Researchers from the City University of New York Graduate School explored whether a diet rich in palm oil could influence multiple sclerosis by studying a mouse model that mirrors the human condition. The work, published in Glia, suggests that palm oil intake may affect nerve health by pushing the production of a specific lipid called ceramide, which can influence cellular energy and inflammatory responses in the nervous system.
Multiple sclerosis is an inflammatory autoimmune disorder characterized by damage to the protective myelin sheath around nerve fibers. This disruption impairs signal transmission and leads to a range of symptoms that can steadily worsen over time. Common manifestations include progressive muscle weakness, difficulty with fine motor tasks, speech and vision problems, dizziness, and numbness. Understanding how dietary factors might modulate this process is an ongoing area of research because lifestyle choices could potentially influence disease activity and quality of life for people living with MS.
To examine palm oil’s impact on disease development, researchers used mice that develop autoimmune encephalomyelitis, a well-accepted stand‑in for human MS. The animals were fed a diet high in palm oil to determine whether this fat source could intensify inflammatory demyelination. The results showed that the palm oil–rich diet aggravated the severity of symptoms and the underlying pathology in this MS-like model. These findings point to a connection between a palm oil–based dietary pattern and the trajectory of neuroinflammatory damage in MS.
The team traced the cause to a metabolic pathway in which palmitic acid, a major fatty acid found in palm oil, is converted into C16-ceramide. This lipid molecule was found to disrupt mitochondria, the energy hubs of the cell, which in turn reduces the energy available to neurons to counteract inflammation. Mitochondrial dysfunction is a known contributor to neuronal vulnerability in inflammatory conditions, and these results provide a plausible mechanism linking dietary fat to nerve injury in MS. By starving neurons of energy at a critical moment during inflammation, the ceramide pathway appears to amplify neural damage in the diseased brain and spinal cord.
Crucially, the researchers demonstrated that preventing ceramide buildup could blunt the negative effects of a palm oil–rich diet. When the CerS5 and CerS6 enzymes, responsible for producing ceramide, were inhibited, the animals showed markedly improved outcomes. Even on a diet high in palmitic acid, health and neurological function were better compared with untreated controls. This finding underscores the potential of targeting ceramide synthesis as a therapeutic approach to slowing or halting neurodegeneration in MS and related disorders.
From a therapeutic perspective, the study opens new avenues for developing treatments that address lipid-derived stress in neurons. By limiting ceramide production or shielding mitochondria from ceramide‑related damage, there could be a way to preserve neuron energy during inflammatory episodes and reduce the rate of disease progression. While the results come from an animal model, they provide a compelling rationale for translating ceramide-focused strategies into human research, with the aim of complementing existing MS therapies and lifestyle interventions.
Context matters. Earlier work in this field has explored connections between multiple sclerosis and other diseases, including cancer, highlighting how metabolic and inflammatory pathways can intersect across conditions. The current findings contribute to a broader understanding of how fats influence neural resilience and inflammatory responses, offering researchers new angles to investigate in hopes of improving outcomes for people affected by MS. These findings also invite careful consideration of dietary patterns as part of a comprehensive approach to managing inflammatory CNS disorders.
In summary, this study from CUNY’s graduate program demonstrates that a palm oil–rich diet can worsen MS-like pathology in mice by promoting ceramide production, which damages mitochondria and drains neuronal energy. Blocking the CerS5 and CerS6 enzymes mitigates these effects, suggesting a potential target for future therapies. The work invites further investigation into whether similar mechanisms operate in humans and how dietary fat modulation might fit with emerging treatments to slow the progression of multiple sclerosis.