Latest news with #KetoDiet
Daily Mail
9 hours ago
- Entertainment
- Daily Mail
The weirdest (and unhealthy) lengths celebs go to in order to get their red carpet looks from questionable cookie diets to uncomfortable colonics
They say it takes a village to get celebrities red carpet ready. Some superstars have succumbed to a series of increasingly unorthodox and occasionally unhealthy methods in a bid to get their red carpet looks proving it's not always fun and games being a celebrity. From colonic irrigation to questionable cookie diets, extreme carb-cutting, obsessive calorie counting and rigorous juice cleansing, there's not much your average celebrity hasn't tried in their quest for what they deem to be the perfect body. But many of the strict dieting techniques come with some little-known side effects, and some A-list stars have opened up about their own shocking stories trying out these unconventional methods. 1. KOURTNEY KARDASHIAN - THE KETO DIET WHAT IS THE KETO DIET? The Ketogenic diet defines a low-carb, high-fat way of eating. Following this eating plan forces the body into a metabolic state, known as ketosis, which starves the body of carbohydrates but not calories. Carbs are shunned in the keto diet as they cause the body to produce glucose, which is used as energy over fat. Keto diets therefore lead to weight loss as they make the body burn fat as its primary energy source. On the diet, followers can eat: Meat Leafy greens and most vegetables Full-fat dairy Nuts and seeds Avocadoes and berries Fats, such as coconut oil People cannot eat: Grains, including rice and wheat Sugar, like honey and maple syrup Most fruit White or sweet potatoes Image-conscious Kourtney Kardashian made two attempts at losing weight on the keto diet, but in 2020 confirmed she had given it up for good. She now focuses on well-balanced meals and engaging in regular exercise to achieve a healthy, well-toned body. According to Medical News Today, the keto diet refers to a ketogenic diet, which is a high-fat, adequate-protein, low-carb diet. The main goal of the food plan is to get more calories from protein and fat than from carbs. It works by depleting your body of its store of sugar, so it will start to break down protein and fat for energy, causing ketosis. Ketosis is a metabolic process that involves fat providing most of the fuel for the body, rather than energy coming from foods eaten. Speaking to Health magazine in 2020, Kourtney revealed she had quit the keto diet but confirmed her household remains gluten and dairy-free. She said: 'I noticed that my body changed for the better when I quit the Keto.' 2. ASHTON KUTCHER - THE FRUITARIAN DIET In 2013 Ashton was hospitalized after trying a fruitarian diet in preparation for his role as Steve Jobs in the biopic Jobs. The actor said at the time that he was rushed to hospital before shooting his new movie Jobs about the late entrepreneur after embarking on a fruit-only diet for the biopic, favoured by the Apple co-founder who died of pancreatic cancer in 2011. He told USA Today newspaper at the premiere of the movie at the Sundance Film Festival: 'First of all, the fruitarian diet can lead to like severe issues. 'I went to the hospital like two days before we started shooting the movie. I was doubled over in pain. 'My pancreas levels were like completely out of whack. It was really terrifying... considering everything.' He studied hundreds of hours of footage of Steve for the role and claimed he discovered they had a lot in common. A fruitarian diet is a vegan diet primarily focused on consuming raw fruits, with some variations including nuts, seeds, and some vegetables. It's considered a restrictive eating pattern and may pose nutritional risks if not carefully planned. 5. KATY PERRY - THE M PLAN American singer Katy Perry was thought to have tried a mushroom based diet in a bid to lose weight as far back as 2012. Dubbed the 'M-Plan', the diet was devised to help women lose weight from their tums, bums, thighs and upper arms, but still keep their bust intact. It promised to help women lose weight from the stubborn areas over a 14-day period by replacing just one regular lunchtime snack or dinner with a mushroom inspired dish. Other celebrities to have been linked with the fad include Emmerdale and Waterloo Road star, Roxanne Pallett and Kelly Osbourne, who both previously claimed to have lost dress sizes from eating raw mushrooms regularly. Speaking in 2013, Katy admitted she had cut all junk food out of her diet while shaping up for a forthcoming tour. She told Rolling Stone: 'After this interview I'm going to have a nice healthy breakfast. I'm on a meal plan, which absolutely sucks...' 