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Dean Ornish

Dean Ornish

For decades, Dr. Dean Ornish has been talking to anyone who will listen about the power of lifestyle changes to avoid some of the chronic diseases that lead to the most drastic health-care costs and consequences: heart disease, diabetes, obesity, and cancer. In 2024, he extended his work to show that a vegan diet, daily aerobic exercise, a meditation and stress-reduction practice, and social engagement can together slow the progression of another increasing health concern as the population ages—Alzheimer's disease.
In his study, published in the journal Alzheimer's Research & Therapy, people who were diagnosed with mild cognitive impairment or early Alzheimer's disease and adopted Ornish's program for 20 weeks showed significant improvements in three of four standard measures of their cognitive function, compared to another group that maintained their current habits and recorded worsening scores. The results don't surprise Ornish. 'I have a unifying theory that many different chronic diseases share the same underlying biological mechanisms,' he says. 'That's why what is good for the heart is good for the brain—these same mechanisms affect different conditions, and lifestyle choices can make them better or worse.'

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Meera Syal: When Dad mistook me for Mum, I played along not to upset him
Meera Syal: When Dad mistook me for Mum, I played along not to upset him

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Meera Syal: When Dad mistook me for Mum, I played along not to upset him

The fact that there isn't even a word in the Punjabi language that means 'dementia' says a lot about the stigma and ignorance surrounding the disease in Indian communities. And yet ironically, incidences of Alzheimer's are much higher in minority ethnicgroups compared to white people. So as a group, we are actually more at risk – and yet we know less. In Asian communities, when signs of memory loss are apparent, it's often just dismissed as old age: 'They're forgetful,' people say. Or 'their minds are going.' But actually there's a huge difference between just age-appropriate forgetfulness and signs of this critical disease. My father, Surendra, really was the most wonderful dad – very loving, playful, sociable, and he adored music. Our house in Walsall, where I grew up, was always full of people singing. Originally a philosophy graduate, Dad worked as an accountant for years in order to provide for our family, my mum Surinder, me and my brother Rajeev, who is seven years younger than me. He was a very bright man who had endured great hardship as a refugee from the partition in 1947, when the British government withdrew from India. Dad's entire family had to abandon their home and flee across the border, so he started from literally nothing and became a self-made man. I'm sure all the stresses he'd suffered going through immigration – and then adaptation – made him more vulnerable to Alzheimer's eventually. It wasn't until 2012 when it became clear to me that Dad wasn't himself. By then I'd long been living in London, as a writer and actor and with two children of my own. Mum had known Dad was unwell for some time, but she had been coping on her own, silently soldiering on for a couple of years before we knew. It started with forgetting where he was driving, the familiar routes he'd taken for years seemed lost. Then in crept a level of paranoia, he became suspicious of even friends he'd known for years. Some days he'd momentarily forget my Mum. Worried, Mum had taken him to the memory clinic several times, but Dad just kept passing the tests, 'maybe because he was having a good day,' she admitted in hindsight. Later, we found out those tests aren't immensely accurate for diagnosing certain different forms of dementia, and actually the only way you can tell is by having a brain scan. In reality, trying to get a brain scan on the NHS is a long and torturous process. You really have to stand your ground and say 'I know something's wrong – and yes he may have passed the memory test – but I know that something is not right.' Ultimately, it was two or three years before Dad's diagnosis was confirmed. That was a long time for my mother to be struggling alone. It must have been isolating. And in that time he could have been taking medication that might have at least been able to help manage his symptoms. Early diagnosis is so crucial. By 2012, Mum could no longer hide it from us or anyone in the wider community. Intervention was needed. Initially we arranged for a carer to come to their home, but that didn't go well as Dad didn't trust them. He didn't want them in the house. And then he kept leaving the house, which meant we had to have security locks fitted to try and keep him safe. He was always restless, and this agitation was hard to live with. Then he became a security risk. One of the cruellest things about this disease is how it affects people's personalities. Becoming ruder or cruder is common with certain types of dementia. Everyone is different so it's impossible to predict. Some people can becalm and