Starting statin therapy as soon as possible can dramatically reduce the risk of heart attack and stroke for patients with diabetes, according to a new study published in the Journal of the American Heart Association. Despite clinicians’ recommendations, nearly one-fifth of diabetic patients choose to delay taking statins, which is a proven and effective way to lower cholesterol levels.

Researchers from Mass General Brigham conducted an analysis of electronic health records of 7,239 patients with diabetes who started statin therapy over a nearly 20-year period. The study found that those who delayed statin therapy for more than a year were significantly more likely to experience heart attacks or strokes compared to those who started taking the medication right away.

The median age of the patients in the study was 55, and about half of them were women. The researchers used artificial intelligence methods to gather data from the electronic health records and found that nearly one-fifth (17.7%) of the patients declined statin therapy when it was first recommended by their clinicians. However, they later accepted the therapy after a median of 1.5 years.

The study’s findings are clear: starting statin therapy on time can save lives. For diabetic patients who delayed taking the medication, the rate of heart attacks or strokes was 8.5%, compared to just 6.4% for those who started taking statins immediately.

Clinicians should use this information to guide shared decision-making conversations with their patients, said senior author Alexander Turchin, MD, MS. “Time is of the essence for your heart and brain health,” he added.

The researchers’ findings are timely, given that heart attacks and strokes remain the leading causes of complications and mortality for patients with diabetes. Statin therapy has been proven to reduce risk by preventing plaque buildup in blood vessels, which can lead to delivery problems for the heart and brain.

The study’s authors emphasize the importance of early intervention and encourage diabetic patients to discuss their individual risks and treatment options with their clinicians. By starting statin therapy on time, patients with diabetes can significantly reduce their risk of heart attack and stroke, and improve their overall health and well-being.

The PREVENT risk calculator has been shown to accurately estimate 10-year cardiovascular disease (CVD) risk and identify individuals with plaque buildup in their heart’s arteries, according to new research published in the Journal of the American Heart Association. The study found that combining the PREVENT score with a coronary calcium score further improved risk prediction, matching patients with the highest risk of heart attack to those who actually experienced one during the follow-up period.

The PREVENT calculator, released by the American Heart Association in 2023, estimates CVD risk based on age, blood pressure, cholesterol levels, body mass index, Type 2 diabetes status, social determinants of health, smoking, and kidney function. This tool can help tailor care and determine who may benefit from treatment to prevent a heart attack.

Another important factor in screening heart health is coronary computed tomography angiography (CCTA), a non-invasive imaging test that visualizes plaque buildup in the heart’s arteries. The CCTA provides a coronary artery calcium (CAC) score, which helps inform decisions about heart disease prevention and treatment.

The researchers analyzed electronic health records for nearly 7,000 adults who had undergone CCTA screening at NYU Langone Health between 2010 and 2024. They found that the PREVENT score accurately matched the level of calcium buildup according to the CAC score. The study also used the PREVENT risk assessment and coronary artery calcium scores, separately and in combination, to predict future heart attack risk and assess the accuracy of each with the participants who had a heart attack during the follow-up period.

Study co-author Sadiya Khan emphasized that the CAC score can help classify risk for heart disease by analyzing calcium buildup. The study’s findings are important in shaping future guidelines on the use of the PREVENT calculator and CCTA, particularly for patients uncertain about starting lipid-lowering therapy or intensifying it.

The study had several limitations, including a single institution as the data source and a predominantly white participant population, which may not be generalizable to other groups. The analysis only included people who had undergone coronary calcium screening, and electronic health records were the sole source of data. Additionally, the follow-up time was relatively short at 1.2 years, and the presence of non-calcified plaque in the heart’s arteries was not assessed.

Despite these limitations, the study demonstrates that the PREVENT risk calculator is accurate in identifying individuals with subclinical risk for CVD, meaning blocked arteries before symptoms develop. This research contributes to shaping future guidelines on the use of the PREVENT calculator and CCTA.

Researchers at NYU Grossman School of Medicine have made a groundbreaking discovery that sheds light on how cells process energy from food. A study published online in Nature reveals a novel mechanism that enables drastic weight loss by manipulating cellular energy processing. The findings, which detail the effects of cysteine depletion on mammalian metabolism, have far-reaching implications for our understanding of how to induce weight loss.

In the study, mice genetically engineered to lack cysteine, an essential amino acid found in most foods, were fed a diet devoid of cysteine. Within one week, these animals experienced significant weight loss, dropping 30% of their body weight on average. This drastic reduction was achieved by disrupting normal metabolic pathways used by cells to convert food into energy.

The researchers identified coenzyme A (CoA), a small molecule involved in over 100 intermediate metabolic reactions and serving as a partner for nearly 4% of all enzymes in the body, as the key factor contributing to this weight loss. By depleting CoA levels through cysteine restriction, cells were forced to rapidly burn stored fat reserves, leading to the observed weight reduction.

What is remarkable about this study is that it was previously impossible to directly examine CoA’s function due to the fact that mice with defective CoA synthesis typically do not survive beyond three weeks of age. The researchers have now been able to detail how CoA shapes metabolism in adult mice, providing new insights into cellular energy processing.

While achieving a truly cysteine-free diet would be challenging for most people, this study highlights the potential benefits of reducing cysteine intake through dietary modifications. For example, fruits, vegetables, and legumes contain lower levels of cysteine compared to red meat.

The authors caution that eliminating cysteine or inhibiting its production could have unintended consequences on organ function, particularly in vulnerable individuals who may be more susceptible to everyday toxins, including medications. However, this research opens up new avenues for understanding how cellular energy processing can be manipulated to induce weight loss without completely removing cysteine from the diet.

Future studies will focus on hijacking parts of this process to safely and effectively induce weight loss in humans while minimizing potential risks associated with cysteine depletion. This breakthrough mechanism has far-reaching implications for our understanding of how to tackle obesity, a major public health concern worldwide.