3. JENNIFER LOPEZ & GWYNETH PALTROW - COLON HYDROTHERAPY It's a treatment that can be traced back to ancient times and has celebrity fans including Jennifer Lopez and Gwyneth Paltrow. But the term colonic irrigation - not the mention what the procedure actually involves - is far from glamorous. In an attempt to make it sound more appealing, the treatment has since been rebranded as 'colonic hydrotherapy'. The practice, which involves flushing the colon with about 60 litres of water via a tube inserted into the rectum, is said to promote health and well-being by ridding the body of toxins. The idea is that for around £90 a time, people can have their digestive tract cleansed and purified leaving them feeling fresh and not bloated with a flatter stomach and renewed energy. Advocating the procedure on her Goop lifestyle website, Gwyneth wrote: 'For the uninitiated, a colonic is essentially a way to hydrate and irrigate your colon – a section of your intestines that's approximately five feet long – by filling it with warm water and then flushing it out repeatedly.' Other celebrity fans reportedly include supermodel Cindy Crawford, TV personality Paris Hilton and R&B singer Beyoncé. But despite its popularity, re-branding, and claims at being good for you, there have been no studies that prove a scientific benefit. 4. GWYNETH PALTROW (AGAIN) - THE GOOP CLEAN PROGRAM The three-week long $475 cleanse was designed by cardiologist and detoxification expert Dr. Alejandro Junger. The program, tried and tested by Paltrow, 'involves an easy-to-follow formula' of daily shakes, supplements, and whole food recipes, and it calls for participants to eliminate soy, dairy, gluten, plant-based protein, refined sugars, grains, several different fruits, and alcohol. The program includes two vegan meal-replacement shakes per day, one 'solid, clean' meal for lunch, and a daily regimen of 24 supplements. According to Gwyneth, the cleanse made her feel 'pure and happy and much lighter', with the Goop founder gushing that the program is 'amazing'. Posting on her Goop lifestyle blog in 2020, she wrote: 'I've used Clean in the past with great results, losing a few pounds and kickstarting a healthier and more energetic New Year.' It's not for everyone, and with good reason, but the prospect of eating 14 jars of baby food a day apparently appealed to the likes of Jennifer Aniston It's not for everyone, and with good reason, but the prospect of eating 14 jars of baby food a day apparently appealed to the likes of Jennifer Aniston and Reese Witherspoon. As the name suggests, the Baby Food Diet involves substituting adult foods for soft, spoon fed jars of baby food. Each one contains roughly 80 calories, meaning 14 consumed each day will provide users with a daily intake of around 1,000 calories. The diet be offset with one adult low-calorie meal per day, but the minimal calorie intake calls into question its long-term benefits. Regardless, sales in dry baby food were given a significant 59% boost, while wet baby food sales went up by 20% following claims that Reese Witherspoon had tried the diet. Reports of the diet began to circulate in 2010 when Jennifer was said to be using it to get in shape for her rom-com Just Go With It. Aniston, it was reported, was eating 14 portions of baby food purees a day followed by a grown-up dinner of grilled fish and green vegetables in the evening and had managed to lose 7lbs in a week - not recommended at all. Pictures of her with co-star Brooklyn Decker showed then then 41-year-old Aniston looking every bit as toned as the Sports Illustrated model, 18 years her junior. Cheryl Cole, in preparation for her appearance as a judge on the U.S. version of the X Factor, also reportedly turned to the outrageous diet. 6. NICOLE 'SNOOKI' POLIZZI - THE COOKIE DIET On paper it sounds perfect, but could you really live on a diet of cookies? Originally trademarked by Australian Dr. Sanford Siegal in 1975, the bizarre diet is based on meal replacement... in the form of a biscuit. Featuring ingredients including milk, sugar, eggs, wheat and a 'secret amino acid protein mix' that kerbs hunger pangs, the diet has been tried and tested by a number of celebrities - notably Jersey Shore star Nicole 'Snooki' Polizzi. Snooki reportedly tried the diet in 2010, with the reality TV personality consuming just six 90-calorie cookies and one small meal each day. The diet involves swapping breakfast, lunch and any snacks in between for just six of the brand's special biscuits - available in flavours including butterscotch, cinnamon oatmeal, chocolate brownie, blueberry, banana and maple syrup - or nine of the little 60-calorie ones. You are permitted to eat a healthy, sensible dinner - just so long as your daily calorific intake does not top 1,200 calories. The cookies - which, according to Madonna, made her then-husband Ritchie lose his sex drive in 2008 - are made from fibrous grains such as oats, fruit and amino acids, and the diet claims to help you drop 10lb per month. In 2009, Kim Kardashian publicly denied turning to the diet after an article on named her as a celebrity advocate. 'Not true! I would never do this unhealthy diet! I do QuickTrim!' she tweeted at the time.
