tripsis

Bring it, bitch!

I suppose I could always do this... + 1 @ Kind of painful on the eyes however. And then everyone will desperately want to neg the shit out of me if I keep doing the above all the time. And then they won't be able be able to! It'll be a vicious cycle of endless negless frustration!

But don't you wish you could neg my post? You do, don't you? C'mon admit it. It did cause disharmony, but it was only because it was childishly abused. Are we a community of adults or a bunch of immature prats? Edit: typo

Ohhhh, if only could neg you!! No, but really, the neg function would be nice to have back. And tipz, dude, stick around. It's good seeing you posting again. Just behave. Plenty of great plants and good conversations to be had on the right side of the law.

Go play with your rank vag business, incog ya cunt!

I love a good heated discussion or debate. Where's the fun in being so chill you blithely accept something that may completely contradict your world view? What do you learn from failing to engage in someone who has differing viewpoints to you? What's the problem with questioning your own views and beliefs? Fuck that. Bring on the heated discussion and debates, engage in other's viewpoints, question what you believe and what you think. Just keep it rational and don't let it degenerate into flaming, personal insults and name calling.

Shame that TBM crest is no longer cresting.

Phobias may be memories passed down in genes from ancestors December 3, 2013 - 12:01AM A fear of spiders may in fact be an inherited defence mechanism laid down in a families genes by an ancestors' frightening encounter with an arachnid. Photo: Kitty Hill Memories can be passed down to later generations through genetic switches that allow offspring to inherit the experience of their ancestors, according to new research that may explain how phobias can develop. Scientists have long assumed that memories and learned experiences built up during a lifetime must be passed on by teaching later generations or through personal experience. However, new research has shown that it is possible for some information to be inherited biologically through chemical changes that occur in DNA. Researchers at the Emory University School of Medicine, in Atlanta, found that mice can pass on learned information about traumatic or stressful experiences – in this case a fear of the smell of cherry blossom – to subsequent generations. The results may help to explain why people suffer from seemingly irrational phobias – it may be based on the inherited experiences of their ancestors. So a fear of spiders may in fact be an inherited defence mechanism laid down in a families genes by an ancestors' frightening encounter with an arachnid. Dr Brian Dias, from the department of psychiatry at Emory University, said: "We have begun to explore an underappreciated influence on adult behaviour – ancestral experience before conception. "From a translational perspective, our results allow us to appreciate how the experiences of a parent, before even conceiving offspring, markedly influence both structure and function in the nervous system of subsequent generations. "Such a phenomenon may contribute to the etiology and potential intergenerational transmission of risk for neuropsychiatric disorders such as phobias, anxiety and post-traumatic stress disorder." In the study, which is published in the journal of Nature Neuroscience, the researchers trained mice to fear the smell of cherry blossom using electric shocks before allowing them to breed. The offspring produced showed fearful responses to the odour of cherry blossom compared to a neutral odour, despite never having encountered them before. The following generation also showed the same behaviour. This effect continued even if the mice had been fathered through artificial insemination. The researchers found the brains of the trained mice and their offspring showed structural changes in areas used to detect the odour. The DNA of the animals also carried chemical changes, known as epigenetic methylation, on the gene responsible for detecting the odour. This suggests that experiences are somehow transferred from the brain into the genome, allowing them to be passed on to later generations. The researchers now hope to carry out further work to understand how the information comes to be stored on the DNA in the first place. They also want to explore whether similar effects can be seen in the genes of humans. Professor Marcus Pembrey, a paediatric geneticist at University College London, said the work provided "compelling evidence" for the biological transmission of memory. He added: "It addresses constitutional fearfulness that is highly relevant to phobias, anxiety and post-traumatic stress disorders, plus the controversial subject of transmission of the ‘memory’ of ancestral experience down the generations. "It is high time public health researchers took human transgenerational responses seriously. "I suspect we will not understand the rise in neuropsychiatric disorders or obesity, diabetes and metabolic disruptions generally without taking a multigenerational approach.” Professor Wolf Reik, head of epigenetics at the Babraham Institute in Cambridge, said, however, further work was needed before such results could be applied to humans. He said: "These types of results are encouraging as they suggest that transgenerational inheritance exists and is mediated by epigenetics, but more careful mechanistic study of animal models is needed before extrapolating such findings to humans.” It comes as another study in mice has shown that their ability to remember can be effected by the presence of immune system factors in their mother's milk. Dr Miklos Toth, from Cornell University in New York, found that chemokines carried in a mother's milk caused changes in the brains of their offspring, affecting their memory in later life. The Telegraph, London Source.

