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Keywords:

test cortisol, high cortisol symptoms, low cortisol, stress hormone testing, burnout biomarker, neurostress profile, DHEA cortisol, ORY Analyse

Kurz:

Cortisol too high or too low? Find out how the stress hormone affects your metabolism, sleep and energy – and what a test shows.

Tryptophan – the small amino acid with a big impact on mood, sleep & energy

You are sitting in a meeting, nodding professionally – and inside, your body is going wild. Cortisol and adrenaline flood your blood as if a pride of lions were after you. Except there is no lion. There is a Slack message with the subject “Urgent”.

That is exactly the problem. The Stanford neurobiologist Robert Sapolsky puts it well in his classic “Why Zebras Don't Get Ulcers”: zebras respond to stress acutely and efficiently – a short sprint, the lion is gone, cortisol settles. We humans spend another three days turning over what the boss might have meant. The result: chronically raised cortisol, quietly doing damage.

How cortisol acts in metabolism

Cortisol is not an enemy. It is a vital steroid hormone, produced in the adrenal cortex, that affects almost every metabolic process in the body. In the morning, shortly after waking, it rises steeply – the cortisol awakening response, which brings the body up to operating readiness. It raises blood sugar, mobilises fat reserves as an energy source, dampens inflammatory responses and sharpens concentration for a short while. At the right dose, cortisol is a high-performance hormone. The problem starts when the dose never comes down.

If the spark doesn't ignite

If tryptophan levels are low – or if it doesn't reach the brain effectively because it competes with other large amino acids for entry – this can manifest as mood swings, restlessness, poor sleep, and difficulty concentrating. Studies show that tryptophan supplementation can slightly improve mood and reduce anxiety in healthy individuals; overall, the effect is moderate but measurable.

Also interesting: Not only the quantity, but also the protein source matters. Different proteins significantly alter the ratio of tryptophan to other amino acids in the blood – and thus potentially the production of serotonin in the brain.

Magazine expert: When mood, energy or sleep fluctuates, it's worth thinking outside the box – the gut, neurotransmitters, and micronutrients work as a team.


Why this matters for your health – and what you can do

This is the side of the story hardly anyone knows – and it is often missed. Cortisol that is too low, known as adrenal insufficiency or, in milder form, as adrenal fatigue, brings lasting exhaustion despite enough sleep, low blood pressure, dizziness on standing, muscle pain with no clear cause and a strong craving for salt. Many people are written off for years as “just tired”, because a low cortisol level is not routinely picked up in a standard blood count. This is one of the most common diagnostic gaps in modern medicine.

Lifestyle impulses that can be implemented immediately

  1. Combine smartly: In the evening, opt for tryptophan-rich snacks plus a little carbohydrates – for example, natural yogurt with rolled oats, whole-grain bread with cottage cheese, or a small chicken wrap. This improves absorption by the brain.
  2. Colorful food makes you cheerful: An antioxidant-rich diet (berries, colorful vegetables, nuts) can also have a positive influence on mood and cognition – especially in the case of “silent inflammation”.
  3. Sleep ritual instead of sleep scroll: Dark, cool, regular – and little alcohol late in the evening (disrupts the sleep rhythm and neurotransmitter balance).
  4. Gut health is key: A healthy microbiome mix supports the tryptophan-serotonin axis (the "gut-brain axis"). Fiber, fermented foods (yogurt, kimchi), and exercise help.

Which values really count

To understand how your stress system really works, you need more than a single value. What matters is cortisol across the day, measured in saliva at four points – morning, late morning, afternoon and evening. That pattern shows whether the body powers up properly in the morning and really winds down in the evening. DHEA-S goes with it as the direct counterweight to cortisol: if DHEA is low and cortisol high, the ratio has shifted – an early sign of exhaustion and accelerated ageing. Neurotransmitters in urine – serotonin, dopamine, adrenaline and noradrenaline – show how much the nervous system has already suffered under the cortisol load. Melatonin tells you whether sleep still brings real recovery or only numbness.

Why ORY Analyse makes the difference here

Most people sense that they are too stressed. But a hunch is not a diagnosis. ORY Analyse puts together a full neurostress profile: cortisol across the day, DHEA, neurotransmitters and melatonin – interpreted, set out clearly and with concrete recommendations. Prevention does not begin with the symptom. It begins with the right value.

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Test your cortisol level

Do you know your cortisol level? This one hormone shapes how well you sleep, how much energy you have – and whether your body is stuck in constant stress.

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Fact check & sources

  • ory-berlin.de – Laboratory diagnostics & health checks: Overview and approach to modular analyses (e.g. basic panels, vitamin check, gut check-up).
  • Scientific:

    Richard et al. L-Tryptophan: Basic Metabolic Functions… – Basic functions, serotonin relationship, behavior. (Open-access review; also listed in PubMed.)

    Jenkins et al. Systematic Review: Tryptophan supplementation, mood/anxiety (moderate effects).

    Dietary proteins & TRP ratio: Proteins influence the tryptophan ratio – relevant for uptake into the brain.

    Gut-Brain-Axis & TRP: Interaction of gut bacteria–tryptophan–serotonin.

    Overview of serotonin & mood (Layman's explanation, Harvard Health).

  • Background notes from your file: Food sources, role in protein synthesis & serotonin, notes on sleep & mood are additionally based on the provided manuscript "ATP Energy and Tryptophan".

