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Your genes can play a role in eczema, but there’s much more to its origins than that.

Unlike, say, the flu or a bacterial infection, eczema (also known as atopic dermatitis) doesn’t have an exact cause. But there are certain factors that may make you more likely to develop it—and one of these factors is your family history. That brings us to the big question: Is eczema genetic? It’s complicated. “Genetics definitely play a role, but so does the environment,” says Geeta Yadav, M.D., a board-certified dermatologist at Facet Dermatology in Toronto, Canada. This combination—plus luck—can contribute to the onset of eczema, although it doesn’t necessarily guarantee it. Here, experts explain the ins and outs of the genetic predisposition to eczema.

Genetic Predisposition to Eczema

There’s a strong link between genetics and eczema, says JiaDe (Jeff) Yu, M.D., a board-certified dermatologist at Massachusetts General Hospital in Boston. The exact connection between the two, though, is unclear. “While there have been some identified genetic mutations that predispose you to eczema, such as mutations in the filaggrin gene [filaggrin is a protein essential for the formation and proper functioning of the skin’s outermost layer], there are many other unidentified genetic causes of eczema,” he says.

So far, there seems to be two different ways through which genetics can contribute to eczema: “Genetic factors [may] influence the skin barrier—how well the skin protects against irritation from the environment and locks in fluid. And the immune system can also predispose people to eczema,” says Jocelyn Gandelman, M.D., a board-certified dermatologist at Schweiger Dermatology in New York City. Let’s look at these factors in more detail.

Genes Coding for Skin Function

Some genes can dictate skin barrier function—and, in the case of eczema, skin barrier dysfunction. One such example is the filaggrin mutation, which is hereditary, says Dr. Yu. “Filaggrin is a protein that helps the skin build a strong barrier to keep water in and keep the skin hydrated,” says Dr. Gandelman. “People with a filaggrin mutation are much more likely to develop eczema than people without one.”

Meanwhile, one 2022 study concluded that mutations of the KIF3A gene also led to impaired skin barrier function, which can in turn contribute to the onset of eczema.

Genes Coding for Immune System Function

For context, eczema is a disease of type 2 inflammation, which is “the kind of inflammation that involves a set of immune cells that release specific inflammatory signals that can cause itch and thickening of the skin,” says Dr. Yadav. Research has shown that the overexpression of certain interleukins, which are molecules that regulate the body’s immune response—such as IL-4, IL-13, and IL 31—seem to predispose people to eczema. Unlike the filaggrin mutation, this isn’t hereditary.

What Family History Can Tell You

Beyond the mutation of certain genes, a family history of eczema can also increase the likelihood of developing the disease. “In families where one or both parents have atopic dermatitis, the likelihood of children having atopic dermatitis is three to five times higher than the general population,” says Dr. Yu. Currently, though, there’s no specific set of genes one can look for in families, since “the exact hereditary nature of atopic dermatitis is still TBD,” he says.

Still, he takes family history seriously when making a diagnosis. “If there is a relative with an atopic disease—eczema, hay fever, food allergies, asthma—then I know the child has a much higher risk of developing atopic dermatitis and other atopic-related disorders,” he says. (Atopic means an allergy-related disorder.)

That family history of eczema is also helpful when diagnosing people of color, who are disproportionately affected by eczema. “Eczema frequently goes underdiagnosed in certain populations, especially patients of color, as a lot of dermatology literature often portrays skin conditions on fair complexions,” says Dr. Yadav. Having markers like a family history to work from, then, can help providers catch it earlier, she says.

How Environmental Factors Influence Genetics

There are also environmental factors that influence genes, particularly during pregnancy. “Environmental factors can lead to an increased risk of eczema in babies; these are factors in the surroundings that impact the body,” says Dr. Gandelman. However, she says, genetic and environmental factors can merge. For instance, “if someone has a genetic predisposition to eczema through family history of eczema or allergies or asthma, plus environmental exposure to things that further put them at risk, this together can very much increase the chance of getting eczema,” she says. These include:

Maternal stress during pregnancy: When an expecting person experiences stress or anxiety during pregnancy, the baby then has a higher risk of eczema, according to a 2018 review. The thinking is that stress interferes with the immune system of a growing fetus, creating the ideal conditions for eczema down the line.

