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  1. [Admin Note: This is a series of posts originally on another thread that started on the topic of how cold exposure can have beneficial effects for health and longevity despite increasing calorie expenditure. I debated where to move them, since they seem to fit General Health & Longevity, CR Practice, and CR Science. I finally opted for CR Science, since you'll see if you haven't been reading them already, they bear directly on CR and CR mimetics. If anyone feels strongly this was the wrong choice, I'll be happy to move the thread to another forum. --Dean] Rodney, Whenever I see someone use the word "surely", I figure the writer isn't very sure about, or doesn't have real evidence to support, what they are about to say. I'm guilty of it sometimes myself. People's appetites differ for a lot of reasons, many of them without negative health implications. Genetics is one example that can alter metabolic rate and therefore hunger (remember the ob/ob mice who ate more but didn't live shorter lives). Exercise or exposure to cold (and extra brown fat that cold exposure can create/promote) will increase calorie expenditure without detrimental effects. In fact, perhaps my favorite study of all time (except for the suffering of the animals involved) was the famous "rats with cold feet" study [1] by John Holloszy. Holloszy found that rats who lived their lives standing in a cold puddle of water ate 44% more than normally-housed rats, but nonetheless stayed thin and didn't live any shorter lives than the normally-housed rats. In fact they lived slightly longer and got less cancer. Our friend Josh Mitteldorf did a whole blog post about the hormetic benefits of cold exposure, and how it casts serious doubt (if not debunks) the popular "rate of living" theory of aging. --Dean (who composed this post while pedalling shirtless and wearing just bike shorts on his stationary bike in his 59 degF basement to maximize hormesis... ) -------- [1] J Appl Physiol (1985). 1986 Nov;61(5):1656-60. Longevity of cold-exposed rats: a reevaluation of the "rate-of-living theory". Holloszy JO, Smith EK. It has been postulated that increased energy expenditure results in shortened survival. To test this "rate-of-living theory" we examined the effect of raising energy expenditure by means of cold exposure on the longevity of rats. Male 6-mo-old SPF Long-Evans rats were gradually accustomed to immersion in cool water (23 degrees C). After 3 mo they were standing in the cool water for 4 h/day, 5 days/wk. They were maintained on this program until age 32 mo. The cold exposure resulted in a 44% increase in food intake (P less than 0.001). Despite their greater food intake, the cold-exposed rats' body weights were significantly lower than those of control animals from age 11 to 32 mo. The average age at death of the cold-exposed rats was 968 +/- 141 days compared with 923 +/- 159 days for the controls. The cold exposure appeared to protect against neoplasia, particularly sarcomas; only 24% of the necropsied cold-exposed rats had malignancies compared with 57% for the controls. The results of this study provide no support for the concept that increased energy expenditure decreases longevity. PMID: 3781978 [PubMed - indexed for MEDLINE]
  2. All, I've been engaged in an off-forum Q&A dialog with a CR friend, and I figured some of you other crazies might appreciate reading about (and hopefully commenting on / criticizing) some of the details of my current diet & exercise regime, as well as tips & my motivation for them. If not, feel free it skip this post! I've only included my sided conversation, but I think from my answers it is pretty clear what the questions were. Feel free to ask for clarification on anything that's unclear. Regarding eating once per day. It's very hard, especially when just starting out on this regime, to eat once per day in the afternoon. It takes a lot of willpower. So I recommend, and always try myself, to wait a couple / few hours after waking before I eat, but then eat in the morning rather than waiting until afternoon, and definitely never try to grocery shop on a (very) empty stomach! For large scale chopped veggie storage, I use glass containers because I'm a bit paranoid about leeching from plastics. The glass jar I use is from Anchor Hocking. Turns out it is only 2gal. Here is a link. I believe both Target and Walmart have them as well, although I'm not sure about in-store availability. I chop my "chunky" veggies once per week, and store them in this glass jar, all mixed up, between layers of paper towels to absorb moisture and keep them fresh. I chop my "leafy green" veggies at the same time, throughly spin-dry them using salad spinner, and then store them in another containing between layers of paper towels to preserve freshness. Both go into my fridge, which I temperature control to maintain a very steady 34degF. Vegetable prep takes me just over one hour per week, but after many years I've got it down to an art/science. It used to take me about 2 hours. I find meditation and practices that cultivate mindfulness are helpful for fostering one's self-discipline. Other