Chronic Fatigue Initiative has mounted the first scientifically-rigorous and statistically-significant wide-scale research into the underlying infectious, immunological and toxicological causes of Chronic Fatigue Syndrome ("CFS"), which had previously attracted little to no resources for basic research. As the causes of the illness are deciphered, CFI's goal is to disseminate its findings in order to equip the broader research community to work on mechanisms of the disease as well as diagnostics, treatment and prevention. CFI, which is located in New York City, was created and funded by the Hutchins Family Foundation.

Hutchins Family Foundation was established by Debbie and Glenn Hutchins to support initiatives that have personal meaning to their family. To date, it has focused on programs in public policy, education, and health. The HFF seeks to have the greatest impact in the shortest period of time with the most efficient use of its resources. It insists that the outcome of its philanthropy is as tangible, measurable and valuable as possible.

CFI’s unique private funding strategy brings together a variety of scientific and academic partners to ensure that the best minds can collaborate and drive new solutions. Its comprehensive strategy includes funding for an epidemiology study; a well-characterized cohort recruitment; pathogenesis discovery research; and a Mechanism of Illness grant program that will fund additional research.

CFI ensures that the best minds can collaborate and drive new solutions for CFS patients.

Participating institutions include the Center for Infection and Immunity at Columbia University, Harvard School of Public Health, Harvard Medical School, Duke University, NewYork-Presbyterian/Columbia University Medical Center, Brigham & Women’s Hospital, Massachusetts General Hospital, University of Miami and University of Utah.

By simultaneously seeking the causes and treatment of CFS and leading research to understand the breadth of the affected population, CFI aims to build awareness, reduce social stigma connected to the disease, and ultimately improve patient lives in a comprehensive way.

CFI believes that as more policy makers and industry experts grasp the full scale of CFS, they will more likely respond in kind and increase efforts to promote research surrounding the disease.

CFI provided substantial financial support to explore the causes of the disease.

• Neither foundations, nor institutions, nor government funded a proportionate amount

Lit the path / created the tools for researchers to follow the science

• Creation of a well-characterized, large cohort of 200 subjects and 200 controls
• Gathered bio-samples and data
• Funded largest epidemiological study performed to date (see Operating Budget)
• Study helped lead a 15-member panel of the Institute of Medicine to conclude that Chronic Fatigue Syndrome is a physical illness, not a psychological disorder.
• Directs physicians to treat CFS as a physical illness

Scientists discover robust evidence that CFS is a biological illness

• Columbia - cerebrospinal fluid:  levels of most cytokines/antibodies, including the inflammatory immune molecule interleukin 1, were depressed in individuals with CFS
• Columbia - plasma: Specific biomarker patterns in patients of fewer than three years. Early onset patients had increased amounts of many different types of cytokines with an unusually strong manifestation of Interferon Gamma.
• Cornell - Analysis of mitochondrial genomes in CFS cases indicates that individuals of a certain haplogroup or carrying specific SNPs are more likely to exhibit certain neurological, inflammatory, and/or gastrointestinal symptoms. No increase in susceptibility to CFS of individuals carrying particular mitochondrial genomes or SNPs was observed
• Stanford – In patients the ATP levels levels are higher and mitochondrial cristae are more condensed compared to their paired controls, while the mitochondrial crista length, mitochondrial size, shape, density, membrane potential, and enzymatic activities of the complexes in the electron transport chain remain intact. Further, the increased ATP largely comes from non-mitochondrial sources. The fatigue symptom in this cohort of patients is unlikely caused by lack of ATP and severe mitochondrial malfunction; it might be linked to a pathological mechanism by which more ATP is produced by non-mitochondrial sources.

Ongoing research

• Columbia - Immuno-phenotyping (TruCulture) - We will examine 600 mRNA segments and 60 Cytokine/Chemokine profiles pre and post exercise with 20 CFS and 20 controls.
• Columbia – Microbiome - Microbiome study quantifying differences in the families of ‘gut’ bacteria and DNA of CFS/Control patients.
• Columbia – Epigenetics - Study of DNA methylation and histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. We will use the Cohort samples to measure Methylation in CFS/Control samples.
• Columbia - Specific Biomarkers in Allergic Phenotype of CFS patients
• Columbia - Specific Biomarkers in High Cognitive Disorder CFS patients
• Columbia - Significant cytokine differences in cerebrospinal fluid between atypical and classical CFS cases