Mind & body, in brief

Multiple sclerosis, or MS, is an illness in which the immune system attacks myelin. Myelin is the fatty coating around nerves in the brain and spinal cord, and without it signals travel badly. [1][2]

MS affects more than 2.8 million people worldwide. It is the leading cause of neurological disability in adults aged 18 to 40. [3]

The Epstein-Barr virus causes glandular fever, also called mono. More than 95% of people catch it, and it then hides for life inside B cells, the immune cells that make antibodies. [4][1]

A 2022 study followed 10 million people in the US military for 20 years. Among the 955 who developed MS, the risk had risen 32-fold after they caught the virus. [5]

Nearly all people with MS, 99.9%, carry signs of a past infection, and the risk in people who never caught it is close to zero. [6] Still, only about one infected person in 1,000 gets MS, usually 5 to 10 years after infection. [7]

The first way the virus may do it is look-alike parts. A 47-piece stretch of a virus protein called EBNA1 matches parts of three proteins in the brain, so antibodies made against the virus can hit them too. [4]

Two papers in the journal Cell in 2026 found more of this. B cells infected with the virus display pieces of myelin on their surface, which switches on T cells that then enter the brain and cause inflammation there. [7]

The same papers found immune T cells that react to both the virus and a brain protein called anoctamin-2. These double-reacting cells were more common in people with MS. [7]

The virus can also keep harmful cells alive. In lab animals, a virus protein called LMP1 let B cells that react against myelin escape the death that normally removes them, and they went on to strip myelin. [7]

A team led from Stanford University found the virus directly infects B cells that target the brain and turns them into cells that rouse other immune cells. That work is a preprint, not yet checked by other scientists. [8]

A Harvard-led study in July 2026 looked at helper T cells in 30 people with MS. Most targeted virus proteins made while the virus is actively copying itself, and there were twice as many as in 30 people without MS. [9][1]

Drugs that remove B cells cut that T-cell response almost to healthy levels in 60 people. They also cleared the virus from saliva in most, which suggests these drugs work partly by emptying the virus's hiding place. [6][1]

Signs of the virus waking up in B cells appeared up to three months before an MS relapse, in a 2026 study that followed patients' blood over time. [10] People at their very first MS symptoms carried more double-stranded RNA, a mark of viruses copying, than healthy people. [11]

Most MS drugs weaken the immune system, and some are linked to the virus waking up again. A review asks whether that could make MS worse, while drugs that remove B cells may shrink the virus's hiding place. [3]

An Australian trial called STOP-MS is now testing famciclovir, an antiviral, and spironolactone, a heart and blood-pressure drug that also blocks the virus copying itself, in people with progressive MS. Its first patient joined in April 2025. [12]

Vaccines against the virus are in development. One Harvard researcher points out that about 1,000 people would need vaccinating to prevent one case of MS. [1]

Why it matters. The next test is STOP-MS. Its first stage asks whether two existing drugs lower the virus in 150 people, and only a drop of at least 10% moves it on to testing disability. [12]

Lupus is an illness in which the immune system attacks the body's own organs, often the kidneys. CAR T-cell therapy changes a patient's immune cells in a lab to hunt down B cells. In the CARLYSLE trial at University College London Hospitals, five of the first six people on the lower dose reached remission. [13] B cells that grew back months later were mostly young cells, not the kind linked to lupus. [13] At Cleveland Clinic, a woman treated in May 2025 has been in remission with no drugs for more than a year. [25]

Why it matters. Lupus has usually meant lifelong drugs that weaken the immune system. A one-off treatment that ends them would change that, but only if the remissions last longer than the year or two seen so far.

Making CAR T cells from each patient's own blood is costly, and the illness can worsen while the cells are made. [26] A team in China instead used cells from a healthy donor, altered to target B cells, in three people with severe lupus affecting several organs. [26] None developed graft-versus-host disease, where donor cells attack the patient, or the dangerous inflammation CAR T cells can cause. [26] The cells removed B cells, antibodies against the body fell, and all three reached remission on a standard lupus score. [26]

Why it matters. Ready-made donor cells could make the treatment quicker and cheaper to give. Three patients is a very small start, and the same approach has to be tested in many more.

Before CAR T-cell therapy, patients usually stop their other lupus drugs so the altered cells can work. A 22-year-old woman in the US with lupus kidney disease had a severe flare during that gap: fever, rash and painful joints. [27] Doctors gave a short burst of high-dose steroids, which calmed it without stopping the new cells growing. [27] Twelve months after the infusion she was in remission with no drugs and back at full-time work. [27]

Why it matters. The pause before treatment is a risky gap for people whose lupus is already severe. This case shows one way through it, in one person.