than that, I don't have much specific advice on that topic. I used to cook for my family when we were 4 rather than 3 . But now that it is just the three of us, and my daughter has an extremely busy schedule, my wife and daughter's eating schedule is pretty irregular. So they cook for themselves. I also found it hard to cook for them. Not because I was particularly tempted by the food I was making for them (although on occasion that too was the case), but more that I was conflicted by the opposing goals of cooking as healthy meals as possible for them, but also meals they would enjoy, and not waste by not eating. When practicing CR for a while, I've found you become extremely averse to wasting anything, but especially food. Plus I'm an ethical vegan. Both kids are (were) vegetarian, and my wife eats mostly vegetarian. But they enjoy quite a bit of dairy, which I had trouble buying/cooking for them for ethical reasons. Regarding exercise, I'll enumerate everything I do in a day, in order: [Get up at 2:45am - yes I'm kind of a early riser ] 4min - straight arm planking 2min - 100 body weight squats 10min - "10 minute abs" workout - Originally from YouTube video of that name, but after doing it several thousand times, I've got it memorized. . Video embedded at bottom. Warning - this will really hurt anyone not used to doing an ab workout, but her accent is strangely compelling... 20min - Jogging on treadmill at 4mph and 15% incline (very steep). 1.07miles, 200 kcal 120min - Stationary road bike. Modest intensity. HR around 95bpm. My Resting HR is about 45bpm. [breakfast - 1.5 hours] 10min - One mile run outdoors. Moderate pace . usually with my dog. 20min - Resistance training. 4day split to work all body parts on successive days, but giving each enough time to recover. Little rest between sets to keep it mildly aerobic. Pretty light weights. Pull-ups, pushups, light squats, triceps extensions, curls, shrugs, etc. All the standard exercises. Using dumbbells and body weight. 4min straight arm planking 2min - 100 body weight squats 2min - Ab Slide machine. Quite a good Ab exerciser 90min - Stationary road bike again. [Time now around 10:30am - Shower & 6min inversion therapy (to decompress spine and stretch back) & 20min power nap] [Puttering around for a while, light food prep, errands etc - 1-2 hours] 10min - One mile run outdoors. With dog. ~240min - pedalling at my bike desk while reading, surfing web, posting to CR forums [Off and on throughout afternoon evening - spend time with wife and daughter, especially when they eat dinner] 30min - brisk walk with my wife (and dog) [8:00pm - bedtime. 8:15 sound asleep] So in total I run for about 40min, do resistance training / calisthenics for about 45min, walk 30-45min, and then pedal for about 7h per day. On an average day, my Fitbit tells me I log about 45K steps (or step equivalents, including bike pedal revolutions), and about 23 miles. All of it at home, by myself (except if you count the mile walk with my wife and jogging with my dog ). I don't enjoy the hassle of working out with others at a gym. I don't seem to need the motivation of having other people around to exercise with. What motivates me to such extreme exercise? Hmmm... A few ideas: I like to eat, and to stay slim. Extreme exercise let's me do both. I'm exploring the possibility of getting CR benefits while eating lots of calories, but burning them off via lots of exercise and cold exposure. It makes me feel good. I like the endorphins, opiates, whatever makes exercise feel good. With my stationary bike and bike desk, I'm able to do other things while pedaling, like composing this message! I like being different from other people. I like pushing myself to extremes, to see what's possible. Pushing the envelope of human possibliity. I think exercising one's abilities and strengths is why we are here, and what makes life meaningful and significant. My biggest strength is probably self-discipline / conscientiousness. Exercising discipline strengthens the will. As Nietzsche said in Twilight of the Idols, "From life's school of war, what does not kill me makes me stronger." He was a big proponent of hormesis before it became fashionable. I hope being very different from others, and sharing my results, will enable people (like you!) to learn from my experiences and experiments, and figure out what might work best for them. Regarding sleep. I sleep for 6.5 hours per day (8:15pm - 2:45am) + a 20min power nap. Lately I've been sleeping like a baby, without my former problem of early waking (unless you count 2:45am as early ). I hope this is helpful. --Dean