vacant, while others become very verbose and front-footed. While Dad was never aggressive, the paranoia was hard, and it was painful when he started insisting Mum had been replaced by a stranger. At that stage we realised we couldn't cope at home, not with Dad escaping, and Mum not being able to keep him safe. For me the worst part was this intermediate stage, when the disease came in and out, because there were times when Dad was completely lucid and cogent and wanted to know what was happening, when he knew something was wrong. This is when families really need support from places like the Alzheimer's Society, because how do you know how to have that conversation with a loved one who is confused and frightened? How do you say the right thing? They have trained, experienced people who can advise you on those difficult talks. What I learnt was that one of the biggest mistakes people make – quite understandably – is trying to correct someone when they are in their own version of reality. Saying to them things like 'No, that's not right' or 'you did that yesterday, remember?' actually distresses a loved one more, because they're coping with two or three different realities in their heads. Instead, it's better to enter into their world with them, even if that means playing along that you are their long-lost friend. Dad would often think I was my mother when she was younger, instead of his daughter. So I'd go along with that as it calmed and reassured him. That has to be the aim. Sometimes, five minutes later after he'd stopped being distressed, he'd find his own way back and know who I was. I came to believe that actually, there are many different kinds of reality in life. I mean, how do we know who's in the right one? Him or me? It becomes quite a Matrix kind of question! I had to open my mind a little bit to try and find the understanding and compassion – and go with whatever he was giving me. When a loved one has dementia it's a long, slow goodbye. You're losing them bit by bit. It's like a little light going off gradually, or a mechanism winding down. You become the parent, not the daughter. While that is certainly awful, there can be many moments of joy along the way, when the light is still on. For Dad, the thing that never left him until the very end, was his passion for music. He loved ghazals, Indian poetry and ballads, which we played and he would sing along. We also put old films from the 1950s and 60s from his youth on the iPad, essentially making our own memory pack for him. Photographs and anything that keeps the memories and the connections going is useful. Dad always had a great sense of humour, so we tried to make him laugh, and be upbeat. Mum visited my dad in the care home every single day and they had a routine, where they'd practise throwing and catching a ball (to keep up his motor skills) and then look at old photos together. You find your own ways of connecting, but the Alzheimer's Society is an amazing resource of information and advice, and through the Dementia Friends network, we found incredible volunteers who would even offer to give relatives a break by sitting and talking to your loved one. Dad was in the care home for six years, so it became the new normal in some ways. You learn to live with the upset, but I hated that in their golden years, when they should have been growing old together, they were separated, with Dad remaining in the home until he died in 2018. When I remember my Papa, I don't try to forget his illness; you can't, it's part of the journey we all had together. I just hope we did everything we could to make his quality of life as good as we could in those last years. You reach a stage where it's actually worse for the family than it is for the person with the disease, because they're in their own world. I took advice about genetic testing, but looking at the rest of my family history, it's highly unlikely to be genetic. There's no history of dementia on my father's side, his older brother is still alive and well, his own father died in his mid-nineties unaffected by dementia. My mother's own mum died at the grand age of 103 (in India!) and she has sisters who are still alive with all their faculties. Losing my parents has made me more health conscious. I'm alert to the increased risks in South Asians of hypertension, obesity, diabetes, and cardiovascular health. And actually there's now more awareness of the massive link between gum disease and Alzheimer's. My father suffered with terrible gums for many, many years. The older I get I take better care of myself, watching my cholesterol levels and cardiovascular health and I regularly exercise and look after my gums with hygienist appointments three times a year. I can't change my genetic hand down, but I can try my best with my lifestyle to try and prevent my kids going through this with me one day. As told to Susanna Galton Meera Syal CBE is an Ambassador for Alzheimer's Society and is supporting the charity's appeal. Donate at Broaden your horizons with award-winning British journalism. Try The Telegraph free for 1 month with unlimited access to our award-winning website, exclusive app, money-saving offers and more.