None taken, but do feel free to make a poll if it bothers you. A single thread would be pretty confusing when it come to comments.

Himalayan flowers shed light on climate change2 December 2013 The steep terrain in Nepal that acted as a natural filter for testing how flower might evolve differently in different climates. Flower colour in some parts of the world, including the Himalayas, has evolved to attract bees as pollinators, research has shown for the first time. In a study published in the Journal of Ecology, biologists from Monash University and RMIT University have investigated the evolution of flower colours due to the bee’s colour vision. They researched in the understudied Nepalese steep mountainous terrain, and other subtropical environments. The study also has implications for understanding the effects of climate change on plant pollination. Associate Professor Adrian Dyer of Monash and RMIT said previous studies had shown that flower colour evolved to attract bees as pollinators in temperate environments, but the story for either subtropical or steep mountainous environments had been unknown. “Mountainous environments provide an ideal natural experiment to understand the potential effects of changing climatic conditions on plant-pollinator interactions, since many pollinators show preferences for localised conditions, and major pollinators like honeybees do not tend to forage at high altitudes,” Associate Professor Dyer said. Dr Mani Shrestha from Monash University and his colleague Prakash Bhattrai from the Tribhuvan University, Kathmandu, collected spectral data from more than 100 flowering plants in Nepal over a range of altitudes, from 900 metres to over 4000 metres. Using computer models to examine flower colours as bees would see them, the team addressed how pollinator vision had shaped flower evolution. Then, with Associate Professor Martin Burd, of the School of Biological Sciences, they did phylogenetic analyses to identify how altitude zones affected results. Dr Shrestha said flowers from both subtropical (900-2000m) and alpine (3000-4100m) regions showed evidence of having evolved colour spectral signatures to enhance discrimination by bee pollinators. “The finding was a surprise as flies are thought to be the main pollinator in many mountain regions, but it appears that in the Himalayas several bee species are also active at high altitude, and these insects have been such effective pollinators that they have led to the evolution of distinctive bee-friendly colours,” Dr Shrestha said. The research could shed light on how flower colours may continue to evolve in particular environments, depending upon the availability of the most effective pollinators. While ‘bee colours’ were prevalent at all elevations, flower colours in high altitude zones were more diverse and had more often undergone larger steps of evolutionary change than those at lower elevation, Associate Professor Burd said. “Studying these patterns helps scientists understand how plant communities are assembled, and are potentially able to deal with changing conditions.” The work was assisted by a grant from the Australian Research Council.

The research is not conclusive, it merely indicates that there may be an inherited component to fears. There is nothing saying that such inherited "memories" would be passed down on the scale that you're talking about either, i.e. going back to where various human lineages evolved.

Start a poll, see what others think. Until then, I'll continue making this forum more interesting in the way I see fit.

I love heights, snakes and spiders. So what happened there? Guess my ancestors were a bunch of awesome, fearless types. ;)

You are all forgetting that by the very nature of being monstrose, growth in unpredictable. Nitrogen's hybrid mutants are a perfect example. One seedling can produce several different morphological forms. If that one seedling was then cut up and propagated, the resulting clones would resemble completely different plants from diverse genetic backgrounds, yet would all in fact still be clones. There is nothing saying that the TBM crest is not the same clone as one of the purely monstrose TBM forms. M S Smith has commented that he's noticed that the TBM crest often reverts to monstrose growth, but almost never does the reverse happen. The phenotypic range you see amongst either form doesn't imply that they originated from more than two clones; that is pure conjecture.

Fascinating, I did not know that. I'm curious how bacteria make their way into the gut of an unborn foetus. That is more than a little concerning for me personally. A little over two months ago, a podiatrist messed up a simple wedge resection and as a result, I now have a bone infection. I was on oral antibiotics for two weeks before being put on IV antibiotics for 3 weeks. I've now been on double dose oral antibiotics for over a month, with close to another month to go before finishing the course. Suffice to say, my microbiome is taking an absolute hammering. I seriously hope this does not lead to any further complications. I hope for your sake you don't have to go down the path of a faecal transplant.