Medical News Today
31-05-2025
- Health
- Medical News Today
Keto vs. Mediterranean: Both diets may help lower blood pressure
Keto vs. Mediterranean: Which diet gets better results for weight loss and blood pressure? Design by MNT; Photography by& Westend61/Getty Images Hypertension, or high blood pressure, can be managed through a number of lifestyle changes, including eating a healthy diet. Past studies have linked the Mediterranean and ketogenic diets as a way to help lower blood pressure. A new study offers further evidence that both the Mediterranean and keto diets can help lower a person's blood pressure and improve cardiovascular health measurements in people who have obesity or overweight. Clinically known as hypertension, this medical condition occurs when the force with which blood flows through the arteries is too high. A study published in April 2024 reported that following the Mediterranean diet was linked to a lower risk for high blood pressure. Another study published in July 2019 showed that following a low carbohydrate diet like the keto diet helped lower blood pressure readings in people with type 2 diabetes. Now, a new study offers further evidence that both the Mediterranean and keto diets can help lower a person's blood pressure and improve cardiovascular health measurements in people who have obesity or overweight. The findings were published in the journal Nutrients. Eleven of the study participants were randomly assigned to follow the Mediterranean diet, and the remaining 15 followed the keto diet over a period of three months. At the study's conclusion, researchers found that participants in both diet groups experienced a decrease in blood pressure and weight loss after three months. There was one area where researchers reported a difference between the Mediterranean and keto diets. They reported that participants following the keto diet had a higher level of 'nocturnal dipping' than those in the keto group. 'Nocturnal dipping refers to the natural decrease in blood pressure that occurs when we sleep,' Cheng-Han Chen, MD, a board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA — who is not associated with this study — told Medical News Today . 'It is a measure of healthy blood pressure regulation, and abnormal nocturnal dipping patterns have been associated with increased risk of heart disease,' he said. A 10-20% dip in blood pressure while you sleep is considered normal. Past studies show that not experiencing nocturnal dipping, or the reverse of it, known as nocturnal hypertension , can increase a person's risk for cardiovascular disease. When asked about his reaction to this study's findings, Chen commented that while the Mediterranean and keto diets are somewhat different in their food restrictions, the study results suggest that there may be different dietary techniques that can achieve the same beneficial outcome, depending on the food preferences of an individual. 'Metabolic syndrome — including high blood pressure, abdominal obesity, high blood sugar, and disordered lipids — remains a significant risk factor for cardiovascular disease,' he explained. 'Lifestyle modification, such as diet improvements, will be essential in order to help control the burden of heart disease in our society.' 'Further research including larger controlled studies with a more diverse population will be necessary to confirm these findings, and to evaluate for any potential benefit to clinical outcomes,' Chen added. MNT also spoke with Mir Ali, MD, a board certified general surgeon, bariatric surgeon, and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, about this research, who commented that its findings are in line with what he recommends to patients. 'Both the keto and the Mediterranean diets emphasize a reduction in carbohydrate and sugar intake, and that's what we found is the best way to kind of shift the body into burning fat is by reducing all the carbohydrates and sugars.' — Mir Ali, MD 'Unfortunately, obesity is an increasing problem in the U.S. and other westernized countries, so the more we can find ways to combat that, find foods that are going to help people lose weight and head to a healthier diet, then maybe some of these larger food manufacturers will start shifting their focus to foods that just taste good to foods that may actually be helpful,' Ali continued. Because this was a smaller study, Ali suggested expanding it to a larger patient base or population to refine it further. 'What is it about these two types of diets that are helpful?,' he asked. 'Is it reducing processed foods or is it more reducing the carbohydrates and sugars? So there are some differences between the diets, and trying to define further what is optimal between these two diets.' While both the Mediterranean and keto diets are popular dietary plans for people to follow, they may not be right for everyone. We asked Monique Richard, MS, RDN, LDN, a registered dietitian nutritionist and owner of Nutrition-In-Sight, for her top tips for readers on how to decide which diet is personally best for them to follow if they want to lose weight and lower their blood pressure. 'Meeting with a registered dietitian nutritionist (RDN) is recommended to further explore which dietary pattern may be most appropriate for an individual's needs, current health condition, preferences, goals, genetics and lifestyle,' Richard said. 'RDNs are trained to bridge the gap between science and everyday life. If you're looking to manage weight or blood pressure in a way that's realistic and sustainable, working with an RDN can be a game-changer.' 'It is also important to consider if the specific dietary pattern is sustainable for a long period of time and can be a lifestyle versus a controlled experiment or 'temporary fix',' she continued. 'Think of dietary patterns like a playlist — the right mix can set the tone for a healthier rhythm in your body and the days ahead.' Richard suggested honing in on increasing foods rich in nutrients with many health benefits, such as: Healthy fats like olives, extra-virgin olive oil, avocados, nuts, and seeds. Non-starchy vegetables such as leafy greens, beets, peppers, onions, garlic, scallions, tomatoes, cabbage, and Brussels sprouts. Herbs such as chives, basil, mint, rosemary, thyme, and sage. Proteins from plants and animals, such as goat cheese, yogurt, beans and lentils, fish, hummus, and tzatziki. High fiber foods from whole grains like oats, whole wheat, and rye, and fresh fruits in season such as peaches, plums, apples, grapes, berries, pears, oranges, figs, dates, and cherries. Incorporation of green, black, white, or herbal teas. 'There's no 'one-size-fits-all' when it comes to dietary patterns — unless it's a kitchen apron. I encourage clients and patients to try to move away from chasing labels —'Mediterranean,' 'low-carb,' 'plant-based'— and move toward tuning into how food functions for our unique needs.' — Monique Richard, MS, RDN, LDN
