In the 1980s, eggs were the dietary equivalent of slow-acting poison.
Over the next 20 years, a mountain of research showing that eggs do not have a major impact on cholesterol levels, combined with pricey marketing campaigns from egg producers, helped to clear their name. Now, eggs occupy coveted positions on brunch menus across the country and are even growing popularity as producers fortify them with omega-3 fatty acids and offer organic, cage-free and free-run varieties.
Then, a few days ago, Canadian researchers made waves when they said one egg yolk is worse, cholesterol-wise, than KFC’s Double Down sandwich, a notorious fast-food legend that replaces the traditional bun with two pieces of chicken slathered with bacon, sauce and cheese. The researchers published a report in the Canadian Journal of Cardiology warning that egg consumption can be dangerous to a person’s health and that it is wrong to assume that dietary cholesterol from eggs is harmless.
“Dietary cholesterol, including egg yolks, is harmful to the arteries,” the report says. “Stopping the consumption of egg yolks after a stroke or [heart attack] would be like quitting smoking after a diagnosis of lung cancer: a necessary action, but late.”
“Dietary cholesterol, including egg yolks, is harmful to the arteries,” the report says. “Stopping the consumption of egg yolks after a stroke or [heart attack] would be like quitting smoking after a diagnosis of lung cancer: a necessary action, but late.”
The more things change, it seems, the more they stay the same.
But does this new report mean that egg-yolk naysayers were right all along?
Cholesterol emerged as a nutritional bogeyman in the 1960s, pushing some Canadians to reject butter in favour of margarine and to abandon eggs altogether. Sweeping public-health campaigns were launched to warn citizens of the perils of egg consumption amid fears that cholesterol in the yolks was a major contributor to cardiovascular problems.
The thinking was that the dietary cholesterol found in eggs could significantly boost levels of blood cholesterol found naturally in the body and consequently raise an individual’s risk of developing heart disease.
Over time, however, a growing amount of research began to suggest that dietary cholesterol – or the cholesterol found in food we eat – has less of an impact than originally believed on the body’s overall levels.
Most of the cholesterol circulating in the bloodstream is actually produced in the liver, research has shown. The rest is derived from dietary sources, such as the cholesterol found in egg yolks, dairy products, meats and other foods.
Although cholesterol has long suffered from a negative public image, it plays an essential role in the proper function of cell membranes and helps the body produce important vitamins and bile and perform other processes.
Although cholesterol has long suffered from a negative public image, it plays an essential role in the proper function of cell membranes and helps the body produce important vitamins and bile and perform other processes.
There are two types of cholesterol: low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL carries cholesterol to the body’s cells from the liver and is known as “bad” cholesterol because when there is too much of it, it promotes the build-up of plaque in arteries, which is a risk factor for cardiovascular disease. HDL cholesterol, on the other hand, is considered “good” because it helps to carry LDL cholesterol away from artery walls.
A study published in the Journal of the American Medical Association in April, 1999, found that people who consumed an egg a day did not face an increased risk of heart attack or stroke. It was a definitive piece of evidence that helped to repair the reputation of eggs as part of a healthy diet, when consumed in moderation.
David Spence, a stroke-prevention expert at the University of Western Ontario and co-author of the new report questioning the value of eggs, said the study, and others like it, are flawed. He pointed out that diabetics in the 1999 study faced higher cardiovascular risks with increased egg consumption. Similar problems may not have been detected in healthy patients because the study did not follow them long enough, he added.
Dr. Spence said marketing campaigns have wrongly convinced Canadians that they can safely consume eggs without a fear of long-term health risks.
But his opinions clash with a wider consensus in the medical community.
In the years since the 1999 study was published, more research has shown that saturated and trans fats are much more likely to raise an individual’s blood cholesterol levels and fuel the risk of heart problems.
Of course, there are some caveats. Certain people are more sensitive to the effects of dietary cholesterol than others and need to watch their consumption to avoid potential problems. People who are at an increased risk of heart attack, stroke or other cardiovascular problems should also watch their intake of dietary cholesterol, said Rosie Schwartz, a Toronto-based dietitian and author.
