Every cell needs energy to function.
The heart needs energy to contract. Muscles need energy to move. Neurons need energy to transmit signals. Even cells at rest require energy to maintain their internal environment.
Most sustained cellular ATP production occurs in mitochondria through a process called oxidative phosphorylation.
How mitochondria generate ATP
When the body metabolizes carbohydrates and fats, it produces electron-carrying molecules, primarily NADH and FADH₂.
These supply electrons to the mitochondrial electron transport chain, a series of protein complexes embedded in the inner mitochondrial membrane.
CoQ10 plays a central role in this process:
Electrons enter the transport chain through Complex I or Complex II.
CoQ10 accepts these electrons and carries them through the membrane to Complex III.
Subsequent reactions move electrons toward oxygen, while several complexes pump protons across the mitochondrial membrane.
The resulting electrochemical gradient drives ATP synthase, which produces ATP.
CoQ10 is effectively a mobile electron shuttle connecting important components of the mitochondrial energy-production system.
Without sufficient functional CoQ10, electron transport and ATP production can become impaired.
Does taking CoQ10 increase energy?
Not necessarily.
This is one of the biggest misconceptions surrounding CoQ10 supplementation.
The fact that a molecule is essential for energy production does not mean increasing its concentration will increase energy output.
Consider an engine that requires oil. Having too little oil causes serious problems, but adding more oil than the engine requires does not make it more powerful.
Similarly, CoQ10 supplementation may be useful when availability is inadequate or a disease process makes the system dysfunctional.
In otherwise healthy individuals with adequate CoQ10, additional supplementation has not consistently demonstrated improved energy, endurance, or athletic performance.
Furthermore, raising CoQ10 concentrations in the bloodstream does not guarantee that additional CoQ10 reaches the relevant mitochondrial membranes.
3. CoQ10’s Second Major Function: Antioxidant Protection
The body’s energy-producing machinery has an unavoidable byproduct: reactive oxygen species (ROS).
These include superoxide and hydrogen peroxide.
Reactive oxygen species are not inherently harmful. At controlled concentrations, they perform important signaling functions.
Problems emerge when the production of reactive species exceeds the body’s capacity to regulate them—a condition called oxidative stress.
Excessive oxidative stress can damage:
Cell membranes and their constituent lipids
Proteins and enzymes
Mitochondrial structures
DNA and other cellular components
CoQ10 contributes to the body’s defense against this damage.
The role of ubiquinol
Ubiquinol, the reduced form of CoQ10, can donate electrons to certain reactive molecules and help interrupt lipid oxidation reactions.
It also participates in antioxidant networks, including the regeneration of vitamin E.
Because CoQ10 is fat-soluble, it is particularly suited to protecting lipid-rich structures such as cellular membranes.
This antioxidant function is separate from, but closely connected to, its role in mitochondrial energy metabolism.
Healthy mitochondria require efficient electron transport and carefully regulated oxidative signaling.
CoQ10 participates in both.
4. The Connection Between CoQ10 and Nitric Oxide
One of the most interesting proposed cardiovascular benefits of CoQ10 involves a small signaling molecule called nitric oxide (NO).
Nitric oxide is essential for normal blood-vessel function.
The endothelial cells lining blood vessels generate nitric oxide using an enzyme called endothelial nitric oxide synthase (eNOS).
Nitric oxide then travels into the surrounding vascular smooth muscle, activating an enzyme called soluble guanylate cyclase.
This increases cyclic GMP (cGMP), triggering a series of molecular events that allow smooth muscle to relax.
The result is vasodilation: blood vessels widen, blood flows more easily, and vascular resistance falls.
Nitric oxide also helps regulate platelet activity, inflammation, and vascular health.
The problem: Oxidative stress consumes nitric oxide
Superoxide, one type of reactive oxygen species, reacts very rapidly with nitric oxide:
NO + O₂⁻ → ONOO⁻
In this reaction:
NO is nitric oxide.
O₂⁻ is superoxide.
ONOO⁻ is peroxynitrite.
The reaction has two important consequences.
First, it consumes nitric oxide, reducing the amount available to signal blood vessels to relax.
Second, it produces peroxynitrite, a reactive molecule capable of damaging cellular components and disrupting normal vascular signaling.
When these processes become excessive, blood vessels can lose some of their normal ability to relax.
This is a feature of endothelial dysfunction, which is associated with hypertension, diabetes, atherosclerosis, and other cardiovascular disorders.
How CoQ10 may help
CoQ10 may help preserve nitric oxide signaling by reducing oxidative stress and supporting the cellular systems that regulate reactive oxygen species.
The proposed mechanism is:
CoQ10 → Improved antioxidant defenses → Reduced oxidative consumption of NO → Greater NO bioavailability → Better vascular relaxation
This is not the same as CoQ10 directly producing nitric oxide.
