Atherosclerosis is a chronic inflammatory disease that is characterized by plaque build-up in the arteries. This condition has been reported to be the underlying cause of over 50% of deaths in the Western world. In the United States specifically, about 610,000 people die from cardiovascular disease annually. To state this another way, one out of every four deaths in the US is due to cardiovascular disease. Atherosclerosis is a significant risk factor for myocardial infarction, cerebrovascular accidents, and peripheral artery disease . Hypercholesterolemia, hypertriglyceridemia, hypertension, smoking, type-1 diabetes, obesity, sedentary lifestyle, and diets high in saturated fat are all commonly recognized risk factors for atherosclerosis. Additionally, human research suggests that there are inflammatory and infectious contributors to the development of atherosclerotic plaque.
What is the link between inflammation and atherosclerosis?
Although the readily identifiable sequelae of atherosclerosis are typically observed in middle-aged patients, evidence suggests that the earliest developments of atherosclerosis actually begin in childhood adolescence, and young adulthood. Risk factors for the development of atherosclerotic changes in this age group include childhood obesity, hypertension, hyperlipidemia, smoking, and the presence of conditions like diabetes mellitus and Kawasaki disease. 
Post-mortem autopsies of children and young adults suggest that atherosclerosis first develops in childhood when lipid-engorged macrophages and T lymphocytes accumulate in the intima of the arteries and form fatty streaks. From there, these fatty streaks may or may not progress into atherosclerosis. The fatty streaks may also regress.
For some people in whom the fatty streaks progress, the accumulation of the lipids increases with time. Over time, the fatty streaks are covered by a fibromuscular cap, and this forms a fibrous plaque. The fibrous caps then enlarge, and they become calcified. They can then hemorrhage, ulcerate or rupture, and thrombose. If thrombotic occlusion occurs, this can result in well-known sequelae, such as myocardial infarction, cerebrovascular accident, or gangrene. As expected, the sequelas are contingent upon which arteries are affected.
To summarize, the earliest stages of atherosclerosis begin because of white blood cells phagocytosing excess lipids. Indeed, atherosclerosis has been described as a chronic inflammatory disorder that is largely driven by an innate immune response through monocytes and macrophages.  Nonetheless, both clinical and pre-clinical studies demonstrate that mechanisms involved in both the innate and adaptive immune systems can either accelerate or curb atherosclerosis.
How do infectious disease processes contribute to atherosclerosis?
Because there is a common underlying inflammatory response between infection and atherosclerosis, researchers have sought to evaluate whether or not the two were linked, and whether or not it would be beneficial to use anti-atherogenic interventions to address atherosclerosis if the scenario also involved infectious burden. To answer this question, researchers designed a pre-clinical study involving a hypercholesterolemic diet-induced atherosclerotic mouse model. The mice in this experiment were fed a diet high in cholesterol for 12 weeks in order to facilitate the development of atherosclerosis, and scientists accounted for inflammatory stimulation during the development of atherosclerosis by injecting the mice with lipopolysaccharide intraperitoneally during the first week of the study.  The researchers treated the experimental mice with alpha lipoic acid (ALA) and observed the results.
By the study’s conclusion, treatment with ALA led to a reduction in inflammatory cytokines and serum cholesterol levels, as well as alleviation of atherosclerotic pathology. The mechanism identified by researchers by which ALA accomplished this was by reducing the proliferation and migration of vascular smooth muscle cells upon platelet-derived growth factor stimulation by targeting the Ras-MEK1/2-ERK1/2 pathway. 
This study demonstrated that anti-atherogenic interventions, and particularly those like ALA that are also capable of normalizing pro-inflammatory cytokines, are efficacious in cases of atherosclerosis that involve infectious burden or immunological complications.
The therapeutic application of ALA in humans
Alpha lipoic acid is a naturally occurring nutrient found in small amounts in green leafy vegetables, potatoes, and some meats.  Within the body, ALA plays roles in regulating the transcription of genes associated with anti-oxidant and anti-inflammatory pathways. 
As humans, our bodies also produce small amounts of ALA. Although healthy young adults usually make enough ALA to meet the body’s needs, the amount of ALA our bodies produce decreases as we age. The evidence currently suggests that this age-dependent decrease in ALA may contribute to dysfunction of the endothelium and atherosclerosis. For this reason, ALA supplementation is an important consideration when it comes to addressing atherosclerotic changes and cardiovascular disease risk.
Atherosclerosis is a significant risk factor for myocardial infarction, cerebrovascular accidents, and peripheral artery disease. In addition to commonly recognized risk factors, research suggests that inflammatory and infectious factors are important contributors to the development of atherosclerotic plaque. As a means of addressing atherosclerotic changes that involve infectious burden or immunological complications, anti-atherogenic interventions like ALA that are also capable of normalizing pro-inflammatory cytokines, can be an effective portion of a comprehensive treatment plan. While our bodies produce ALA, levels decline with age making supplementation an important consideration.
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