Smoking while pregnant or breastfeeding: Smoking is already considered off-limits during this time because of the risk of birth defects (among other serious health issues), but it can also lead to either eczema or allergies to pollen and dust mites. In one study, 52% of children whose moms had smoked experienced symptoms, compared to 36% of those with nonsmoking mothers.

Maternal use of antibiotics: Antibiotics are known for throwing off the balance of the gut microbiome, since they can inadvertently target good bacteria. But a meta-analysis found that taking antibiotics before the third trimester led to a modest increase in eczema risk. That may be because the microbiome of the mom (which the baby is exposed to) can influence the immune system and gut microbiome of the baby, too.

Maternal exposure to air pollution: Even the air mom breathes can impact eczema risk. A big meta-analysis found that exposure to nitrogen dioxide (better known as smog) during the first and second trimesters led to a higher risk of eczema in the baby. Again, the idea is that the exposure to pollutants can impact immune function in both mom and baby, resulting in a higher risk of eczema for the latter in childhood.

Additional environmental factors may include:

Air pollution, Climate, like humidity and precipitation, Hard water, Irritants, like fragrances and nickel, Tobacco smoke, Urban environments

Still, if you get diagnosed with eczema out of nowhere, you’re not alone, since you don’t necessarily have to have an inherited eczema risk to develop the disease. “I also see many patients who have no family history of eczema—and if their skin rash looks like eczema, then they can be diagnosed with eczema as well,” says Dr. Gandelman.

Triggers For Eczema

What specifically triggers your eczema is related to, but not the same as, your risk factors. “Genetics determine the risk for eczema—as do some unknown and not fully understood contributors—but then triggers will cause a flare,” says Dr. Gandelman, who notes that flares can also happen without a specific trigger or reason for it.

Confused? Keep in mind that it’s a complex topic, even for experts. “For example, changes in the bacteria in the skin may be seen in patients with eczema, and food allergies are more common in patients with eczema—but these conditions are complicated, and it is not fully understood if these are true triggers of eczema,” says Dr. Gandelman. That said, the best-known triggers include:

Allergens, like fragrance and metals, Certain chemicals, Diet, Dry skin, Stress

Takeaways

When it comes to eczema, hereditary factors are important, but they don’t tell the whole story. And it’s helpful to remember that even if you do have a family member with asthma or a mutation that predisposes you to eczema, that doesn’t mean that you’ll definitely get it. Ultimately, these genetic markers for eczema are just one piece of the puzzle in fully understanding its causes.

(Source : HealthCentral.com)

New research finds a link between the skin condition and eosinophilic esophagitis—especially if you have certain food allergies.

Eczema and eosinophilic esophagitis (EoE) affect two different parts of the body: the skin and the digestive tract. But if you have the former, you may be at higher risk for the latter, especially if you also have an allergy to milk, wheat, or egg, reports a new study published in the journal International Archives of Allergy and Immunology.

“We knew that people with EoE often have atopic [genetically predisposed to allergies] conditions. But the reverse—how often EoE occurs in those with atopic diseases—was unclear. Knowing this helps clinicians screen earlier, identify symptoms sooner, and prevent long-term issues [caused by EoE] like esophageal scarring,” says the study’s coauthor Micheal Tadros, M.D., a gastroenterologist at Albany Medical Center in New York.

Study Findings

A Strong Link Between Eczema and EoE

The cross-sectional study looked at electronic healthcare data from the nationwide Veteran’s Affairs (VA) records database, which consists of around 1.1 million adults. Dr. Tadros and his coauthors randomly selected 10% of these patients to include in the study. Within the randomly selected group, 26% had eczema and less than 1% had EoE. The team also noted whether the people in the study group had allergies to milk, eggs, or wheat.

From there, the researchers analyzed the data to see how often the conditions occurred together. As it turned out, people with eczema were around three times more likely to also have EoE compared to those without eczema. The odds were even higher for people with eczema who also had certain food allergies: The risk for EoE was four times higher for patients with an egg allergy, nearly six times higher for patients with a wheat allergy, and a whopping 20 times higher for patients with a milk allergy.
The findings send a clear message: “People with [eczema] are at higher risk of EoE, especially with food allergies,” Dr. Tadros says.