Kelun-Biotech Announces Breakthrough Therapy Designation Granted for Sacituzumab Tirumotecan (Sac-TMT) in Combination With Tagitanlimab in China for Certain Types of Non-Small Cell Lung Cancer
Kelun-Biotech Announces Breakthrough Therapy Designation Granted for Sacituzumab Tirumotecan (Sac-TMT) in Combination With Tagitanlimab in China for Certain Types of Non-Small Cell Lung Cancer

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Kelun-Biotech Announces Breakthrough Therapy Designation Granted for Sacituzumab Tirumotecan (Sac-TMT) in Combination With Tagitanlimab in China for Certain Types of Non-Small Cell Lung Cancer

CHENGDU, China, June 10, 2025 /PRNewswire/ -- Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd. (the "Company") today announced that its TROP2-directed antibody-drug conjugate (ADC) sacituzumab tirumotecan (sac-TMT) (佳泰莱®) in combination with the PD-L1 monoclonal antibody tagitanlimab (科泰莱®) was granted Breakthrough Therapy Designation by the Center for Drug Evaluation (CDE) of the National Medical Products Administration (NMPA) of China for the first-line treatment of locally advanced or metastatic non-squamous non-small cell lung cancer (NSCLC) without actionable genomic alterations. Breakthrough Therapy Designation is granted for treatment options that demonstrate significant clinical advantages over currently available treatments and is aimed at expediting the research, development and marketing of innovative treatment options that address clinically urgent medical needs. This designation is based on the efficacy and safety data from the non-squamous cohort of the Phase II OptiTROP-Lung01 study. This marks the fifth Breakthrough Therapy Designation granted to sac-TMT by the NMPA. Sac-TMT has previously received this designation for: Locally advanced or metastatic triple-negative breast cancer (TNBC) in July 2022; EGFR-mutant, locally advanced or metastatic NSCLC after progression on EGFR-TKI therapy in January 2023; Locally advanced or metastatic hormone-receptor positive (HR+) and human epidermal growth factor receptor 2-negative (HER2-) breast cancer (BC) in patients who have previously received at least two lines of systemic chemotherapy in June 2023; First-line treatment of unresectable locally advanced, recurrent or metastatic PD-L1 negative TNBC in March 2024. Results from a Phase 2 OptiTROP-Lung01 study of sac-TMT in combination with tagitanlimab in first-line advanced or metastatic non-squamous NSCLC patients were presented in a poster session at the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting[1]. Dr. Michael Ge, CEO of Kelun-Biotech said, "This designation by the NMPA highlights the importance of developing novel therapeutic options for diverse NSCLC subtypes. Sac-TMT in combination with tagitanlimab demonstrated clinically meaningful outcomes in key endpoints for patients with non-squamous NSCLC without actionable genomic alterations as a first-line treatment. We are excited about the therapeutic potential of TROP2 ADC- immunotherapy combinations, and we look forward to working with regulatory authorities in China to bring this combination therapy to patients in need as soon as possible." [1] Abstract #8529: Lung Cancer – Non-Small Cell Metastatic, ASCO Annual Meeting, 2025 About sac-TMT (佳泰莱®)Sac-TMT, a core product of the Company, is a novel human TROP2 ADC in which the Company has proprietary intellectual property rights, targeting advanced solid tumors such as NSCLC, BC, gastric cancer (GC), gynecological tumors, among others. Sac-TMT is developed with a novel linker to conjugate the payload, a belotecan-derivative topoisomerase I inhibitor with a drug-to-antibody-ratio (DAR) of 7.4. Sac-TMT specifically recognizes TROP2 on the surface of tumor cells by