Instead, CoQ10 may help protect nitric oxide that the body already makes.
This distinction matters because cardiovascular health depends on both producing adequate nitric oxide and preserving its biological activity.
Some randomized controlled trials have reported improvements in endothelial function with CoQ10 supplementation, often assessed through flow-mediated dilation.
However, these findings have not consistently translated into substantial improvements in blood pressure or demonstrated reductions in cardiovascular events among otherwise healthy adults.
The mechanism is plausible and supported by some experimental evidence, but its clinical importance remains uncertain.
5. What Benefits Does CoQ10 Actually Have?
The biological mechanisms of CoQ10 are well established. Its clinical benefits, however, vary considerably depending on the condition being studied.
Heart failure
Heart muscle consumes enormous amounts of ATP because it contracts continuously throughout life.
People with heart failure may have altered mitochondrial function, increased oxidative stress, and reduced CoQ10 availability.
Researchers have therefore investigated CoQ10 as an additional treatment alongside standard heart-failure medications.
A Cochrane review of 11 randomized trials involving 1,573 participants found evidence suggesting reductions in mortality and heart-failure hospitalizations. However, the studies had important limitations, and the authors emphasized the need for further research.
CoQ10 is not a replacement for established heart-failure therapies. <Cite ref=”turn351140search1″/>
Endothelial function and blood pressure
CoQ10’s effects on oxidative stress and nitric oxide signaling provide a plausible mechanism for improving vascular function.
A 2024 systematic review of 12 randomized trials involving 489 participants found improvements in flow-mediated dilation, particularly after eight or more weeks of supplementation.
However, improved endothelial function does not necessarily translate into meaningful blood-pressure reductions.
Research on CoQ10 for hypertension remains inconsistent. <Cite refs={[“turn351140search0″,”turn351140search2”]}/>
Statin-associated muscle symptoms
Statins lower cholesterol by inhibiting an enzyme involved in the mevalonate pathway.
This same biochemical pathway contributes to CoQ10 synthesis, meaning statins can reduce circulating CoQ10 concentrations.
This observation led to the hypothesis that reduced CoQ10 contributes to muscle pain sometimes associated with statin therapy.
Although some small trials have reported improvements, the overall evidence remains mixed. CoQ10 has not consistently demonstrated a clinically meaningful benefit for statin-associated muscle symptoms. <Cite ref=”turn351140search2″/>
Exercise performance and recovery
Because CoQ10 is involved in mitochondrial energy production, researchers have studied whether supplementation improves endurance, physical performance, or recovery.
Some studies report improvements in particular measures of fatigue or oxidative stress.
However, results are inconsistent, and there is insufficient evidence that CoQ10 reliably improves athletic performance in healthy individuals.
Migraine prevention
CoQ10 has also been investigated for migraine prevention, partly because mitochondrial energy metabolism may contribute to migraine biology.
Some small randomized trials suggest that supplementation can reduce migraine frequency.
The evidence is promising but limited, and CoQ10 is generally considered a possible adjunct rather than a first-line preventive treatment.
Metabolic health and insulin sensitivity
Mitochondrial dysfunction and oxidative stress are associated with insulin resistance and metabolic disease.
This has prompted investigations into whether CoQ10 supplementation improves glucose regulation, insulin sensitivity, or inflammatory biomarkers.
Some small clinical trials and meta-analyses report modest improvements in particular metabolic markers, but findings vary across populations and study designs.
There is currently insufficient evidence to recommend CoQ10 as a primary treatment for insulin resistance, prediabetes, or diabetes.
Longevity and aging
CoQ10 levels in some tissues tend to decline with age, although this is not uniform across all organs.
Because mitochondrial dysfunction and oxidative stress are associated with aging, CoQ10 is sometimes marketed as an anti-aging supplement.
The biological rationale is interesting, but there is no convincing human evidence that CoQ10 supplementation extends lifespan or meaningfully slows biological aging.
An important scientific principle emerges: improving a biomarker or supporting a plausible mechanism is not equivalent to demonstrating a longer or healthier life.
6. Ubiquinone vs. Ubiquinol: Which Form Is Better?
CoQ10 supplements generally contain one of two forms.
Ubiquinone
Ubiquinol
Chemical state
Oxidized
Reduced
Primary characteristic
Accepts electrons
Donates electrons
Antioxidant activity
Requires reduction to ubiquinol
Directly functions as an antioxidant
Supplement cost
Generally lower
Generally higher
Absorption
Depends on formulation
Sometimes higher
Proven clinical superiority
Not established
Not established
Both forms participate in the same biochemical cycle and can be converted into one another by the body.
Although ubiquinol may provide higher blood concentrations in certain comparisons, differences in formulation and absorption complicate the evidence.
Higher blood levels also do not necessarily translate into better clinical outcomes.