But she emphasized that Canadians should not fixate on cholesterol alone. High blood pressure, a diet high in fat, being overweight and a sedentary lifestyle are all factors that can contribute to serious health problems.
“We need to really look at all the issues of heart disease,” Ms. Schwartz said.
Wednesday
High-density lipoproteins and cardiovascular disease: 2010 update.
Abstract
High-density lipoprotein-cholesterol (HDL-C) is a continuous inverse cardiovascular risk factor. The mechanisms by which HDLs protect against atherosclerosis are multiple. The major effect is thought to be reverse cholesterol transport, the mechanism by which excess cellular cholesterol is returned to the liver for excretion in the bile.
HDLs also have pleiotropic roles: they decrease inflammation, prevent low-density lipoprotein oxidation, vascular endothelial cell apoptosis and thrombosis, and improve vascular endothelial function. Recent studies suggest that nascent HDL particles are metabolized rapidly and that their components (Apo AI, cholesterol and phospholipids) are rapidly exchanged within lipoprotein classes. There are many causes of HDL-C deficiency. Using Mendelian randomization, several groups have concluded that many genetic forms of HDL deficiency do not increase cardiovascular risk.
This raises the controversial issue of the causality of low HDL-C as a cardiovascular risk factor, rather than a marker of cardiovascular health. This is reflected in the importance of lifestyle in determining HDL-C levels. The treatment of low HDL-C remains controversial, in part because the only currently available effective medication, niacin, is relatively poorly tolerated and outcomes studies on cardiovascular disease prevention are still pending
Alwaili K, Awan Z, Alshahrani A, Genest J.
Cardiovascular Research Laboratories, McGill University Health Centre/Royal Victoria Hospital, 687 Pine Avenue West, Montréal, Quebec, Canada.
Expert Rev Cardiovasc Ther. 2010 Mar;8(3):413-23.
High-density lipoprotein-cholesterol (HDL-C) is a continuous inverse cardiovascular risk factor. The mechanisms by which HDLs protect against atherosclerosis are multiple. The major effect is thought to be reverse cholesterol transport, the mechanism by which excess cellular cholesterol is returned to the liver for excretion in the bile.
HDLs also have pleiotropic roles: they decrease inflammation, prevent low-density lipoprotein oxidation, vascular endothelial cell apoptosis and thrombosis, and improve vascular endothelial function. Recent studies suggest that nascent HDL particles are metabolized rapidly and that their components (Apo AI, cholesterol and phospholipids) are rapidly exchanged within lipoprotein classes. There are many causes of HDL-C deficiency. Using Mendelian randomization, several groups have concluded that many genetic forms of HDL deficiency do not increase cardiovascular risk.
This raises the controversial issue of the causality of low HDL-C as a cardiovascular risk factor, rather than a marker of cardiovascular health. This is reflected in the importance of lifestyle in determining HDL-C levels. The treatment of low HDL-C remains controversial, in part because the only currently available effective medication, niacin, is relatively poorly tolerated and outcomes studies on cardiovascular disease prevention are still pending
Alwaili K, Awan Z, Alshahrani A, Genest J.
Cardiovascular Research Laboratories, McGill University Health Centre/Royal Victoria Hospital, 687 Pine Avenue West, Montréal, Quebec, Canada.
Expert Rev Cardiovasc Ther. 2010 Mar;8(3):413-23.
Thursday
Liver X receptor agonist inhibits proliferation of ovarian carcinoma cells stimulated by oxidized low density lipoprotein
Abstract
Objectives
We previously observed an association between ovarian cancer outcome and statin use and hypothesized lipoproteins have direct effects on ovarian cancer proliferation. Here we investigate the direct effects of low density lipoprotein (LDL) and oxidized LDL (oxLDL) on proliferation and the inhibitory effects of fluvastatin and a liver X receptor (LXR) agonist.
Methods
The effects of LDL, oxLDL, the LXR agonist TO901317, fluvastatin and cisplatin on cellular proliferation were determined using MTT assays. LXR pathway proteins were assayed by immunoblotting. Cytokine expression was determined by antibody array.