recombinant anti-TROP2 humanized monoclonal antibodies, which is then endocytosed by tumor cells and releases KL610023 intracellularly. KL610023, as a topoisomerase I inhibitor, induces DNA damage to tumor cells, which in turn leads to cell-cycle arrest and apoptosis. In addition, it also releases KL610023 in the tumor microenvironment. Given that KL610023 is membrane permeable, it can enable a bystander effect, or in other words kill adjacent tumor cells. In May 2022, the Company licensed the exclusive rights to MSD (the tradename of Merck & Co., Inc., Rahway, NJ, USA) to develop, use, manufacture and commercialize sac-TMT in all territories outside of Greater China (includes Mainland China, Hong Kong, Macao, and Taiwan). To date, two indications for sac-TMT have been approved and marketed in China for the treatment of adult patients with unresectable locally advanced or metastatic TNBC who have received at least two prior systemic therapies (at least one of them for advanced or metastatic setting) and EGFR mutation-positive locally advanced or metastatic non-squamous NSCLC following progression on EGFR-TKI therapy and platinum-based chemotherapy. Sac-TMT became the first domestic ADC with global intellectual property rights to be fully approved for marketing. It is also the world's first TROP2 ADC to be approved for marketing in a lung cancer indication. In addition, two new indication applications for sac-TMT for the treatment of adult patients with EGFR-mutant locally advanced or metastatic NSCLC who progressed after treatment with EGFR-TKI therapy and with unresectable locally advanced, metastatic HR+/HER2- BC who have received prior endocrine therapy and other systemic treatments in the advanced or metastatic setting were accepted by the CDE, and were included in the priority review and approval process. As of today, the Company has initiated 8 registrational clinical studies in China. MSD has initiated 14 ongoing Phase 3 global clinical studies of sac-TMT as a monotherapy or with pembrolizumab2 or other agents for several types of cancer. These studies are sponsored and led by MSD. About Tagitanlimab (科泰莱®)Tagitanlimab is the first PD-L1 mAb globally to receive authorization for the first-line treatment of NPC. Previously, the NMPA has approved the marketing in China of tagitanlimab used in combination with cisplatin and gemcitabine for the first-line treatment of patients with R/M NPC and monotherapy for the treatment of patients with recurrent or metastatic NPC who have failed after prior 2L+ chemotherapy, respectively. About Kelun-BiotechKelun-Biotech ( is a holding subsidiary of Kelun Pharmaceutical ( which focuses on the R&D, manufacturing, commercialization and global collaboration of innovative biological drugs and small molecule drugs. The company focuses on major disease areas such as solid tumors, autoimmune, inflammatory, and metabolic diseases, and in establishing a globalized drug development and industrialization platform to address the unmet medical needs in China and the rest of world. The Company is committed to becoming a leading global enterprise in the field of innovative drugs. At present, the Company has more than 30 ongoing key innovative drug projects, of which 3 projects have been approved for marketing, 1 project is in the NDA stage, and more than 10 projects are in the clinical stage. The company has established one of the world's leading proprietary ADC platforms, OptiDC™, and has 1 ADC project approved for marketing, 1 ADC project in NDA stage, and multiple ADC and novel DC assets in clinical or preclinical research stage. For more information, please visit Media: klbio_pr@ View original content to download multimedia: SOURCE Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd.