Medscape
09-05-2025
- Health
- Medscape
May 09 2025 This Week in Cardiology
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending May 9, 2025, John Mandrola, MD, comments on the following topics: the controversial KETO-CTA study, tough decisions in subclinical AF, and potentially huge benefit for GLP-1 receptor agonists. Meta-analysis The journal JACC Advances published a study looking at plaque progression in people eating a ketogenic diet (KD). It stirred all sorts of controversy on social media. I will review it this week. A few background comments. An obstacle to the broad clinical implementation of carbohydrate-restricted diets (CRDs) and KD are lipid changes that occur in a minority of patients upon carbohydrate restriction. Bad lipid changes. As in large increases in LDL cholesterol (LDL-C) and associated apolipoprotein B (ApoB). While there are many factors contributing to increases in LDL-C and ApoB in the KD, "leanness" seems important. Get this: The authors cite a meta-analysis of 41 studies that reports that mean baseline BMI had a strong inverse association with LDL cholesterol change [whereas saturated fat amount was not significantly associated with LDL-C change. For trials with mean baseline BMI <25, LDL cholesterol increased by 41 mg/dL (95% CI, 19.6-63.3) on the low carbohydrate diet (LCD). By contrast, for trials with a mean of BMI 25 to less than 35, LDL cholesterol did not change, and for trials with a mean BMI ≥35, LDL cholesterol decreased by 7 mg/dL (95% CI, –12.1 to –1.3). I did not know that lipid changes with CHD was modified by BMI. These observations have given rise to the characterization of the lean mass hyper-responder (LMHR) phenotype. From the authors: the aim of the study was "to examine the association between plaque progression and its predicting factors." I know; it is a bit confusing. 100 people who were on a KD (for years actually), and had a "keto-induced" LDL-C ≥190 mg/dl and HDL ≥60 mg/dl and TG ≤ 80 mg/dl were followed for 1 year using coronary artery calcium (CAC) scan and coronary computed tomography angiography (CCTA). I say "keto-induced" because the LDL-C had to be less than 160 before adapting the KD. Entry criteria also included an increase in ≥ 50% in the LDL-C. Plaque progression predictors were assessed with linear regression and Bayes Factors. Study subjects had to have normal glucose and A1c and normal CRP. Patients on the KD had a normal BMI at 22 and very high LDL of 254, HDL 89 and triglycerides of 67. Pause there: average LDL 254, so many were higher. These were 55-year-old mostly men who were adherent to KD as documented with beta-hydroxybutyrate (BHB) measures. Over the year, there was no substantial changes in ApoB or BMI. The study was actually pre-registered, and the primary endpoint was originally the change in noncalcified plaque burden. They did not formally present this endpoint. Instead, they gave the median change in percent atheroma volume, which they said was 0.8%. Who knows what this means? They tells us that this value is comparable with those observed in other cohorts. The thing is…the primary endpoint of change in noncalcified plaque volume (NCPV) was presented in a figure which you could look at and see that most individuals have an increase in NCPV. This lack of data on the PEP caused a stir online and the lead author offered the data in a video on Twitter/X. The numerical pooled NCPV change value was an in increase of 18.8 mm³. If this means nothing to you, don't worry. I will come back to it. Weird though that we had to get the primary endpoint in a Twitter video. The main thrust of the paper were the correlations. Neither the change in ApoB throughout the study nor the ApoB at the beginning of the study were associated with the change in NCPV. There was also no correlation between LDL-C and NCPV. What was correlated? The baseline CAC was positively associated with a change in NCPV. So also were baseline plaque measures. Simplifying: if there was plaque or CAC at baseline, there was a positive correlation with NCPV. The authors make the case that while both LDL-C and ApoB are independent risk factors for atherosclerosis, the absolute risk associated with elevated LDL-C and ApoB is context-dependent and may not apply to this lean mass hyper-responder (LMHR) group. Thus, they write, "these data are consistent with the observation that high LDL-C and ApoB among a metabolically healthy population have different cardiovascular risk implications than high LDL-C among those with metabolic dysfunction." Gosh, that is a big conclusion because these people had total cholesterol of 350 and LDL-C of 255. The authors make the case that the lean mass hyper-responders are different from the person with abnormal lipids from metabolic syndrome: Difference 1 : LDL-C and ApoB elevations are dynamic and result from the metabolic response of carb restriction and this is not a genetic defect. Difference 2 : LMHR are normal weight and metabolically healthy; they don't have obesity, diabetes, or insulin resistance. Difference 3 : The high LDL-C and ApoB in this phenotype emerge as part of a lipid triad, also inclusive of high HDL-C and low triglycerides, representing a