Ozone high dose therapy (OHT) improves mitochondrial bioenergetics in peripheral blood mononuclear cells

Background: why mitochondrial function matters in chronic and acute disease

Mitochondria are the structures inside cells that convert oxygen and nutrients into usable energy. When their performance falls - a state described as mitochondrial dysfunction - cells have less capacity to meet demand and to withstand stress. This decline is a feature of many chronic and acute conditions, which has prompted interest in whether therapies that influence cellular metabolism might help restore reserve. Ozone high dose therapy (OHT), a form of ozone autohaemotherapy in which blood is treated with an ozone-oxygen mixture and returned to the patient, has been proposed as one such approach. Until this study, its effect on the energy-producing machinery of human immune cells had not been measured directly.

Study design: mitochondrial testing of blood cells from six patients

The researchers followed six people receiving preventive ozone therapy. Each was given two OHT sessions within one week, using a ten-pass protocol delivering roughly 140,000 micrograms of ozone per session. Blood was sampled at three points - before treatment, immediately after the first session, and one week after the second - and peripheral blood mononuclear cells (a group of immune cells that includes lymphocytes and monocytes) were isolated from each sample. In the laboratory these cells were analysed with a Seahorse extracellular flux analyser, an instrument that measures how quickly cells consume oxygen. A mitochondrial stress test was used to derive basal, ATP-linked and maximal oxygen consumption, spare reserve capacity, and non-mitochondrial oxygen use. These figures were combined into a Bioenergetic Health Index, a single summary score of mitochondrial performance. Because the analysis was carried out on cells outside the body, the study measures a laboratory marker of cellular energy rather than any clinical outcome.

Findings: higher bioenergetic health index and reserve capacity after two sessions

After the two sessions the cells showed measurable changes. The Bioenergetic Health Index rose significantly (p=0.045). The largest shifts were in maximal oxygen consumption and spare reserve capacity - the extra output cells can call on under stress - both of which increased markedly (p<0.001). Non-mitochondrial oxygen consumption also rose (p=0.014), which the authors interpreted as a sign of activated antioxidant enzymes. With six participants and no untreated comparison group, these results describe a short-term change in a laboratory measure rather than a demonstrated health benefit.

What the authors concluded

The authors reported this as the first demonstration of a beneficial effect of OHT on mitochondrial parameters in human blood cells. They suggested that OHT could be a safe and effective therapeutic option, either alone or as integrative and complementary support alongside pharmacological therapy, in the range of chronic and acute diseases in which mitochondrial dysfunction plays a central role. This is the authors' interpretation of a small mechanistic study, and it reaches well beyond what six patients and a single laboratory marker can establish.

Limitations of this study

The study is small and preliminary. It included only six patients, had no control or placebo group, and was not randomised, so any change over time cannot be separated from natural variation or other influences. It measured cellular energy in isolated blood cells in the laboratory - a mechanistic marker - and did not track symptoms, disease progression or any clinical endpoint, so it cannot show that patients felt or fared better. Follow-up extended only to one week after the second session, leaving durability unknown. Readers should also be aware that the journal has attached an editorial note (15 January 2025) recording that concerns were raised about the lack of full informed consent for using patients' blood samples and about an undeclared conflict of interest - the first author's financial interest in the facility where the mitochondrial experiments were performed - and urging readers to take these points into account. Taken together, this is early, mechanistic laboratory evidence that should be read as hypothesis-generating rather than proof of clinical benefit.