High prevalence of atherosclerosis found in lower risk patients

Image shows examples of whole-body angiograms. A, Normal study with no disease evident in a 45-year-old woman. B, Evidence of extensive disease including left carotid bulb stenosis (black arrow), bilateral renal artery stenosis (white arrows), and occluded right superficial femoral artery (arrowhead) in a 53-year-old woman. Credit: Radiological Society of North America

Researchers using whole-body magnetic resonance angiography (MRA) have found a surprisingly high prevalence of atherosclerosis in people considered to be at low to intermediate risk for cardiovascular disease, according to a study appearing online in the journal Radiology. Almost half of all study participants had at least one narrowed artery.

06 may 2018--Atherosclerotic disease is characterized by a narrowing of the arteries caused by plaque buildup. The condition often progresses to cardiovascular disease, the leading cause of death in the United States. Early intervention can slow or reverse disease progression, but standard imaging techniques for early detection focus on specific artery segments, potentially missing evidence of disease elsewhere in the body.
Whole-body MRA allows clinicians to take a broader view of the vascular system.
"The key advantages of this MRA technique include the 'whole-body' approach, which detects systemic disease that would be missed by modalities assessing single vascular sites," said study co-author Graeme Houston, M.D., from the University of Dundee in Dundee, Scotland. "The results offer a validated quantitative score of atherosclerotic burden, and the technique does not use ionizing radiation, which is an advantage over CT angiography."
Professor Houston and colleagues used whole-body MRA to quantify the burden and distribution of asymptomatic atherosclerosis in 1,513 people, average age 53.5 years old. The participants were considered in the low-intermediate risk group, with a 10-year cardiovascular disease risk of less than 20 percent. The researchers assessed 31 arterial segments in each participant.
The plaque burden, or overall amount of atherosclerotic plaque, and number of narrowed vessels correlated with age, blood pressure and cholesterol—all known risk factors for cardiovascular events like heart attacks. But the prevalence of atherosclerosis in the study group was surprisingly high. Almost half of the participants had at least one narrowed vessel, and more than a quarter had multiple narrowed vessels.
"This is surprising, given that the study group was made up of asymptomatic individuals without diabetes who had low to intermediate risk of future cardiovascular events by standard risk factor assessment," Prof. Houston said.
With whole-body MRA, the researchers were able to detect early atherosclerotic disease throughout the body, disease that would have been missed by methods that evaluate only a single vascular territory. The technique's high technical success rate—researchers were able to interpret 99.4 percent of the potentially analyzable arterial segments—underscores its potential for more widespread use.
"The results confirm the feasibility for MRA as an imaging method for detecting early atherosclerotic disease in individuals at low to intermediate risk of cardiovascular events," Prof. Houston said. "This approach could stratify individuals for the presence of disease burden, which could inform further preventative therapy in the future."
The researchers plan to conduct follow-up studies to look for links between whole-body MRA findings and long-term health outcomes.

More information: "Prevalence and Distribution of Atherosclerosis in a Low- to Intermediate-Risk Population: Assessment with Whole-Body MR Angiography" Radiology, 2018.


Provided by Radiological Society of North America

LDL cholesterol found to be the main modifiable predictor of atherosclerosis in individuals with no risk factor

Cholesterol plaque in a carotid artery, visualized by vascular magnetic resonance imaging.

LDL cholesterol (LDL-C), known as 'bad' cholesterol, is the underlying reason why many apparently healthy individuals have heart attacks or strokes during middle age despite not having cardiovascular risk factors such as hypertension, smoking, obesity, dyslipidemia or diabetes. Even at levels considered normal, LDL-C, after age and male sex, is the main predictor of the presence of atherosclerotic plaques in the arteries.

