Hidden Liver Protein Controls Cholesterol and Heart Disease Risk

Scientists Identify Master Switch for Cholesterol Control

Researchers at UT Southwestern Medical Center identified a protein that acts as a key regulator. This protein controls how the liver releases cholesterol carrying particles into the bloodstream. The discovery may transform treatment approaches for heart disease and fatty liver disease. Scientists found that the protein HELZ2 helps control activity of a crucial gene. This gene produces proteins responsible for transporting cholesterol through the body.

Researchers published the study in the American Heart Association journal Circulation. The research focused on how HELZ2 regulates apolipoprotein B. Cells need this gene to produce apoB proteins that form lipoproteins. These particles transport cholesterol and fats throughout the body. According to researchers, these particles significantly contribute to plaque buildup in arteries.

Zhao Zhang, Ph.D., Assistant Professor at UT Southwestern, explained the significance. He serves in the Center for the Genetics of Host Defense. He also works in Internal Medicine. Zhang stated that HELZ2 acts as a powerful control point. The protein determines how many cholesterol carrying particles enter the bloodstream.

How the Hidden Protein Reduces Harmful Cholesterol

The research team discovered that HELZ2 works through a specific mechanism. It shortens the lifespan of APOB messenger RNA inside liver cells. This mRNA carries instructions needed for cells to make proteins. When HELZ2 activity rises, the APOB message breaks down more quickly. This results in lower production of apoB proteins. Fewer cholesterol carrying lipoproteins enter the blood as a consequence.

Most previous research focused on what happens after apoB production. Researchers examined processes that occur after cells already make the protein. Yiao Jiang, Ph.D., a postdoctoral researcher, noted the surprising finding. He works in the Zhang Lab as study co author. Jiang explained that HELZ2 acts much earlier in the process. The protein controls how long the apoB message survives. This happens before cells even produce the protein.

Researchers used a large scale genetic screening system to uncover HELZ2’s role. Bruce Beutler, M.D. developed this system. He directs the Center for the Genetics of Host Defense. He also serves as Professor of Immunology and Internal Medicine at UT Southwestern. The screening technology enabled scientists to identify this hidden regulatory mechanism.

Food Preservatives Linked to Heart Disease in Major Study

A separate massive study identified another concerning factor affecting heart health. Researchers found that specific preservative additives show independent links to cardiovascular problems. These additives appear in thousands of packaged foods. The study tracked participants for nearly eight years. Findings held up even after researchers accounted for overall diet quality. Scientists also controlled for sodium intake and ultra processed food consumption.

The research appeared in the European Heart Journal. Scientists tracked adults in France from 2009 through 2024. Researchers analyzed participants’ diets and health outcomes throughout this period. The analysis included 112,395 adults with median follow up of 7.9 years. During that time, researchers identified 2,450 cardiovascular disease cases. They also documented 5,544 high blood pressure cases.

Detailed Tracking Reveals Preservative Dangers

This study stood out because of its exceptional detail level. Researchers did not broadly label foods as ultra processed. Instead, they tracked exposure to 58 individual preservative additives. Scientists used brand specific food records collected over up to 15 years. Additive content varies significantly from one brand to another. This variation occurs even within the same food category. The detail level allowed unusually precise estimates. Researchers determined how much of each preservative participants actually consumed over time.

Scientists grouped participants into lower, medium, and higher consumers of preservative food additives. Those with highest intake showed alarming results. Participants with highest total non antioxidant preservative intake faced a 16% higher risk of cardiovascular disease. They also showed a 26% higher risk of coronary heart disease. Researchers compared these individuals to those with lowest intake. Higher intake of total preservatives overall showed association with a 24% higher risk of high blood pressure.

Specific Additives Pose Serious Heart Risks

Researchers specifically flagged several individual additives for high blood pressure risk. Potassium sorbate, listed as E202, showed the highest risk increase. It demonstrated a 39% higher risk of hypertension. Citric acid, known as E330, linked to a 25% higher risk. Sodium nitrite (E250) showed a 16% higher risk. Potassium metabisulphite (E224) also demonstrated a 16% higher risk increase.

Ascorbic acid, labeled as E300, showed particularly concerning results. It linked to a 14% higher risk of high blood pressure. The same additive showed a 15% higher risk of cardiovascular disease. Sodium erythorbate (E316) demonstrated a 14% higher risk. Sodium ascorbate (E301) showed a 12% higher risk. Sulphites overall raised significant concerns among researchers.

Women Face Unique Heart Disease Challenges

Acute coronary syndromes affect women differently than men. Over 3.2 million women in the United States live with myocardial infarction history. More than 41,000 annual deaths occur from acute coronary syndromes among women. Women compared to men with these conditions face significant biases. Knowledge gaps result in missed and late diagnoses. Undertreatment leads to poorer outcomes for female patients.

Significant sex based and gender based disparities persist in cardiovascular care. These disparities affect epidemiology, diagnosis, management, and outcomes. The differences reflect biological and pathophysiological variations in disease manifestation. Evidence gaps exist due to longstanding lack of focus. Historical exclusion affects cardiovascular clinical trials. Women remain underrepresented, especially those of reproductive age and elderly women.

Sex differences in acute coronary syndromes encompass a spectrum of mechanisms. These range from coronary atherosclerosis to spontaneous coronary artery dissection. Vasospasm, coronary microvascular dysfunction, and embolic phenomena also play roles. Non atherosclerotic and non obstructive mechanisms occur more prevalently in women. Traditional diagnostic algorithms frequently miss these mechanisms. Women’s symptoms more likely include non chest pain presentations. This occurs especially at younger and older ages.