Results
Concentrations of oxLDL as small as 0.1 μg/ml stimulated CAOV3 and SKOV3 proliferation, while LDL had no effect. TO901317 inhibited the proliferation of CAOV3, OVCAR3 and SKOV3 cells stimulated by oxLDL. Fluvastatin inhibited oxLDL mediated proliferation of CAOV3 and SKOV3. Cardiotrophin 1 (CT-1) was mitogenic to CAOV3 and SKOV3, was induced by oxLDL, and was reversed by TO901317. OxLDL increased cisplatin IC50s by 3.8 μM and > 60 μM for CAOV3 and SKOV3 cells, respectively. The LXR pathway proteins CD36, LXR, and ABCA1 were expressed in eight ovarian carcinoma cell lines (A2780, CAOV3, CP70, CSOC882, ES2, OVCAR3, SKOV3).
Conclusions
OxLDL reduced ovarian carcinoma cell chemosensitivity and stimulated proliferation. These effects were reversed by LXR agonist or fluvastatin. The LXR agonist also inhibited expression of the ovarian cancer mitogen CT-1. These observations suggest a biologic mechanism for our clinical finding that ovarian cancer survival is associated with statin use. Targeting LXR and statin use may have a therapeutic role in ovarian cancer.
Daniel R. Scolesa, b, , , Xuan Xua, Haimei Wangc, Hang Trana, Barbie Taylor-Hardingb, Andrew Lia, b and Beth Y. Karlana, b
aWomen's Cancer Research Institute and Division of Gynecologic Oncology, CSMC Burns and Allen Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA, USA
bDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA, USA
cDivision of Cardiothoracic Surgery, CSMC Burns and Allen Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA, USA
Received 17 April 2009. Available online 24 October 2009.
Objectives
We previously observed an association between ovarian cancer outcome and statin use and hypothesized lipoproteins have direct effects on ovarian cancer proliferation. Here we investigate the direct effects of low density lipoprotein (LDL) and oxidized LDL (oxLDL) on proliferation and the inhibitory effects of fluvastatin and a liver X receptor (LXR) agonist.
Methods
The effects of LDL, oxLDL, the LXR agonist TO901317, fluvastatin and cisplatin on cellular proliferation were determined using MTT assays. LXR pathway proteins were assayed by immunoblotting. Cytokine expression was determined by antibody array.
Results
Concentrations of oxLDL as small as 0.1 μg/ml stimulated CAOV3 and SKOV3 proliferation, while LDL had no effect. TO901317 inhibited the proliferation of CAOV3, OVCAR3 and SKOV3 cells stimulated by oxLDL. Fluvastatin inhibited oxLDL mediated proliferation of CAOV3 and SKOV3. Cardiotrophin 1 (CT-1) was mitogenic to CAOV3 and SKOV3, was induced by oxLDL, and was reversed by TO901317. OxLDL increased cisplatin IC50s by 3.8 μM and > 60 μM for CAOV3 and SKOV3 cells, respectively. The LXR pathway proteins CD36, LXR, and ABCA1 were expressed in eight ovarian carcinoma cell lines (A2780, CAOV3, CP70, CSOC882, ES2, OVCAR3, SKOV3).
Conclusions
OxLDL reduced ovarian carcinoma cell chemosensitivity and stimulated proliferation. These effects were reversed by LXR agonist or fluvastatin. The LXR agonist also inhibited expression of the ovarian cancer mitogen CT-1. These observations suggest a biologic mechanism for our clinical finding that ovarian cancer survival is associated with statin use. Targeting LXR and statin use may have a therapeutic role in ovarian cancer.
Daniel R. Scolesa, b, , , Xuan Xua, Haimei Wangc, Hang Trana, Barbie Taylor-Hardingb, Andrew Lia, b and Beth Y. Karlana, b
aWomen's Cancer Research Institute and Division of Gynecologic Oncology, CSMC Burns and Allen Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA, USA
bDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA, USA
cDivision of Cardiothoracic Surgery, CSMC Burns and Allen Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA, USA
Received 17 April 2009. Available online 24 October 2009.
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