A Possible Mechanism

Shared Immune System Dysfunction

The findings also reinforce what many experts in the allergy and immunology world have long suspected, namely that eczema, EoE, and food allergies exist along a shared immune system pathway. “It’s not just a coincidence; it’s a reflection of how the immune system behaves across multiple organ systems,” says Inderpal Randhawa, M.D., a board-certified allergist and immunologist and founder of the Food Allergy Institute in Long Beach, CA. (Dr. Randhawa was not involved in the study, but reviewed its results.)
These shared pathways seem to involve similar cytokines (inflammatory immune proteins) and immune cells. Eczema’s “association with a defective skin barrier is mirrored by epithelial barrier defects in EoE, possibly predisposing patients to both,” Dr. Tadros explains. (Epithelial tissue is the thin tissue lining the esophagus and other parts of the GI tract.) 
Food allergens could also trigger or worsen esophageal inflammation, setting off barrier dysfunction that ends up affecting both the skin barrier and the GI tract lining. “Milk, wheat, and egg are among the first foods infants are exposed to and the most common allergens in early life,” says Dr. Randhawa. “The immune system’s memory of these allergens is deep, and when combined with an impaired barrier, these proteins can repeatedly trigger inflammation, both in the skin and the esophagus.”

Significance

Helping With Early Detection

There’s no known way to prevent EoE (or eczema or food allergies, for that matter). But knowing that eczema and food allergies up EoE risk may make it easier to catch new cases of EoE sooner, before they become severe. “Early detection is crucial,” Dr. Tadros says. When unmanaged, EoE can lead to long-term complications like esophageal scarring or narrowing, which can make it harder to swallow, according to the American Gastroenterological Association.

“As we learn more about EoE, and the population most likely to develop it, we are able to home in on clinical questions and be more selective about [screening] patients,” says Nicole Nudelman, M.D., the lead study author and Ophthalmology Resident Physician at Albany Medical College in New York.

For example, doctors can ask their eczema and food allergy patients about symptoms known to occur with EoE, like swallowing problems, a feeling like food is sticking in the throat, or acid reflux that doesn’t get better with the usual treatments. “From there, we can start proactive testing or early interventions,” says Dr. Randhawa. You also can (and should) bring up those symptoms with your doctor if you start to experience them.

In addition to being on the lookout for possible EoE symptoms if you’re at higher risk, you can take steps to manage your existing conditions: Follow your eczema treatment plan and steer clear of any known food allergens to keep inflammation levels as low as possible, Dr. Tadros recommends. That said, you don’t need to actively avoid egg, wheat, or milk if you don’t have a known allergy, he adds. But do let your doctor know if you start to notice any unusual reactions after eating those foods, such as hives, itching, swelling, or stomach cramps; seek emergency medical attention for severe symptoms such as mouth or tongue swelling or trouble breathing.

Future Impacts

Looking Forward

How might these findings impact future research and treatments? Experts maintain more studies are needed to better understand how eczema, food allergies, and EoE are intertwined. Additional data can help clinicians determine whether their patients with eczema or food allergies should routinely be screened for EoE, and whether it may one day be possible to prevent EoE in people who are high-risk.

(Source : HealthCareCentral)

Rocatinlimab is an experimental biologic medicine being developed to treat moderate-to-severe atopic dermatitis (eczema). It is a fully human monoclonal antibody that binds the immune receptor called OX40 (also written OX40/OX40L), a protein found on activated T cells — the immune cells that drive much of the inflammation in eczema. By attaching to OX40, rocatinlimab blocks the OX40–OX40L signalling that helps pathogenic T cells survive and expand, and it also reduces the number of these activated OX40-positive T cells. The net idea is “T-cell rebalancing”: damp the harmful T-cell activity that fuels skin inflammation while leaving other immune functions as intact as possible. (PMC)

Because of that mechanism, the health effect most consistently reported in clinical studies is reduced skin inflammation and rapid improvement in the signs and symptoms of atopic dermatitis. Large randomized trials and subsequent reports have shown that patients treated with rocatinlimab experienced clinically meaningful reductions in eczema severity scores (for example EASI and Investigator Global Assessment measures) compared with placebo, and many patients reported less itch and clearer skin during the trial periods. These benefits reflect the drug’s targeted action against the specific T-cell pathway that helps sustain chronic skin inflammation. (The Lancet)