Outside Magazine, March 2013 Tuesday, March 5, 2013 Your Fat Has a Brain. Seriously. And It's Trying to Kill You. Body fat is just an inert layer of blubber, right? If only. New research shows that it's more like a toxic parasite that doesn't want to let go. The good news: if you exercise and eat right, you can force it to. By: Bill Gifford Photo: Joe Baran Phil Bruno was super-sizing again. It was just past 5:30 on a spring evening in 2004, and he was driving home from work. He pulled into a White Castle, one of many fast-food outlets lining Route 100 in his hometown of Manchester, Missouri, a suburb of St. Louis. He was only a mile from his house, where his wife, Susan, was cooking the usual big Italian dinner for their family of five, but he was hungry now. The urge was automatic. Ten minutes later, with a bag of burgers steaming on the seat beside him, he pulled into a McDonald’s and ordered a Double Quarter Pounder with Cheese, an apple pie, and a chocolate shake to wash it all down. “I did this because I would be embarrassed to order too much from one drive-through,” Phil explained to me. “I didn’t want the person at the window to look at me funny.” Phil had always loved food, which was part of the fabric of his tight-knit Sicilian-American family: Grandma and her lasagna were right down the street. But he’d been athletic in his youth, playing high school football and carrying a robust but reasonable 215 pounds on a six-foot-three-inch frame. Then, in his mid-twenties, he’d stopped working out, as many of us do when life starts to chew up our time. Over the years, his regular meals and high-calorie bingeing had turned him into a physical and emotional wreck. His joints ached whenever he used the stairs, his heart hammered, and he was possessed by a strange, burning thirst that no amount of ice water could quench. “I was 47 years old,” he says, “but I felt like I was 80.” Prodded by a friend, Bruno finally went to see his long-time family physician, Don Livingston, in early 2004. The results were harrowing: his blood pressure was at a firehose-like 230 over 150, his blood sugar was off the charts, and his A1C—an important blood marker for diabetes—was 16. (It should have been under six.) He weighed a scale-crushing 470 pounds. Phil had developed Type 2 diabetes, but that was just one of his problems. He walked out of the doctor’s office with prescriptions for 12 different medications and supplements, from fish oil to blood-pressure medicine to Lipitor for his cholesterol to Glucophage for his diabetes. And he never forgot Dr. Livingston’s ominous words at the end of the visit. “Bruno,” he had said, “you should be dropping dead any second.” Everyone knows that being fat is bad for you, but most people can’t explain exactly why. Some reasons are obvious. Fat tends to go hand in hand with diabetes, and more weight means increased stress on joints and the heart. More puzzling to researchers is that excess fat seems to be linked with cancer of the kidneys, colon, and liver, and even to cognitive decline. Until fairly recently, fat was thought to be inert, evolution’s wobbly way of letting humans store energy for lean times. And we’ve long known that it’s better to be slightly overweight than underweight, as a recent study in the Journal of the American Medical Association reiterates. Starting in the 1990s, though, scientists began to realize that fat is best understood as a single huge endocrine gland, one that wields powerful influence over the rest of the body. “For a typical North American, their fat tissue is their biggest organ,” says James Kirkland, M.D., director of the Robert and Arlene Kogod Center on Aging at the Mayo Clinic. Not everything about fat is bad, of course. Fat tissue under the skin, known as subcutaneous fat—the kind that makes young people look succulent and ripe—is essentially padding that protects the body from injury, and it also helps fight infection and heal wounds. “Sub-q” fat produces an important hormone called adiponectin, which appears to help control metabolism and protect against certain cancers, notably breast cancer. The bad news is that, as we age, we gradually lose this good fat, which is one reason why our hands get bonier. Instead, men and women alike tend to build up blobby fat on our midsections. Over the past decade or so, Kirkland and other scientists have discovered that this so-called visceral fat infiltrates our vital organs, bathing them in a nasty chemical stew that wreaks havoc in the body. Visceral fat produces an array of cell-signaling proteins called cytokines, including interleukin-6 (IL-6), which causes chronic inflammation, and TNF-alpha, for tumor necrosis factor, which has been linked to cancer. Kirkland and other researchers have come to believe that, in addition to the problems associated with diabetes and heart disease, fat may actually help accelerate the aging process. In a 2008 experiment, scientists at the Albert Einstein College of Medicine at Yeshiva University surgically removed abdominal fat from obese lab rats and found that the rodents lived significantly longer than their chubby cousins. In a more recent study, not yet published, the Einstein team found that surgical fat removal prevented