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Preventive lab testing for the whole family – Ory experts.

from microbiome through neurotransmitters to nutrient status. Functional medicine for more energy, resilience and long-term health – conveniently from home.

test - IDO, serotonin and melatonin in interaction in depressive disorders

IDO, serotonin and melatonin in interaction in depressive disorders

Modern research into the development of depressive disorders is increasingly recognizing that, in addition to psychological factors, biological factors also play a crucial role. A central biochemical approach is tryptophan metabolism, which encompasses not only the synthesis of neurotransmitters such as serotonin, but also the formation of other active metabolites such as melatonin and kynurenines. The enzyme indolamine 2,3-dioxygenase (IDO), in particular, plays a key role in this process, as its increased activity promotes the degradation of tryptophan into kynurenine metabolites, which can lead to an imbalance in the neurochemical system.

1. IDO and its influence on tryptophan metabolism
IDO is predominantly expressed in monocytes and dendritic cells and is induced by proinflammatory cytokines, particularly interferon-gamma (IFN-γ). This mechanism represents a physiological defense response to impede the proliferation of invading pathogens by depriving them of the essential amino acid tryptophan. However, persistent activation of IDO can occur in chronic, TH1-dominated inflammation or in the context of interferon-based therapy (e.g., in HCV infections).

Increased IDO activity and its consequences:

  • Tryptophan deficiency: Due to the increased conversion of tryptophan to kynurenine, less tryptophan is available for serotonin synthesis.

  • Reduced serotonin production: Since serotonin in the central nervous system (CNS) is involved in the regulation of mood, sleep and pain, its decrease can promote depressive symptoms.

  • Formation of kynurenines: Metabolites such as quinolinic acid and 3-OH-kynurenine, which result from tryptophan degradation, have neurotoxic properties and can also cause disturbances in the neuronal control circuits.

2. Serotonin: More than just a “happiness hormone”
Serotonin plays a multifunctional role in the brain and influences numerous physiological processes:

  • Mood regulation: A lack of serotonin is often associated with depressive states.

  • Sleep-wake rhythm: By regulating sleep, serotonin contributes to a stable internal clock.

  • Pain processing and appetite: In addition to emotional regulation, serotonin is also involved in the modulation of pain perception and eating behavior.

The limitation of serotonin synthesis due to a lack of tryptophan as a result of increased IDO activity can therefore lead to a number of neurological and psychological symptoms that are typical of depressive disorders.

3. Melatonin: The sleep regulator in the context of tryptophan metabolism
The hormone melatonin is synthesized from serotonin in the pineal gland. This hormone is essential for:

  • Regulation of the circadian rhythm: Melatonin helps to control the sleep-wake cycle and adapt it to daylight conditions.

  • Antioxidant effects: Melatonin also has protective properties against oxidative stress in the nervous system.

A balanced ratio of serotonin and melatonin is therefore crucial not only for mood, but also for healthy sleep and adequate stress management. Disturbed tryptophan metabolism, caused by increased IDO activity, can also indirectly impair melatonin synthesis, leading to sleep disorders and other secondary psychological stress.

4. Therapeutic approaches and diagnostics

4.1 Tryptophan supplementation
One possible therapeutic approach for depressive symptoms is targeted tryptophan supplementation to stabilize serotonin production. However, the following must be considered:

  • No increased IDO activity: Supplementation should only be used if there is no persistent inflammatory activation that promotes tryptophan degradation towards kynurenines through increased IDO activity.

  • Low tryptophan levels: The patient's actual tryptophan status should be determined using appropriate laboratory methods.

Supplementation may be particularly useful in disorders such as fructose malabsorption, which impede the absorption of tryptophan in the intestine, provided that other metabolic activations are not present.

4.2 Anti-inflammatory therapy
Elevated serum levels of TNF-α and IFN-γ (or measurable via IP-10) indicate systemic inflammation, which can lead to IDO overactivation. In such cases, if targeted causal therapy of the inflammation is not possible, general anti-inflammatory treatment can help alleviate the depressive symptoms mediated by increased IDO activity.
Especially patients with the IFN-γ polymorphism 874T/A, who produce increased levels of IFN-γ independent of an external inflammatory stimulus, can benefit from an anti-inflammatory therapeutic approach.

4.3 Diagnostics
Modern diagnostics include:

  • Analysis of tryptophan degradation: The inflammation-induced tryptophan degradation rate is investigated in isolated blood cells.

  • Measurement of inflammatory markers: Tryptophan, IP-10 and TNF-α are determined using immunological methods to assess the extent of inflammatory activity.

  • Genetic analyses: Determination of the IFN-γ polymorphism (874T/A) by DNA sequencing provides important information on individual inflammatory predisposition.


    5. Conclusion
    Research clearly shows that tryptophan metabolism and its regulation via IDO play a crucial role in the development of depressive disorders. By influencing serotonin and melatonin synthesis, neurochemical imbalances arise that can contribute to the development of depressive symptoms. A differentiated diagnostic approach that considers both inflammatory parameters and genetic predispositions is therefore essential for developing targeted treatment concepts.
    Therapeutic approaches range from individualized tryptophan supplementation—excluding elevated IDO activity—to anti-inflammatory measures, particularly in cases of genetically determined overproduction of IFN-γ. Ultimately, the integration of neuroendocrine-immunological aspects into clinical practice opens up new possibilities for the individualized treatment of depressive disorders.

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