  3. Email Facebook Twitter Pinterest Pocket Reddit Print By Cassandra Willyard 11 hours ago The internet is rife with advice for keeping the brain sharp as we age, and much of it is focused on the foods we eat. Headlines promise that oatmeal will fight off dementia. Blueberries improve memory. Coffee can slash your risk of Alzheimer’s disease. Take fish oil. Eat more fiber. Drink red wine. Forgo alcohol. Snack on nuts. Don’t skip breakfast. But definitely don’t eat bacon. One recent diet study got media attention, with one headline claiming, “Many people may be eating their way to dementia.” The study, published last December in Neurology, found that people who ate a diet rich in anti-inflammatory foods like fruits, vegetables, beans and tea or coffee had a lower risk of dementia than those who ate foods that boost inflammation, such as sugar, processed foods, unhealthy fats and red meat. Sign Up For the Latest from Science News Headlines and summaries of the latest Science News articles, delivered to your inbox E-mail Address* But the study, like most research on diet and dementia, couldn’t prove a causal link. And that’s not good enough to make recommendations that people should follow. Why has it proved such a challenge to pin down whether the foods we eat can help stave off dementia? First, dementia, like most chronic diseases, is the result of a complex interplay of genes, lifestyle and environment that researchers don’t fully understand. Diet is just one factor. Second, nutrition research is messy. People struggle to recall the foods they’ve eaten, their diets change over time, and modifying what people eat — even as part of a research study — is exceptionally difficult. For decades, researchers devoted little effort to trying to prevent or delay Alzheimer’s disease and other types of dementia because they thought there was no way to change the trajectory of these diseases. Dementia seemed to be the result of aging and an unlucky roll of the genetic dice. While scientists have identified genetic variants that boost risk for dementia, researchers now know that people can cut their risk by adopting a healthier lifestyle: avoiding smoking, keeping weight and blood sugar in check, exercising, managing blood pressure and avoiding too much alcohol — the same healthy behaviors that lower the risk of many chronic diseases. Diet is wrapped up in several of those healthy behaviors, and many studies suggest that diet may also directly play a role. But what makes for a brain-healthy diet? That’s where the research gets muddled. Despite loads of studies aimed at dissecting the influence of nutrition on dementia, researchers can’t say much with certainty. “I don’t think there’s any question that diet influences dementia risk or a variety of other age-related diseases,” says Matt Kaeberlein, who studies aging at the University of Washington in Seattle. But “are there specific components of diet or specific nutritional strategies that are causal in that connection?” He doubts it will be that simple. Worth trying In the United States, an estimated 6.5 million people, the vast majority of whom are over age 65, are living with Alzheimer’s disease and related dementias. Experts expect that by 2060, as the senior population grows, nearly 14 million residents over age 65 will have Alzheimer’s disease. Despite decades of research and more than 100 drug trials, scientists have yet to find a treatment for dementia that does more than curb symptoms temporarily (SN: 7/3/21 & 7/17/21, p. 8). “Really what we need to do is try and prevent it,” says Maria Fiatarone Singh, a geriatrician at the University of Sydney. Forty percent of dementia cases could be prevented or delayed by modifying a dozen risk factors, according to a 2020 report commissioned by the Lancet. The report doesn’t explicitly call out diet, but some researchers think it plays an important role. After years of fixating on specific foods and dietary components — things like fish oil and vitamin E supplements — many researchers in the field have started looking at dietary patterns. That shift makes sense. “We do not have vitamin E for breakfast, vitamin C for lunch. We eat foods in combination,” says Nikolaos Scarmeas, a neurologist at National and Kapodistrian University of Athens and Columbia University. He led the study on dementia and anti-inflammatory diets published in Neurology. But a shift from supplements to a whole diet of myriad foods complicates the research. A once-daily pill is easier to swallow than a new, healthier way of eating. Where diet fits Up to 40 percent of dementia cases could be prevented or delayed by modifying 12 risk factors. Targeting some of these risks reduces nerve cell loss in the brain; other interventions protect the brain’s ability to function and adapt even if some nerve loss has occurred, a concept called cognitive reserve. Diet plays a role in at least four of these risk factors. Twelve modifiable risk factors for dementia Reduce nerve cell damage Minimize diabetes Treat hypertension Prevent head injury Stop smoking Reduce air pollution Reduce midlife obesity Increase or maintain cognitive reserve Maintain frequent exercise Reduce depression Avoid excessive alcohol Treat hearing impairment Maintain frequent social contact Attain high level of education Source: G. Livingston et al/Lancet 2020 Earning points Suspecting that inflammation plays a role in dementia, many researchers posit that an anti-inflammatory diet might benefit the brain. In Scarmeas’ study, more than 1,000 older adults in Greece completed a food frequency questionnaire and earned a score based on how “inflammatory” their diet was. The lower the score, the better. For example, fatty fish, which is rich in omega-3 