Author: Horst Gross
Fasting alters core physiologic processes — including inflammation regulation, energy metabolism, and neuronal plasticity — and these shifts can change the trajectory of chronic pain, particularly when peripheral and central mechanisms interact. At the German Pain and Palliative Care Days 2026, Louise Reisner-Sénélar, MD, medical director at the Schmerzzentrum-Wiesbaden (Pain Centre Wiesbaden), Wiesbaden, Germany, presented the lecture “Fasting and nutrition as a complement in interdisciplinary pain therapy — theory and science,” outlining how therapeutic fasting may be used as an adjunct in outpatient pain care.
Seizing the Opportunity
In primary care, nutrition is discussed mainly in connection with metabolic and cardiovascular diseases. Its potential within pain therapy, however, often goes unused.
Anti-inflammatory Metabolic State
At the core is a metabolic shift: When glycogen stores are depleted, the body switches to fat metabolism and enters ketosis, which measurably modulates inflammatory activity. Levels of proinflammatory cytokines such as TNF-alpha and interleukin-6 (IL-6) fall, while cellular proteostasis and regenerative processes are upregulated, reducing systemic inflammatory burden. Reisner-Sénélar reported that these changes translate into tangible benefits for patients in daily life.
Less Cellular Stress
Unlike pharmacologic strategies, fasting does not selectively target individual signaling pathways. Instead, it fundamentally modulates metabolic homeostasis. A key factor is increased autophagy: Damaged cellular components are degraded more efficiently, and intracellular stress responses are reduced. This could matter particularly in chronic pain syndromes, where such mechanisms are often impaired. The available data is still limited, but the biological connections are plausible.
Chronic pain cannot be explained solely by peripheral causes. Central sensitization and increased neuronal excitability contribute significantly to persistence. At this point, the effects of fasting act indirectly. Under ketosis, concentrations of beta-hydroxybutyrate rise. This is associated with increased expression of brain-derived neurotrophic factor — a neurotrophic factor that influences synaptic adaptation. These neuroplastic changes can weaken maladaptive circuits and thus help deprogram the pain memory. In addition, oxidative stress in nerve cells appears reduced. Sensory processing becomes more stable, and neuronal hyperexcitability may decrease, according to the hypothesis.
Raised Pain Threshold
Clinically, patients often report an increased pain threshold during or after fasting periods. Stimuli are perceived as less intense. These effects affect not only the sensory dimension; mood also improves for some patients, which in turn influences pain processing.
Mixed Study Results
However, the evidence remains heterogeneous. In the Nutrifast study with patients who have rheumatoid arthritis, no significant difference in the Health Assessment Questionnaire Disability Index was observed after 12 weeks compared with a control group on standard nutrition. Notably, the fasting group showed a faster response and a more stable course over time.
Studies on intermittent fasting, for example, in postmenopausal women with rheumatoid arthritis, provide a mixed picture. While reductions in inflammatory markers and oxidative stress are consistently detectable, the effects on subjective pain intensity compared with standard therapy often remain inconsistent.
Effects in Fibromyalgia
Observational studies of multimodal fasting programs in fibromyalgia show short-term improvements in pain and quality of life. From these studies, however, statements about the isolated effect of fasting or about long-term outcomes cannot yet be drawn. Fasting should therefore not be seen as a standalone therapy. Rather, it acts as a metabolic modulator that can complement existing therapeutic approaches. The described effects on C-reactive protein, IL-6, and TNF-alpha, as well as the activation of autophagy, are biologically plausible and potentially clinically relevant, even though robust long-term data are still lacking.
Physician Counseling
Not every patient is suitable for extended fasting periods. Comorbidities, medications, and individual resilience must be considered. At the same time, combining moderate fasting with physical activity can be sensible. Both interventions can synergistically improve mitochondrial function and cellular energy availability. However, this requires a physician to oversee the process. Patients need clear explanations of mechanisms and realistic expectations. Fasting does not produce immediate effects. Those who understand these connections generally show higher adherence and are more likely to benefit from the intervention.