Like all immune-targeting medicines, rocatinlimab also has potential side effects. Across phase 2 and phase 3 trial reports and company safety summaries, the most commonly observed adverse events included upper respiratory infections (nasopharyngitis, pharyngitis), simple viral illnesses (influenza), mouth ulcers (aphthous ulcers), headache, cough and rhinitis; some patients experienced fever or chills shortly after dosing. Overall the safety profile reported so far has been described as clinically acceptable in trial populations, but longer-term monitoring and larger post-approval data (if and when it is approved) will be needed to fully characterize rare or late effects. Because it affects T-cell activity, clinicians watch for infections and other immune-related effects as a precaution. (Amgen)

Rocatinlimab is given by subcutaneous injection according to the schedules tested in trials (for example, every few weeks in the studies reported so far), and it has been studied both alone and in combination with standard topical therapies. The exact dosing regimen and administration details that would be recommended in routine practice depend on final regulatory approvals and prescribing information. (kyowakirin.com)

Finally, it’s important to know the current regulatory status: rocatinlimab has shown promising results in late-phase clinical trials, but as of December 20, 2025 it is an investigational therapy under review and not yet a widely available, approved prescription medicine. That means people cannot obtain it commercially through pharmacies; access is limited to participation in clinical trials or programs authorized by the drug developers and regulators. If it receives regulatory approval, clinicians will be better able to weigh its benefits and risks for individual patients compared with existing therapies. (investors.amgen.com)

(Source : ChatGPT)

An international team of investigators led by Emma Guttman-Yassky, MD, PhD, Waldman Professor and System Chair of the Kimberly and Eric J. Waldman Department of Dermatology at the Icahn School of Medicine at Mount Sinai, has reported results from the first phase 3 clinical trials of rocatinlimab, a novel treatment for moderate-to-severe atopic dermatitis (eczema). The landmark findings from the ROCKET-IGNITE and ROCKET-HORIZON studies were published today in The Lancet. 

Eczema affects hundreds of millions of people worldwide and is notoriously difficult to treat due to its complex and chronic inflammatory pathways. Current biologics focus on blocking “allergy” cytokines but fail to address the memory T cells that sustain disease activity. Rocatinlimab is the first antibody to selectively block the OX40 receptor on effector and memory T cells, rebalancing the immune system and altering the long-term course of disease. 

Across the two global, double-blind, placebo-controlled randomized phase 3 clinical trials, nearly 1,500 patients were followed for 24 weeks, and rocatinlimab showed robust and lasting benefits. Patients receiving the treatment were three times more likely to achieve significant improvement in eczema severity, as measured by EASI and vIGA-AD scores, compared to those on placebo. Improvements continued beyond week 24, suggesting that the benefits strengthen over time. The therapy also led to meaningful reductions in itch, pain, and sleep disturbances, enhancing overall quality of life. Importantly, rocatinlimab was well tolerated, with adverse events comparable to placebo, and demonstrated high selectivity by reducing only the OX40R+ CD4+ T cells responsible for eczema’s persistence, without off-target effects. 

“These findings represent a major advance for patients living with eczema, who often face years of uncontrolled symptoms and few effective options,” said physician scientist, Dr. Guttman-Yassky, lead author of the study. “By targeting memory T cells through OX40, rocatinlimab not only clears the skin and relieves itch, but continues to improve patients’ lives over time with a strong safety profile. This is the first phase 3 proof that rebalancing these immune cells can transform how we treat atopic dermatitis.” 

The results establish OX40 as a validated treatment target in eczema and position rocatinlimab as a potential first-in-class therapy. Patients from the phase 3 trials are now being followed in the ROCKET-ASCEND extension study, which will track outcomes for up to two years. Additional research will explore its role in pediatric patients, in combination with other therapies, and in direct comparisons to existing systemic treatments. 

The studies were conducted with international partners and funded by Amgen Inc. and Kyowa Kirin Co., Ltd. 

