Medical Bulletin 22/ March/ 2024

Can high heat impair the immune system?

According to a study presented at the American Heart Association’s Epidemiology and Prevention│Lifestyle and Cardiometabolic Scientific Sessions 2024, short-term exposure to higher heat may increase inflammation and interfere with normal immune system functions in the body, which may, in turn, increase susceptibility to infections and accelerate the progression of cardiovascular disease.

Inflammation is a normal part of the body’s defence against injury or infection, however, an inflammatory response that is longstanding — lasting weeks to months — or that occurs in healthy tissues is damaging and plays a key role in the build-up of plaque in the arteries. This may lead to atherosclerosis. Heat waves are known to promote inflammation, however, more study is needed.

“Most research only considers temperature as the exposure of interest, which may not be adequate to capture a person’s response to heat. In our study, we used alternative measurements of heat in relation to multiple markers of inflammation and immune response in the body to investigate the short-term effects of heat exposure and produce a more complete picture of its health impact.” said lead study author Daniel W. Riggs, Ph.D., an assistant professor of medicine at the University of Louisville in Kentucky.

In the study, Participants visited various sites during the summer months for a blood test, and were analysed for multiple markers of immune system function. The researchers then examined associations between the markers of immune system function and heat levels, including temperature, net effective temperature (which factors in relative humidity, air temperature and windspeed) and the Universal Thermal Climate Index (UTCI) on that day, which is a thermo-physiological model that factors in temperature, humidity, wind speed and ultraviolet radiation levels, and used to evaluate participant’s physical comfort.

The analysis found:

1.For every 5-degree increase in UTCI, there was an increase in the levels of key markers of inflammation: monocytes (4.2%), eosinophils (9.5%), natural killer T-cells (9.9%) and tumor necrosis factor-alpha (7.0%) in the blood. These immune molecules indicate activation of the body’s innate immune system, to protect against pathogens and injury.

2.A decrease in B-cells (-6.8%), indicating the body’s adaptive immune system that remembers specific viruses and germs and creates antibodies to fight them, was lowered.

3.A lesser impact on the immune system was found when heat was measured by average 24-hour temperature or by net effective temperature, which incorporates humidity and wind but not sunshine.

“Our study participants only had minor exposure to high temperatures on the day of their blood test, however, even minor exposure may contribute to changes in immune markers. With rising global temperatures, the association between heat exposure and a temporarily weakened response from the immune system is a concern because temperature and humidity are known to be important environmental drivers of infectious, airborne disease transmission. Thus, during the hottest days of summer people may be at higher risk of heat exposure, they may also be more vulnerable to disease or inflammation.” said Riggs.

Reference: Heat exposure may increase inflammation and impair the immune system; American Heart Association Epidemiology and Prevention

Pregnancy history offers insights into risk of CV disease mortality: Study

Pregnancy leads to a lot of radical changes within the body. The entire cardiovascular system reorganizes itself to sustain life for a second person inside the womb. The heart starts beating faster, and the total amount of blood in the body doubles. Mothers grow an entirely new organ, the placenta, to feed and protect the growing baby.

A study published in the journal Paediatric and Perinatal Epidemiology revealed that around five to ten percent of people develop a problem with their cardiovascular system during pregnancy in response to the physiological changes occurring and/or problems with the placenta, like “preeclampsia.”

While some disorders are rather benign, like high blood pressure during pregnancy, others are true emergencies, including liver failure, kidney failure, and seizures.

In the study, the researchers looked at the specific order and severity of hypertensive disorders of pregnancy throughout women’s lifetime number of pregnancies with the help of compulsory birth registry and public healthcare system in Norway.

Previous studies have concluded that having a hypertensive disorder of pregnancy doubles your risk of heart attack and stroke. Researchers found that some people have severe risks compared to previous estimates, with almost 10-fold increased risk.

“These people at high risk have a rare pattern of more than one hypertensive disorder in their reproductive history, and they delivered their pregnancies early, which may indicate more severe conditions”, said Sage Wyatt, PhD-candidate at the Department of Global Public Health and Primary Care, University of Bergen.

He also found that some patterns on pregnancy histories that include hypertensive disorders are not associated with heart attack and stroke at all.

“This study adds to the evidence that CVD mortality cannot be predicted by a history of HDP alone but must be predicted in the context of multiple factors across our lifetime reproductive history” concluded Wyatt.

Reference: Sage Wyatt, Liv Grimstvedt Kvalvik, Aditi Singh, Kari Klungsøyr, Truls Østbye, Rolv Skjærven; Heterogeneity in the risk of cardiovascular disease mortality after the hypertensive disorders of pregnancy across mothers' lifetime reproductive history; Journal: Paediatric and Perinatal Epidemiology; DOI: 10.1111/ppe.13059

Research discover potential triggers for inflammatory bowel disease

Abdominal pain, diarrhea, weight loss—these and the other symptoms of inflammatory bowel disease (IBD) can be disruptive and debilitating. And while scientists have figured out that IBD has a genetic component, not everyone with a family history develops the disease. The environmental triggers for Crohn’s disease and ulcerative colitis, known together as IBD, remained largely unknown.

A new study from the University of Michigan discovered a complex interplay between diet, genes, and the gut microbiota that could explain why Inflammatory bowel disease develops.

The study published in the journal Cell Host & Microbe found that a low-fibre diet led to a proliferation of mucin-degrading bacteria—bacteria that thrive by eating the mucus lining of the intestine.

Researchers analyzed the genetic link using mice with identical immune alterations. While some developed intestinal inflammation, its severity varied and worsened with specific bacteria and a low-fibre diet. Manipulating the presence of a human gut microbiome and dietary fibre in mice models allowed the team to regulate inflammation levels. Moreover, inflammation from fibre-free diets intensified with higher levels of mucin-degrading bacteria.

“These bacteria start foraging on the mucus layer for nutrients, reducing its thickness and barrier function and bringing microbes just 10-100 microns closer to the host tissue. That was enough in the context of the mice with IBD genetics to make them sick,” said Martens, professor of microbiology and immunology at U-M Medical School.

Conversely, feeding the mice a fibre-rich diet prevented inflammation from developing and even returning mice fed low fibre to a high-fibre diet led to a peak in inflammation followed by a decline, suggesting fibre can reverse the deleterious effects of mucus erosion on inflammation.

IBD, particularly in children, is frequently managed with exclusive enteral nutrition (EEN), a fiber-lacking formula-based diet. Surprisingly, EEN reduces inflammation without a clear explanation. To understand, researchers administered dried-down formula to mice with IBD genetics. Results showed varying inflammation levels among the mice, with some experiencing notably less inflammation compared to those on a fibre-free diet, despite EEN also reducing mucus thickness.

The team then discovered that elevated amounts of a single branched-chain fatty acid, isobutyrate, was elevated in EEN fed mice and might suppress inflammation. Isobutyrate is produced through fermentation by some bacteria in the gut.

"Our findings suggest a potential new path for treating IBD. By tailoring specific dietary interventions to influence gut microbiome function, we may be able to manipulate these bacterial communities to alleviate inflammation,” said Gabriel Pereira, first author of the study.

Reference: Gabriel Vasconcelos Pereira, Marie Boudaud, Mathis Wolter, Celeste Alexander, Alessandro De Sciscio, Erica T. Grant, Bruno Caetano Trindade, Eric C. Martens; Opposing diet, microbiome, and metabolite mechanisms regulate inflammatory bowel disease in a genetically susceptible host; Journal: Cell Host & Microbe; DOI: 10.1016/j.chom.2024.03.001