A growing number of epidemiological studies confirm the existence of direct and inverse comorbidities between different Alzheimer’s disease (AD) types and certain cancers. Inverse comorbidities such as these provide an ideal opportunity to identify the mechanisms through which protection against both diseases might be conferred and exploited. A number of factors are generally considered to impact comorbidities, such as age, lifetime exposures, and socio-economic factors, but none yet have been found to play a role in cancer and AD comorbidity. Thus, overlapping genetic and molecular mechanisms hold the greatest promise in explaining relationships between these diseases. In this work, we demonstrate using statistical omics that inverse patterns of disrupted gene expression, associated with cellular metabolism and associated with inverse comorbidity, are detectable in the blood of cancer and Alzheimer’s patients. However, this is the first time these changes have been demonstrated to be detectable outside of the disease tissues. This suggests the possibility of blood markers that can identify certain individuals with reduced or increased risk for either disease.