fatty acids, was considered an anti-inflammatory food and earned negative points. Cheese and many other dairy products, high in saturated fat, earned positive points. During the next three years, 62 people, or 6 percent of the study participants, developed dementia. People with the highest dietary inflammation scores were three times as likely to develop dementia as those with the lowest. Scores ranged from –5.83 to 6.01. Each point increase was linked to a 21 percent rise in dementia risk. Such epidemiological studies make connections, but they can’t prove cause and effect. Perhaps people who eat the most anti-inflammatory diets also are those least likely to develop dementia for some other reason. Maybe they have more social interactions. Or it could be, Scarmeas says, that people who eat more inflammatory diets do so because they’re already experiencing changes in their brain that lead them to consume these foods and “what we really see is the reverse causality.” To sort all this out, researchers rely on randomized controlled trials, the gold standard for providing proof of a causal effect. But in the arena of diet and dementia, these studies have challenges. Dementia is a disease of aging that takes decades to play out, Kaeberlein says. To show that a particular diet could reduce the risk of dementia, “it would take two-, three-, four-decade studies, which just aren’t feasible.” Many clinical trials last less than two years. As a work-around, researchers often rely on some intermediate outcome, like changes in cognition. But even that can be hard to observe. “If you’re already relatively healthy and don’t have many risks, you might not show much difference, especially if the duration of the study is relatively short,” says Sue Radd-Vagenas, a nutrition scientist at the University of Sydney. “The thinking is if you’re older and you have more risk factors, it’s more likely we might see something in a short period of time.” Yet older adults might already have some cognitive decline, so it might be more difficult to see an effect. Many researchers now suspect that intervening earlier will have a bigger impact. “We now know that the brain is stressed from midlife and there’s a tipping point at 65 when things go sour,” says Hussein Yassine, an Alzheimer’s researcher at the Keck School of Medicine of the University of Southern California in Los Angeles. But intervene too early, and a trial might not show any effect. Offering a healthier diet to a 50- or 60-year-old might pay off in the long run but fail to make a difference in cognition that can be measured during the relatively short length of a study. And it’s not only the timing of the intervention that matters, but also the duration. Do you have to eat a particular diet for two decades for it to have an impact? “We’ve got a problem of timescale,” says Kaarin Anstey, a dementia researcher at the University of New South Wales in Sydney. And then there are all the complexities that come with studying diet. “You can’t isolate it in the way you can isolate some of the other factors,” Anstey says. “It’s something that you’re exposed to all the time and over decades.” Food as medicine? In a clinical trial, researchers often test the effectiveness of a drug by offering half the study participants the medication and half a placebo pill. But when the treatment being tested is food, studies become much more difficult to control. First, food doesn’t come in a pill, so it’s tricky to hide whether participants are in the intervention group or the control group. Imagine a trial designed to test whether the Mediterranean diet can help slow cognitive decline. The participants aren’t told which group they’re in, but the control group sees that they aren’t getting nuts or fish or olive oil. “What ends up happening is a lot of participants will start actively increasing the consumption of the Mediterranean diet despite being on the control arm, because that’s why they signed up,” Yassine says. “So at the end of the trial, the two groups are not very dissimilar.” Second, we all need food to live, so a true placebo is out of the question. But what diet should the control group consume? Do you compare the diet intervention to people’s typical diets (which may differ from person to person and country to country)? Do you ask the comparison group to eat a healthy diet but avoid the food expected to provide brain benefits? (Offering them an unhealthy diet would be unethical.) And tracking what people eat during a clinical trial can be a challenge. Many of these studies rely on food frequency questionnaires to tally up all the foods in an individual’s diet. An ongoing study is assessing the impact of the MIND diet (which combines part of the Mediterranean diet with elements of the low-salt DASH diet) on cognitive decline. Researchers track adherence to the diet by asking participants to fill out a food frequency questionnaire every six to 12 months. But many of us struggle to remember what we ate a day or two ago. So some researchers also rely on more objective measures to assess compliance. For the MIND diet assessment, researchers are also tracking biomarkers in the blood and urine — vitamins