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Your body cannot make tryptophan on its own. You get it from food, and once it reaches your bloodstream, your cells route it in three very different directions: toward building proteins, toward making mood and sleep molecules like serotonin and melatonin, and toward making compounds that shape how your immune system reacts. The level circulating in your blood reflects the balance of all three, and when that balance tips, it often shows up years before any disease has a name.
Lower blood tryptophan has been linked in large studies to higher risk of heart attacks, earlier death, faster kidney decline, and depression. But this is not a simple high-is-good story. In some settings, such as obesity and prediabetes, tryptophan moves in the opposite direction. Reading it well means tracking it over time and in the context of other markers.
Trp (tryptophan) is one of the nine essential amino acids, meaning your body depends on your diet to supply it. Once absorbed, the large majority of your tryptophan (roughly 90 to 95 percent) gets pulled down a path called the kynurenine pathway, which makes immune-signaling molecules and compounds your cells use for energy production. A small slice is used to make serotonin and melatonin, the molecules your brain and gut use to regulate mood, appetite, and sleep. Another portion is handed to your gut microbes, which turn it into substances that help keep your intestinal lining intact.
Inflammation is the main reason a blood tryptophan level drops. When your immune system is active, enzymes called IDO and TDO (the proteins that start breaking tryptophan down) speed up the conversion of tryptophan into kynurenine. So a low level can reflect ongoing inflammatory activity in your body, not just low dietary intake. This is why tryptophan is increasingly studied as a window into immune and metabolic stress, not just nutrition.
Across many cohorts, people with lower circulating tryptophan tend to develop more heart attacks, strokes, and cardiovascular deaths. A meta-analysis combining thirteen studies with 34,370 participants found that higher tryptophan levels were linked to about a 15 percent lower risk of future cardiovascular disease. The EPIC-Norfolk study, tracking 11,972 adults for a median of 22 years, found that people with higher tryptophan had roughly 27 percent lower all-cause mortality and 24 percent lower fatal cardiovascular disease per standard deviation, after adjusting for classical risk factors and inflammation.
In a Chinese cohort of 1,829 people with coronary artery disease, people in the highest quartile of plasma tryptophan had roughly 38 percent lower risk of cardiovascular death and 33 percent lower all-cause death compared to those in the lowest quartile, over a median follow-up of 9.2 years. In the PREDIMED trial of 985 high-cardiovascular-risk adults, a one-year increase in plasma tryptophan translated into about 21 percent lower risk of a major cardiovascular event per standard deviation rise.
In 184 adults with chronic kidney disease tracked for a median of two years, higher baseline tryptophan was associated with about 68 percent lower odds of developing new cardiovascular disease. In a separate study of 1,915 people with type 2 diabetes, every one standard deviation higher tryptophan was tied to about 38 percent lower risk of progressing to end-stage kidney disease.
A 10-year follow-up of 492 adults undergoing coronary angiography found that kynurenine, the main breakdown product of tryptophan, sharply predicted long-term mortality: 17.6 percent in the lowest tertile, 28.2 percent in the middle, and 42.9 percent in the highest. A high kynurenine-to-tryptophan ratio (meaning your body is breaking tryptophan down faster than it is coming in) is consistently a warning sign for both cardiovascular events and early death.
A meta-analysis of blood metabolites in major depressive disorder found that people with depression have lower blood tryptophan and lower kynurenic acid, along with shifts in related molecules. In a pilot study of 34 first-episode, drug-naive adults with depression, plasma tryptophan alone had an area under the curve of 0.74 for distinguishing people with depression from healthy controls, which is a moderate signal.
When inflammation is active, more of your tryptophan gets siphoned into the kynurenine path and less is available to make serotonin. That shift is thought to be one reason chronic inflammation tracks so closely with low mood. A blood tryptophan level cannot diagnose depression, but it can add context about the biology that clinical symptom scores cannot see.
In most disease states, lower tryptophan looks worse. But in a 10-year prospective study of 213 adults, higher baseline tryptophan actually predicted higher risk of developing type 2 diabetes, and adding tryptophan to an amino acid risk panel improved prediction. Obesity and fatty liver disease are also associated with higher circulating tryptophan, alongside more activity in the kynurenine pathway.
This is not a contradiction. Tryptophan is not a simple good-number-versus-bad-number marker. It reflects the balance between how much you take in from food and how fast your body is burning through it. In chronic inflammation, intake stays steady while breakdown speeds up, so the level falls. In overnutrition, intake rises faster than breakdown, so it climbs. Either direction can signal a problem. The useful question is not whether your number is high or low in isolation, but how it moves in relation to inflammation markers and your overall metabolic picture.
No major guideline body has set a clinical cutpoint for blood tryptophan. Tryptophan is primarily used in research settings, and reported values vary by lab method and population. The numbers below come from a published study of malnourished medical inpatients and are offered as orientation, not a target. Your own lab will likely report different numbers, possibly in different units, and the clinical meaning of any single reading depends on why you are testing.
| Tier | Plasma Tryptophan | What It Suggests |
|---|---|---|
| Low | Below 36.2 μmol/L | In a study of malnourished inpatients, associated with higher 30-day mortality and weaker response to nutritional support. |
| Higher | 36.2 μmol/L or above | Better short-term survival in the same study, but high readings should be interpreted alongside inflammation and metabolic markers, since very high values can also signal overnutrition. |
Compare your results within the same lab over time for the most meaningful trend. A single reading carries far less information than your own trajectory.
Tryptophan levels shift meaningfully with diet, inflammation, hormones, and time of day, which makes one-time snapshots easy to misread. The clinical value of this test comes from repeated measurement: getting a baseline when you are feeling well, retesting in 3 to 6 months if you are making dietary or medical changes, and then at least annually. A rising kynurenine-to-tryptophan ratio over time, even within normal-looking absolute numbers, is often the first sign of a drift toward higher inflammatory activity.
For preventive use, pair tryptophan with an inflammatory marker and amino acid panel so you can see whether movement in the number reflects real changes in your biology or just day-to-day noise. If you are making a specific dietary or lifestyle change, retest about 12 weeks later to check whether the change has actually shifted your level.
A single tryptophan reading can be distorted by factors that have nothing to do with your underlying health:
A single unusual tryptophan reading is almost never enough to act on. If your level is low, retest on a fasting morning after at least 72 hours without major illness or strenuous exercise, and get an inflammation panel including hs-CRP (high-sensitivity C-reactive protein, a blood marker of low-grade inflammation) at the same time. A persistently low tryptophan alongside elevated inflammation markers points toward chronic inflammatory activity that deserves a broader workup, potentially including evaluation of gut, autoimmune, or cardiometabolic drivers.
If your level is high and you are in a metabolic risk category (elevated BMI, prediabetes, fatty liver markers), the right next step is a metabolic workup including fasting insulin, HbA1c (a marker of average blood sugar over the past 2 to 3 months), and liver enzymes. A high tryptophan in the context of rising insulin resistance carries a different meaning than a high reading in a lean, inflammation-free adult. If results are persistently outside research-derived ranges and you cannot explain them with diet, medication, or illness, consider looping in a specialist familiar with amino acid metabolism, such as a metabolic physician or endocrinologist.
Evidence-backed interventions that affect your Tryptophan level
Tryptophan is best interpreted alongside these tests.