16 dec 2017--This is the finding of research conducted at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) and published today in the Journal of the American College of Cardiology (JACC). The results of the new study, led by CNIC Director Dr. Valentín Fuster, support the use of more aggressive strategies to reduce LDL-C, including for individuals considered at minimum risk. Fortunately, LDL-C is the main risk factor that can be modified in order to avoid the appearance of atherosclerotic plaques.
As study first author Dr. Leticia Fernández-Friera explained, "Although the absence of classical cardiovascular risk factors is linked to a low risk of cardiovascular events, people in this situation still have heart attacks and strokes. We therefore need to define new markers of early atherosclerosis in these apparently healthy individuals."
This subanalysis of the PESA study (Progression of Early Subclinical Atherosclerosis) evaluated 1779 study participants who had no classical risk factors. The main goal of the study was to define predictors of subclinical atherosclerosis in this population. The research team evaluated the association of a battery of biometric, analytical, and lifestyle parameters with the presence of atherosclerotic plaques. The results demonstrate that, after age and male sex, the most prominent association is shown by LDL-C. Study author Dr. Javier Sanz commented that "even in people with optimal blood pressure, blood sugar, and total cholesterol, we detected an independent association between the level of circulating LDL-C and the presence and extent of subclinical atherosclerosis."

Calcium deposits (white) in the coronary arteries.

Cardiovascular prevention

The JACC study shows a relationship between LDL-C levels that are considered healthy in current clinical guidelines and the extent of atherosclerosis in multiple vascular territories: the aorta and the carotid, iliofemoral, and coronary arteries. Using the latest noninvasive vascular imaging technology, the study demonstrates that "atherosclerotic plaques are present in 50 percent of middle-aged individuals (40-54 years old) with no classical cardiovascular risk factors: non-smokers with no hypertension, diabetes mellitus, or dyslipidemia. These findings could help to improve cardiovascular prevention in the general population even before the appearance of conventional risk factors, an example of primordial prevention," explained Dr. Leticia Fernandez-Friera.
Cardiovascular disease is the principal cause of death in the world, and the worldwide high prevalence of cardiovascular diseases makes the development of effective prevention strategies a major health care priority. Current guidelines from the US National Cholesterol Education Program categorize LDL-C levels above 160 mg/dL as high and levels from 130 mg/dL 159 mg/dL as borderline high. The research team on the JACC article believe that the new findings will have important societal and clinical implications because they demonstrate the importance of aggressively reducing LDL-C, both on an individual level and in the general population. Drs. Valentín Fuster and Borja Ibañez affirm that "we should be more restrictive, and consider lowering the threshold values stipulated in the guidelines." The new results point the way to defining new lower levels of normal LDL-C.
This ambitious project was made possible through the shared commitment of the CNIC and Banco Santander and the leadership of principal investigator Dr. Fuster. The PESA study uses the latest noninvasive vascular imaging technology (magnetic resonance, PET, CT, and 2D and 3D ultrasound) in an attempt to answer important unresolved questions about cardiovascular disease: when and how it begins and what has to happen for it to manifest clinically. As study author Dr. Antonio Fernández-Ortiz explained, "Thanks to vascular ultrasound, we can directly visualize the presence of cholesterol plaques in the carotid arteries, the aorta, and the iliofemoral arteries; and with computed tomography, we can detect calcification in the coronary arteries. With these approaches, we are able to evaluate the progress of the disease in an individual."
Normally, atherosclerosis is detected at an advanced stage, after it has provoked clinical events such as a heart attack, stroke, or another condition. Treatment options after the event are limited, and affected patients experience a permanent decline in quality of life. Moreover, the long term care of these patients places a major cost burden on health care systems. Drs. Fuster and Sanz conclude that "the ability to identify patients with the disease before the appearance of symptoms could help to avoid or reduce the associated complications and translate into an enormous societal and economic benefit. The major impact of the PESA project will felt over the long term, 15 or 20 years after its launch. At that stage, we will be able to relate the initial study findings to participants' clinical progress."


Provided by Centro Nacional de Investigaciones Cardiovasculares

Fundamental research is paving the way for development of first vaccine for heart disease

Researchers at Wayne State University have made a fundamental discovery and, in subsequent collaboration with scientists at La Jolla Institute for Allergy and Immunology (LIAI), are one step closer to the goal of developing the world's first T-cell peptide-based vaccine for heart disease—the number one killer in the nation.