such as folate, B12 and vitamin E, plus levels of certain antioxidants. Weighty survey Lengthy food frequency questionnaires (a snapshot of some questions below) are a common tool for assessing an individual’s eating habits over time. But the accuracy of results depends on how well participants can recall what they ate and how often. NIH Another difficulty is that these surveys often don’t account for variables that could be really important, like how the food was prepared and where it came from. Was the fish grilled? Fried? Slathered in butter? “Those things can matter,” says dementia researcher Nathaniel Chin of the University of Wisconsin–Madison. Plus there are the things researchers can’t control. For example, how does the food interact with an individual’s medications and microbiome? “We know all of those factors have an interplay,” Chin says. The few clinical trials looking at dementia and diet seem to measure different things, so it’s hard to make comparisons. In 2018, Radd-Vagenas and her colleagues looked at all the trials that had studied the impact of the Mediterranean diet on cognition. There were five at the time. “What struck me even then was how variable the interventions were,” she says. “Some of the studies didn’t even mention olive oil in their intervention. Now, how can you run a Mediterranean diet study and not mention olive oil?” Another tricky aspect is recruitment. The kind of people who sign up for clinical trials tend to be more educated, more motivated and have healthier lifestyles. That can make differences between the intervention group and the control group difficult to spot. And if the study shows an effect, whether it will apply to the broader, more diverse population comes into question. To sum up, these studies are difficult to design, difficult to conduct and often difficult to interpret. Kaeberlein studies aging, not dementia specifically, but he follows the research closely and acknowledges that the lack of clear answers can be frustrating. “I get the feeling of wanting to throw up your hands,” he says. But he points out that there may not be a single answer. Many diets can help people maintain a healthy weight and avoid diabetes, and thus reduce the risk of dementia. Beyond that obvious fact, he says, “it’s hard to get definitive answers.” A better way In July 2021, Yassine gathered with more than 30 other dementia and nutrition experts for a virtual symposium to discuss the myriad challenges and map out a path forward. The speakers noted several changes that might improve the research. One idea is to focus on populations at high risk. For example, one clinical trial is looking at the impact of low- and high-fat diets on short-term changes in the brain in people who carry the genetic variant APOE4, a risk factor for Alzheimer’s. One small study suggested that a high-fat Western diet actually improved cognition in some individuals. Researchers hope to get clarity on that surprising result. “I get the feeling of wanting to throw up your hands.” Matt Kaeberlein Another possible fix is redefining how researchers measure success. Hypertension and diabetes are both well-known risk factors for dementia. So rather than running a clinical trial that looks at whether a particular diet can affect dementia, researchers could look at the impact of diet on one of these risk factors. Plenty of studies have assessed the impact of diet on hypertension and diabetes, but Yassine knows of none launched with dementia prevention as the ultimate goal. Yassine envisions a study that recruits participants at risk of developing dementia because of genetics or cardiovascular disease and then looks at intermediate outcomes. “For example, a high-salt diet can be associated with hypertension, and hypertension can be associated with dementia,” he says. If the study shows that the diet lowers hypertension, “we achieved our aim.” Then the study could enter a legacy period during which researchers track these individuals for another decade to determine whether the intervention influences cognition and dementia. One way to amplify the signal in a clinical trial is to combine diet with other interventions likely to reduce the risk of dementia. The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability, or FINGER, trial, which began in 2009, did just that. Researchers enrolled more than 1,200 individuals ages 60 to 77 who were at an elevated risk of developing dementia and had average or slightly impaired performance on cognition tests. Half received nutritional guidance, worked out at a gym, engaged in online brain-training games and had routine visits with a nurse to talk about managing dementia risk factors like high blood pressure and diabetes. The other half received only general health advice. After two years, the control group had a 25 percent greater cognitive decline than the intervention group. It was the first trial, reported in the Lancet in 2015, to show that targeting multiple risk factors could slow the pace of cognitive decline. Now researchers are testing this approach in more than 30 countries. Christy Tangney, a nutrition researcher at Rush University in Chicago, is one of the