Chlorine dioxide (CDS) is often described by proponents like Andreas Kalcker as a selective oxidant, capable of targeting harmful pathogens while sparing human cells. This purported selectivity is central to claims about its therapeutic potential. Understanding its mechanism requires a dive into basic chemistry and the biological environments where CDS operates.

Chlorine dioxide (ClO₂) functions through oxidation, a process where it accepts electrons from other molecules. Unlike stronger oxidants like bleach (sodium hypochlorite), which non-specifically damage tissues, ClO₂ is argued to be selective due to its reaction preferences. It primarily targets electron-rich compounds, such as those found in the cell walls of pathogens (bacteria, viruses, fungi, and parasites), while leaving human cells relatively unaffected. This selectivity is attributed to differences in pH and redox potential between microbial and human cells.

Pathogens often thrive in acidic environments and possess simpler biochemical structures without robust antioxidant defenses. When ClO₂ encounters these cells, it disrupts their membranes and critical proteins through oxidation, leading to cell death. In contrast, human cells operate at a near-neutral pH and are equipped with advanced antioxidant systems (e.g., glutathione, superoxide dismutase) that neutralize mild oxidative stress. Additionally, human cell membranes lack the same electron-rich targets, reducing the risk of damage.

Kalcker and others cite studies suggesting that ClO₂’s oxidative effects are concentration-dependent. At low, controlled doses (as used in CDS protocols), it may selectively eliminate pathogens without overwhelming human defenses. However, these claims are largely based on in vitro experiments and anecdotal reports rather than robust clinical trials. Critics argue that the margin of error is narrow, and improper dosing can still cause harm, such as oxidative damage to healthy tissues or methemoglobinemia—a condition where oxygen transport in blood is impaired.

While the theory of selective oxidation is plausible in principle, the scientific consensus remains skeptical due to limited human data and documented risks. Nonetheless, understanding this mechanism is key to evaluating the ongoing debate around CDS—a debate that hinges on balancing potential benefits against known dangers.

Chlorine dioxide (CDS) is often described by proponents like Andreas Kalcker as a selective oxidant, capable of targeting harmful pathogens while sparing human cells. This purported selectivity is central to claims about its therapeutic potential. Understanding its mechanism requires a dive into basic chemistry and the biological environments where CDS operates.

Chlorine dioxide (ClO₂) functions through oxidation, a process where it accepts electrons from other molecules. Unlike stronger oxidants like bleach (sodium hypochlorite), which non-specifically damage tissues, ClO₂ is argued to be selective due to its reaction preferences. It primarily targets electron-rich compounds, such as those found in the cell walls of pathogens (bacteria, viruses, fungi, and parasites), while leaving human cells relatively unaffected. This selectivity is attributed to differences in pH and redox potential between microbial and human cells.

Pathogens often thrive in acidic environments and possess simpler biochemical structures without robust antioxidant defenses. When ClO₂ encounters these cells, it disrupts their membranes and critical proteins through oxidation, leading to cell death. In contrast, human cells operate at a near-neutral pH and are equipped with advanced antioxidant systems (e.g., glutathione, superoxide dismutase) that neutralize mild oxidative stress. Additionally, human cell membranes lack the same electron-rich targets, reducing the risk of damage.

Kalcker and others cite studies suggesting that ClO₂’s oxidative effects are concentration-dependent. At low, controlled doses (as used in CDS protocols), it may selectively eliminate pathogens without overwhelming human defenses. However, these claims are largely based on in vitro experiments and anecdotal reports rather than robust clinical trials. Critics argue that the margin of error is narrow, and improper dosing can still cause harm, such as oxidative damage to healthy tissues or methemoglobinemia—a condition where oxygen transport in blood is impaired.

While the theory of selective oxidation is plausible in principle, the scientific consensus remains skeptical due to limited human data and documented risks. Nonetheless, understanding this mechanism is key to evaluating the ongoing debate around CDS—a debate that hinges on balancing potential benefits against known dangers.