17 july 2014--Atherosclerosis is a chronic inflammatory disease of the arterial walls, which thicken due to accumulation of fatty materials such as cholesterols and triglycerides. Blocking of arteries supplying blood to the heart is the underlying cause of many heart diseases. Nearly 600,000 Americans die of heart disease every year. Although cholesterol is believed to be a major factor in creating the plaque that leads to heart disease, immune inflammation is another important contributor in arterialplaque buildup. The goal of the vaccine is to reduce immune-based inflammation in the arteries, leading to decreased plaque buildup.

The scientists published their findings in the December 2013 issue of Frontiers in Immunology, entitled "Atheroprotective vaccination with MHC-II restricted peptides from ApoB-100." These experiments show proof of concept for the development of an autoantigen-specific vaccine for reducing the amount of atherosclerotic plaques in mice. If successful, the vaccine could aid in preventing heart disease and stop or reduce disease progression. In addition to heart disease, the vaccine could target strokes, which are also a product of plaque buildup in arteries.

The published work, performed in the laboratory of Klaus Ley, M.D., a prominent vascular biologist of LIAI, was based on the fundamental discovery made by Harley Tse, Ph.D., professor of immunology and microbiology in Wayne State's School of Medicine, and professor in Wayne State's Cardiovascular Research Institute, and Michael Shaw, Ph.D., adjunct assistant professor of immunology and microbiology at Wayne State. Shaw and Tse are the first to demonstrate that two T cell epitopes of the autoantigen apoB100 are deeply involved in the development of the disease. Their novel discovery is reported in the article, "Identification of two Immunogenic T cell Epitopes of ApoB-100 and their Autoimmune Implications," published in the April – June 2014 issue (volume 2) of Journal of Immunology and Clinical Research.

"ApoB100 is an apolipoprotein of the LDL (low-density lipoprotein) particle which is the notorious 'bad cholesterol' that contributes to the formation of plaques in the vessel wall," said Tse. "Although T cells of the immune system are known to participate in the development of heart disease, by what and how these T cells are directed to act have not been elucidated. The lack of this knowledge has greatly hampered the development of immune peptide-based therapeutics to control the disease. With the discovery of the disease-causing T cell epitopes, we can now manipulate the activities of the T cells responding to these epitopes to control the disease."

Since immune T cells are normally activated by a short sequence (called an epitope), and not by the whole molecule of an antigen, Shaw and Tse conceptualized that finding the apoB100 epitopes capable of stimulating the disease causing (atherogenic) T cells is a prerequisite for understanding how these T cells are involved in heart disease development and for finding ways to control their adverse effects.

Based on this idea, they identified two short sequences (3501–3515 and 978–992) of ApoB100 (ApoB3501-3515 and ApoB978-992, also designated peptides P3 and P6, respectively) that were able to direct specific T cells to proliferate as well as to cause worsening atherosclerosis. This discovery is significant because it identifies the target T cells and makes it possible to manipulate this population of pathologic T cells away from their harmful activities.

The subsequent collaboration with Ley's laboratory bears the first fruits of this effort.

Provided by Wayne State University

Disturbance in blood flow leads to epigenetic changes and atherosclerosis

This image shows the effects of 5aza on atherosclerosis model. Credit: Dunn et al JCI (2014)

Disturbed patterns of blood flow induce lasting epigenetic changes to genes in the cells that line blood vessels, and those changes contribute to atherosclerosis, researchers have found. The findings suggest why the protective effects of good blood flow patterns, which aerobic exercise promotes, can persist over time. An epigenetic change to DNA is a chemical modification that alters whether nearby genes are likely to be turned on or off, but not the letter-by-letter sequence itself.

30 may 2014--The results are scheduled for publication in the Journal of Clinical Investigation.

Atherosclerosis is the buildup of fats and inflammatory cells in arteries, a process that can lead to heart attacks and strokes. The curvature of arteries and resulting disturbed flow influence where atherosclerotic plaques develop. Biomedical engineer Hanjoong Jo and his colleagues have developed a model that allows them to see the inflammatory effects of disturbed blood flow quickly. Jo is professor of biomedical engineering in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.

