IGF-1 (Insulin-like Growth Factor 1) is a hormone produced mainly by the liver in response to growth hormone signaling from the pituitary gland. Once released into the bloodstream, it acts on nearly every tissue in the body, driving cell growth, tissue repair, and metabolic regulation. It’s especially important for muscle protein synthesis, bone density, and the general maintenance of lean tissue as we age.

Levels of IGF-1 rise through childhood and adolescence, peak in early adulthood, and then decline steadily from there. That decline is a normal part of aging, but the rate and degree vary a lot from person to person, shaped by nutrition, sleep, exercise, and body composition. Abnormally low levels can point to growth hormone deficiency, malnutrition, or liver dysfunction, since the liver is where most of the production happens. Abnormally high levels can be associated with growth hormone excess or, in some research contexts, have been studied in relation to other long-term health considerations. A single number rarely tells the full story on its own, which is why we treat IGF-1 as one input among many rather than a standalone verdict.

Why it’s especially relevant right now

IGF-1 has become a more interesting marker to watch as GLP adoption has climbed. Rapid weight loss changes the hormonal environment in ways that don’t show up on a scale. Appetite suppression can mean lower overall caloric and protein intake, and lower protein intake is one of the biggest levers affecting both IGF-1 production and muscle retention. That connection matters because muscle isn’t just about strength. Lean mass plays a direct role in metabolic rate, glucose regulation, and how well the body holds onto its progress.

This ties directly into one of the most consistent findings from recent industry research on GLP users: most people losing weight on these medications are losing some amount of muscle along with fat, and most aren’t tracking it. Cardio activity tends to increase, but strength training, the single best lever for preserving lean mass, is often the most neglected part of the routine. IGF-1 sits right at the intersection of that story. It’s a hormonal signal that reflects whether the body is in a state that supports muscle maintenance or one that’s working against it.

What this means in practice

Tracking IGF-1 alongside body composition gives a more complete picture than either one alone. Body composition scanning shows what’s changing (the ratio of fat loss to muscle loss). IGF-1 offers a window into part of why that’s happening on a hormonal level, and whether protein intake and resistance training are keeping pace with the rate of weight loss. Watched over time, a downward trend paired with disproportionate muscle loss is a signal worth acting on, whether that means adjusting protein intake, adding resistance training, or flagging it for a conversation with a prescriber.

That’s the same logic behind pairing IGF-1 with metabolic, thyroid, and nutritional markers in a single panel rather than testing it in isolation. Hormones don’t operate independently, and neither does weight loss. A marker like IGF-1 is far more useful in context than as a standalone data point.

Getting the full picture

We offer IGF-1 as an optional upgrade alongside our core panels, collected through our EasyDraw arm-based draw and processed at a CLIA-certified, CAP-accredited lab, so it’s easy to add to your existing testing routine without a separate blood draw or lab visit.

Want to see where your IGF-1 stands? Add it to your next panel and track it alongside your other biomarkers over time.

References

1. MedlinePlus. “IGF-1 (Insulin-like Growth Factor 1) Test.” National Library of Medicine. https://medlineplus.gov/lab-tests/igf-1-insulin-like-growth-factor-1-test/
2. Kouvari M, et al. “About 31% of weight lost by adults during GLP-1 therapy comes from lean mass.” Healio, reporting on a systematic review and meta-analysis of 9 RCTs. https://www.healio.com/news/endocrinology/20250313/about-31-of-weight-lost-by-adults-during-glp1-therapy-comes-from-lean-mass
3. “Greater lean-body-mass decline with tirzepatide than semaglutide in routine care, revealed by body-composition digital phenotyping.” medRxiv preprint, nference, 2026. https://www.medrxiv.org/content/10.64898/2026.04.11.26350687.full.pdf

Heart rate variability (HRV) is the variation in time between consecutive heartbeats. A heart beating 60 times a minute does not beat exactly once per second: the intervals fluctuate, and that fluctuation is the measurement. HRV is used as a non-invasive index of cardiac autonomic regulation, particularly the parasympathetic (vagal) branch that slows the heart between breaths. The 1996 ESC/NASPE Task Force standards remain the reference document for how HRV is calculated and interpreted.

Higher HRV generally indicates greater vagal activity and a more flexible autonomic response. Lower HRV indicates the opposite: a system biased toward sympathetic activation, which is what you would expect during stress, illness, sleep deprivation, or heavy training load.

Most wearables report HRV as RMSSD – the root mean square of successive differences between beat intervals – expressed in milliseconds. RMSSD is the standard choice for short recordings because it is dominated by parasympathetic activity and is relatively robust in brief windows. Devices typically average it across your sleep period, which is why the metric is often labelled “average HRV.” Some research uses SDNN instead, which captures total variability across a longer recording; the two are not interchangeable.

Why heart rate variability matters

Low HRV is an established risk marker. A meta-analysis and dose–response meta-regression of eight prospective studies covering 21,988 people with no known cardiovascular disease found that those in the lowest HRV category had a 32–45% higher risk of a first cardiovascular event than those in the highest. The same analysis estimated that a 1% higher SDNN corresponded to roughly 1% lower risk of a fatal or non-fatal event.

HRV also responds quickly to short-term physiological stressors, which is what makes it useful day to day. A meta-analysis of randomized trials found that sleep deprivation significantly reduced RMSSD while increasing low-frequency power and the LF/HF ratio: a pattern consistent with vagal withdrawal and sympathetic predominance.

One important nuance: higher is not universally better. Very high RMSSD values can be produced by ectopic beats, arrhythmia, or motion artifact rather than by robust vagal tone, and in older cohorts, both reduced and increased HRV on a short resting ECG have predicted cardiac mortality. An unexpectedly high reading is a reason to check data quality, not to celebrate.

How can I better understand my HRV levels?

There are no universally accepted clinical reference intervals for HRV measured by Fitbit, Oura, WHOOP, Garmin, or any other consumer wearable. The closest defensible reference intervals come from ECG-based RMSSD population studies.

The best available reference is the Lifelines Cohort Study, published in the European Journal of Preventive Cardiology. It derived RMSSD from 10-second resting ECG recordings in 84,772 relatively healthy adults aged 13 to 91. Participants with cardiovascular disease, hypertension, type 2 diabetes, or obesity were excluded, along with anyone taking antidepressants, beta-blockers, or vagally active medications, and recordings with excessive noise or non-sinus beats were discarded.

SiPhox scores HRV in age-based bands. All values are in milliseconds.

The source measurement is a resting ECG in a clinical setting, whereas your reading comes from optical (PPG) sensing during sleep. We recommend comparing HRV to your own baseline and avoiding comparison across devices. For wearable-scale context, a cross-sectional study of 8 million Fitbit users published in The Lancet Digital Health characterized PPG-derived HRV by age, sex, time of day, and activity level, and confirmed a strong circadian rhythm in the measure. It remains the largest description of HRV as consumer devices actually measure it.