metabolic signature of a distinct physiological state. Difference 4: The degree of this phenotype appears inversely related to BMI ("leanness"), consistent with the idea that it is a metabolic response to carbohydrate restriction that is accentuated in leaner, more metabolically healthy persons. The authors really are not shy in their conclusions. And I call them Whoppers No. 1, No. 2, and No. 3: Whopper 1: The LMHR population constitutes a unique and important natural experiment evaluating the lipid heart hypothesis in an unprecedented manner. Whopper 2: Our data are consistent with the notion that elevated ApoB, even at extreme levels, does not drive atherosclerosis in a dose-dependent manner in this population of metabolically healthy individuals. They qualify this conclusion by saying that LHMR may still have risk. For instance, they noted that PAV increase comparable to what has been observed in other studies on populations with lower LDL-C across the cardiovascular disease risk spectrum. They offer no citation here. Whopper 3: Quote: "These insights can facilitate personalized treatment and risk mitigation strategies based on modern, cost-effective cardiac imaging." For instance, they say, despite profound elevations in LDL-C and ApoB, based on their data, LMHR subjects with CAC = 0 at baseline (n = 57) constitute a low-risk group for percent atheroma volume (PAV) progression, even as compared to other cohorts with far lower LDL-C and ApoB. By contrast, LMHR subjects with elevated baseline CAC, possibly from a history of metabolic damage and dysfunction prior to adopting a CRD, appear to constitute a relatively higher risk group for PAV progression even where LDL-C and ApoB are equal to their CAC = 0 counterparts. Before closing they coin the phrase " plaque begets plaque. " I see why this paper generated angst online. The idea of the study is reasonable; what's unreasonable are the conclusions. First, if you look at the primary endpoint of change in noncalcified plaque volume, it went up. A lot. 18.8 mm3. That was 2.5x higher than they predicted in their study protocol. So, if you believe that the delta of NCPV is a great surrogate, it looks quite ominous. Second, imaging tests are almost always a terrible surrogate measure. Images are images. To assess risk, you need to measure events. Heart attacks. Stroke. CV death. I realize this is a small uncontrolled study, and it's fine to look at these things (in fact, I am curious), but you cannot claim clinical importance just because you weaved a nice story about high LDL-C in LMHR being different from high LDL-C in metabolic syndrome patients. Third, there is like 50 years of data supporting LDL-C being causal for atherosclerosis. Like every Bradford Hill criteria is met. So…. If you are going to claim an exception, you need more rigorous evidence than this. The priors here — the priors being that these LMHR are an exception — have to be extremely pessimistic, so you'd need really strong data to change your posterior view. This study surely was not strong evidence. Fourth, assuming you believe the plaque images are precise and reproducible and clinically relevant, this study really suffers from a lack of control. All they had to do is recruit a group of people eating a Mediterranean diet. Let's see what happens to them relative to the Keto people. Fifth, the authors don't tell us how many people they screened to find these 100 people. I get the sense they are highly selected bunch. Finally, the question of heart health from a specific diet is going to be really hard to sort out. Nutritional studies always are. An RCT in a prison might work, but cardiac event rates in young people—even with KD-induced LDL will be infrequent. What's more, the LMHR will surely do other things that affect heart disease, like exercise, not smoking etc. If the authors are wrong, and actually eating a diet that causes crazy high LDL levels and maintaining a lean body mass is actually harmful , then, given the popularity of carbohydrate-restricted diets, this could be a public health disaster. As for diet, I do think Americans eat too many carbs, but the KD seems extreme. Why not just eat a balanced diet, like they do in Sicily? JAMA Network Open has published an interesting modeling study from a Finnish group on the matter of net benefit of oral anticoagulation (OAC) in subclinical device-detected atrial fibrillation (AF). The background here is known to anyone practicing cardiology. It's perhaps the most common question I receive: John, Mrs Smith had 4 hours of AF on her pacemaker. Her CHA 2 DS 2 VASc score is 4; should we anticoagulate? And if we don't anticoagulate, how much AF does she have to have before we do? The short answer is that I have no idea. Your comeback is…come on Mandrola, we have two trials. And it is true. We have the NOAH trial. Edoxaban vs placebo in 2500 patients with a median duration of AF 2.8 hours. The primary outcome of CV death, stroke, and systemic embolism (SE) was 19% lower in the edoxaban group. The confidence intervals (CI) were wide, and the difference did not reach significance. Major bleeding was 31% higher and this did reach statistical significance. We also have the ARTESIA trial. Apixaban vs acetylsalicylic acid (ASA) in 4000 patients with median duration AF 1.5 hours. The primary outcome of stroke and SE was 37% lower with apixaban and this did meet statistical significance. Major bleeding however was 80% higher and this met statistical significance. Some have said NOAH was negative and ARTESIA was positive. Perhaps, technically, this is true. But I think they both show the same thing. OAC reduces stroke and increases bleeding. It leaves us with the question of net benefit. I've heard Jeff Healey, the PI of ARTESIA, rightly say that we should favor OAC because strokes are worse than bleeds. This is certainly true. The tension in subclinical AF is that the yearly stroke rates were low—in the 1% range. Far lower than what would be predicted in the CHA 2 DS 2 VASc assessment for clinical AF. And if that is true, even if OAC reduces the