Researchers at the University of North Carolina argue that CAR T-cell therapy for lupus is being kept as a last resort. [16] When it is given late, the kidneys may already be scarred, and that damage can remain even if the treatment works. [16] So a patient who does not improve may be showing old damage rather than a treatment that failed. [16] They propose trials in early severe lupus instead; the paper was accepted on 10 September 2026. [16]

Why it matters. Where a treatment sits in the queue changes what its results seem to show. Moving it earlier would also expose patients who might have done well on safer drugs to its risks.

A review counted 56 trials of CAR T-cell therapy in autoimmune rheumatic diseases, conditions like lupus where the immune system attacks joints and organs. [28] Of these, 64% were phase 1, the first safety step, and only 7% had reached phase 2. [28] China ran 48% of the trials and the US 34%, and only two were joint projects between the two countries. [28] A group of doctors, companies, regulators and patients has called for long-term tracking of everyone treated. [29]

Why it matters. Most of what is known comes from small, early studies in a few countries. How long remissions last will only show up if patients are followed for years.

Researchers used genome data from two huge health studies, the UK Biobank with 490,560 people and the US All of Us programme with 245,394. [30] They measured Epstein-Barr virus DNA left in blood samples, and found it in 11.9% of the All of Us group. [30] Carrying it was linked to rheumatoid arthritis, lung disease and lupus, but a link with MS did not hold up after statistical checks. [30] Genes that control how cells show virus pieces to the immune system shaped how much virus stayed. [30]

Why it matters. It shows a person's genes help decide how well they keep the virus quiet. It also shows the link to MS does not appear in every kind of measurement.

A review looked at why autoimmune illnesses flare suddenly. Flares often come with surges of plasmablasts, short-lived cells that pour out antibodies. [31] Three kinds of trigger keep appearing: sleeping herpes viruses waking up, including Epstein-Barr and the chickenpox virus; chest or gut infections, including COVID; and imbalanced gut bacteria. [31] These all act through the same alarm sensors on immune cells. [31]

Why it matters. It links flares in lupus, arthritis and MS to ordinary infections. It is a review of existing evidence, so it points to a pattern rather than proving a cause.

A review proposes a common thread between two known MS risks: the Epstein-Barr virus and low vitamin D. [32] Both raise hepcidin, a hormone that blocks the body taking in iron. [32] Older studies suggested iron builds up in the brain in MS, but newer work suggests it is actually low in deep brain areas. [32] That could starve the cells that make myelin, which need iron for energy. [32]

Why it matters. If it holds, iron levels could matter in MS care. For now it is an idea built from other studies, and no trial has tested it.

Inflammatory bowel disease covers Crohn's disease and ulcerative colitis, long-term inflammation of the gut. Johnson & Johnson, the US drug company, tested two of its drugs together in two mid-stage trials. [33] The combination did better than either drug alone but missed its main target of remission, in results presented on 5 May 2026. [33] A 2022 trial had nearly doubled remission rates, and the company is still moving into late-stage testing in one group of patients. [33]

Why it matters. Combining drugs was one of the field's big hopes for people whom single drugs fail. This result makes that hope smaller for now.

Crohn's disease is inflammation that can appear anywhere in the gut. A review of 14 trials with 3,139 patients compared people whose disease sat only in the large bowel with those whose disease sat at the end of the small intestine. [34] Drugs beat placebo far more strongly in large-bowel disease. [34] One class of pills, JAK inhibitors, worked only in the large bowel and showed no benefit at the end of the small intestine. [34]

Why it matters. Where the disease sits may matter as much as which drug is picked. It also means trial results that mix both groups can hide a drug that fails in one of them.

A network analysis, which compares treatments across many trials at once, pooled 79 trials with 20,724 people with Crohn's disease. [35] The strongest result came from adalimumab, an injected antibody, combined with a thiopurine, an older immune-calming pill. [35] For every three people treated with that pair, one more reached remission than on placebo. [35] Guselkumab and adalimumab alone needed about four people treated for one extra remission. [35]

Why it matters. Doctors choosing a first drug have few direct comparisons. A ranking like this helps, though the trials lasted only 2 to 30 weeks. [35]

Upadacitinib is the first pill of its kind approved for Crohn's disease, cleared by England's health technology body NICE in 2023. [19] Nineteen UK hospitals reported on 312 patients, 64% of whom had already failed three or more injected drugs. [19] Half reached remission by 12 weeks and 45% by 24 weeks. [19] Serious side effects affected 18%. [19]

Why it matters. These were some of the hardest cases in UK care, not trial volunteers. Half reaching remission in that group is the kind of result a trial cannot show.