NIH Director Struggles To Defend His Own Plan To Slash $18 Billion In Medical Research
NIH Director Struggles To Defend His Own Plan To Slash $18 Billion In Medical Research

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NIH Director Struggles To Defend His Own Plan To Slash $18 Billion In Medical Research

WASHINGTON ― National Institutes of Health director Jayanta Bhattacharya got a cool reception from Democratic and Republican senators on Tuesday as he defended his agency's budget request for 2026, which would slash billions in cutting-edge biomedical research on cancer, Alzheimer's disease, diabetes and other health conditions. NIH is considered the crown jewel of American science and the global leader in biomedical research and innovation. Senators in both parties are proud of its success and of their own roles in boosting its funding over the years in support of medical breakthroughs. So Bhattacharya had to know his budget request would land with a thud as he presented it to a Senate appropriations subcommittee. He kept trying to square two things that didn't make sense: that Trump is committed to preserving America's role as the leader in biomedical research, and that his proposed $18 billion in cuts to the agency next year ― or 40% of its entire budget ― won't hamper that. Senators didn't buy it. At times, Bhattacharya didn't seem to want to defend it, either. Sen. Susan Collins (R-Maine), who chairs the full Senate Appropriations Committee, called the administration's proposed cuts to NIH 'so disturbing.' 'It would undo years of congressional investment in NIH, and it would delay or stop effective treatments and cures from being developed for diseases,' Collins said. 'We also risk falling behind China and other countries that are increasing their investment in biomedical research.' In particular, she asked why the administration is calling for the cutting of funding by 40% for the National Institutes of Aging, which funds most Alzheimer's research, when it's been successfully developing breakthrough drugs and blood tests. Bhattacharya, without defending his own proposed cuts, said 'the intention' of the Trump administration is to lead the world in biomedical research, suggesting Congress could make a counteroffer and potentially propose more spending. 'The budget is a collaborative effort between the Congress and the administration,' he said. Collins simply replied, 'We look forward to working with you to remedy these problems and the deficiencies in the budget.' Sen. Patty Murray (D-Wash.), the top Democrat on the appropriations panel, ripped the administration's 'catastrophic' cuts to NIH to date. She said Trump has so far forced out nearly 5,000 employees, prevented nearly $3 billion in grants from being awarded, and terminated nearly 2,500 grants totaling almost $5 billion for life-saving research. 'The Trump administration is already systematically dismantling the American biomedical research enterprise that is the envy of the world, throwing away billions in economic activity in every one of our states,' Murray fumed. 'This budget proposal would effectively forfeit our leadership in research innovation and competitiveness to China.' She tangled with Bhattacharya over one of dozens of clinical trials that have been halted due to frozen NIH funds: a 23-year research effort to develop an HIV vaccine. Scientists there are on 'the cusp of a functional cure for HIV,' she said, and now 6,000 people in that trial have been cut off from treatment. Bhattacharya jumped in to say he is 'absolutely committed' to supporting research on HIV. 'But you did terminate the HIV research at Fred Hutch that, again, was on the cusp of a treatment for 6,000 patients nationwide,' Murray replied, referring to the Fred Hutchinson Cancer Research Center in Seattle. 'You did do that,' she said, as they talked over each other. 'I'd have to get back to you on that,' said Bhattacharya. 'You did do that,' she repeated. After more back and forth, the NIH director said again, 'The budget request is a work of negotiation between Congress and the administration.' Minutes later, he said it yet again, as Murray pressed for details on how many fewer clinical trials there would be next year because of the Trump administration's proposed cuts. 'I'll say this,' Bhattacharya declared. 'The budget itself is a negotiation between Congress and the administration.' He said it several other times, too. In fact, it became clear this was the NIH director's go-to line for defending his own devastating budget request. It simultaneously allowed him to stand by his bosses ― Trump, and Health and Human Services Secretary Robert F. Kennedy Jr. ― while not exactly arguing in support of its specific cuts. 'President Trump has committed that the U.S. be the leading nation in biomedicine in the 21st century,' he said at one point. 'I entirely support that goal.' 'Well, I do too, but it's hard to understand how we're going to get there when the budget slashes funding,' replied Sen. Jeanne Shaheen (D-N.H.). 'Particularly in critical areas of research where our most critical competitor, the Chinese, are increasing funding in those areas and we're slashing the budgets.' Bhattacharya didn't respond. It's possible he may not have agreed with some of his own budget's cuts. Bhattacharya certainly had a hand in crafting his agency's budget, but so did other officials at the White House and the Department of Health and Human Services. Before becoming NIH director in April, Bhattacharya was a professor of medicine, economics and health research policy at Stanford University. He knows how vital and highly esteemed NIH is, worldwide. Why not put it on Congress to save it? 'You say this is a collaborative effort, and you're absolutely right, and I encourage Congress to exert its authorities,' said Sen. Jerry Moran (R-Kansas). 'If Congress were to provide additional dollars above and beyond the president's budget request, how would we as a committee and how would you as NIH recommend for us to prioritize that spending?' Bhattacharya said he's focused on the 'real health needs' of Americans, like diabetes and cancer, and on the 'need to think big' for advancing science. 'Again, the budget, it's a collaborative effort,' he said. 'But I think it's going to be important that we address the real problems in science and the real needs of the American people with whatever budget comes out. That's my job.' Moran redirected Bhattacharya back to the need for more funding at NIH. 'I assume that means we need more resources,' said the Republican senator. 'And that you would put them to good use. Is that accurate?' 'That's my job,' replied the NIH director.

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