(Source : MountSinai.org)

People with eczema sometimes notice that eating certain foods makes their skin worse. To understand why, it helps to see food-related flares as one part of a larger immune-and-barrier problem rather than as a single, universal cause. In plain scientific terms: some foods can trigger immune reactions that show up on the skin, but this happens only in some people and by several different biological routes — so food is a real trigger for some patients (especially young children with severe eczema) and much less important for others. (PubMed Central)

The most clearly understood route is classical IgE-mediated food allergy. In that situation the immune system has made IgE antibodies to a food protein (for example, milk, egg, peanut, tree nuts, fish or shellfish). When the person eats that food, the antibodies rapidly trigger a Type-2 allergic response that can cause hives, swelling, vomiting, breathing problems — and in some people it can also make eczema flare. These reactions usually happen quickly after eating and are the same type of allergy that can sometimes cause anaphylaxis. Because the immune mechanism is well defined, testing and diagnosis follow established allergy pathways. (nhs.uk)

A second, less immediate route is a delayed or non-IgE immune response. Some people develop eczematous flares a day or two after eating a particular food without the classic rapid allergic symptoms. These delayed reactions can be driven by other parts of the immune system (T cells and cytokines) and are harder to detect with standard blood or skin IgE tests. In practice this means that a food can be a real trigger for skin inflammation even when routine allergy tests are negative, but proving that requires careful clinical work such as elimination diets followed by supervised food re-challenge. (AAAAI)

A key biological reason why food can affect the skin in eczema is the “leaky barrier” problem. When the outer skin barrier is damaged or immature (for genetic reasons such as filaggrin deficiency, or because of inflammation and scratching), proteins and tiny particles on the skin surface get through more easily. Animal and human studies show that allergens that touch or sit on inflamed, leaky skin are more likely to sensitize the immune system — a process called epicutaneous sensitization — which raises the chance that ingesting the same protein later will produce an allergic reaction or make eczema worse. In other words, eczema’s broken skin barrier both allows allergic sensitization to develop and amplifies the immune response that makes flares happen. (PubMed Central)

Not every reported “food trigger” has the same scientific backing. In infants and very young children with early, severe eczema, true food allergies are relatively common and can be an important cause of flares. In school-age children and adults, however, broad claims that foods such as dairy, wheat, or gluten are major causes of eczema are not supported for most people; many adults who think food is to blame will not improve with unsupervised elimination diets. Some foods or additives (for example, highly processed foods, foods high in sugar, or foods that release histamine) are sometimes named by patients and small studies suggest they might worsen inflammation in some individuals, but the evidence is weaker and more variable than for classical food allergy. That’s why specialist evaluation is important before removing foods long-term — elimination diets can cause nutritional problems and sometimes give a false sense of cause-and-effect. (HealthyChildren.org)

Finally, practical implications follow directly from the biology. When food is genuinely triggering eczema, the foods most commonly involved in children are cow’s milk, eggs, peanuts/tree nuts, soy, wheat, fish and shellfish — though any food can theoretically be a problem for a sensitized person. Because mechanisms differ (immediate IgE reactions versus delayed non-IgE responses versus skin-sensitization pathways), testing should be targeted: a careful clinical history is the first step, followed by selective testing (skin or blood IgE) and, when needed, a supervised oral food challenge to confirm whether the food truly causes flares. For most older children and adults with eczema, however, routine broad food avoidance is not recommended; treating the skin barrier and controlling inflammation are central, and only when the history or testing points to a food allergy should dietary changes be pursued under medical guidance. (ouh.nhs.uk)

In short: certain foods can cause or worsen eczema in people who are immunologically sensitized to them, through rapid IgE-mediated allergy, slower T-cell mediated responses, or as a consequence of epicutaneous sensitization across a damaged skin barrier. The exact foods and mechanisms vary from person to person, which is why diagnosis and any elimination plan should be individualized and supervised by clinicians experienced in allergy and eczema. (PubMed Central)

(Source : ChatGPT)

A recently approved injectable eczema drug provides quick itch relief to patients with the maddening skin disease, a new study says.

Nemolizumab (Nemluvio) relieved itchiness within two days for three times as many patients as a placebo, researchers reported Tuesday in the Journal of the European Academy of Dermatology and Venereology.
The drug also helped twice as many eczema patients sleep better within a couple of days, researchers said.
"These new data reinforce our understanding of nemolizumab's rapid onset of action in relieving itch and, in turn, improving sleep in patients living with atopic dermatitis and prurigo nodularis," researcher Dr. Christophe Piketty said in a news release. He's program head of therapeutic dermatology for the Swiss pharma company Galderma. Galderma, the developer of nemolizumab, funded the study.