Risankizumab is an injected drug that blocks one immune signal in Crohn's disease. In 60 patients in the United Arab Emirates, 69.6% of those who had never had such drugs reached remission after the first doses, against 32.4% of those who had. [17] In 49 patients in Taiwan, 42.9% reached remission by week 12. [36] There the gap between earlier and later users was not statistically clear. [36]

Why it matters. Both groups are outside the trials that won the drug its approval. The UAE result shows the same drug doing about half as well when it comes later.

Mirikizumab blocks an immune signal called interleukin-23. In the VIVID-2 study, 430 people with Crohn's disease kept taking it for a second year after a one-year trial. [37] At two years, 73.4% were in remission on a standard symptom score. [37] Most people who had responded at one year still had at two. [37] In the second year, 7.7% had a serious side effect. [37]

Why it matters. Crohn's disease lasts for decades, and trials usually stop at one year. Two-year results like these are part of what patients and doctors need to judge a drug.

Ulcerative colitis is long-term inflammation of the large bowel. Two hospitals followed 74 adults who started mirikizumab outside a trial, and 93% had already tried other advanced drugs. [21] Overall, 70.3% had responded and 17.6% were in remission. [21] Results were about the same whether or not people had tried other drugs first. [21]

Why it matters. It is a counter-example to the pattern in the Crohn's studies. Coming later does not always mean doing worse.

Few trials test two gut-disease drugs directly against each other. French researchers compared three head-to-head trials with what earlier placebo trials had predicted. [38] Placebo trials suggested vedolizumab would beat adalimumab by 17.3 points in colitis, but the direct trial found 8.8. [38] In Crohn's, placebo trials suggested adalimumab would beat ustekinumab, and the direct trial found the two drugs about equal at 52 weeks. [38]

Why it matters. Doctors often choose between drugs using indirect comparisons. This study shows those comparisons can be wrong in both size and direction.

Thyroid-stimulating hormone, or TSH, is the brain's signal telling the thyroid to work harder, and a high reading is used to label the thyroid underactive. In 1,626 people aged 65 to 84 in Japan's Bunkyo Health Study, TSH rose with age. [39] Mildly raised readings were not linked to any of the health problems of old age that were checked. [39] In the TRUST trial of 737 people over 65 with mildly raised readings, a year of thyroid tablets did not improve tiredness or symptoms. [40]

Why it matters. Many older people may be labelled with an underactive thyroid for a normal change of ageing. Treating them adds a daily tablet without clear benefit.

Levothyroxine is the tablet that replaces thyroid hormone. Researchers in England used one city's records to compare 47,869 people taking it with 393,101 people not taking it, over 14 years of blood tests. [41] Even at the lowest doses, treated people had higher thyroid hormone levels than untreated people, and many had TSH readings pushed very low. [41] Too much replacement hormone in older people is linked to irregular heartbeat and bone loss. [40]

Why it matters. A tablet dose judged on one number may leave many people over-replaced. That matters most for older people, whose bones and hearts carry the risk.

Researchers in Colombia reviewed the records of 398 people prescribed levothyroxine and followed each for at least a year. [20] At the first blood check, 52% were not at their target level. [20] Only 36.4% had a second check, and fewer than half were still taking their tablets after a year. [20]

Why it matters. A tablet only helps if it is taken and checked. In 31.7% of cases, doctors did not change a dose that had missed its target. [20]

Tourette syndrome causes tics, sudden movements or sounds, usually starting between ages 3 and 8. [42] Ecopipam blocks one type of receptor for dopamine, a brain chemical. In a trial at 77 sites in 12 countries, 216 people took it, and those who improved were then switched at random to ecopipam or a dummy pill. [42] Children who stayed on ecopipam had about half the risk of their tics coming back. [42] Sleepiness affected 11%, and weight was not affected. [42]

Why it matters. Current Tourette drugs are often stopped because of side effects. [42] The adult group was too small to show a clear result.