relative risk, the absolute risk reduction is tiny, in the order of 4 per 1000, with a number needed to treat (NNT) of 250. Therefore, any increase in bleeding may mitigate the net benefit. Led by senior author Konsta Teppo, the group set out to estimate the "net benefit" of OAC in SCAF. They used modeling. It's technical. A Medscape colleague, nephrologist F. Perry Wilson, covered this paper, and he wrote: The study was done using a computer. I know — all studies are done with computers. But here I mean literally. The authors used a decision analytical model run with 10,000 patients with subclinical AF on OAC and 10,000 without OAC. They then used a "Markov decision model" to estimate net outcomes of NOACs. You all know that doctors who ablate AF and put in pacers and defibrillators don't know much about Markov modeling. I was going to ask Professor Teppo. He would have told me. But to make life easier, I just asked Claude. Who said: A Markov model consists of multiple health states individuals can move between based on specific transition probabilities. Think of it as a simulation where: Patients exist in various health states (e.g., well, post-stroke, bleeding event, death) In each cycle (1 month in this study), patients can transition between states with certain probabilities The model tracks what happens to a cohort of simulated patients over time The model was constructed in multiple steps: Base Case Patient: The researchers created a model patient, aged 77 years (matching the average age in the clinical trials), and applied the untreated stroke and bleeding rates from the NOAH-AFNET 6 and ARTESIA trials. Health States: The model included states for: Being Well with subclinical AF Ischemic stroke (with varying severities) Major bleeding events (hemorrhagic stroke, other intracranial bleeding, extracranial bleeding) Development of clinical AF Death Transition Probabilities: The pooled point risk estimates from the meta-analysis combining the two trials were used as the effect sizes for anticoagulation on stroke (32% decrease) and major bleeding (62% increase). The model assigned an 80% weight to nonintracranial bleedings for the increase in bleedings caused by the DOACs. The numbers come from the McIntyre et al meta-analysis of NOAH and ARTESIA in Circulation . Event Severity: Probabilities for the severity of stroke and bleeding events in the anticoagulation and non-anticoagulation groups of the model were approximated from previous observations in patients with and without anticoagulation. Quality of Life Weights: The net benefit outcome was assessed in terms of QALYs (Quality-Adjusted Life Years), where clinical events reduced patients' quality of life based on the type and severity of the event according to previously published quality of life data. Time Horizon: The simulation was run for a 10-year period with 10,000 samples in both decision groups (with and without the DOACs). The main outcome measure for net benefit was the cumulative quality-adjusted life-years (QALYs) during the simulation. This included things like severity of ischemic strokes, hemorrhagic strokes, other intracranial bleeds, and extracranial bleeds, as well as the number of deaths during a 10-year simulation. It's really neat way to look at net benefit. As I said, I don't know anything more than what I read about Markov modeling, but the thing that strikes me, and perhaps you too, is that there are a lot of degrees of freedom of choices. That said, here is what the model shows: Over the 10-year period, you would have 1076 strokes in nontreated subclinical AF vs 843 with treatment. The delta of 233 strokes saved seems like a lot but it's only 2.3% per year. There would be 1213 major bleeds without OAC vs 1664 with OAC. The 453 more bleeds that would be 4.5% per year. Deaths were nearly the same. 55 fewer in the anticoagulation (AC) arm but it's only 0.6% delta per year. OK, what about the primary endpoint of quality-adjusted life years. It was, drumroll… Per patient, the differences listed led to 1 additional quality-adjusted week of life (0.024 QALYs) with DOAC treatment during the 10-year simulation. When the 95% CIs of treatment effect sizes were considered in probabilistic sensitivity analysis, there was a 66% probability that DOAC treatment leads to more QALYs than withholding treatment. The authors did an exploratory analysis looking at higher risk patients and as you would expect, in patients with CHADSVASC score >4, the increase QALY with DOAC was now a month, not a week. But they note caution because this estimate came from subgroup analyses in the two trials, neither of which met statistical significance for interaction. The authors concluded that "initiating DOACs in patients with device-detected subclinical AF was associated with a minimal increase in QALYs. However, the benefits were uncertain, and the effect size of the overall net benefit does not appear to be clinically meaningful." I loved this paper and the authors' discussion. The modeling and estimates make intuitive sense, right? The trials find extremely low rates of stroke with SCAF. The average age of patients was 77. Older patients have many competing risks. Andrew Foy has a nice model thinking about domains acting on treatment effect. They are overlapping circles where you have the risk of the primary outcome vs competing risk, and the treatment benefit and treatment harm. Treating subclinical AF is a perfect example of these four domains coming together to almost cancel themselves out. The Markov model basically quantifies this to 1-week extra of good quality of life. Perhaps a few weeks longer if the patient has extremely high stroke risk. The clear conclusion I make from this paper is that subclinical AF is a different entity than clinical AF of old. I co-authored a paper on that in Stroke . The Finnish group has shown very little net benefit in treating SCAF. This contrasts with the famous Singer et al net benefit paper in Annals of Internal Medicine in 2010, where they showed clear net benefit of warfarin in patients in the ATRIA