The U.S. Food and Drug Administration approved nemolizumab in 2024 for treatment of moderate-to-severe atopic dermatitis, commonly known as eczema, as well as for itchy bumps that often appear alongside eczema in a condition called prurigo nodularis, according to Drugs.com.

Eczema occurs due to immune system problems that hamper the skin's defenses against allergens and irritants, the Cleveland Clinic says.

A monoclonal antibody, nemolizumab targets a receptor which activates an inflammatory immune system chemical that drives itch and other symptoms in eczema, researchers said in background notes.

For the new study, researchers performed a follow-up analysis of the clinical trial data that led to FDA approval of the drug. They reviewed data from trials involving nearly 2,300 people.

Results showed that nemolizumab reduced itch within 48 hours for nearly 11% of patients, compared to 3% of patients taking a placebo.

It also reduced itch that swiftly for 17% of patients with prurigo nodularis, compared to just under 4% of those on placebo.

Sleep also improved within two days for 10% of eczema patients on nemolizumab compared to under 5% of those on a placebo, and more than 13% of prurigo nodularis patients compared to about 4% of those on placebo.

By two weeks, a quarter of patients with eczema and more than a third with prurigo nodularis had shown clinically meaningful improvements in itch and sleep, the study said.

"Itch is the most burdensome symptom reported by patients with moderate-to-severe atopic dermatitis and patients with prurigo nodularis, and rapid improvement in itch intensity is a key treatment goal," researchers concluded.

"Treatments that rapidly reduce itch and provide clinically meaningful improvements in disease severity and patients' quality of life are key in the current treatment landscape for both AD and PN," they wrote.

(Source :  UnitedPressInternational)

Glutathione is made inside your cells from three amino acids — cysteine, glutamate and glycine — so the easiest way diet helps is by supplying those building blocks and the nutrients that let the body make and recycle glutathione. Of the three precursors, cysteine is usually the most limiting, so eating foods that supply sulfur-containing amino acids supports production. Good dietary sources include protein-rich foods such as eggs, poultry, lean meat, fish, dairy (whey protein is particularly rich in cysteine), and legumes; these provide the amino-acid raw material your liver and other tissues need to synthesise glutathione.

Beyond precursors, several vitamins and minerals help glutathione work and be renewed. Vitamin C and vitamin E act as complementary antioxidants and help recycle oxidized glutathione back to its active form. Selenium is an essential cofactor for glutathione peroxidase, an enzyme that uses glutathione to remove harmful peroxides; selenium-rich foods like Brazil nuts, seafood and whole grains therefore support the system. B-group vitamins and adequate overall protein intake also help because they support general metabolism and the pathways that supply glutamate and glycine.

Certain plant compounds stimulate the body’s own glutathione production by turning on protective genes. Compounds found in cruciferous vegetables (for example broccoli, Brussels sprouts, and kale) — especially sulforaphane — activate cellular antioxidant response pathways (commonly called Nrf2), which upregulate enzymes involved in glutathione synthesis and regeneration. Allium vegetables (garlic, onions), green tea polyphenols, and some other phytochemicals have similar mild activating effects. Eating a variety of colorful vegetables and fruits therefore provides both direct precursors and signals that encourage cells to make and preserve glutathione.

What you avoid in your diet matters too. Chronic alcohol intake, a diet very high in processed foods and refined sugars, and long periods of overeating or nutrient-poor eating increase oxidative stress and can deplete cellular glutathione. Conversely, dietary patterns associated with lower inflammation and oxidative stress — for example Mediterranean-style diets rich in vegetables, fruits, whole grains, nuts, fish and modest amounts of lean protein — are more likely to preserve glutathione over the long term.

Finally, while some fresh foods (asparagus, avocado, spinach) contain measurable glutathione, most ingested glutathione is broken down during digestion; the main benefit of food is supplying precursors and activating protective pathways rather than delivering ready-made glutathione. For people with specific clinical needs or suspected deficiency, clinicians sometimes recommend targeted supplements (such as N-acetylcysteine) because they reliably raise cysteine availability; for general health, a balanced, protein-adequate, plant-rich diet that includes sulfur-containing foods, cruciferous vegetables, vitamin-C rich fruits, and selenium sources is the practical, evidence-based way to boost and preserve your body’s glutathione system.