"This new study shows that disturbed blood flow induces epigenetic changes that lead to atherosclerosis," Jo says. "It had been known for a long time that plaques preferentially develop in curved and branched arteries, but our lab has been able to prove that disturbed blood flow can actually trigger atherosclerosis, in the presence of risk factors such as high blood cholesterol."

Despite the demonstrated importance of blood flow patterns in atherosclerosis, it can be blocked in mouse models with a drug that interrupts the process of DNA methylation, an epigenetic change that often turns genes off. Jo's team has identified several genes that become turned off under disturbed flow conditions, in a way that requires DNA methylation. Some of these genes may represent new therapeutic targets in atherosclerosis.

The co-first authors of the JCI paper are biomedical engineering graduate students Jessilyn Dunn and Haiwei Qiu, and postdoc Soyeon Kim, PhD.

In the Jo lab's mouse model, researchers restrict blood flow in three carotid arteries on one side, in the presence of a high-fat diet. In a 2010 paper in Blood, they had found that one of the genes induced by disturbed blood flow is DNMT1, encoding a DNA methyltransferase enzyme.

DNMT1 carries out DNA methylation, an epigenetic modification of DNA. Changes in DNA methylation are important for cells differentiating into different tissues such as blood, muscle or bone, and for the development of cancer.

Dunn and her colleagues found that treatment with 5-aza-2'-deoxycytidine, a drug that is now used to treat acute myeloid leukemia, can prevent atherosclerotic plaques fr om forming in the mouse model.

"While we do not envision using 5-aza for atherosclerosis treatment clinically, our results do revealpotential therapeutic targets," Jo says.

A broader implication is that improving blood flow patterns, through aerobic exercise for example, can induce a lasting imprint on gene expression in the blood vessels, he says.

Provided by Emory University

Heart disease, stroke risk estimator app now available for health care professionals

20 feb 2014—The American College of Cardiology and the American Heart Association have released a mobile and Web-based app for health care professionals to use with their patients in determining 10-year and lifetime risks for developing atherosclerotic cardiovascular disease (ASCVD), the major cause of heart attack and ischemic stroke.

"This tool is meant to facilitate a conversation between the health care provider and the patient about the patient's risk of heart attack and stroke and how best to reduce those risks," said John G. Harold, MD, MACC, president of the American College of Cardiology. "While we hope the app will make the risk assessment guidelines more accessible, it is not a substitute for face-to-face engagement. It is a tool to help health professionals and patients work together as part of a discussion of the patient's medical history and lifestyle."

The ASCVD Risk Estimator, a mobile and Web version of the Excel-based calculator released with the ACC/AHA Cardiovascular Risk Guideline released in November 2013, uses a patient's age, sex, race, total cholesterol, HDL cholesterol, systolic blood pressure, blood pressure-lowering medication use, diabetes status and smoking status to estimate their 10-year and lifetime risk of heart attack and ischemic stroke. The app also helps health care professionals determine whether statin therapy is appropriate, what intensity of statin therapy is needed, how to address safety concerns of statin therapy, and what lifestyle changes should be made.

"We are pleased the risk assessment guidelines are now available in easy to access tools," said Mariell Jessup, MD, president of the American Heart Association. "The guidelines were broadened late last year to include the assessment for risk of stroke as well as heart attack. This app incorporates the stroke risk as well as the new gender- and ethnicity-specific formulas for predicting risk in African-American and white women and men found in the guidelines, and it looks beyond traditional short-term (10-year) risk estimates to predict an individual's lifetime risk of developing heart disease and having a stroke."

The ASCVD Risk Estimator mobile app can be downloaded for free from the iTunes and Google Play app stores. The Web version is available on CardioSource.org and on myamericanheart.org

Provided by American Heart Association

Researchers discover new link between heart disease and red meat

An uncooked rib roast. Credit: Michael C. Berch/Wikipedia

A compound abundant in red meat and added as a supplement to popular energy drinks has been found to promote atherosclerosis – or the hardening or clogging of the arteries – according to Cleveland Clinic research published online this week in the journal Nature Medicine.