What changes HRV?

Age. The dominant factor, and not modifiable.

Sleep. Sleep loss reduces RMSSD, per the randomized-trial meta-analysis cited above. Because most devices measure HRV during sleep, poor or short sleep affects both the physiology and the measurement window.

Alcohol. The 5-million-person-day wearable analysis found dose-dependent reductions in nocturnal HRV alongside increases in resting heart rate. Drinking earlier in the evening attenuated the effect.

Training load. HRV is widely used to monitor adaptation, but it is not a simple “higher means fitter” readout. A review in Sports Medicine documented that both decreases and increases in vagal HRV indices have accompanied negative adaptation in elite endurance athletes, and that gains in fitness have sometimes coincided with falling HRV.

Slow breathing. A systematic review and meta-analysis of 223 studies found that voluntary slow breathing increased vagally mediated HRV during the session, immediately after a single session, and after multi-session interventions. It is a low-cost, low-risk practice with consistent short-term effects on the measure.

Illness and recovery. Suppressed HRV accompanies acute infection and can persist afterward. A retrospective study of more than 12,000 individuals found that persistent physiological changes after COVID-19 most commonly presented as elevated nightly heart rate together with reductions in some HRV metrics.

Measurement context. More than resting heart rate, HRV is sensitive to body position, time of day, breathing rate, recording length, and artifact handling. Two readings taken under different conditions are not comparable, even on the same device.

Where can I learn more?

1. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Heart rate variability: standards of measurement, physiological interpretation, and clinical use. Eur Heart J. 1996;17(3):354–381. (full text PDF)
2. Tegegne BS, Man T, van Roon AM, Snieder H, Riese H. Reference values of heart rate variability from 10-second resting electrocardiograms: the Lifelines Cohort Study. Eur J Prev Cardiol. 2020;27(19):2191–2194.
3. Hillebrand S, Gast KB, de Mutsert R, et al. Heart rate variability and first cardiovascular event in populations without known cardiovascular disease: meta-analysis and dose–response meta-regression. EP Europace. 2013;15(5):742–749.
4. van den Berg ME, Rijnbeek PR, Niemeijer MN, et al. Normal values of corrected heart-rate variability in 10-second electrocardiograms for all ages. Front Physiol. 2018;9:424.
5. Natarajan A, Pantelopoulos A, Emir-Farinas H, Natarajan P. Heart rate variability with photoplethysmography in 8 million individuals: a cross-sectional study. Lancet Digit Health. 2020;2(12):e650–e657.

If you have both results in your dashboard, you may notice they don’t always agree. That is expected, and it is not a sign that one of them is wrong. They are built to answer two different questions.

Biological Age asks: which age does my biomarker pattern most resemble?

Advanced Biological Age asks: my predicted long-term disease risk matches the average person of what age?

Those sound similar. The difference in how each number is built is what makes them useful together.

What Biological Age measures

Biological Age is a machine learning model trained on publicly available CDC data paired with internal SiPhox Health data to recognize how biomarker patterns shift with chronological age across large populations. When your results come in, the model compares your pattern to the patterns it learned and estimates the age your profile most closely resembles.

Key characteristics:

• One whole-body number. It summarizes the combined shape of your biomarker profile into a single trackable figure.
• Broad marker set. It draws on a wide panel including metabolic, lipid, liver, kidney, inflammatory, nutrient, and hormonal markers, with sex-specific inputs. At least about half of the eligible markers are needed to generate a result.
• Trained on age itself. The target the model learned to predict is chronological age.

Biological Age is best used as a general wellness summary and a trend line. It answers “is my overall biomarker picture drifting older or younger over time?”

What Advanced Biological Age measures

Advanced Biological Age comes from our partnership with VOLO Health, whose modeling platform we use to generate the Advanced BioAge Report. The underlying models were trained on long-term health outcome data from large longitudinal cohorts, including the UK Biobank and a large body of US clinical records. Rather than learning to predict age, the models learned which biomarker patterns are associated with the development of specific conditions over a multi-year observation window, using standardized diagnostic code definitions for each condition.

The result is a predicted long-term risk estimate, compared against people of your same age and sex. That estimate is then translated back into an age frame: if your profile carries the predicted risk typical of someone four years younger, your delta reads as four years younger.

Key characteristics:

• Eleven results, not one. You get an Overall Advanced Biological Age plus a separate age for each of ten body systems: cardiovascular, metabolic, respiratory, brain, liver, kidney, bone, thyroid, blood, and inflammation.
• Trained on outcomes, not on age. The age number is the final translation step, not the modeling target.
• Peer-relative by design. Every result is calibrated to your age and sex, and each system also comes with a peer group ranking.
• Attribution built in. Each system shows which of your biomarkers are pushing that age up or down.

Advanced Biological Age is best used to find out where to focus. Because each system is modeled independently, you can have a strong cardiovascular result and a middling metabolic one, and that pattern tells you something a single number cannot.

Side by side

Why your two results might not match

4. They were trained on different targets. One model learned age. The other learned disease outcomes and converted to age afterward. A biomarker can be strongly age-associated without being strongly outcome-associated, and the reverse is also true. The two models will weight that marker very differently.
5. They use different inputs. The marker sets overlap but are not identical. Biological Age leans more heavily on hormonal and nutrient markers. The Advanced models lean more heavily on markers with long-run outcome evidence behind them. A result that moves one number may barely register in the other.
6. They use different reference points. Advanced Biological Age is always calibrated against people of your exact age and sex. Biological Age compares your pattern against age patterns across the whole population. Being average for your age and being average overall are not the same thing.
7. One is a summary, the other is a set. Advanced Biological Age reports eleven results. Your Overall Advanced Biological Age is its own independently modeled result and is not the average of the ten system ages. Comparing a single whole-body number to one system’s age, or to an overall figure built a different way, will rarely produce a clean match.

If the two numbers differ by a few years, that is normal. If they differ substantially and consistently across several tests, the more useful next step is to look at your contributing factors in each system and bring both results to your healthcare provider.

Which one should I pay attention to?

Both, for different jobs.

• Tracking progress over time: Biological Age is a clean single line to watch, especially if you test consistently under similar conditions.
• Deciding what to work on: Advanced Biological Age is more actionable, because it separates your body into systems and shows which markers are driving each one.
• Talking to your doctor: Bring the contributing factors, not just the ages. The underlying biomarker values are what a clinician can act on.

What neither number is

Both results are wellness and educational tools. Specifically:

• Neither is a diagnosis, and neither should be used on its own to diagnose or treat any condition.
• Neither is a literal measurement of how old your cells or organs are. Both are comparisons expressed in years because years are intuitive.
• The Advanced models have not been reviewed or cleared by the FDA and are not intended as clinical decision support.
• Neither captures everything that shapes aging, including genetics, fitness, body composition, sleep quality, imaging findings, and medical history.