(Source : ChatGPT)

Glutathione is a small molecule your cells make from three amino acids (glutamate, cysteine and glycine) and it works as a central antioxidant and repair molecule inside nearly every cell. It neutralizes harmful reactive oxygen species directly, and it also acts as a required cofactor for enzymes (for example glutathione peroxidases and glutathione S-transferases) that detoxify peroxides and help remove damaged chemicals from cells. This combined activity helps protect DNA, proteins and membranes from oxidative damage that accumulates with stress, toxic exposures, infection and aging. (PubMed)

Beyond simple antioxidant activity, glutathione is a key player in the body’s detoxification system. Many toxins and drug breakdown products are chemically linked to glutathione (a process called conjugation) so they become easier for the liver and kidneys to eliminate. By participating in these conjugation reactions, glutathione helps reduce the chance that reactive chemicals will injure cellular targets. This detox role is especially important in the liver, where glutathione concentrations and turnover are high. (PMC)

Because glutathione levels fall when cells are exposed to oxidative stress or when precursor supply is limited, researchers have asked whether giving glutathione or its precursors can improve health. Clinical studies and randomized trials show that supplementation can raise circulating glutathione in some settings and reduce markers of oxidative damage and inflammation, with demonstrated benefits in selected groups (for example some older adults and people with metabolic stress). Those trials are encouraging but vary in size and quality, so the strength of evidence differs by condition. (PMC)

How glutathione is delivered matters. Standard oral glutathione is variably absorbed, so many studies use precursors such as N-acetylcysteine (NAC), which reliably raises the body’s own glutathione production, or they use formulations designed for better uptake (liposomal or intravenous glutathione) when a rapid, large increase in blood levels is desired. The choice of form affects how much glutathione actually reaches tissues and therefore the likely benefit. (livemomentous.com)

Safety and practical limits are important. Glutathione supplements are usually well tolerated, but they are not free of risk: inhaled forms have worsened breathing in some people with asthma, and improperly compounded injectable products have caused serious adverse events leading to regulatory warnings. Long-term effects, optimal doses for different conditions, and interactions with medications remain areas of active study, so clinical guidance is recommended before starting high-dose or injected glutathione. (Natures Fix)

In plain terms: glutathione is a natural, powerful defender inside cells that supports antioxidant protection and chemical detoxification. Boosting or preserving glutathione—either through diet, supplying building blocks like cysteine, or, in some clinical settings, by targeted supplementation—can help reduce oxidative stress and support organ health, but the benefits depend on the person’s starting status, the form and dose used, and the medical context. For anyone considering supplements, a clinician can help weigh the existing evidence, choose a delivery method, and monitor safety.

(Source : ChatGPT)

Spermidine is a small organic molecule called a polyamine that cells use for growth, repair and many basic processes. In the human gut it comes from three places: the food we eat, the cells of our own body, and the bacteria that live in the intestine. A range of common gut microbes are able to make spermidine themselves, so the community of bacteria in the intestine helps determine how much of this molecule is present in the gut lumen. (Frontiers)

Not every microbe uses the same recipe. Classic laboratory and animal studies have shown that bacteria from genera often found in the human gut — for example Bacteroides and Fusobacterium — can produce putrescine and spermidine when given appropriate food substrates in the gut, and other groups such as Escherichia, Lactobacillus and Bifidobacterium are also associated with polyamine production in different studies. Those are examples rather than an exhaustive list: many species across different bacterial families carry the enzymes needed to make these molecules, and which species are important can vary with diet and the individual’s microbiome composition. (MDPI)

Biochemically, most bacterial spermidine production follows a two-step idea: bacteria first make putrescine from amino acids (arginine or ornithine) and then convert putrescine into spermidine. Putrescine can be generated by enzymes called decarboxylases (ornithine decarboxylase or arginine decarboxylase, depending on the route). To make spermidine a second set of enzymes is used: S-adenosylmethionine decarboxylase provides an activated propylamine donor and spermidine synthase (often called SpeE) transfers that propylamine onto putrescine to form spermidine. These enzymatic steps are well described in reviews of bacterial polyamine metabolism and explain why many different gut bacteria can contribute to the pool of spermidine. (MDPI)

