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Allergy to red meat increases risk for CHD
Immunoglobulin E to galactose-alpha-1,3-galactose increased atheroma burden and plaques, particularly in patients aged 65 years or younger, according to a study published in Arteriosclerosis, Thrombosis and Vascular Biology.
“This novel finding from a small group of subjects from Virginia raises the intriguing possibility that allergy to red meat may be an underrecognized factor in heart disease,” Coleen McNamara, MD, professor of medicine in the Cardiovascular Research Center of University of Virginia Health System in Charlottesville, said in a press release.
Jeffrey M. Wilson, MD, PhD, of the division of allergy and immunology at University of Virginia, and colleagues analyzed data from 118 patients who were undergoing medically warranted cardiac catherization and underwent IVUS of a noninfarct-related artery. Assays were performed for total immunoglobulin E (IgE) and specific IgE to galactose-alpha-1,3-galactose (alpha-gal), oak, dust mite, ragweed, timothy grass and peanut.
IgE to alpha-gal was seen in 26% of patients. Patients who were sensitized had higher atheroma burden (P = .02), and the association was stronger in patients aged 65 years or younger (P < .001). Based on IVUS, patients aged 65 years or younger and who were in the sensitized group had less stable features.
When IgE to peanut and inhalants were assayed, they were not associated with CAD.
Alpha-gal-specific IgE and total IG were strongly associated with each other, although the strength of the association with atheroma burden was stronger with alpha-gal-specific IgE. When adjusted for diabetes, sex, statin use, hypertension and total IgE, this association remained significant (regression coefficient = 12.2; standard error = 5.2; P = .02).
“As the causal agent of a delayed allergic reaction to mammalian meat, which is IgE mediated, the glycolipid form of [alpha-gal] may be particularly relevant to understanding its role in atherosclerosis,” Wilson and colleagues wrote. “Mechanistic studies in animal models are suggested, but ultimately, efforts to translate this finding into clinical relevance will benefit from analysis of larger cohorts, including disparate geographic areas and prospective studies of adult subjects, which include information on diet, allergic history and detailed investigation into [specific] IgE antibodies.” – by Darlene Dobkowski
Disclosures: McNamara reports she received research grants from AstraZeneca. Wilson reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
Perspective
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These results show a provocative finding, which is that individuals who have a specific type of allergic response with immunoglobulin E to a carbohydrate group that is found in red meat are more likely to have an atherosclerotic plaque phenotype that is associated with adverse outcomes.
The results are hypothesis-generating, in that the present studies are associative. They do not prove causation, but they suggests that perhaps in some individuals inflammation driven by an allergic response to a foreign carbohydrate that is found in red meat may help contribute to atherosclerotic CVD.
This study raises questions as to whether or not an immune response to this food antigen could contribute to CVD in places where a tick bite is a common occurrence in a person’s lifetime. You cannot generate an allergy to this carbohydrate that is found in red meat by any way other than direct introduction into the bloodstream. Just by eating red meat, you do not generate the allergy. It is a newly recognized phenomenon, in that people who get a tick bite, with that exposure, can sometimes develop an allergic response to red meat. It is not a common occurrence, but it does happen apparently more frequently than we previously recognized. This study was done in an area where ticks are endemic.
It is a provocative finding, when an antibody, an immunoglobulin E response to a common food allergen, is associated with a worse phenotype of atherosclerotic plaque and a greater degree of atherosclerotic plaque. At this point, the numbers are not sufficient to argue that testing for this IgE response is worthwhile. This may represent a new facet of yet another type of inflammatory and immune pathway that might contribute to the development of CVD. Future research should aim to determine whether the IgE response contributes to cardiovascular disease. There are numerous examples of inflammatory insults triggering enhanced atherosclerotic plaque development. If it does turn out to be potentially a causal contributor in some individuals, it will be of interest to see if this pathway can be targeted as we drive more towards personalized medicine for the treatment of CVD. CVD is a multifaceted disease. Beyond cholesterol, there are many potential factors that enhance susceptibility for accelerated development of atherosclerosis.
As far as I am aware, this study is the first time that a specific allergic response to a food component has been so directly demonstrated to be associated with an adverse CV phenotype. In that sense, it broadly contributes to the idea that what we eat contributes to our health. If causal, this would only be relevant in a subset of people – subjects would have had an exposure to a tick bite and developed an allergic response to this red meat associated carbohydrate group. It is a fascinating environmental exposure.
Cleveland Clinic