some colorectal cancers in mice that were genetically predisposed to those tumors. Unfortunately for Phil Bruno, surgery wasn’t an option: liposuction only removes the good subcutaneous fat, which is why several recent studies have associated the procedure with negative health outcomes. In humans, says Einstein researcher Nir Barzilai, visceral fat can’t be removed safely because it’s so deeply intertwined with blood vessels and organs. So Bruno called on the only thing in his body that was powerful enough to fight it off: muscle. ON JUNE 6, 2004, roughly a month after his grim diagnosis, Bruno did the one thing his doctor hadn’t prescribed: he went to a gym. Dr. Livingston had suggested he lose weight, but he stopped short of recommending exercise. That’s typical. One study found that less than half of U.S. physicians discuss exercise with their patients. After getting his heart checked out via a stress test—it was enlarged, but his arteries were clean, thanks to Grandma’s olive oil—Phil walked into his local Gold’s Gym on a Sunday morning. He looked around uncertainly before settling on the one piece of equipment that seemed feasible for a 470-pound man: the exercise bike. He got himself aboard and managed to pedal for five minutes before he had to stop, wheezing and panting and feeling self-conscious. Yet he came back the next day and the next. Soon he could manage 30 minutes on the bike, leaving a bigger sweat puddle on the floor each time. He saw every drop as a blob of fat exiting his body, one tiny step toward his goal. In those early weeks at the gym, Bruno would often walk past a glass-walled indoor-cycling studio. With its atmosphere of pounding music and lithe bodies pumping away on stationary bikes, the room seemed off-limits to someone like him. It took Bruno another week or two to work up the courage to go in for a class, and he instinctively skulked to a bike in the back corner. The instructor, a fit blonde, came over and greeted him. “I’m Beth,” she said, smiling. “Let’s help you get set up.” Beth Sanborn was a local triathlete who was training for her second Ironman. She helped keep Bruno motivated as he suffered through the 45-minute class, puffing and churning away. He soon became a regular, showing up six times a week. He got to know everyone, and his relentlessly upbeat personality made him a favorite of the instructors. “I had never seen anybody that big,” Sanborn recalls. “He was the hardest-working person in my class. A man on a mission—he really was.” Bruno often rode until his shorts were bloody, because they don’t make bike shorts (or seats) that fit people who weigh more than 400 pounds. “It wasn’t pretty,” he says. By September, he decided to take on an even bigger challenge: he would try a 100-mile bike ride, a century to combat MS, which his wife Susan had been diagnosed with a few years previously. He hadn’t been on a real bike in 20 years, but he dragged his old Trek out of the basement, dusted it off, and took it to the shop. He made it all the way to mile 63, stopping on a slight incline when the road seemed like it was starting to wobble and melt. He felt pains in his chest, and, ominously, he had stopped sweating, a possible sign of heatstroke. The sag wagon pulled up and the event staff rushed to his aid, grabbing his arms to keep him from collapsing. “The thought actually went through my mind that if I die here on the road,” Bruno told me, “at least I’m doing something to change my life.” WITHOUT KNOWING IT, PHIL had kicked off a war for control of his body, with fat on one side and muscle on the other. Just as fat was long thought to be neutral, muscle was considered a passive organ that did what the brain told it to do. But muscle is now known to be one of the most dynamic systems in the body; when it contracts, it undergoes huge changes at the cellular level. And its mortal enemy is fat. In any sedentary, inactive person—including people who aren’t actually obese—fat invades the muscles, slipping in between muscle fibers like the marbling in Wagyu beef. Worse, fat infiltrates individual muscle cells in the form of lipid droplets that make the cells sluggish. According to Gerald Shulman, M.D., a prominent diabetes researcher at Yale, these pools of fat, which occur in both the liver and the muscles, block a key step in the conversion of glucose, leading to the insulin resistance that’s a prerequisite for diabetes. This explains why some sedentary people of normal weight are still at risk for the disease. “It’s not how much fat we have but how it’s distributed,” Shulman says. “When the fat builds up where it doesn’t belong, in the muscle and liver cells, that’s what leads to Type 2 diabetes.” On a strictly mechanical level, more fat means less muscle, which means fewer mitochondria, the cellular power plants that are most plentiful in muscle tissue. The majority of fat contains almost no mitochondria. This explains one of the nagging problems with obesity: the more fat you accumulate, the harder it becomes for your body to burn off that stored energy. With his intense cycling, Bruno was growing new muscle, obviously, and that helped. “The more muscle you have, the more mitochondria you have, so you can burn more