Some bacteria use alternative chemical routes. A notable example is Campylobacter jejuni, which lacks the standard SpeD/SpeE pair yet still makes spermidine by a different “carboxyspermidine” style pathway. More recently, researchers have discovered further alternative bacterial pathways (for example a carboxy-aminopropylagmatine route reported in 2023) that broaden the kinds of microbes we know can make spermidine. Those alternative pathways matter because they show that spermidine production is widespread and biochemically diverse across the microbiome, not confined to a single canonical pathway. (immunenetwork.org)

Finally, production in the gut is dynamic: what bacteria make depends on what substrates are available (the diet, especially amino acids and fermentable fibers), the presence of particular bacterial strains, and interactions between microbes and host cells that can both supply and take up intermediates. Intervention studies show that adding certain probiotics or dietary components can change microbiome-derived spermidine levels, illustrating that bacterial spermidine output can be modified by what we eat or by changing the resident microbes. In short, multiple gut bacterial groups can produce spermidine through one of several biochemical routes, and diet plus microbial ecology determines how much of that bacterial spermidine ends up in the intestine. (PMC)

(Source : ChatGPT)

In a study published in PNAS, scientists reveal that the survival of the bacterium responsible for tuberculosis, Mycobacterium tuberculosis, depends on a specialized transporter that enables it to absorb sulfate, a mineral form of sulfur. This transporter is highly specific to M. tuberculosis and could therefore be a target for drugs without side effects on human cells.

Tuberculosis, still a formidable enemy

Tuberculosis remains one of the deadliest infectious diseases today. Each year, it affects millions of people worldwide and continues to claim many lives, despite the existence of a vaccine and available treatments. In 2023, the World Health Organization reported 10.8 million new cases. The situation is further complicated by the emergence of antibiotic-resistant strains: these bacteria evade current treatments—which are already lengthy and difficult to follow—making the search for new solutions more urgent than ever.

Understanding the bacterium’s lifestyle to fight it more effectively

Tuberculosis is caused by a bacterium known as Mycobacterium tuberculosis. To combat it effectively, it is essential to understand its way of life. How does it survive inside the human body? How does it hijack our immune defenses to its own advantage? And above all, what mechanisms allow it to persist for years in a dormant state before reactivating to cause disease? These are the fundamental questions that a team of French scientists set out to address—leading to a major breakthrough published in the journal PNAS.
A discovery about the bacterium’s sulfur intake

For a long time, the scientific community believed that the bacterium fed mainly on organic sulfur, particularly from methionine, an amino acid taken directly from our cells. But this study overturns that view: the scientists show that M. tuberculosis actually prefers to import “inorganic” sulfate—a form of sulfur present in our bodies—through a specialized transporter named SubI-CysTWA.
To reach this conclusion, they used a highly precise imaging technology called NanoSIMS, which makes it possible to visualize chemical elements—including sulfur—directly within the cells infected by the bacterium. They observed that the bacterium stores large amounts of sulfur derived from sulfate, especially when it is in full activity.

The SubI transporter is required for sulfate import in intracellular bacteria.

The bacteria (M. tuberculosis) were cultured in the presence of glucose labeled with the isotope ¹³C to allow visualization within infected macrophages (left panels). The cells were incubated with sulfate labeled with ³³S in order to track the molecule inside infected cells (right panels). The cells were infected either with wild-type bacteria (top panels) or with a mutant lacking an active SubI transporter (bottom panels). The figure shows sulfate accumulation in the wild-type bacteria, but not in those that do not express the transporter.

A weak point to exploit for future treatments

The scientists then inactivated the gene responsible for producing this transporter. The result: the growth of the bacterium in laboratory cultures slowed down, and its survival decreased in the lungs of infected mice. It also became more sensitive to oxidative stress—a natural reaction of our defenses against pathogens.
This dependency is particularly interesting because the SubI-CysTWA transporter exists only in M. tuberculosis. Drugs targeting this mechanism could therefore weaken the bacterium without harming human cells. Such an approach could also boost the effectiveness of antibiotics already in use, such as isoniazid, and help shorten treatment duration.

A promising breakthrough

In a context where current treatments are lengthy and resistance is on the rise, this discovery opens a new avenue: blocking access to sulfate to prevent the bacterium from defending itself. In the long term, this could improve treatment efficacy, limit resistance, and ultimately save many lives.

(Source : Institute of Biology Paris-Seine)