cohort. Here, even with an annual stroke rate of only 2%, warfarin provided a large net benefit. In clinical AF, stroke reduction for anticoagulation was larger than the bleeding increase. But subclinical AF has a different meaning. Yes, it is electrically the same; the atria is fibrillating. But, and this is my opinion, I am beginning to think that a certain degree of short duration occurs in older people as a matter of normal life. We know that PACs and PVCs increase with age, why not short duration AF? For now, the only solution to the matter is to do what David Sackett described when he coined the term evidence-based medicine. That is, we align care with patient preferences. With our patients we discuss the uncertainty, seek their preferences, and treat accordingly. There can be no algorithm, no guideline. This problem does not fit into those colored boxes in guidelines, and the top people who write guidelines should resist the urge to help us clinicians. If a patient fears stroke and is willing to deal with the disutility of taking a daily pill (that is, the cost and taking it every day), then use OAC. If a patient fears bleeding, then hold off and monitor more. I know, this is a cardiology podcast, but here me out. There is a connection. Plus, the science of this study is striking. In Kentucky, one of the least healthy states in the US, obesity is essentially the norm. I estimate that more than half the patients I see in clinic have some degree of metabolic syndrome—overweight or obese, insulin resistant, type 2 diabetes (T2D). Many of these patients also have fatty liver disease, which used to be called non-alcoholic steatohepatitis, or NASH. But it is now called MASH, or metabolic-associated steatohepatitis. It's a bad condition, and I think it flies under the radar of most of us cardiologists—because we see these patients for hypertension or AF or ischemic heart disease. My friend Claude says that 9-15 million adults in the US have MASH. And it's getting worse. The prevalence of MASH in the US is predicted to increase 63% from 16.5 million cases in 2015 to 27 million cases in 2030. And in patients with T2D and obesity, the prevalence of MASH is as high as 16%, so almost 1 in 5 patients. NEJM recently published the results of the ESSENCE trial of 1197 patients with documented inflammation on liver biopsy of semaglutide vs placebo. This is a two-part trial. Part 1 looks at histology. And it has resolution of steatohepatitis without worsening of liver fibrosis and reduction in liver fibrosis without worsening of steatohepatitis as the primary endpoints. ESSENCE trial is ongoing, and Part 2 will measure clinical outcomes. NEJM published the PART 1 and it is shocking. Patients were young, age 56, and more than half were females. The mean BMI was 34-35. The primary endpoints were twofold: Resolution of steatohepatitis without worsening of fibrosis occurred in 63% vs 34% in the semaglutide vs placebo groups. That is an absolute treatment difference of 29 percentage points, which was highly significant. The second primary endpoint, a reduction in liver fibrosis without worsening of steatohepatitis, was reported in 37% vs 22% in the semaglutide vs placebo arms. That is absolute treatment diff of 14.4 percentage points, also highly significant. All secondary outcomes favored semaglutide. I mention this study because a) oodles of our patients have MASH, whether we know it or not, b) MASH is on the rise, and c) MASH portends a poor prognosis; it is the leading cause of liver transplant, but perhaps most relevant to cardiologists is that most patients with MASH die of cardiovascular (CV) complications. The GLP-1 agonist drug in ESSENCE basically shredded evidence of liver disease, at least histologically, and I suspect the follow-on outcomes portion of ESSENCE will be stopped early for benefit. There is an approved medication for MASH, called resmetirom, but this is a thyroid hormone receptor-beta (THR-β) selective agonist that specifically targets the liver. Other than mild lipid-lowering effects, it has no known CV benefits. This is unlike GLP-1 agonists which have RCT-proven benefits in CV disease and diabetes. I am not yet prescribing GLP-1, but like the SGLT2 inhibitors, I think GLP-1 agonists will soon be a drug that cardiologist will want to prescribe. I realize that some listeners may say we should be treating obesity and obesity-related diseases with weight loss and diet and exercise. The GLP-1 benefit seen in ESSENCE was likely due to weight loss. My answer to that is it doesn't matter why the GLP-1 drugs work. When trials show that something works, an evidenced-based practitioner should embrace it. What's more, clinical medicine is pragmatic. It's pretty obvious that lifestyle interventions have a low success rate. So, if the GLP-1 agonists work, we should prescribe them. And, finally, there is a big difference in using GLP-1 agonists in an adult with diabetes, heart disease, and liver inflammation vs an adolescent who is overweight. The former person is in real trouble. The net benefit calculus favors treatment. The younger person should be counseled aggressively to change lifestyle. In other words, treatment is different from prevention. CABG Still Superior to Stents Despite FAME 3 Endpoint Swap A few weeks ago, I discussed the FAME-3 trial 5-year results. I turned this into a column that is up now. The short story is that FAME-3 was designed as a one-year non-inferiority trial comparing fractional flow reserve (FFR)-guided PCI to coronary artery bypass grafting (CABG) in patients with multivessel disease. Why someone would want to compare revascularization strategies at one year is mysterious, but that is what they did. And CABG was much better. FFR-PCI did not even reach non-inferiority in a four-point composite endpoint of death, myocardial infarction, stroke, and unplanned revascularization. My column pushes back against the claims in 3 and 5-year results that FFR-PCI is now equivalent to CABG. The claims stem from use of a different endpoint. Take a look at my column and see what you think.