09 april 2013--The study shows that bacteria living in the human digestive tract metabolize the compound carnitine, turning it into trimethylamine-N-oxide (TMAO), a metabolite the researchers previously linked in a 2011 study to the promotion of atherosclerosis in humans. Further, the research finds that a diet high in carnitine promotes the growth of the bacteria that metabolize carnitine, compounding the problem by producing even more of the artery-clogging TMAO.

The research team was led by Stanley Hazen, M.D., Ph.D., Vice Chair of Translational Research for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart and Vascular Institute at Cleveland Clinic, and Robert Koeth, a medical student at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University.

The study tested the carnitine and TMAO levels of omnivores, vegans and vegetarians, and examined the clinical data of 2,595 patients undergoing elective cardiac evaluations. They also examined the cardiac effects of a carnitine-enhanced diet in normal mice compared to mice with suppressed levels of gut microbes, and discovered that TMAO alters cholesterol metabolism at multiple levels, explaining how it enhances atherosclerosis.

The researchers found that increased carnitine levels in patients predicted increased risks for cardiovascular disease and major cardiac events like heart attack, stroke and death, but only in subjects with concurrently high TMAO levels. Additionally, they found specific gut microbe types in subjects associated with both plasma TMAO levels and dietary patterns, and that baseline TMAO levels were significantly lower among vegans and vegetarians than omnivores. Remarkably, vegans and vegetarians, even after consuming a large amount of carnitine, did not produce significant levels of the microbe product TMAO, whereas omnivores consuming the same amount of carnitine did.

"The bacteria living in our digestive tracts are dictated by our long-term dietary patterns," Hazen said. "A diet high in carnitine actually shifts our gut microbe composition to those that like carnitine, making meat eaters even more susceptible to forming TMAO and its artery-clogging effects. Meanwhile, vegans and vegetarians have a significantly reduced capacity to synthesize TMAO from carnitine, which may explain the cardiovascular health benefits of these diets."

Prior research has shown that a diet with frequent red meat consumption is associated with increased cardiovascular disease risk, but that the cholesterol and saturated fat content in red meat does not appear to be enough to explain the increased cardiovascular risks. This discrepancy has been attributed to genetic differences, a high salt diet that is often associated with red meat consumption, and even possibly the cooking process, among other explanations. But Hazen says this new research suggests a new connection between red meat and cardiovascular disease.

"This process is different in everyone, depending on the gut microbe metabolism of the individual," he says. "Carnitine metabolism suggests a new way to help explain why a diet rich in red meat promotes atherosclerosis."

While carnitine is naturally occurring in red meats, including beef, venison, lamb, mutton, duck, and pork, it's also a dietary supplement available in pill form and a common ingredient in energy drinks. With this new research in mind, Hazen cautions that more research needs to be done to examine the safety of chronic carnitine supplementation.

"Carnitine is not an essential nutrient; our body naturally produces all we need," he says. "We need to examine the safety of chronically consuming carnitine supplements as we've shown that, under some conditions, it can foster the growth of bacteria that produce TMAO and potentially clog arteries."

This study is the latest in a line of research by Hazen and his colleagues exploring how gut microbes can contribute to atherosclerosis, uncovering new and unexpected pathways involved in heart disease. In a 2011 Nature study, they first discovered that people are not predisposed to cardiovascular disease solely because of their genetic make-up, but also based on how the micro-organisms in their digestive tracts metabolize lecithin, a compound with a structure similar to carnitine.

More information: Paper: dx.doi.org/10.1038/nm.3145

Provided by Cleveland Clinic

Egg yolk consumption almost as bad as smoking when it comes to atherosclerosis

Newly published research led by Dr. David Spence of Western University, Canada, shows that eating egg yolks accelerates atherosclerosis in a manner similar to smoking cigarettes. Surveying more than 1200 patients, Dr. Spence found regular consumption of egg yolks is about two-thirds as bad as smoking when it comes to increased build-up of carotid plaque, a risk factor for stroke and heart attack. The research is published online in the journalAtherosclerosis.