fat,” says Iñigo San Millán, an exercise physiologist at the University of Colorado in Denver, who has worked with elite cyclists for two decades. San Millán notes that slow-twitch muscle fibers, the most prominent muscle type in endurance athletes, are far more mitochondria-dense than any other kind. So they’re much more efficient at burning fat. Second, Bruno’s new muscle tissue was actually changing his body chemistry in ways that science is just beginning to understand. For decades, researchers suspected that muscle exerted some kind of influence on other organs, starting with the liver, which acts as the body’s fuel depot. When we work out intensely or for long periods, the liver is prompted to send out more glucose, the primary fuel for physical activity. It was long thought that those signals traveled via the nervous system and brain, but experiments in the '90s on patients with spinal paralysis revealed that there had to be some other pathway, because their livers still responded to muscle stimulation, as did their brains. They even experienced runner’s high. In 2003, biologists Mark Febbraio, from Australia, and Bente Pedersen, of Denmark, figured out that muscle is an endocrine organ, just like fat, and that exercising muscle produces chemical secretions—which they called myokines—that communicate with the rest of the body. As Pedersen puts it: “Skeletal muscle is the organ that counteracts fat.” Febbraio and Pedersen identified the most common myokine as none other than IL-6, the inflammatory cytokine that’s also produced by excess fat. But when released during exercise, they found, IL-6 actually had beneficial effects, telling the liver to increase the rate of fat oxidation. “When we made this discovery, people really didn’t believe us, because IL-6 was considered a bad actor in many diseases,” says Febbraio, a former professional triathlete. “But the thing is, in exercise it’s actually anti-inflammatory.” The difference had to do with time. Obese patients tended to have low but constant levels of IL-6, which caused chronic inflammation. When patients exercised, their IL-6 levels would spike, then dissipate over a few hours. The patients who exercised had much lower baseline levels of inflammation. Since then, dozens of these myokines have been identified. Febbraio believes there could be hundreds more and that they’re largely responsible for the beneficial effects of exercise. They act on bones, the pancreas (which secretes insulin), and the immune system. Researchers think they may also act on muscle itself, promoting growth and healing, and on the brain, triggering the release of derived neurotrophic factor, which heals and protects neurons. “There’s a growing body of evidence suggesting that healthy muscle may lead to a healthier liver, a healthier gut, a healthier pancreas, and a healthier brain,” says Nathan LeBrasseur, a Mayo Clinic scientist who specializes in muscle tissue. New research from Canada indicates one way this might work. Mark Tarnopolsky, a scientist at McMaster University in Hamilton, Ontario, has identified six muscle-specific compounds that drive mitochondrial growth in every type of human tissue. One newly discovered myokine even tries to convert fat itself into an energy-consuming system like muscle. In 2012, a Harvard-based team identified a hormone called irisin, secreted during exercise, that tricks plain, blobby, “white” fat—and even deep visceral fat—into acting like “brown” fat, a far less common form that is dense with mitochondria and burns energy just like muscle does. Bruce Spiegelman, the Harvard scientist who led the team that discovered irisin, is now looking for a drug compound that might trigger its release. But Febbraio cautions that exercise in a pill is not in the cards. “It’ll never happen, because the benefits of exercise are a multifactor thing,” he says. “You could never design a drug that would replace exercise.” Just ask Bruno. For him, exercise wound up replacing the drugs. FAT IS STUBBORN, DEMANDING stuff. Much of the time it’s telling you to eat more, which is one reason why most attempts at dieting are doomed to fail. Our fat wants to keep us fat, and most of us lack the impressive willpower of the legendary Scotsman who somehow managed to stop eating solid food for more than a year. Known to science only as A.B., this person was 27 years old and weighed 450 pounds when he turned up at a hospital at the University of Dundee in the mid-1960s. With the encouragement of researchers, A.B. began subsisting on nothing but vitamins and brewer’s yeast, and researchers measured his progress regularly. The weight came off, but slowly: he lost less than a pound a day. In the end, he managed to slim down to 180 pounds, but it took him 382 days. João Correia, a 38-year-old publishing executive from New York City who went through a less extreme version of Bruno’s and A.B.’s drastic slim-downs, says that the process transformed not only his body but his mind. “I had a totally different relationship with food when I was fat,” he says. A pro cyclist in his youth, Correia quit riding in his twenties, moved up the ladder of Manhattan publishing, and ate too many expense-account dinners. By age 30, he’d packed 205 pounds