Priorities in obesity, CVD risk: optimizing body weight, atherogenic lipid levels
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Key takeaways:
- Obesity increases heart disease risk, in part due to adverse effects on lipid levels.
- Priorities for patients with obesity are reducing body weight and reduce atherogenic blood lipid levels.
Patients with obesity are at increased risk for CVD, in part due to the promotion of an atherogenic lipid profile, according to a speaker.
Patients with obesity may reduce their risk for CVD through weight reduction and improvements in atherogenic lipoproteins, as noted during the National Lipid Association Scientific Sessions.
Harold E. Bays, MD, DABOM, MFOMA, FTOS, FACC, FASPC, FNLA, the medical director and president of the Louisville Metabolic and Atherosclerosis Research Center and clinical associate professor at the University of Louisville School of Medicine, presented an overview of a joint expert review from the National Lipid Association and the Obesity Medicine Association on the relationship between obesity, dyslipidemia and CVD. In May the document was simultaneously published in Obesity Pillars and the Journal of Clinical Lipidology.
‘A natural integration’
“This joint expert review examines basic connections between obesity medicine and clinical lipidology, representing content I probably should have better known 30 years ago,” Bays said during the presentation. “I suspect many do not fully recognize the foundational relationship between lipids and obesity; a natural integration exists between these two disciplines.”
In a given patient with obesity, adipose tissue may store more than 50% of total body free cholesterol. Perhaps most important, clinically, especially in patients with obesity, adipose tissue is the organ that stores the most amount of body energy in the form of triglycerides, with body fat representing over 50% to 60% of body weight in some individuals, the authors of the expert review wrote. They noted that it is this storage of fat and adipose tissue expansion that accounts for the greatest variance in body weight in most people.
Regarding other lipids, “the role of cholesterol in adipose tissue is similar to the role of cholesterol in other body tissues, which includes cellular structure, signaling, and exchange with circulating lipoproteins,” Bays said.
Perhaps surprisingly, population studies suggest that excess adiposity confers only a modest increase in LDL. More common in patients with obesity is an adiposopathic dyslipidemia that includes elevated triglycerides, reduced HDL, increased non-HDL, higher apolipoprotein B, increased LDL particle concentration, and greater presence of small dense LDL particles, according to Bays and colleagues.
This atherogenic lipid pattern “has the potential for lipid discordance,” Bays said. “That’s why it’s important that when you have patients with obesity, particularly if they have insulin resistance, high triglycerides and low HDL cholesterol, that you look into alternative ways to assessing their atherosclerotic risk from a lipid standpoint; it can’t just be LDL cholesterol. It is better to include non-HDL cholesterol and/or Apo B. As clinical lipidologists, you should be the leaders in how to most accurately assess the atherogenic potential of the lipid profile in the patient with obesity. If you don’t understand how obesity and adiposopathy disrupts the function and mechanisms of the adipocyte and adipose tissue, and how this contributes to adiposopathic dyslipidemia, metabolic syndrome, and increased CVD risk, then it may be time to become more familiar with this joint publication regarding obesity and dyslipidemia.”
As an example, many clinicians assume an increase in waist circumference represents an increase in visceral adiposity. Based on data published decades ago, this may not be true for everyone, such as in female and Black patients. “If you look at females or Black individuals, oftentimes they can have an increase in waist circumference but not so much an increase in visceral fat. This is a frequent finding during our routine evaluation of body composition via dual x-ray absorptiometry (DXA).”
From a therapeutic standpoint, another common treatment principle is that interventions that reduce body weight and reduce risk for CV outcomes are usually linked with improved lipid profiles, so “early interventions to treat both excess adiposity and elevated atherogenic cholesterol (LDL-C and/or non-HDL-C) levels represent priorities in reducing the risk of CVD,” Bays and colleagues wrote in the expert review, noting that such an approach includes nutritional intervention, routine physical activity, behavior modification, anti-obesity medications and potentially bariatric procedures.
Effects of newer anti-obesity drugs
In one of the more important recent breakthroughs, GLP-1 receptor agonists hold promise to not only be highly effective anti-obesity medications, but also have the potential to reduce CVD risk. The SELECT trial of semaglutide 2.4 mg (Wegovy, Novo Nordisk) revealed that this GLP-1 receptor agonist reduces CVD risk and improves blood lipoprotein levels for patients with obesity, the authors wrote.
“It is true that the modest weight reduction often found with lifestyle intervention and/or many older anti-obesity medication only marginally reduces LDL cholesterol. However, the degree of weight reduction we are seeing with some of the newer, more highly effective anti-obesity medications (and bariatric surgery) can sometimes result in more clinically meaningful reductions in LDL cholesterol,” Bays said. “The bottom line is that often only a modest increase in LDL cholesterol occurs with an increase in body weight, while a reduction in body weight results in modest reductions in LDL cholesterol for many individuals. What that means for you as clinical lipidologists is that if you have a patient at high cardiovascular disease risk, you have to look at both weight reduction and reducing atherogenic lipids (LDL cholesterol, Apo B, etc.) if you want to optimize a reduction in CVD risk. In other words, the clinical lipidologist continues to play an important role in this age of evolutionary and revolutionary emerging anti-obesity treatments.”
Reference:
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Bays HE. Session II – Publications from the NLA. Presented at: National Lipid Association Scientific Sessions; May 30-June 2, 2024; Las Vegas (hybrid meeting).
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