investigators on the U.S. arm of the study, enrolling 2,000 people ages 60 to 79 who have at least one dementia risk factor. The study is called POINTER, or U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk. The COVID-19 pandemic has delayed the research — organizers had to pause the trial briefly — but Tangney expects to have results in the next few years. This kind of multi-intervention study makes sense, Chin says. “One of the reasons why things are so slow in our field is we’re trying to address a heterogeneous disease with one intervention at a time. And that’s just not going to work.” A trial that tests multiple interventions “allows for people to not be perfect,” he adds. Maybe they can’t follow the diet exactly, but they can stick to the workout program, which might have an effect on its own. The drawback in these kinds of studies, however, is that it’s impossible to tease out the contribution of each individual intervention. Embracing complexity To untangle the role of diet in dementia, researchers are designing trials that intervene earlier in life and last longer. Some studies combine multiple interventions, like diet, exercise and brain training, as well as measure a wider range of outcomes. Dementia and diet studies are due a makeover Then Now Target one risk factor at a time Target multiple risk factors and disease mechanisms simultaneously Enroll individuals with substantial cognitive impairment Enroll at-risk individuals who do not yet have symptoms of dementia Trials last 6–12 months Trials last 18–24 months Focus on cognitive and functional outcome measures Look at multiple outcome measures, including surrogate measures like biomarkers Source: R. Stephen et al/Frontiers in Neurology 2021 Preemptive guidelines Two major reports came out in recent years addressing dementia prevention. The first, from the World Health Organization in 2019, recommends a healthy, balanced diet for all adults, and notes that the Mediterranean diet may help people who have normal to mildly impaired cognition. The 2020 Lancet Commission report, however, does not include diet in its list of modifiable risk factors, at least not yet. “Nutrition and dietary components are challenging to research with controversies still raging around the role of many micronutrients and health outcomes in dementia,” the report notes. The authors point out that a Mediterranean or the similar Scandinavian diet might help prevent cognitive decline in people with intact cognition, but “how long the exposure has to be or during which ages is unclear.” Neither report recommends any supplements. Plenty of people are waiting for some kind of advice to follow. Improving how these studies are done might enable scientists to finally sort out what kinds of diets can help hold back the heartbreaking damage that comes with Alzheimer’s disease. For some people, that knowledge might be enough to create change. “One of the reasons why things are so slow in our field is we’re trying to address a heterogeneous disease with one intervention at a time. And that’s just not going to work.” Nathaniel Chin “Inevitably, if you’ve had Alzheimer’s in your family, you want to know, ‘What can I do today to potentially reduce my risk?’ ” says molecular biologist Heather Snyder, vice president of medical and scientific relations at the Alzheimer’s Association. But changing long-term dietary habits can be hard. The foods we eat aren’t just fuel; our diets represent culture and comfort and more. “Food means so much to us,” Chin says. “Even if you found the perfect diet,” he adds, “how do you get people to agree to and actually change their habits to follow that diet?” The MIND diet, for example, suggests people eat less than one serving of cheese a week. In Wisconsin, where Chin is based, that’s a nonstarter, he says. But it’s not just about changing individual behaviors. Radd-Vagenas and other researchers hope that if they can show the brain benefits of some of these diets in rigorous studies, policy changes might follow. For example, research shows that lifestyle changes can have a big impact on type 2 diabetes. As a result, many insurance providers now pay for coaching programs that help participants maintain healthy diet and exercise habits. “You need to establish policies. You need to change cities, change urban design. You need to do a lot of things to enable healthier choices to become easier choices,” Radd-Vagenas says. But that takes meatier data than exist now. Questions or comments on this article? E-mail us at feedback@sciencenews.org A version of this article appears in the July 2, 2022 issue of Science News. Citations S. Charisis et al. Diet inflammatory index and dementia incidence: A population-based study. Neurology. Vol. 97. December 2021. doi: 10.1212/WNL.0000000000012973. T. Ngandu et al. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. Lancet. Vol 385. June 2015. doi: 10.1016/S0140-6736(15)60461-5. S. Radd-Vagenas et al. Effect of the Mediterranean diet on cognition and brain morphology and function: a systematic review of randomized controlled trials. The American Journal of Clinical Nutrition, Vol. 107. March 2018. doi: 10.1093/ajcn/nqx070.