The bottom line

Biological Age gives you one number that tracks your overall biomarker aging signal over time. Advanced Biological Age gives you eleven outcome-anchored, peer-calibrated numbers that tell you which systems are strong and which deserve attention, plus the specific markers behind each. They are complementary views, and the most useful thing you can do with either is retest and watch the direction of travel.

References and further reading

On biological age models built from standard blood biomarkers

1. Levine ME, Lu AT, Quach A, et al. An epigenetic biomarker of aging for lifespan and healthspan. Aging (Albany NY). 2018;10(4):573-591. doi:10.18632/aging.101414
2. Liu Z, Kuo PL, Horvath S, Crimmins E, Ferrucci L, Levine M. A new aging measure captures morbidity and mortality risk across diverse subpopulations from NHANES IV: a cohort study. PLoS Med. 2018;15(12):e1002718. doi:10.1371/journal.pmed.1002718
3. Rutledge J, Oh H, Wyss-Coray T. Measuring biological age using omics data. Nat Rev Genet. 2022;23:715-727. doi:10.1038/s41576-022-00511-7

On organ systems aging at different rates within the same person

1. Oh HSH, Rutledge J, Nachun D, et al. Organ aging signatures in the plasma proteome track health and disease. Nature. 2023;624(7990):164-172. doi:10.1038/s41586-023-06802-1
2. Oh HSH, Le Guen Y, Rappoport N, et al. Plasma proteomics links brain and immune system aging with healthspan and longevity. Nat Med. 2025;31:2703-2711. doi:10.1038/s41591-025-03798-1

On the outcome data behind the Advanced models

1. Sudlow C, Gallacher J, Allen N, et al. UK Biobank: an open access resource for identifying the causes of a wide range of complex diseases of middle and old age. PLoS Med. 2015;12(3):e1001779. doi:10.1371/journal.pmed.1001779
2. Khan SS, Matsushita K, Sang Y, et al. Development and validation of the American Heart Association’s PREVENT equations. Circulation. 2024;149(6):430-449. doi:10.1161/CIRCULATIONAHA.123.067626

Your blood work is processed in a CLIA-certified, CAP-accredited laboratory. The Advanced BioAge Report is generated using VOLO Health’s modeling platform and is provided for educational and informational purposes only. It is not intended to diagnose, cure, mitigate, treat, or prevent any disease or medical condition and does not constitute medical advice. Statistical associations described here are population-level findings and are not evidence of causation at the individual level. Always consult a qualified healthcare professional with questions regarding your health.

Your biological age reveals how your body is actually aging, not just how many birthdays you have had. The Advanced BioAge Report translates your blood biomarker results into an age for each major organ system, so you can see where your health is thriving and where it needs attention.

This guide walks through every part of the report and what each piece means.

What’s in your report

• Your Overall Advanced Biological Age
• Ten system-specific biological ages
• A peer group ranking for your overall result and for each system
• Contributing factors showing which biomarkers are most influencing each system

Your Overall Advanced Biological Age

At the top of your report you will see two numbers: your chronological age, and your Overall Advanced Biological Age. The difference between them is your delta, shown as something like “2 years younger.”

One thing worth knowing up front: your overall result is not the average of your ten system ages. It is modeled separately, using biomarker patterns associated with whole-body resilience and long-term susceptibility across multiple systems at once. So it is possible for your overall result to look better or worse than a simple average of the systems below it. That is not an error. It is a different calculation answering a broader question.

The ten body systems

Each system gets its own age, modeled independently. Because each one is calculated the same way, they are directly comparable to each other.

Cardiovascular reflects vascular and cardiac risk physiology, drawing on markers associated with atherosclerosis, endothelial stress, inflammation, and cardiometabolic load.

Metabolic reflects glucose regulation and insulin sensitivity, and how flexible your metabolism looks versus showing signs of strain.

Respiratory reflects patterns in your blood associated with reduced respiratory reserve and chronic airway inflammation.

Brain reflects biomarker patterns associated with brain aging and cognitive resilience, often vascular, metabolic, or inflammatory in nature.

Liver reflects hepatocellular integrity, metabolic liver load, and detoxification-related stress.

Kidney reflects filtration efficiency and renal reserve.

Bone reflects bone remodeling balance and mineral metabolism.

Thyroid reflects thyroid axis physiology and the downstream metabolic signaling it drives.

Blood reflects oxygen-carrying capacity, red cell and iron dynamics, and overall blood system resilience.

Inflammation reflects chronic inflammatory load, sometimes described as inflammaging, which cuts across many age-related conditions.

A note on systems we infer rather than measure directly

Respiratory, bone, and brain deserve a specific caveat. We are not performing a lung function test, a bone density scan, or a cognitive assessment. These ages are derived entirely from patterns in your blood biomarkers that the underlying models found to be associated with long-term outcomes in those areas across large populations.

That association is real and it is useful. It is not the same as a direct measurement of the organ. If one of these systems comes back with an unfavorable result, the appropriate next step is a conversation with your provider about whether direct testing makes sense for you, not a conclusion about your lungs or bones.

What your delta actually means

If your cardiovascular age reads four years younger than your chronological age, it means your cardiovascular biomarker profile looks like the average profile of someone four years younger than you.

What it does not mean:

• It is not a prediction that you will live four extra years.
• It is not a claim that your heart is literally four years younger.
• It is not a diagnosis, in either direction.

It is a comparison, expressed in years because years are the frame most people find intuitive.

Your deltas will often differ across systems, and that variation is the most useful thing in the report. A strong cardiovascular result alongside an average metabolic one tells you something specific about where to focus. A single number would hide that.

Your peer group ranking

Alongside each age, you will see a ranking such as “your cardiovascular health is in the top 14% for your peer group.” Your peer group is people of your same age and sex.

A ranking in the top 14% means roughly 14% of your peers have a result at least as favorable as yours, so you are ahead of about 86% of them. Lower percentages are better.

Why your ranking and your delta can tell different stories. You may see similar deltas across several systems while the rankings vary widely. This happens most often for younger customers, and it is expected. The models have less room to spread results apart at younger ages, when very few people in the reference data have developed the conditions being modeled. The age deltas compress toward a narrow band, while the peer ranking still has plenty of room to differentiate.

If that describes your report, read the ranking as your primary signal and the delta as secondary. As you get older, or as you retest over time, the deltas become more expressive.

Contributing factors

For each system, you can open the contributing factors view to see which of your biomarkers are influencing that age and in which direction. This is the part of the report you can actually act on.

Two things to keep in mind:

The same marker can matter differently in different systems. A given result might be a major driver of one system’s age and barely register in another. That is because the models learned, from outcome data, which markers carry weight for which outcomes.

A result can be inside the standard lab range and still pull your age up. Standard reference ranges were built to flag clinical outliers in a general population. These models are looking for the values associated with the most favorable long-term outcomes for someone your age and sex, which is a narrower target. A value that is clinically normal but not at that optimum can still show up as a contributing factor. That is a signal for proactive attention, not a cause for alarm.

