Latest news with #immunesystem
The Guardian
7 hours ago
- Health
- The Guardian
Is it true that … cold water plunges boost immunity?
'It's a long-held belief that taking to the waters is good for your health,' says Mike Tipton, a professor of human and applied physiology at the University of Portsmouth. From Roman frigidariums to Thomas Jefferson's foot baths, cold immersion has long been seen as curative. But does modern science support the idea that it boosts immunity? The answer: it's complicated. While cold water immersion does activate the body, that's not the same as strengthening the immune system. 'When you immerse yourself in cold water, your body undergoes the cold shock response,' says Tipton. 'You get rapid breathing, a spike in heart rate and a surge of stress hormones such as adrenaline and cortisol.' This may explain why people feel more alert or energised after a cold dip. But does it mean you're less likely to get sick? Many studies into the effects focus on immune cell activity in the blood – which can increase after cold exposure – but that doesn't always translate into fewer infections. 'It's easy to cherry-pick results,' says Tipton. He points to a frequently quoted Dutch study in which people who ended their daily hot showers with at least 30 seconds under cold water took 29% fewer sick days. While it's often used as an example of the powers of cold plunges, those participants actually reported the same number of infections as those who didn't have a cold shower. 'That might reflect increased resilience or just a willingness to push through because of being part of a study,' says Tipton, rather than better immunity. It may also be that regular cold plungers simply have a healthier lifestyle overall. A recent study by Tipton's team found that indoor and outdoor swimmers had fewer respiratory infections than non-swimmers, suggesting it may be the exercise, not the cold, doing the work. Sign up to Inside Saturday The only way to get a look behind the scenes of the Saturday magazine. Sign up to get the inside story from our top writers as well as all the must-read articles and columns, delivered to your inbox every weekend. after newsletter promotion One thing is clear: too much cold is harmful. 'If your core temperature drops too far, it can suppress the immune system,' he says. His advice? Keep it short – no more than 90 seconds.
Medscape
23-05-2025
- Health
- Medscape
Chronic Stress Quietly Speeds Up Immune Aging and Depression
Karin de Punder, PhD, a postdoctoral researcher at the University of Innsbruck, Innsbruck, Austria, has conducted research on how chronic stress accelerates the aging of the immune system and its connection to depression. Traditionally, depression has been diagnosed on the basis of self-reported symptoms; however, reliable clinical biomarkers are lacking. de Punder and colleagues have explored new potential biomarkers in ongoing studies. She recently presented her findings at the German Congress for Psychosomatic Medicine and Psychotherapy in Berlin from March 12 to 14, 2025, during a session titled 'Stress and Aging: A Biological Basis of Trauma and Depression Symptoms?' de Punder stated, 'Chronic stress affects the immune system by accelerating its aging,' highlighting the important implications of the study. The molecular toxic properties of chronic stress promote these processes, including: Changes in stress reactivity, such as decreased sensitivity of cortisol receptors. Increased inflammation, particularly low-grade inflammation caused by chronic overactivity of the innate immune system, particularly when trauma is experienced early in life. Oxidative stress results in increased free radical production due to inflammation, which damages cells. Reduced mitochondrial function leads to less energy available for the repair and regeneration processes. Accelerated telomere shortening due to increased oxidative stress and inflammation. Shortened Telomeres Telomeres, which are the protective caps of chromosomes, shorten during cell division. Stress accelerates this process. When the telomere length falls below a critical threshold, cell death and senescence occur. Senescent cells cannot divide but continue to secrete pro-inflammatory signaling molecules. Accelerated telomere shortening has been linked to a shorter lifespan and various diseases, including coronary artery disease, atherosclerosis, type 2 diabetes, autoimmune diseases, and mental disorders, such as depression. Depression Biomarkers In studies examining how stress contributes to disease risk, researchers often measure the telomere length in peripheral blood mononuclear cells. If leukocyte aging and telomere length are associated with depression, they could serve as potential biomarkers, aiding the identification of depression through physical parameters. To identify these biomarkers, researchers analyzed blood samples from 22 patients diagnosed with depression, all of whom received inpatient treatment. Age-matched women without depression, with an average age of 58 years, served as controls. The severity of depression was measured using the Beck Depression Inventory II, and traumatic stress was assessed using the Essen Trauma Inventory. Blood samples were isolated to measure telomere length, and serum was used for mass spectrometry–based omics analysis to generate the biochemical profiles. In total, 682 metabolites were identified and evaluated for their association with depression and telomere length. Further investigation focused on glyceraldehyde, revealing that blood levels were significantly correlated with the severity of depression and trauma and with the inflammatory marker C-reactive protein, which is often elevated in patients with depression. Notably, higher glyceraldehyde levels were associated with shorter telomeres, particularly in CD8+ cells. These findings remained significant even after adjusting for age and body mass index. Glyceraldehyde and Depression Glyceraldehyde is a triose monosaccharide and an intermediate in carbohydrate metabolism. This highly reactive molecule can modify and bind proteins, resulting in the formation of advanced glycation end products. Glyceraldehyde-modified proteins exert cytotoxic effects by reducing glutathione levels, which protects cells from damage and leads to the production of reactive oxygen species, thereby promoting inflammatory responses. 'These are precisely the processes that negatively affect telomere length,' said de Punder. Glyceraldehyde, with other markers, could serve as a biomarker for a subtype of depression linked to immune system activation. The study also suggested that a slightly elevated C-reactive protein level above 1 mg/L may not always indicate infection but could reflect low-grade chronic inflammation. 'This would give physicians a testing option to determine whether this form of depression is present,' said de Punder. To validate these results, the study requires duplication in a larger cohort with a longitudinal design, a broader age range, and inclusion of both sexes. Further investigations are needed to better understand the mechanisms linking glyceraldehyde to depression, trauma, and telomere biology. 'If we have multiple biomarkers available in the future, we can not only improve the detection of depressive disorders but also better tailor treatment,' de Punder emphasized.
