Fasting, the Immune System, and Inflammation

Why True Healing Requires Order — and How IHHT May Produce Similar Biological Effects

The Nature of Inflammation — A Necessary but Potentially Harmful Mechanism

Inflammation is not a mistake of the body. It is a biological service.

Whenever tissue is injured, pathogens invade, or cells become damaged, the organism activates inflammatory processes. Immune cells are mobilized, repair programs are initiated, and damaged structures are broken down and cleared. Without inflammation, healing would not be possible.

However, inflammation also has a second side. It functions much like a fire department:

At the right moment, it is life-saving.
When it remains active for too long, it begins to damage the very structures it was meant to protect.

This is precisely what we observe today in many chronic diseases. The body is not in a strong acute inflammatory reaction, but rather in a state of low-grade, persistent activation. This condition — often referred to as chronic low-grade inflammation or “silent inflammation” — frequently goes unnoticed for long periods, yet it gradually burdens organ function and regulatory systems.

Systems that are particularly affected are those that depend heavily on energy availability and precise regulation:

• mitochondrial energy production
• nervous system regulation
• central metabolic pathways
• the balance of the immune system itself

The consequences often appear as symptoms that initially seem nonspecific: fatigue, diffuse pain, mental restlessness, reduced resilience, poor sleep, or a persistent feeling of internal exhaustion.

Many people interpret these signals as a psychological problem or simply as a temporary stress reaction. This is not entirely incorrect — stress certainly plays a role. But in many cases a biological imbalance has already developed: a body that continuously expends energy on defense and alertness rather than on regulation and stabilization.

When the Body Never Gets a Break

A key factor in this development is that modern metabolism rarely experiences true periods of rest.

Food is constantly available. Energy is continuously supplied. As a result, many cellular repair programs that historically became active during metabolic pauses are now activated only to a limited degree.

This is where the topic of fasting becomes particularly interesting.

Why Fasting Can Have Immunoregulatory Effects

Fasting is often perceived as a stressor for the body — or as a necessary sacrifice for weight reduction. In reality, however, it triggers a series of biological adaptation processes that may relieve stress on many physiological systems.

When the body does not receive external nutrition for a certain period of time, metabolism undergoes fundamental changes. Energy and organic resources are used more efficiently, cellular repair programs are activated, and processes that are normally less active during continuous nutrient intake become more prominent.

One of these processes is autophagy, a cellular recycling system in which damaged proteins and defective cellular components are degraded and reused.

At the same time, several immune signaling pathways shift. Pro-inflammatory signaling molecules may decrease, while regulatory mechanisms become more prominent.

Put simply:
The immune system no longer operates in a constant alarm mode, but instead has the opportunity to reorganize its processes.

A well-regulated immune system is not aggressive — it is precise.

And it certainly does not work against the body. This is a topic I will explore in greater depth in a future article.

The Immunological Intelligence of Metabolic Pauses

During metabolic pauses such as fasting, numerous studies have observed changes associated with improved regulation of inflammatory processes.

These include reductions in specific inflammatory signaling pathways — including those associated with cytokines such as IL-6 or TNF-α — as well as reductions in oxidative stress.

At the same time, mitochondrial function tends to stabilize. Because mitochondria play a central role not only in cellular energy production but also in immune signaling, their efficiency directly influences the body’s ability to distinguish between defense and repair.

In such phases, the body does not necessarily work harder — it works more economically.

Energy is no longer predominantly consumed by alarm reactions, but can instead be redirected toward stabilization and repair.

A Different Approach: Intermittent Hypoxia Training (IHHT / IHT)

Not every person can or should fast.

In clinical practice, there are many situations — such as states of exhaustion, certain metabolic disorders, or ongoing pharmacological therapies — in which prolonged fasting periods may not be appropriate.

This is where another physiological stimulus becomes relevant: controlled alterations in oxygen availability.

During Intermittent Hypoxia-Hyperoxia Training (IHHT or IHT), the body is repeatedly exposed to short phases of reduced oxygen concentration followed by phases of normal or elevated oxygen supply.

These controlled stimuli trigger adaptive responses throughout the organism — including within the mitochondria.

Mitochondria respond to these signals by improving their efficiency, regulating oxidative stress more effectively, and stabilizing their function over time.

Because mitochondrial activity is closely linked to immunological signaling pathways, this adaptation may also influence inflammatory processes.

IHHT does not replace fasting.
However, through a different biological pathway it may support similar regulatory effects: improved energy efficiency, reduced oxidative burden, and more stable cellular communication.

Clinical Perspective: Regulation Rather Than Suppression

Many conventional therapeutic approaches focus on pharmacologically blocking or suppressing inflammation. In acute situations this can be life-saving and remains an indispensable component of modern medicine.

Regenerative and regulatory medicine, however, often pursues an additional objective: not merely suppressing inflammation, but improving the regulatory capacity of the system itself.

Fasting and IHHT belong to the class of interventions that target precisely this level.

They do not primarily alter individual symptoms, but rather the energetic conditions under which the body operates.

When energy production becomes more stable and oxidative stress decreases, the immune system can respond in a more differentiated manner — less chaotic, less exhausting, and more precise.

Conclusion

Chronic inflammation is rarely an isolated immune problem.
It is closely connected to energy metabolism, metabolic regulation, and mitochondrial function.

Fasting may help regulate these relationships by shifting metabolism into a state that promotes repair and efficiency.

Intermittent hypoxia training takes a different approach: targeted mitochondrial adaptation through controlled oxygen stimuli.

Ultimately, both strategies pursue the same goal — the restoration of biological order.

How these mechanisms can be applied in practice and which clinical decision criteria are relevant will be discussed in detail in our online courses on Intermittent Hypoxia Training together with hypoxia expert and cellular medicine specialist Dr. med. Egor Egorov.

Recommended Courses on This Topic

Online Course:
IHHT/IHT Coaching Intensive with Dr. med. Egor Egorov

Online Course:
Effects of IHHT/IHT on Autophagy and Metabolic Pathways — Activating the Cellular Program for Regeneration and Healthy Aging

Online Course:
IHHT/IHT – Application-Oriented Perspectives in Neurodegeneration with Dr. med. Egor Egorov
Marion Massafra-Schneider

Scientific References

1. Mizushima N, Komatsu M. Autophagy: renovation of cells and tissues. Cell. 2011;147(4):728–741.
2. Longo VD, Mattson MP. Fasting: molecular mechanisms and clinical applications. Cell Metabolism. 2014;19(2):181–192.
3. de Cabo R, Mattson MP. Effects of intermittent fasting on health, aging, and disease. New England Journal of Medicine. 2019;381(26):2541–2551.
4. Brandhorst S, et al. A periodic diet that mimics fasting promotes multi-system regeneration and healthspan. Cell Metabolism. 2015;22(1):86–99.
5. West AP, Shadel GS. Mitochondria in innate immune responses. Nature Reviews Immunology. 2017;17(6):363–375.
6. Navarrete-Opazo A, Mitchell GS. Therapeutic potential of intermittent hypoxia: a matter of dose. Experimental Neurology. 2014;256:45–55.
7. Serebrovska ZO, et al. Intermittent hypoxia training as non-pharmacological therapy. Frontiers in Physiology. 2019;10:123.

Note
The cited studies are provided for scientific contextualization of the described biological mechanisms. They do not constitute individualized therapeutic recommendations and do not replace medical diagnosis or treatment.

Additional Articles on Related Topics

• Neuroinflammation, Fasting & Intermittent Hypoxia Training
• mTOR, Autophagy & Fasting
• AMPK and Metabolic Regulation
• Autophagy & Cellular Recycling