7. Supplementation: Dosage, Absorption, and Safety
Common supplemental doses range from 100 to 200 mg per day, although clinical studies have used doses outside this range.
Because CoQ10 is fat-soluble, absorption is generally improved when taken with a meal containing fat.
CoQ10 is generally well tolerated. Reported side effects include digestive discomfort, nausea, and occasional sleep disturbances.
Important interactions include warfarin, whose anticoagulant effect CoQ10 may reduce, and medications used to lower blood glucose. CoQ10 may also be unsuitable alongside certain cancer treatments without medical supervision. <Cite ref=”turn351140search2″/>
Importantly, there is no established universal target blood level of CoQ10 for healthy adults, and routine testing is not generally recommended.
Supplementation should be considered in the context of a specific clinical objective rather than simply because CoQ10 participates in important biological pathways.
8. The Bigger Picture: Mitochondria, Oxidative Stress, and Vascular Health
CoQ10 sits at the intersection of three important physiological systems:
Energy metabolism: Mitochondria use CoQ10 to transfer electrons and generate ATP.
Oxidative regulation: CoQ10 participates in antioxidant defenses, helping protect membranes and cellular structures.
Cardiovascular signaling: By influencing oxidative stress, CoQ10 may help preserve the biological availability of nitric oxide, supporting normal blood-vessel function.
These systems are interconnected.
For example, metabolic dysfunction can contribute to excessive oxidative stress. Oxidative stress can impair endothelial nitric oxide signaling. Reduced nitric oxide availability can interfere with normal vascular relaxation.
At the same time, chronic cardiovascular and metabolic diseases may involve changes in mitochondrial function.
CoQ10 is compelling precisely because it participates in several parts of this network.
However, the body is not a simple system where supplying more of a beneficial molecule necessarily produces better results.
Health depends on maintaining a regulated balance between energy production, cellular signaling, antioxidant defenses, and repair.
Regular exercise, adequate sleep, good nutrition, healthy blood-pressure control, and management of metabolic risk factors influence several of these systems simultaneously.
These interventions have substantially stronger evidence for improving long-term cardiovascular health than CoQ10 supplementation in otherwise healthy adults.
Conclusion
CoQ10 is an essential molecule with two well-established biological functions: supporting mitochondrial energy production and participating in antioxidant protection.
Its proposed ability to preserve nitric oxide signaling provides an additional explanation for why researchers are interested in its cardiovascular effects.
There is encouraging clinical evidence in certain conditions, particularly heart failure, and preliminary evidence for improvements in endothelial function and migraine prevention.
But the distinction between biological importance and supplemental benefit is crucial.
CoQ10 is indispensable to the body’s normal functioning. Whether taking additional CoQ10 improves health depends on the individual, the condition, and the outcome being measured.
For most healthy adults, it remains a scientifically interesting supplement rather than an established necessity.
Educational content only. This article is not medical advice. Readers should consult a qualified healthcare professional before using supplements to manage a medical condition or alongside prescription medication.
Weight loss becomes so much easier when you realize this.
Let’s say a bodybuilder decides to wake up on Thanksgiving and eat in excess of 10,000 calories. I mean, he goes crazy eating when he wakes up tomorrow morning. Will he still be a bodybuilder? Yes, of course he will. He might be a few pounds over what he was, but he will still look like a bodybuilder, and he will still be a bodybuilder if you overeat and binge tomorrow after doing well all week. Will you regain all your weight that you worked so hard to lose? No, you won’t. Now let’s say both of these people do these things for multiple months. The bodybuilder eats an excess of 10,000 cal every day, and you binge every day. That is when the bodybuilder will no longer be a bodybuilder anymore. My point is if you have a bad day and overeat, let’s say an excess of 1200 cal or 2000, it doesn’t matter. Forgive yourself. Continue on the same diet that you’ve been on and move on. Hating yourself won’t do anything.
Peter Attia’s glucose framework is less about whether a number is technically “normal” and more about maintaining low average glucose, small post-meal excursions, and low variability.
His rough targets are: fasting glucose in the 80s, average glucose below 100 mg/dL, standard deviation below ~15 mg/dL, and very few—ideally no—excursions above 140 mg/dL. A single fasting reading matters less than the overall pattern, since sleep, stress, illness, cortisol, and the dawn phenomenon can temporarily raise glucose.
For meals, 140 mg/dL is better viewed as a ceiling than a target. A curve like 88 → 110 → 95 → 88 is preferable to 88 → 155 → 105 → 68, even if both produce a similar daily average. The first shows a modest rise and smooth recovery; the second shows high variability and a possible post-meal crash.
The drop after eating is not inherently bad. Glucose should return toward baseline. The concern is overshooting well below baseline, particularly after a large spike. Large post-meal dips may also correlate with greater hunger and subsequent food intake.