What to do with your results

1. Start with the systems that ranked least favorably, not the ones with the biggest headline deltas.
2. Open the contributing factors for those systems and note which markers appear.
3. Cross-reference those markers with your individual biomarker insights in your dashboard for context on what each one reflects.
4. Retest. A single report is a snapshot. The direction of travel across two or three reports carries far more signal than any one result, and normal variation between tests is expected. 
5. Bring the report to your healthcare provider, especially the contributing factors rather than just the ages.

An unfavorable result in any system is not a diagnosis. It is a prompt for attention, and a starting point for a better conversation with your provider.

References and further reading

On different organ systems aging at different rates

1. Oh HSH, Rutledge J, Nachun D, et al. Organ aging signatures in the plasma proteome track health and disease. Nature. 2023;624(7990):164-172. doi:10.1038/s41586-023-06802-1
2. Oh HSH, Le Guen Y, Rappoport N, et al. Plasma proteomics links brain and immune system aging with healthspan and longevity. Nat Med. 2025;31:2703-2711. doi:10.1038/s41591-025-03798-1

On the Inflammation domain

1. Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci. 2014;69(Suppl 1):S4-S9. doi:10.1093/gerona/glu057
2. Franceschi C, Bonafè M, Valensin S, et al. Inflamm-aging: an evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:244-254. doi:10.1111/j.1749-6632.2000.tb06651.x

On the Kidney domain

1. Shlipak MG, Matsushita K, Ärnlöv J, et al. Cystatin C versus creatinine in determining risk based on kidney function. N Engl J Med. 2013;369(10):932-943. doi:10.1056/NEJMoa1214234

On the Brain domain

1. Livingston G, Huntley J, Liu KY, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet. 2024;404(10452):572-628. doi:10.1016/S0140-6736(24)01296-0

On the Respiratory domain

1. Ellingsen J, Janson C, Bröms K, et al. CRP, fibrinogen, white blood cells, and blood cell indices as prognostic biomarkers of future COPD exacerbation frequency: the TIE cohort study. J Clin Med. 2024;13(13):3855. doi:10.3390/jcm13133855

On the Thyroid and Bone domains

1. Rodondi N, den Elzen WPJ, Bauer DC, et al. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA. 2010;304(12):1365-1374. doi:10.1001/jama.2010.1361
2. Blum MR, Bauer DC, Collet TH, et al. Subclinical thyroid dysfunction and fracture risk: a meta-analysis. JAMA. 2015;313(20):2055-2065. doi:10.1001/jama.2015.5161

Your blood work is processed in a CLIA-certified, CAP-accredited laboratory. The Advanced BioAge Report is generated using VOLO Health’s modeling platform and is provided for educational and informational purposes only. It is not intended to diagnose, cure, mitigate, treat, or prevent any disease or medical condition and does not constitute medical advice. It has not been reviewed or cleared by the FDA. Statistical associations described here are population-level findings and are not evidence of causation at the individual level. Always consult a qualified healthcare professional with questions regarding your health.

There is no single lab test that directly measures biological age. Any biological age result is a model, and models differ enormously in how they are built. This guide explains how the Advanced BioAge Report is calculated, and what that method can and cannot tell you.

The Advanced BioAge Report is powered by VOLO Health’s modeling platform. We collect and process your blood work, and VOLO’s models turn those results into system-by-system age estimates.

We chose this platform for one reason above all others: the models are anchored to real health outcomes rather than to expert consensus about what “healthy” should look like. The model was never told which values are good. It learned that from data on what actually happened to hundreds of thousands of people over many years.

Step 1: Your blood work

Everything starts with measurement. Your sample is processed in a CLIA-certified, CAP-accredited laboratory, and the resulting biomarker values are the only inputs to your report.

The models draw on markers across several categories, including metabolic and glycemic markers, a full lipid picture, liver and kidney function, inflammatory markers, and blood count markers. Report completeness scales with panel breadth: the more of these markers your panel includes, the more confident each system result becomes.

Step 2: Removing the effect of age and sex

Age is by far the strongest predictor of most chronic disease, and sex matters substantially too. If a model does not handle this carefully, it mostly ends up rediscovering that older people get sick more often, which tells you nothing about you.

So the first modeling step builds a baseline expectation of disease prevalence as a function of age and sex, separately for each condition. Every individual in the training data is then measured against their own demographic baseline rather than against everyone else. What comes out is a relative signal: how does this person’s risk compare to what would be expected for someone of their age and sex?

This is why your report is explicitly peer-calibrated. Two people with identical lab values but different ages will receive meaningfully different reports, because the question being asked is always relative to your own demographic group.

Step 3: Learning from outcomes, not from age

The models were trained on two large bodies of data: a major long-term population health study following roughly half a million participants with linked medical records, plus a much larger set of US clinical records used for external validation and calibration.

For each health system, the outcomes being modeled are defined using standardized diagnostic code sets applied to those linked medical records, over a multi-year observation window following the original blood draw. In other words, the model looked at people’s biomarkers at one point in time, then looked at what conditions they went on to develop years later, and learned which biomarker patterns preceded which outcomes.

This is the single most important thing to understand about the method. The model was not trained to guess your age. It was trained to estimate long-term disease risk. The age you see in your report is the final translation step, not the modeling target.

Step 4: Capturing how markers interact

The models used are gradient-boosting machines, chosen specifically because they handle two things that simpler models struggle with:

Nonlinear relationships. Risk does not always rise in a straight line as a marker rises. Some markers carry risk at both ends of their range. Some have a threshold effect. The model can represent those shapes rather than forcing a straight line through them.

Interactions between markers. This is the part that a marker-by-marker reading of your labs cannot give you. Certain combinations carry more risk together than the sum of their individual contributions. Two people can have similar-looking individual results and meaningfully different combined risk pictures. Because the models were trained on the whole panel at once, those combinations are captured.

Step 5: Modeling each system separately

Every system in your report is modeled independently, using the same underlying data and the same set of biomarker inputs. No single condition gets privileged treatment.

This matters more than it sounds. Because the systems are modeled simultaneously on the same population, the models can capture trade-offs where a biomarker value that looks favorable for one outcome is less favorable for another. A single-condition model would miss that entirely.

It also means your ten system results are directly comparable to each other. A given ranking in the kidney system means the same thing, relative to your peers, as the same ranking in the brain system.

Step 6: Translating into an age

Once your relative risk estimate exists for a system, it is converted into an age by working backwards through the reference curve for people of your sex. The model asks: at what age would the average person in the reference population carry this same level of predicted risk?

If the answer is four years below your chronological age, your delta reads as four years younger. That is the whole of what the number means.