  4. Interesting article which investigates the synergy of exercise and sleep. To interpret with caution, since it's an epidemiological study. According to the association underlined in the study, we may theoretically counteract bad sleep problems with exercise. In cases like mine, where sleep is poor and fragmented, exercise according to this study would constitute at least in part sort of an antidote. undeniably, it also tends to improve sleep by building up adenosine. Sleep and physical activity in relation to all-cause, cardiovascular disease and cancer mortality risk
  5. Does exercise prevent major non-communicable disease and premature mortality? A critical review based on results from randomized controlled trials. Ballin M, Nordström P. J Intern Med. 2021 Jul 9. doi: 10.1111/joim.13353. Online ahead of print. PMID: 34242442 Review. Abstract Observational studies show that physical activity is strongly associated with reduced risk of premature mortality and major non-communicable diseases (NCDs). We reviewed to which extent these associations have been confirmed in randomized controlled trials (RCTs) for the outcomes of mortality, cardiovascular disease (CVD), type 2 diabetes (T2D), and fracture. The results show that exercise does not reduce all-cause mortality and incident CVD in older adults or in people with chronic conditions, based on RCTs comprising ∼50,000 participants. The results also indicate a lack of effect on cardiovascular mortality in people with chronic conditions, based on RCTs comprising ∼11,000 participants. Furthermore, there is inconsistent evidence regarding the effect of exercise on fractures in older adults, based on RCTs comprising ∼40,000 participants. Finally, based on RCTs comprising ∼17,000 participants, exercise reduces T2D incidence in people with prediabetes when combined with dietary modification, although evidence for the individual effect of exercise is lacking. Identified shortcomings of the current evidence include risks of publication bias, lack of high-quality studies in certain high-risk populations, and inconstant evidence with respect to some outcomes. Thus, additional large trials would be of value, especially with fracture as primary outcome. In conclusion, according to current RCT evidence, exercise can prevent T2D assuming it is combined with a dietary intervention. However, the evidence show that exercise does not prevent premature mortality or CVD, with inconsistent evidence for fractures. Keywords: Exercise; Health; Morbidity; Mortality; Physical activity.
  6. [This is a new thread to discuss the topic of "Extreme" amounts of exercise. The first 15 posts have been moved from the Blood Pressure thread where the discussion started - DP] Dean is that a misprint? 20 miles! And on top of 2 miles of running. I cannot help but quote Kenneth Cooper. I paraphrase: jogging more than 15 miles a week will not improve health.
  7. This new study [1] in JAMA found that walking 8000 steps per day was associated with a ~50% reduction in all-cause mortality relative to 4000 steps per day. Boosting steps to 12,000 per day appeared to be even better. It was associated with a 65% reduction in all-cause mortality. Linearly extrapolating to 45,000 steps per day (~20 miles - you were close Drew!) would equate to about a 168% reduction in all-cause mortality. 😉 Interestingly, walking intensity (i.e. steps per minute) didn't seem to matter much at all. -Dean ----------- [1] JAMA. 2020;323(12):1151–1160. doi:10.1001/jama.2020.1382 Association of Daily Step Count and Step Intensity With Mortality Among US Adults. Saint-Maurice PF, Troiano RP, Bassett DR, et al. Abstract Importance It is unclear whether the number of steps per day and the intensity of stepping are associated with lower mortality. Objective Describe the dose-response relationship between step count and intensity and mortality. Design, Setting, and Participants Representative sample of US adults aged at least 40 years in the National Health and Nutrition Examination Survey who wore an accelerometer for up to 7 days ( from 2003-2006). Mortality was ascertained through December 2015. Exposures Accelerometer-measured number of steps per day and 3 step intensity measures (extended bout cadence, peak 30-minute cadence, and peak 1-minute cadence [steps/min]). Accelerometer data were based on measurements obtained during a 7-day period at baseline. Main Outcomes and Measures The primary outcome was all-cause mortality. Secondary outcomes were cardiovascular disease (CVD) and cancer mortality. Hazard ratios (HRs), mortality rates, and 95% CIs were estimated using cubic splines and quartile classifications adjusting for age; sex; race/ethnicity; education; diet; smoking status; body mass index; self-reported health; mobility limitations; and diagnoses of diabetes, stroke, heart disease, heart failure, cancer, chronic bronchitis, and emphysema. Results A total of 4840 participants (mean age, 56.8 years; 2435 [54%] women; 1732 [36%] individuals with obesity) wore accelerometers for a mean of 5.7 days for a mean of 14.4 hours per day. The mean number of steps per day was 9124. There were 1165 deaths over a mean 10.1 years of follow-up, including 406 CVD and 283 cancer deaths. The unadjusted