Behavioural therapy teaches people with tics to notice the urge that comes before one and respond differently. A UK review pooled two trials with 445 participants, comparing online therapy with online education alone. [43] Tic scores were lower with therapy at 3 and at 12 months. [43] A wrist device called Neupulse was tested for only four weeks. [43]

Why it matters. The review could not settle whether the online therapy is good value for England's health service, because long-term data are thin. The chance it was good value ranged from 52% to 89%. [43]

Deep brain stimulation places wires in the brain that send steady electrical pulses, and it is used only in severe Tourette syndrome. [18] Doctors at 12 centres pooled 115 patients stimulated in three different brain areas. [18] The best results lined up along three bundles of nerve fibres linking two deep brain regions. [18] That pattern explained about a fifth of the difference between patients. [18]

Why it matters. Surgeons could aim more precisely. Most of the difference between patients is still unexplained, and patients were followed for a median of six months.

Cannabis-based medicine is recommended for adults with Tourette syndrome when other treatments fail, but evidence in children is very limited. [44] Doctors described two boys who started it at ages 8 and 12 and were followed for five and six years. [44] Both had lasting improvement in tics, without severe side effects or harm to school performance. [44]

Why it matters. It is two cases, so it cannot show the medicine works or is safe for other children. The authors suggest it be considered before brain surgery in severe cases.

Vitiligo causes white patches where skin loses its colour, and it affects about 0.36% of people worldwide. [14] The colour-making cells are destroyed by immune T cells that settle in the skin and stay there. [14] Ruxolitinib cream blocks a signalling route those immune cells use. [45] It was the first cream approved for vitiligo, for people over 12 with patches on the face. [45]

Why it matters. The attack also harms the stem cells that could replace lost colour cells. [14] Treatment aims to stop the patches spreading, bring colour back, and then keep it. [14]

Cosmo Pharmaceuticals, a Dublin-based drug company, tested a cream called clascoterone in men with common male-pattern hair loss. [46] After six months, men on the cream had 168% more hair than the placebo group in one trial and 539% more in the other. [46] Experts were underwhelmed by the data, and the company planned to seek approval in the US and Europe after gathering a full year of safety results. [46]

Why it matters. Large percentages can describe small gains when the starting number is low. The full data will show how much hair people actually regrow.

In pattern baldness, a hormone called DHT, made from testosterone, shrinks hair follicles until they grow only fine, short hairs. [47] By age 70 it affects about 80% of white men and nearly half of white women, and about half of men in Korea. [47] Minoxidil and finasteride are the most used treatments, and both have to be used long-term. [47]

Why it matters. Because the shrinking carries on, the two main treatments depend on long-term use. Their side effects and inconvenience have pushed interest in other options. [47]

A review of newer treatments found platelet-rich plasma, made from a person's own blood and injected into the scalp, is the most studied. [48] Its studies are short and describe what was injected inconsistently. [48] In a separate randomised trial, 33 women with female-pattern hair loss had stem cells from their own fat injected into the scalp, and hair count and thickness improved at 12 and 24 weeks. [49]

Why it matters. The review calls for standard methods and clearer reporting before firm claims are made. [48] The stem-cell trial had 33 women and six months of results.

Saw palmetto is a plant extract sold for thinning hair. A six-month trial gave 40 adults an extract and 20 a dummy pill. [50] Hair counts rose by an average of 18.6 hairs in the extract group and fell by 10.1 in the placebo group. [50] The study was written by one doctor who runs a private skin clinic in California, and she declared no conflicts. [50]

Why it matters. The result is reported as a 283% greater improvement, which sounds bigger than a difference of about 29 hairs in the patch counted. The trial was small and short. [50]

The International Society of Hair Restoration Surgery found 95% of its members' patients were aged 20 to 35 when they sought surgery. [51] A UK hair surgeon told the BBC that social media and dating apps have made men more aware of their looks. [51] More UK men now travel abroad, to countries like Turkey, where the surgeon says transplants cost a fraction of UK prices. [51]

Why it matters. Pattern baldness keeps going after a transplant, so a young man may need more surgery later. One consultant told the BBC reporter his hair could recede further after the procedure. [51]

NutriNet-Sante is a French study that has followed 108,723 adults since 2009 through repeated food diaries. [52] Of 17 widely eaten preservatives, 12 were linked to a higher chance of developing type 2 diabetes, including potassium sorbate, sodium nitrite and citric acid. [52] In total 1,131 people developed diabetes. [52] The authors call for the safety of these additives to be looked at again. [52]

Why it matters. Each of the 17 preservatives studied was eaten by at least a tenth of the group. [52] This kind of study shows a link, not that the additives cause diabetes.