The Sun
08-05-2025
- Entertainment
- The Sun
Danielle Lloyd shows off incredible 1.5 stone weight loss and six-pack as she poses in skintight gym gear
Beth Allcock Published: Invalid Date, DANIELLE Lloyd has stripped to her sports gear to reveal her 1.5 stone weight loss. The model, 41, flashed her ripped abs in a beige co-ord as she took a mirror selfie following an intense reformer Pilates class. 6 6 6 Danielle, who oozed a natural glow after going make-up free for the session, captured her ripped look following her body transformation. She finished off her gym kit with pink socks, tying her brunette locks in a half-up style. In her Instagram image caption, she wrote: "Spray tans and pilates Wednesday's are my favourite." Revealing she had shed more than a stone, she added: "Feeling so body confident 23lb down." Her online following were quick to support her wellbeing mission and one posted: "Gorgeous hard working Mum and keeping fit at the same time love you." A second put: "Wow! You look incredible," as a third gushed: "Looking fab beaut." One then added: "Omg looking amazing." The star, who is mum to Archie, 13, Harry, 12, George, 10, Ronnie, six, and Autumn Rose, two, trains up to four times a week, follows a keto diet and rarely touches alcohol. Danielle Lloyd breaks down in tears in heartbreaking post as she reveals skin cancer diagnosis As a result, she admitted that she feels in better shape now than she did at the peak of her modelling career. She said: 'I'm a totally different person and I feel the best I ever have. 'Back in the day, I didn't care what I put into my body. I thought I was living life to the full, but I was totally lost. 'I was on the front pages of the magazines and everyone automatically thought I must love myself, but the truth was I was one of the most insecure people on the planet. What is melanoma, what are the symptoms and how can you prevent it? Melanoma is the most serious type of skin cancer that has a tendency to spread around the body. It is diagnosed 16,000 times per year, and tragically takes the lives of 2,340 people per year. The number of people being diagnosed with melanoma is increasing, and it is the 5th most common cancer in the UK. But it is also one of the most preventable cancers, with 86 per cent of cases in the UK avoidable. The best way to protect yourself from melanoma is to be sun safe - wear SPF every day, wear a hat and sunglasses and keep out of the sun in the hottest hours. It is also advised to avoid sunbeds. People who are fair-skinned, have blue or green eyes, blonde or red hair and a large number of freckles or moles are more likely to get skin cancer. Surgery is the main treatment for melanoma, particularly if it is found early. This will involve removing the affected tissue in the skin. Radiotherapy, medicines and chemotherapy are also sometimes used to try and stop the cancer from growing. Treatment depends on the severity of the disease. What are the symptoms? The key thing to look out for are changes to an existing mole, or a new mole on your skin. Most experts recommend using the simple 'ABCDE' rule to look for symptoms of melanoma skin cancer, which can appear anywhere on the body. There are five letters/words to remember: A symmetrical – melanomas usually have two very different halves and are an irregular shape B order – melanomas usually have a notched or ragged border C olours – melanomas will usually be a mix of two or more colours D iameter – most melanomas are usually larger than 6mm in diameter E nlargement or elevation – a mole that changes size over time is more likely to be a melanoma A mole that changes size, shape or colour may be a melanoma. But other signs to look out for include moles that are: Swollen and sore Bleeding Itchy Crusty How deadly is it? Melanoma is a deadly form of skin cancer. The outlook of a person's disease depends on the stage of the cancer when it was diagnosed. Survival is better for women than it is for men. 'We don't know exactly why this is. It may be because women are more likely to see a doctor about their melanoma at an earlier stage,' says Cancer Research UK. The charity says that generally, statistics show that in England, more than 85 out of every 100 people (more than 85 per cent) will survive their melanoma for 10 years or more after they are diagnosed. Around 100 per cent in England diagnosed with melanoma at stage 1 - when the cancer cells are only in the top layer of skin - will survive for five years or more after drops to 80 per cent for stage 2. Some 70 per cent live for a further five years when they are diagnosed in stage 3, which is when the cancer has started to spread to nearby lymph nodes. At stage 4, when the melanoma has spread elsewhere in the body, almost 30 per cent survive their cancer for 5 years or more. Cancer Research says the stage 4 data does not account for age differences. Age can affect outlook and younger people have a better prognosis than older people. Age can affect outlook and younger people have a better prognosis than older people. What is melanoma? Melanocytes are cells in the skin that give us the colour of our skin because they produce a pigment, known as melanin. When you sit in the sun, melanocytes produce more pigment (a sun tan), which spreads to other skin cells to protect them from the sun's rays. But melanocytes are also where cancer starts. Too much UV causes sunburn, and this is a sign of damage to the skin's DNA. The UV triggers changes in the melanocytes, which makes the genetic material become faulty and cause abnormal cell growth. People who burn easily are more at risk of skin cancer because their cells do not produce as much pigment to protect their skin. Those with albinism are at the most risk because their skin produces no pigment at all. 'I did not feel good about myself and I was using drink and drugs to mask a lot of that.' The star previously also wowed in a glam sauna selfie. HEALTH HORROR Yet Danielle's new look comes after she opened up on her skin cancer battle. Danielle shared graphic photos alongside a candid health update to raise awareness of the disease - admitting her own patch was smaller than a 5p coin. The model underwent an operation after being diagnosed with a form of skin cancer several weeks ago. She had an operation to remove a cancerous patch from just above her collarbone, after spotting a change in a small freckle. She said the freckle was 'smaller than a five pence coin' but had started to raise alarm bells after she saw how much it had evolved over time. She responded to one fan in the comments: "Mine was melenoma which was sun damage x". Danielle admitted she believed her tanned skin tone gave her some protection from cancer. She admitted she rarely wore sunscreen with a high SPF, saying: "Honestly, if I did, it was very low factor as I go so brown very quickly. I never thought my skin tone could get skin cancer and if I did anyone can". The mum also said she had ditched sunbeds for the first time in her life. Posting the update to her fans, Danielle urged others to be vigilant about any skin changes, especially those that may seem minor at first glance. She said in the comments: "I used to be a total sun worshiper, never really thinking about the risk of skin cancer. "Sunbeds before holidays? Absolutely! But now, I've decided it's better to fake the glow because my health and being there for my kids are what truly matter. "I'm still waiting on the results from my second operation". Danielle rose to prominence as a beauty queen who was crowned Miss England 2004 and later Miss Great Britain 2006. In 2007, she featured on the fifth series of the reality show Celebrity Big Brother. She made it to the final three of Celebrity SAS: Who Dares Wins in 2023 alongside singer Gareth Gates and former health secretary Matt Hancock, but missed out on completing the course at the final stage. 6 6