20 aug 2012--Atherosclerosis, also called coronary artery disease, is a disorder of the arteries where plaques, aggravated by cholesterol, form on the inner arterial wall. Plaque rupture is the usual cause of most heart attacks and many strokes. The study looked at data from 1231 men and women, with a mean age of 61.5, who were patients attending vascular prevention clinics at London Health Sciences Centre's University Hospital. Ultrasound was used to establish a measurement of total plaque area and questionnaires were filled out regarding their lifestyle and medications including pack-years of smoking (number of packs per day of cigarettes times the number of years), and the number of egg yolks consumed per week times the number of years consumed (egg yolk-years).

The researchers found carotid plaque area increased linearly with age after age 40, but increased exponentially with pack-years of smoking and egg yolk-years. In other words, compared to age, both tobacco smoking and egg yolk consumption accelerate atherosclerosis. The study also found those eating three or more yolks a week had significantly more plaque area than those who ate two or fewer yolks per week.

"The mantra 'eggs can be part of a healthy diet for healthy people' has confused the issue. It has been known for a long time that a high cholesterol intake increases the risk of cardiovascular events, and egg yolks have a very high cholesterol content. In diabetics, an egg a day increases coronary risk by two to five-fold," says Dr. Spence, a Professor of Neurology at Western's Schulich School of Medicine & Dentistry and the Director of its Stroke Prevention and Atherosclerosis Research Centre (SPARC) at the Robarts Research Institute. "What we have shown is that with aging, plaque builds up gradually in the arteries of Canadians, and egg yolks make it build up faster - about two-thirds as much as smoking. In the long haul, egg yolks are not okay for most Canadians."

Dr. Spence adds the effect of egg yolk consumption over time on increasing the amount of plaque in the arteries was independent of sex, cholesterol, blood pressure, smoking, body mass index and diabetes. And while he says more research should be done to take in possible confounders such as exercise and waist circumference, he stresses that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease.

Provided by University of Western Ontario

Inflammation worsens danger due to atherosclerosis

Stockholm, Sweden, 22 jan 2009 — Current research suggests that inflammation increases the risk of plaque rupture in atherosclerosis. The related report by Ovchinnikova et al, "T cell activation leads to reduced collagen maturation in atherosclerotic plaques of ApoE-deficient- mice," appears in the February 2009 issue of The American Journal of Pathology.

Atherosclerosis is a disease of arterial blood vessels where fats, cholesterol, blood cells, and fibers form hardened plaques on the artery wall. These plaques restrict blood flow to tissues such as the heart and brain by narrowing the artery. Atherosclerosis can be caused by high blood pressure, high fat and high cholesterol diets, smoking, and diabetes. People with atherosclerotic plaques often show no symptoms for decades.

Atherosclerotic plaques consist of lipid cores covered by collagen fiber caps. These plaques can suddenly rupture, resulting in blood clots that completely block blood flow and lead to heart attack or stroke in otherwise healthy individuals. One potential cause of plaque rupture is the thinning of the collagen fiber cap covering the plaque.

Inflammatory cells are often observed at the site of plaque rupture. Researchers led by Dr. Göran K Hansson at the Karolinska Institute explored the role of inflammatory cells in atherosclerotic plaque rupture using an animal model of atherosclerosis with hyper-activated immune cells. They found that inflammation leads to a reduction of mature collagen in atherosclerotic plaques, leading to thinner caps that are more likely to rupture. They then identified a collagen-maturing enzyme, lysyl-oxidase (LOX), which represents a novel target in inflammation-induced plaque rupture.