Why this differs from your standard lab reference range

The reference range printed next to a lab value is designed to flag clinical outliers in a general population. It is typically the central range of a healthy reference group, sometimes adjusted for perceived healthy limits.

These models are looking for something different: the biomarker values associated with the most favorable long-term outcomes across multiple systems at once, for someone of your specific age and sex. That target range is usually narrower than the standard lab range and can sit in a different place within it.

The consequence is that a value can be entirely normal on your lab report and still appear as a contributing factor pulling a system’s age upward. Both things are true at once. The lab range is telling you there is no immediate clinical concern. The model is telling you the value is not at the modeled optimum for your profile. Only the second one is a target for proactive attention, and neither is a diagnosis.

Honest limitations

• This is a model, not a measurement. Every result is an estimate built on population-level associations, and population associations are not evidence of causation for any individual.
• Blood biomarkers cannot see everything. Genetics, fitness, body composition, sleep quality, imaging findings, and medical history all shape aging and none of them are inputs here.
• Some systems are inferred, not measured. The respiratory, bone, and brain results are derived from blood patterns, not from lung function testing, bone density scanning, or cognitive assessment.
• Single results are snapshots. Lab values move with hydration, fasting state, time of day, sleep, illness, medication, and training load. The trend across multiple reports is more informative than any single one.

References and further reading

1. Sudlow C, Gallacher J, Allen N, et al. UK Biobank: an open access resource for identifying the causes of a wide range of complex diseases of middle and old age. PLoS Med. 2015;12(3):e1001779. doi:10.1371/journal.pmed.1001779
2. Levine ME, Lu AT, Quach A, et al. An epigenetic biomarker of aging for lifespan and healthspan. Aging (Albany NY). 2018;10(4):573-591. doi:10.18632/aging.101414
3. Rutledge J, Oh H, Wyss-Coray T. Measuring biological age using omics data. Nat Rev Genet. 2022;23:715-727. doi:10.1038/s41576-022-00511-7
4. Oh HSH, Rutledge J, Nachun D, et al. Organ aging signatures in the plasma proteome track health and disease. Nature. 2023;624(7990):164-172. doi:10.1038/s41586-023-06802-1
5. Oh HSH, Le Guen Y, Rappoport N, et al. Plasma proteomics links brain and immune system aging with healthspan and longevity. Nat Med. 2025;31:2703-2711. doi:10.1038/s41591-025-03798-1

Your blood work is processed in a CLIA-certified, CAP-accredited laboratory. The Advanced BioAge Report is generated using VOLO Health’s modeling platform and is provided for educational and informational purposes only. It is not intended to diagnose, cure, mitigate, treat, or prevent any disease or medical condition and does not constitute medical advice. Statistical associations described here are population-level findings and are not evidence of causation at the individual level. Always consult a qualified healthcare professional with questions regarding your health.

Symptoms and biomarkers work together

Thyroid symptoms are famously nonspecific, and no two people have exactly the same set. That is precisely why lab tests sit at the center of your report: the biomarkers show what your thyroid is doing, and your symptoms add the human context of how it is affecting you. Read together, they are far more informative than either alone.

When your thyroid slows down (hypothyroid)

An underactive thyroid slows your metabolism, so the symptoms tend to be ones of “slowing down”:

• Fatigue and sluggishness
• Feeling cold when others don’t
• Weight gain or fluid retention
• Constipation
• Dry skin and thinning hair
• Low mood, brain fog, or poor memory

When your thyroid speeds up (hyperthyroid)

An overactive thyroid does the opposite, revving your system up:

• Feeling hot, sweaty, or restless
• Weight loss despite a normal or bigger appetite
• A racing or irregular heartbeat
• Anxiety, nervousness, or irritability
• Trembling hands
• Trouble sleeping

Specific vs non-specific symptoms

Some symptoms are non-specific: tiredness, low mood, or weight change could stem from many causes and don’t point to the thyroid on their own. They gain meaning when they line up with your labs. Others are more specific (for example, a racing heartbeat with heat intolerance, or neck fullness) and point more directly toward a particular thyroid pattern. Your report groups them this way so the more telling signals carry appropriate weight.

How your report uses them

Your symptoms are scored for severity and combined with your biomarker results to build your overall picture: whether things look balanced, underactive, or overactive, and how strongly the signals agree. When your symptoms and your labs point the same way, that adds confidence; when they disagree, that is useful too, and worth discussing with your doctor.

What this means for you

If your labs are normal but you still feel off, that doesn’t mean your experience isn’t real: it means the answer may lie elsewhere, or may be worth rechecking over time. And if your labs are abnormal but you feel fine, your report helps flag it early. Either way, the goal is to bring the two together into one clear, personalized read.

Key takeaway

Hypothyroid symptoms are about slowing down; hyperthyroid symptoms are about speeding up. Neither is diagnosed on feeling alone. Your report pairs how you feel with what your biomarkers show to give you the fullest picture.

Where to read more

• American Thyroid Association: Hypothyroidism, Hyperthyroidism
• Mayo Clinic: Hypothyroidism, Hyperthyroidism.

This article is for general wellness and educational purposes and is not medical advice. For anything specific to your health, please speak with your doctor.

Sleep is one of the most important aspects of physical and mental health, yet it is one of the aspects of health and wellness that is first neglected even when it helps to support the brain, heart, immune system, metabolism, hormones, memory and our energy and mood during the day. Sleep is vital yet overlooked.

During sleep, the brain activates the glymphatic system, which help to clear metabolic waste. This helps with memory consolidation, allowing the brain to gain and retain new information and connect it to already existing information.

Sleep also influences hormones such as leptin and ghrelin which are involved with hunger and appetite. Have you ever pulled an “all nighter”. Did you notice how much more hungry you were and the urge to constantly snack? When sleep is continually interrupted, it can become increasingly difficult to regulate appetite which can contribute to overeating and weight gain.

Sleep also benefits the cardiovascular system by giving it time to recover. Blood pressure usually decreases during sleep which in turn reduces the workload placed on the heart. Chronic and poor sleep is associated with high blood pressure, cardiovascular disease as well as impaired immune function, weight gain (as mentioned earlier) and poor cognitive function.

How Much Sleep Do You Need?

The general guideline for healthy adults is to aim for 7-9 hours of sleep each night.

Of course, life can get in the way sometimes and while the occasional poor night’s sleep is okay, regular sleep of less than 7 hours can result in decreased daytime performance and increased long term health risks. On the other hand, constantly sleeping more than 9 hours per night may also be associated with negative health outcomes for some people. Keep in mind that sleep is highly personal and varies from person to person.

The main goal is to get enough consistent, high quality sleep that makes you wake up feeling fresh and reenergized, not solely spending more time in bed. The actual sleep matters most.

Why Sleep Consistency Matters

Maintaining a regular sleep schedule is one of the most important habits to support the body’s internal clock.

