The question of whether COVID-19 can lead to high cholesterol is complex, reflecting the virus’s widespread impact on the body’s metabolic systems. Cholesterol and other lipids are fundamental components of cell membranes and play a role in the immune system, meaning any severe systemic infection can disrupt their balance. Evidence from patients and research studies suggests a clear, dynamic relationship where the virus first causes a temporary drop in blood lipids during the acute illness, followed by a potential and sustained increase in cholesterol levels weeks or months after recovery. This dual effect highlights the necessity of monitoring metabolic health in patients who have recovered from the infection.
Understanding Dyslipidemia and COVID-19
Dyslipidemia describes abnormal levels of lipids in the bloodstream, including cholesterol and triglycerides. These lipids are transported by lipoproteins, such as low-density lipoprotein (LDL, “bad” cholesterol) and high-density lipoprotein (HDL, “good” cholesterol). The primary concern with dyslipidemia is its link to cardiovascular disease, making healthy lipid levels important for long-term health.
COVID-19, caused by the SARS-CoV-2 virus, is a systemic disease that triggers widespread inflammation throughout the body. This inflammatory response is a key factor in how the infection interacts with lipid metabolism. The virus’s systemic reach and immune activation explain why lipid levels fluctuate significantly during and after the illness.
Acute Viral Impact on Lipid Levels
During the active phase of a COVID-19 infection, the body experiences acute systemic stress and intense inflammation. This immediate response is characterized by a sharp, temporary drop in total cholesterol, LDL cholesterol, and HDL cholesterol levels. Studies consistently reported lower cholesterol levels in hospitalized COVID-19 patients compared to healthy individuals.
This phenomenon, called “hypolipidemia of infection,” is a common response to severe inflammation. The body rapidly consumes or redistributes cholesterol, especially HDL, as part of the acute immune response. Lower HDL levels during the acute phase have been associated with a more severe disease course. While total and LDL cholesterol decrease, triglyceride levels often show an opposite trend, frequently rising during the acute infection.
Long-Term Changes Post-Infection
The most significant finding relates to the sustained changes observed after the acute infection has passed. For many patients, the temporary drop in lipids reverses, leading to a rebound where cholesterol and triglyceride levels become persistently elevated. This sustained elevation in LDL and triglycerides, known as new-onset hyperlipidemia, is increasingly recognized as a complication in the post-acute phase of SARS-CoV-2 infection (PASC), often referred to as Long COVID.
Research examining the long-term health of COVID-19 survivors shows an increased risk for new cholesterol problems. One large-scale study found that infected individuals were significantly more likely to develop elevated levels of total cholesterol, LDL cholesterol, and triglycerides months after recovery. This finding was often present in people who had no history of metabolic issues before their infection.
In contrast to the acute phase, the post-recovery period is often marked by an unfavorable lipid profile, including persistent high LDL and triglycerides, along with a sustained low level of the protective HDL cholesterol. These lingering abnormal lipid levels contribute to an increased overall cardiovascular risk in the months following infection. Therefore, medical guidelines now recommend that lipid panels be checked as part of the cardiovascular risk evaluation for patients recovering from COVID-19, especially those experiencing Long COVID symptoms.
Biological Mechanisms Linking COVID-19 and Cholesterol
The mechanism behind these changes involves both direct viral activity and the systemic immune response. Widespread systemic inflammation, often referred to as a cytokine storm, disrupts the liver’s normal lipid processing. Inflammatory molecules interfere with pathways regulating the synthesis and clearance of cholesterol and triglycerides, leading to a temporary acute drop and then a dysregulated, pro-atherogenic state afterward.
The SARS-CoV-2 virus also directly manipulates cellular cholesterol to facilitate its own life cycle. The virus requires cholesterol to successfully enter host cells and to complete its replication process. The virus’s spike protein interacts with the host cell receptor ACE2, which resides in cholesterol-rich areas of the cell membrane.
The virus appears to hijack the cell’s internal cholesterol trafficking system. Viral proteins, like ORF3a, cause cholesterol to become sequestered within cellular compartments called lysosomes, disrupting the normal flow and utilization of cholesterol. This manipulation contributes to both the immediate metabolic disturbances and the sustained changes seen weeks later, leading to long-term hyperlipidemia.