incidence density for all-cause mortality was 76.7 per 1000 person-years (419 deaths) for the 655 individuals who took less than 4000 steps per day; 21.4 per 1000 person-years (488 deaths) for the 1727 individuals who took 4000 to 7999 steps per day; 6.9 per 1000 person-years (176 deaths) for the 1539 individuals who took 8000 to 11 999 steps per day; and 4.8 per 1000 person-years (82 deaths) for the 919 individuals who took at least 12 000 steps per day. Compared with taking 4000 steps per day, taking 8000 steps per day was associated with significantly lower all-cause mortality (HR, 0.49 [95% CI, 0.44-0.55]), as was taking 12 000 steps per day (HR, 0.35 [95% CI, 0.28-0.45]). Unadjusted incidence density for all-cause mortality by peak 30 cadence was 32.9 per 1000 person-years (406 deaths) for the 1080 individuals who took 18.5 to 56.0 steps per minute; 12.6 per 1000 person-years (207 deaths) for the 1153 individuals who took 56.1 to 69.2 steps per minute; 6.8 per 1000 person-years (124 deaths) for the 1074 individuals who took 69.3 to 82.8 steps per minute; and 5.3 per 1000 person-years (108 deaths) for the 1037 individuals who took 82.9 to 149.5 steps per minute. Greater step intensity was not significantly associated with lower mortality after adjustment for total steps per day (eg, highest vs lowest quartile of peak 30 cadence: HR, 0.90 [95% CI, 0.65-1.27]; P value for trend = .34). Conclusions and Relevance Based on a representative sample of US adults, a greater number of daily steps was significantly associated with lower all-cause mortality. There was no significant association between step intensity and mortality after adjusting for total steps per day. Full Text
  8. Dear ALL, Today is my 80th birthday. I continue to be in excellent health. Several factors that I think are important for prolonged healthspan and (possibly) lifespan: I've been practicing CR since April, 1996 (so about 23 years). I do vigorous aerobic exercise for half an hour or longer six days a week at my gym (in my case, on the latest Precor elliptical cross trainer with hand motion, at the maximum resistance and a fast speed). I continue to be fully employed at the University of Rochester as a Professor of Mathematics (a position that I've held since 1974): I'm the oldest member of the Math Department. I teach two courses every term (both in the Fall and Spring -- I'm off for the Summers). I enjoy the teaching, and attending seminars and colloquia. Here is a recent health assessment from my Endocrinologist: (Note: The weight is incorrect -- weight was taken after I'd eaten a huge breakfast of 1 pound of raw Nappa cabbage, and 64 ounces of carefully brewed Chinese white tea -- that's always my breakfast): Wittlin, Steven D, MD at 5/7/2019 10:00 AM Status: Signed HPI: Saul Lubkin is a 79 y.o. male who presents for follow up of Osteoporosis. He now takes Forteo. . He denies any pain , fractures, muscle weakness or kidney stones. He continues on low calorie diet. Patient's medications, allergies, past medical, surgical, social and family histories were reviewed and updated as appropriate. ROS: CONSTITUTIONAL: Appetite good, no fevers, night sweats or weight loss HEENT: No double or blurry vision; denies severe headache CV: No chest pain, shortness of breath or peripheral edema RESPIRATORY: No cough, wheezing or dyspnea NEURO: No MS changes, no motor weakness, no sensory changes ENDO: No polyuria or polydipsia PE: BP 110/60 | Pulse 71 | Ht 1.55 m (5' 1.02") | Wt 61.2 kg (135 lb) | BMI 25.49 kg/m² GENERAL APPEARANCE: well developed, well nourished, no acute distress; aware and alert HEENT: PERLA, EOMI, no lid lag, pink conjunctiva ; no proptosis NECK: supple, no thyromegaly, no lymphadenopathy HEART: RRR, normal S1, S2 CHEST: lungs clear to auscultation bilaterally, no spinal tenderness EXTREMITIES: no clubbing, cyanosis, or edema. Pedal pulses 2+ bilaterally. Both feet clean without deformity, callous, ulceration, or fungal infection. NEUROLOGICAL: Alert and oriented x 3. Normal DTRs SKIN: Orange color. ASSESSMENT/PLAN: Forteo. Mr Lubkin will repeat his DXA . He continues to appear hypercarotenemic. Saul and I had a long discussion. As per usual he is on top of recent research in osteoporosis. He wants Forteo, acknowledging that we have no good data on its use for this long, that convention is that he should be using A bisphosphonate, and that he has had a very small decrease in BMD.. RTC one year with DXA
  9. An interesting article in University of Illinois Urbana-Champaign Health News It alleges to show that mice (and people) on the same diet, that exercise, have improvements in their gut microbiota, over sedentary mice (and people). Interestingly, the improvement that comes from exercise is much more pronounced in lean, vs obese, subjects. https://www.mdlinx.com/gastroenterology/top-medical-news/article/2017/12/06/7496068/?utm_source=in-house&utm_medium=message&utm_campaign=epick-gastro-dec07 Note: The article was brought to my attention by my wife, who is a Nurse Practitioner specialized in gastroenterology. (Unlike most of her colleagues, she tries to get her patients to improve their diet, with more fruits and vegetables. -- Saul
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