You can help support your internal clock by going to bed and waking up at roughly the same time each day, including the weekends. Having an inconsistent sleep/wake routine can disrupt circadian rhythms and make it harder to fall asleep, make it harder to wake up leaving you feeling groggy and impair daytime energy.

Consistently waking up at the same time each day is particularly useful as it gives your brain a reliable signal that the day has started.

Morning Sunlight and Exercise

The habits that support good sleep begin in the morning.

Morning sunlight

Natural sunlight in the morning helps to sync your circadian rhythm which controls alertness, sleepiness and melatonin production.

Aim for 20-30 minutes of morning sunlight before 10am or after 3pm whereas sunlight between 10-3 is best for vitamin D production. Morning sunlight signals to your brain that the day has started and can help you to fall asleep earlier later in the evening.

Research also suggests that greater morning light exposure is associated with an earlier sleep midpoint and over better sleep quality.

Regular exercise

Physical activity can improve sleep quality and increase the amount of deep sleep you get.

Aim for approximately 150 minutes of moderate intensity activity per week of 75 minutes of intense activity. A single bout of 30 minute moderate intensity activity can help to improve sleep the same night.

Check out this link on The Minimum Effective Workout Plan for Maintaining Muscle as You Age – SiPhox Health.

Exercise should help support sleep and sleep should help to support exercise and recovery. Avoid sacrificing sleep to fit in a workout.

Sleep Hygiene and Evening Habits

Sleep hygiene refers to the habits and environment that prepares your body for quality, restful sleep.

Make sure your bedroom is:

• Cool
• Dark
• Quiet
• Comfortable

Use a pillow and mattress that are right for you. Blackout curtains, earplugs and a white noise machine can also help to create a more restful sleep environment. Consider going around and taping up any light that may be emitting from power outlets and charging devices.

Try reserving the bed for sleep and intimacy only and avoid using the bed as a space for working, studying, eating, watching T.V. and scrolling on your phone. This can help strengthen the association between going to bed and falling asleep.

Screens

Phones, tablets, televisions and all of the other light emitting devices around can suppress melatonin and increase awakeness near to bedtime.

Try to turn off and avoid screens 30-60 minutes before bed. This is also a good time to start dimming the light around the house.

Caffeine

Caffeine blocks adenosine receptors which is one of the signals that helps your body feel sleepy. Try to avoid caffeine after midday (2pm) when possible. The half life of caffeine is around 8 hours meaning that 8 hours after caffeine consumption, half will still be circulating in your system.

Alcohol

Alcohol may initially make you feel drowsy, but it can disrupt the second half of the night. It may reduce REM sleep, increase awakenings, and leave you feeling less refreshed the next morning.

Avoid relying on alcohol as a sleep aid and avoid alcohol 4 hours before time. This would mean the last call is at 7pm for an 11pm bedtime.

Evening meals

Avoid large, heavy, or unhealthy meals approximately 2 hours before bedtime. Eating too much too close to bedtime may cause digestive discomfort, or acid reflux, making it harder to stay and fall asleep.

Stress Management and Bedtime Journaling

A racing mind is a common reason people struggle to fall asleep. Relaxation practices can help shift the body away from a high-alert “fight or flight” state and toward a calmer resting state.

Helpful options include:

• Mindfulness meditation
• Slow breathing
• Progressive muscle relaxation
• Mindful walking in nature
• Bedtime journaling

Progressive muscle relaxation

Progressive muscle relaxation involves gently tensing and then releasing different muscle groups.

Tense each muscle group for approximately 5–10 seconds, then slowly release it while focusing on the feeling of relaxation. Work gradually through the feet, legs, hips, abdomen, shoulders, face, and hands.

Avoid tensing the muscles to the point of pain.

The five-minute to-do list

If unfinished tasks keep running through your mind, spend five minutes before bed writing a specific to-do list for the next day or coming days.

Writing future tasks down may help “off-load” them from your mind so you do not have to keep mentally rehearsing them.

Be specific. Instead of writing “work on project,” list the individual actions you need to complete. Journaling about completed tasks may not provide the same sleep-onset benefit.

Nature walking

A mindful nature walk may also improve mood and sleep difficulties. One studied approach used approximately 35 minutes of mindful walking, with attention directed toward the surroundings and present moment.

Supplements That May Support Sleep

Behavioral changes should remain the foundation of a sleep-improvement plan. Supplements may provide additional support, but they should not replace a consistent sleep schedule, morning light, exercise, stress management, or a supportive bedroom environment.

Magnesium Bisglycinate

Magnesium supports nervous system function and relaxation.

A study using 250 mg of elemental magnesium daily for four weeks found a modest improvement in insomnia severity.

The evidence remains limited and mixed. Benefits may be greater in people with low dietary magnesium intake.

Holy Basil

Holy basil, also called tulsi, is an herb that has been studied for stress and sleep support.

A standardized extract taken at 250 mg daily for eight weeks was associated with reduced perceived stress and improved subjective sleep quality.

The supplement was well tolerated in the study, but individual responses may vary.

L-Theanine

L-theanine is an amino acid naturally found in tea.

Research suggests it may support:

• Sleep quality
• Daytime function
• Sleep onset

However, the evidence is mixed because many studies combine L-theanine with other ingredients, making it difficult to determine its independent effect.

Speak with a healthcare professional before using supplements if you take medications, have a chronic health condition, are pregnant, or are breastfeeding.

What to Track

Tracking a few simple measures can help you understand whether your sleep routine is working.

Sleep duration

The total amount of time you spend asleep.

Aim for 7–9 hours per night.

Sleep latency

The amount of time it takes to fall asleep after going to bed.

A sleep latency of less than 30 minutes is a useful general target.

Sleep efficiency

The percentage of your time in bed that you are actually asleep.

A sleep efficiency above 85% is a useful general target.

Daytime energy

Pay attention to your alertness, focus, mood, and sleepiness during the day. How you feel and function can be just as important as the numbers recorded by a device.

A sleep diary, app, or wearable may help you monitor trends. Wearable devices are useful for patterns but may not measure total sleep time or sleep stages with clinical accuracy.

When to Seek Professional Help

General sleep habits may not be enough when an underlying sleep disorder is present.

Speak with a healthcare professional if you experience:

• Persistent difficulty falling or staying asleep
• Excessive daytime sleepiness
• Loud or chronic snoring
• Gasping or choking during sleep
• Frequent nighttime awakenings
• Sleep problems that interfere with work, driving, safety, or daily functioning
• Feeling unrefreshed despite spending enough time in bed

Snoring, gasping, and choking may be signs of obstructive sleep apnea. Persistent insomnia may also require targeted clinical treatment rather than sleep hygiene alone.

Simple Daily Sleep Plan

Morning

• Wake up at approximately the same time every day
• Get 20–30 minutes of natural light before 10 a.m.