The data from Ovchinnikova et al suggest "a novel mechanism by which adaptive immunity can modulate plaque stability - impairment of collagen maturation by T cell-dependent inflammation." These studies help unraveling the cause of myocardial infarction and stroke, and provide "interesting new targets for plaque stabilization therapy." In future studies, Dr. Hansson's group will explore the role of insufficient collagen maturation in human atherosclerosis. They hope that components of collagen and the LOX enzyme will become useful both to identify patients at risk for plaque rupture and to develop new therapy to prevent plaque rupture and thrombosis.

###

This work was supported by grants from the Swedish Heart-Lung Foundation and Swedish Medical Research Council, the Academy of Finland, and S. Jusélius foundation.

Ovchinnikova O, Robertson A-KL, Wågsäter D, Folco EJ, Hyry M, Myllyharju J, Eriksson P, Libby P, Hansson GK: T cell activation leads to reduced collagen maturation in atherosclerotic plaques of ApoE-deficient- mice. Am J Pathol 2009 174: 693-700

ADA: Cheap Fructose May Exact High Metabolic Price

CHICAGO, June 25 -- Fructose in sodas and other beverages -- but not glucose -- can set patients on the fast track to atherosclerosis, investigators here reported.
Overweight men and women assigned to drink fructose-sweetened beverages as 25% of their energy intake developed atherogenic lipid profiles in just two weeks, whereas those who drank glucose-sweetened drinks did not, said Kimber Stanhope, M.S., of the University of California at Davis, and colleagues.
"Compared with consumption of glucose, 10 weeks of fructose consumption as 25% of energy requirements promoted the development of an atherogenic lioproprotein phenotype and glucose intolerance/insulin resistance in older, overweight and obese men and women," Stanhope said at the American Diabetes Association meeting.
Fructose, which in the U.S. is mostly derived from corn syrup, is a common ingredient in soft drinks, including sodas and sweetened juices. It is about twice as sweet pound for pound as sucrose, and is relatively inexpensive, making it attractive to soft-drink makers.
Consumption of fructose-sweetened beverages increased by 135% from 1977 to 2001, Stanhope said. He speculated that the increased consumption could in part explain the rise in the rate of metabolic syndrome.
The investigators enrolled 23 overweight men and women into a randomized study. The patients were told that were participating in a diet study, but did not know that they would be getting drinks with one of two types of sugars.
The 23 patients, ranging in age from 43 to 70, had body mass-indices ranging from 25 to 35 kg/m2. They spent the first two weeks of the study on an inpatient unit for baseline measures, including 24 hour blood monitoring, while the patients ate an energy balanced diet. Additional 24-hour blood readings were collected at eight and 10 weeks.
The patients were then randomly assigned on an outpatient basis to eat their normal diets, with 25% of their energy requirements to come from either fructose-sweetened drinks (13 patients) or glucose-sweetened beverages (10 patients).
During the ninth week the patients came back to the clinical trials center for and additional two weeks to drink their assigned beverages while on the energy balanced diets.
The authors found that after just two weeks of fructose drinking, 24-hour postprandial triglycerides more than doubled, increasing by 212% + 59% (P<0.0001). In contrast, there was a non-significant trend toward decrease in triglycerides among the patients who drank glucose-sweetened beverages.
Neither fructose nor glucose consumption affected fasting triglyceride levels, however.
In addition, patients who took fructose had increases in fasting plasma concentrations of LDL (up 17% + 4%), Apolipoprotein B (up 28% 7%), small dense LDL (up 27% + 11%), postprandial concentrations of remnant lipoprotein (up 77% + 19%) and of remnant-like particle cholesterol (up 53% + 12%; P for each <0.01). None of these parameters was unchanged in patients who drank glucose.
"These effects appear to be exacerbated when fructose sweetened-beverages are consumed with a typical ad labium western diet compared with an energy-balanced moderate fat diet," she said.
No information on study funding sources or author conflicts of interest was available.Primary source: American Diabetes Association 2007 Scientific SessionsSource reference: Stanhope K et al. "Consumption of Fructiose-, but not Glucose-Sweetened Beverages Produces an Atherogenic Lipid Profile in Overweight/Obese Men and Women." Abstract 062, presented June 23.\