Metal Exposure Can Increase Cardiovascular Disease Risk

Metal exposure from environmental pollution is associated with increased calcium buildup in the coronary arteries at a level comparable to traditional risk factors, according to a new study. The findings support that metals in the body are associated with the progression of plaque buildup in the arteries and potentially provide a new strategy for managing and preventing atherosclerosis. The findings highlight the importance of considering metal exposure as a significant risk factor for atherosclerosis and CVD. This could lead to new prevention and treatment strategies that target metal exposure. This can restrict blood flow and cause clots to form. This groundbreaking study underscores the critical associations of metal exposure from environmental pollution to cardiovascular health. Exposure to environmental pollutants like metals is a newly recognized risk factor for CVD, but there isn't a lot of research on its association with CAC. Researchers in this study sought to determine how urinary metal levels, biomarkers of metal exposure and internal doses of metals impact CAC. Researchers used data from the Multi-Ethnic Study of Atherosclerosis (MESA) prospective cohort, tracking 6,418 men and women aged 45-84 from diverse racial backgrounds free from clinical CVD, to measure urinary metal levels at the beginning of the study in 2000-2002. They examined non-essential (cadmium, tungsten, uranium) and essential (cobalt, copper, zinc) metals, both common in U.S. populations and associated with CVD. Widespread cadmium, tungsten, uranium, cobalt, copper, and zinc pollution occurs from agricultural and industrial uses such as fertilizers, batteries, oil production, welding, mining, and nuclear energy production. Results provided evidence that metal exposure may be associated with atherosclerosis over 10 years by increasing coronary calcification. Comparing the highest to lowest quartile of urinary cadmium, CAC levels were 51% higher at baseline and 75% higher over the 10-year period. For urinary tungsten, uranium and cobalt, the corresponding CAC levels over the 10-year period were 45%, 39%, and 47% higher, respectively. For copper and zinc, the corresponding estimates dropped from 55% to 33% and from 85% to 57%, respectively, after adjustment for clinical factors. Non-essential and essential urinary metal levels also varied by demographic characteristics. Higher urinary metal levels were seen in older participants, Chinese participants and those with less education. Participants from Los Angeles had markedly higher urinary tungsten and uranium levels, and somewhat higher cadmium, cobalt, and copper levels. The study's analysis also considered traditional CVD risk factors such as smoking, diabetes, and LDL-cholesterol levels. The associations between metals and CAC progression were comparable in magnitude to those for traditional risk factors. Addressing environmental risk factors like metal exposure will significantly reduce the global burden of cardiovascular disease and address long-standing health disparities.

Return to top

  Can Having a Stroke Change Sleep Pattern

People who have had a stroke may be more likely to sleep too much or too little compared to those without prior stroke, according to a new study. The study does not prove that stroke causes abnormal sleep; it only shows an association. Sleeping the right amount is considered essential for ideal brain and heart health. Abnormally long or short sleep after stroke can affect recovery and deteriorate quality of life, so these results should prompt us to screen for these issues and look at how we can help people improve their sleep habits. The study involved 39,559 people. Of the group, 1,572 people had a stroke and 37,987 people did not have a stroke. Every two years, participants were asked how much sleep they usually get at night on weekdays or workdays. Sleep duration was divided into three categories: short, less than six hours; normal, six to eight hours; and long, eight or more hours of sleep. Researchers looked at how often participants had normal sleep, defined as six to eight hours. Normal sleep duration was less common for people who had a stroke than for those with no prior stroke for all age groups with 32% vs. 54% for people age 18-44; 47% vs. 55% for people age 45-64; and 45% vs. 54% for people over age 65. After adjusting for factors that could affect sleep such as age, weight and high blood pressure, researchers found people who had a stroke were 54% more likely to report more than eight hours of sleep per night compared to those without stroke. Those with stroke were 50% more likely to get less than six hours of sleep per night when compared to those without stroke. In previous research, stroke has been linked to abnormal sleep, in particular sleep apnea. Conditions like insomnia and excessive sleepiness are common in stroke patients and may occur as a direct or indirect consequence of stroke itself. Future research should explore the links between stroke and duration of sleep and determine the effect of sleep duration on outcomes after stroke. A limitation of the study was that hours of sleep were self-reported, so participants may not have remembered accurately how much they slept.

SOURCE: American Academy of Neurology, September 2024

Return to top

                                            A New Therapies for Inflammatory Bowel Disease (IBD) 

There is a critical unmet need to help tighten and maintain a healthy intestinal barrier and treat a leaky gut. Researchers have now found that a unique strain of probiotic bacteria, Bifidobacterium bifidum BB1, enhances intestinal barrier function and protects against penetration of bacteria and various harmful agents in the intestine. The findings can help advance the development of novel, targeted, naturally occurring probiotic therapy for patients with inflammatory bowel disease (IBD) and other inflammatory diseases, such as fatty liver disease or alcoholic liver disease, that are associated with a leaky or disordered intestinal barrier. Patients with active IBD have elevated proinflammatory cytokines, including tumor necrosis factor (TNF)-α and IL1β. TNF-α levels are markedly elevated in intestinal tissue, serum, and stool of patients with IBD and at elevated levels produce an increase in intestinal tight junction permeability. TNF-α plays a central role in promoting intestinal inflammation in patients with IBD, and anti-TNF-α antibodies are highly effective in the treatment of the active disease. Previous studies from the laboratory at Penn State College of Medicine have shown that BB1 caused a marked enhancement of the intestinal epithelial barrier function and protects against the development of dextran sulfate sodium-induced intestinal inflammation. The results show that BB1 prevented the TNF-α increase in intestinal tight junction permeability via a toll-like receptor (TLR)-2 signal transduction pathway inhibition of NF-kB p50/p65 activation and MLCK gene. We also found that a protein called PPAR-γ was a critical intestinal cell mediator that regulated the intestinal barrier protection. Treatment of patients with active ulcerative colitis with a PPAR-γ agonist, rosiglitazone, significantly reduced the ulcerative colitis disease activity index score and resulted in an improved quality of life. These studies unravel novel intracellular mechanisms of BB1, a unique probiotic bacterial strain, demonstrating the promise of promoting health and treating inflammatory diseases including inflammatory bowel disease by maintaining a healthy intestinal barrier and protecting against leaky gut or intestinal barrier disruption. IBD, which includes Crohn's disease and ulcerative colitis, is characterized by inflammation affecting the gastrointestinal tract. The defective intestinal epithelial tight junction barrier is an important pathogenic factor contributing to the development of IBD. Patients with IBD have a defective intestinal tight junction barrier, characterized by increased intestinal permeability and increased luminal antigen penetration. Intestinal epithelial cells cover the entire intestinal mucosal surface and serve as a physical and functional barrier against the intestinal permeation of noxious luminal substances, including bacterial antigens, toxins, digestive enzymes, and food by-products.

Return to top