During the day

• Exercise regularly
• Aim for approximately 150 minutes of moderate aerobic activity per week
• Stop caffeine around midday

Evening

• Finish large meals at least two hours before bed
• Limit alcohol
• Keep the bedroom dark, cool, quiet, and comfortable

Thirty minutes before bed

• Turn off screens
• Dim the lights
• Use breathing, mindfulness, or progressive muscle relaxation

At bedtime

• Spend five minutes writing a specific to-do list for the next day
• Aim for 7–9 hours of sleep
• Maintain the same wake-up time on weekdays and weekends

Summary / Key Takeaways

Improving sleep usually starts with consistent daily habits rather than a single supplement or quick fix.

✓ Sleep duration: Aim for 7–9 hours each night
✓ Consistency: Keep a regular bedtime and wake-up time
✓ Morning light: Get 20–30 minutes of sunlight before 10 a.m.
✓ Exercise: Work toward 150 minutes of moderate activity each week
✓ Sleep environment: Keep the bedroom dark, cool, quiet, and comfortable
✓ Evening habits: Reduce late caffeine, alcohol, screens, and heavy meals
✓ Mental relaxation: Use mindfulness, progressive muscle relaxation, or a five-minute to-do list
✓ Supplements: Consider magnesium, holy basil, or L-theanine only as additions to healthy sleep habits

Bottom line: Better sleep is built through consistency. Start with one or two manageable changes, practice them daily, and gradually add more habits as they become part of your routine.

Book a call with one of our health coaches today to learn more about improving your sleep and building a routine that supports your long-term health.

What your panel measures, and why it is enough

Your panel is built around the questions that matter: is your thyroid working at the right pace, and if it isn’t, then in which direction and by how much, and is an autoimmune process involved? Five core markers answer those questions clearly:

• TSH is the most sensitive early signal of how actively your thyroid is working, and it usually moves first, before the other markers shift.
• Free T4 is the main hormone your thyroid makes, and read alongside TSH it adds context to how the gland may be working.
• Free T3 is the active hormone that sets your metabolic pace, and it is most informative when your thyroid may be running fast.
• TPO and thyroglobulin antibodies can suggest whether an autoimmune process, such as Hashimoto’s or Graves’, may be involved.

Together, these markers give a clear picture of how your thyroid may be working, one that you and your doctor can use to decide on any next steps. That is the same core set thyroid specialists rely on, and every test in it earns its place by adding real insight rather than extra uncertainty.

What reverse T3 is

Your thyroid mostly produces T4, a storage form of the hormone that your body activates as needed. To use it, the body removes a single iodine atom from T4. Take it from one spot and you get T3, the active hormone that speeds your metabolism up. Take it from the other spot and you get reverse T3, an inactive look-alike that does nothing. One way to picture it: T4 is a dimmer switch, and the body can turn it up to T3 or leave it off as rT3. Both are normal, everyday products of a healthy thyroid.

Why reverse T3 rises, and why that usually isn’t a thyroid problem

Most of the time, a high reverse T3 has nothing to do with thyroid disease. When your body is under stress, during an illness, after surgery, while fasting or dieting, or under heavy physical strain, it deliberately steers more T4 toward inactive rT3 and less toward active T3. Doctors call this non-thyroidal illness, sometimes “euthyroid sick syndrome,” and the telling detail is in that name: euthyroid, meaning the gland itself is working normally. It is a sensible energy-saving response to a hard stretch, not a fault to correct. Some medications, including beta-blockers, steroids, and amiodarone, nudge the body the same way. So in an otherwise well person, a raised rT3 usually just reflects that the body has recently been stressed, unwell, or underfed.

Why we leave reverse T3 out of your panel

Put simply, reverse T3 would add noise rather than signal. Four reasons stand behind that.

It rarely reflects your thyroid. As above, a high rT3 usually tracks stress, illness, or fasting rather than a gland that is genuinely under- or over-active, so it is hard to interpret as a thyroid test at all.

It would not add anything to act on. Understanding an underactive thyroid rests on TSH, supported by Free T4. As one clinical review put it, there is “no rationale for measuring reverse T3” when starting or adjusting treatment, which is always best worked through with your doctor. A result that adds no useful information does not belong on the panel.

The test itself is shaky. Reverse T3 is a specialized assay that laboratories do not measure consistently, and it lacks validated reference ranges for this use. It cannot reliably tell true hypothyroidism apart from the harmless stress-related shift described above.

The popular “Free T3 to reverse T3 ratio” is not validated. You will see this ratio in some wellness circles, but there is no agreed cutoff, the “ideal” numbers swing widely from one source to the next, and the answer even depends on the units used. No major medical society backs it.

Specialists advise against it. The American Thyroid Association states plainly that, in healthy, non-hospitalized people, measuring reverse T3 “does not help determine whether hypothyroidism exists or not, and is not clinically useful.”

A note on “Wilson’s syndrome”

Reverse T3 testing often travels with a label called “Wilson’s temperature syndrome,” the idea that a low body temperature plus vague symptoms come from a conversion problem, supposedly fixable with T3. The American Thyroid Association looked at this directly, found “no scientific evidence” that it exists, and cautioned that the T3 regimens sold to treat it can affect the heart and bones and prove “potentially dangerous.” It is not something we build your care around.

Key takeaway

Your panel of TSH, Free T4, Free T3, and thyroid antibodies already covers what matters: it gives a clear, useful picture that you and your doctor can act on. Reverse T3 is a genuine molecule, but as a test it mostly reflects stress, fasting, or illness, it is not measured reliably, and it would not add anything you or your doctor would act on. Leaving it out is not a gap. It is what keeps your results clear and your decisions anchored to the markers that count.

Where to read more

• Understanding Your Thyroid Biomarkers: a closer look at each marker on your panel and how they fit together

This article is for general wellness and educational purposes only. It explains why reverse T3 is not part of the SiPhox panel; it is not medical advice, it is not a diagnosis, and it does not replace care from your own clinician. For decisions about thyroid testing or treatment, please speak with your doctor.

Sources: American Thyroid Association: Thyroid Function Tests, Statement on “Wilson’s Syndrome”, Clinical Thyroidology for the Public (Jan 2019); “Reverse T3 or perverse T3?” Cleveland Clinic Journal of Medicine (2018); Merck Manual: Euthyroid Sick Syndrome; The Non-Thyroidal Illness Syndrome, Endotext.

Why movement helps

When your thyroid is well managed, regular activity does just what you would hope: steadier energy, a brighter mood, easier weight control, and better protection for your heart and bones. Those happen to be the areas a thyroid imbalance tends to hit hardest, which is why movement is such a useful part of feeling like yourself again once your levels sit in a reasonable range.

If your thyroid is underactive (running slow)

An underactive thyroid slows your metabolism, so when it is undertreated you may feel tired, cold, and quick to run out of steam during exercise. The trick is not to force it. Start gentle and build up over time, with walking, light strength work, and easy cardio as good first steps.

Here is the encouraging part: as treatment brings your levels back to normal, energy and stamina usually climb with them, and activity then helps with any leftover fatigue and with weight. If you still feel wiped out by ordinary movement once things have settled, mention it to your clinician rather than pushing through.

If your thyroid is overactive (running fast)

This is where a little caution pays off. An overactive thyroid already keeps your body revved up, with a faster heartbeat and higher energy burn even at rest. Piling intense exercise on top of uncontrolled hyperthyroidism can strain the heart, raise the risk of irregular rhythms, and worsen overheating, anxiety, and poor sleep. Uncontrolled overactivity also drains muscle and speeds up bone loss.

So the order matters: it is best to have your levels well controlled first, which is something to work through with your doctor, and to hold off on high-intensity training until then. Check with your clinician before you start or restart a program, and once things are steady you can build back up safely.

Exercise supports your treatment, it does not replace it

Activity is a real tool for energy, mood, weight, and long-term heart and bone health. What it cannot do is take the place of getting your thyroid levels right in the first place. Treatment is the foundation, and movement is what you build on top of it, so the two work best together.

Simple ways to start

• Begin low: walking, gentle cycling, or light resistance work
• Add time or intensity slowly, as your energy allows
• Include some strength training to protect muscle and bone
• Listen to your body: unusual breathlessness, a racing heartbeat, or lasting exhaustion is your cue to ease off and check in with your clinician

Key takeaway

If your thyroid is running slow, start gently and let treatment rebuild your energy before you ramp up. If it is running fast, make sure it is well controlled, with your doctor’s guidance, before any intense exercise. Either way, movement is there to support your treatment, not to stand in for it.

Where to read more

• Hypothyroid vs Hyperthyroid Symptoms: how your symptoms and biomarkers fit together
• Eating Well for Thyroid Health: nutrition that supports your thyroid

This article is for general wellness and educational purposes only. It is not medical advice, it is not a diagnosis, and it does not replace care from your own clinician or a personalized exercise or treatment plan. Please get your clinician’s guidance before starting or changing an exercise program, and do not adjust any treatment on your own, especially if your thyroid levels are not yet controlled. If you have chest pain, a severe or irregular heartbeat, fainting, or breathlessness at rest, stop and seek medical care.

Sources: Cleveland Clinic: Exercise and an Uncontrolled Thyroid; American Thyroid Association: Hyperthyroidism, Hypothyroidism.

Why food matters for your thyroid

Your thyroid runs on nutrients from what you eat. It uses iodine to build thyroid hormone, then relies on a handful of other nutrients to activate and protect it. Get enough of the right ones, without overdoing it, and the gland has what it needs. For most people that comes from everyday balanced meals, not from a stack of pills.

Iodine: enough, but not too much

Iodine is the one nutrient your thyroid cannot do without, since it is the raw material for its hormones. The important nuance is that both too little and too much can cause problems, so the aim is a steady, adequate intake rather than the highest amount you can manage.

Most people who use iodized salt get plenty from ordinary foods like dairy, eggs, and seafood. Adults need about 150 micrograms a day, and a little more in pregnancy. The usual source of trouble is the opposite of deficiency: high-dose iodine or kelp and seaweed products, which can deliver many times a safe amount and tip the gland off balance. Unless your clinician has recommended it, there is no need to add iodine, and kelp supplements are best left on the shelf.

Selenium: the quiet helper

Selenium helps your body switch thyroid hormone into its active form and shields the gland from everyday wear, so getting enough matters. More is not better, though. A few studies hint that selenium supplements can slightly lower thyroid antibodies in Hashimoto’s, but the evidence is mixed, does not clearly help people feel better, and is not something major guidelines recommend across the board. Selenium also has a narrow safe range. The simplest approach is to get it from food, where a couple of Brazil nuts already cover a full day, and to add a supplement only in discussion with your clinician.

Iron, zinc, and vitamin D: the supporting cast

A few other nutrients play backup. Iron powers the enzyme that makes thyroid hormone, and running low on it often accompanies an underactive or autoimmune gland, so it is worth checking if you feel tired a lot. Zinc helps your body process thyroid hormone. Vitamin D tends to run low in people with autoimmune thyroid conditions, though that is a link rather than proof a supplement fixes anything. For all three, aim for enough through a varied diet, and correct a genuine shortfall only if you have one.

Broccoli, kale, and soy are fine

You may have heard that cruciferous vegetables like broccoli, cabbage, and kale, along with soy, are “goitrogens” that harm the thyroid. In the amounts people normally eat, they are safe, and cooking softens any effect even further. The theoretical worry only applies alongside iodine deficiency or genuinely extreme habits, such as drinking large amounts of raw cruciferous juice daily. These are nutritious foods, so keep them on your plate as part of a varied diet.

If you take levothyroxine: keep the timing steady

If you take levothyroxine, food and some supplements can affect how much your body absorbs. The notes below are general background, not instructions for your dose, so keep taking your medication exactly as prescribed and check any timing questions with your doctor or pharmacist. As a rule of thumb, levothyroxine is usually absorbed best on an empty stomach; coffee and soy-heavy meals are kept a little apart from it; and calcium or iron supplements are spaced several hours away, because they can bind it. Whatever schedule you settle on with your clinician, keeping it the same each day is the part that helps most.

The bottom line: a balanced, whole-food pattern

No single food makes or breaks thyroid health. What the evidence keeps pointing to is an overall pattern: plenty of vegetables and fruit, quality protein, whole grains, and enough (not extra) iodine, selenium, iron, zinc, and vitamin D. One myth worth retiring is going gluten-free to help thyroid disease. On its own it does not, and it only makes a difference if you also have celiac disease, which is worth ruling out if you have symptoms of it, since the condition turns up more often in people with autoimmune thyroid conditions.

Key takeaway

Get enough iodine without going overboard, aim for a solid baseline of selenium, iron, zinc, and vitamin D from food, and keep broccoli and soy on your plate. If you take medication, hold its timing steady and separate from coffee, calcium, and iron. A consistent, balanced diet will do far more for your thyroid than any restrictive plan.

Where to read more

• Understanding Your Thyroid Biomarkers: what each marker means in your report
• Preparing for Your Thyroid Test: how to get a clean, accurate result
• Staying Active & Thyroid Health: movement that supports your thyroid

This article is for general wellness and educational purposes only. It is not medical advice, it is not a diagnosis, and it does not replace care from your own clinician. Do not start, stop, or change any supplement or medication based on it. Individual needs vary, so please speak with your doctor, pharmacist, or a registered dietitian before making major dietary changes or starting supplements.

Sources: NIH Office of Dietary Supplements: Iodine, Selenium; American Thyroid Association: Statement on Excess Iodine, Selenium & Hashimoto’s; Harvard Nutrition Source: Iodine; Mayo Clinic: hypothyroidism diet & levothyroxine; AAFP/FPIN: gluten-free diet & thyroid disease.