onto his five-eight frame, and he was still always hungry. “My ability to consume food at that weight was huge,” he recalls. “I used to be able to go to a restaurant and have six courses and a bottle or two of wine.” The reason was a hormone called leptin, which is produced by fat tissue. Ordinarily, leptin tells the brain, “Dude, we’re fat. It’s time to stop eating.” But the brains of obese people often become deaf to leptin, so they don’t get the message. When Correia started working for a fitness-oriented publisher, he realized he had to do something, so he got back on the bike, doing laps in Central Park before and after work. He cut back on eating, which wasn’t easy at first. Unexpectedly, as Correia’s waistline shrank, so did his appetite. You’d think that, as the fat melted off, his leptin levels would decline, making him hungrier. But research has shown that exercise actually helps restore sensitivity to leptin. So his body knew when it was time to stop eating. “I wasn’t ever hungry,” he says. Within three years, he’d lost so much weight—and gotten so fast on the bike—that he actually turned pro again, riding first in the U.S. for the Bissell team, then in Europe for the high-level (but short-lived) Cervélo Test Team. Things weren’t quite as easy in Bruno’s case. For one thing, unlike Correia, he’d never been an elite athlete. And while Correia’s body mass index peaked at 31, just above the threshold for obesity, Phil’s BMI had been 58. His immense size meant that he may have been unusually insensitive to leptin and other signals of satiety. Going on a conventional diet was out of the question for him; he’d tried that before. This time around, he proved himself to be every bit the equal of A.B., though his strategy was different. Rather than starve himself, he started by simply cutting out fried food, fast food, and soda. Instead, he and Susan would cook grilled chicken or fish for dinner with some greens; they snacked on fresh fruit and unsalted almonds rather than potato chips. He also (mostly) said goodbye to lasagna. “The first 50 pounds melted off,” he says. “But when you’re eating three Quarter Pounders with Cheese at a time, any change is an improvement.” Bruno’s initial goal was just to be able to use his home scale. (At first, he was still so big that he had to go to the grocery store to weigh himself, on the same scales used to weigh food pallets.) But he also loved food, and he would still eat an extra chicken breast at dinner if he felt like it. Better that than a Quarter Pounder. He drew inspiration from motivational figures ranging from Jesus Christ to football coach Tony Dungy. As he kept exercising, Bruno found that he not only lost weight but also felt less hungry. His burning thirst was gone, too, and his long-suffering knees and hips felt better. He threw himself into his spin classes. “We saw quite a remarkable change,” says Jim Wessely, a spin-class friend who is head of emergency medicine at St. Luke’s Hospital in St. Louis. “When he first came in, he was this huge, morbidly obese guy who could barely spin for more than a few minutes. Now he would really go at it.” A year after Bruno was diagnosed with Type 2 diabetes, he went back to Dr. Livingston for tests. The doctor was astonished: Bruno’s insulin resistance was gone, and his blood values were almost back to normal. His A1C, which had been 16, was now down to 5.5. Livingston had never seen anyone do that. Bruno no longer needed his medications. Yet Bruno knew he was far from fixed. Because of his individual metabolism, he’d been primed for weight gain his entire life. He had to fight a constant, escalating battle against his morphological fate. He remained dedicated to him regimen, going to spin class five or six days a week; eventually, he got certified, and he soon became one of the most popular instructors at that branch of Gold’s Gym. Relentlessly positive and a born organizer, he led a regular outdoor group ride on Sundays, and he captained the Golden Flyers, a 100-strong fundraising team for charity rides like the Tour de Cure (for diabetes) and the MS 150. Fitness consumed him. “I’m a financial adviser with Wells Fargo,” he says, “but most people think I’m a spinning instructor with Gold’s Gym.” In four years, he had lost more than 200 pounds, whittling his body down below 260. He was still big, and he still wasn’t satisfied: he wanted to lose that last 50, to get down to where he’d been in high school. He kept moving, kept riding, knowing he could never stop. “It’s kind of like holding a beach ball under the water,” he told me last winter. “As long as you keep doing what you’re doing, it’s easy. As soon as you quit, then boom—it’ll pop right up.” AND THEN, LAST SUMMER, he had to stop. He was walking out to his car after work one day in July when his legs suddenly gave out. He couldn’t stand; they were pretty much paralyzed. He managed to crawl over to a nearby car and haul himself up onto the bumper. With the help of two friendly strangers, he hobbled over to his car and got in. He had just enough sensation in his right leg that he could drive himself home. Bruno went to the hospital that night, and doctors were mystified. He had a spinal tap, and an MRI, that revealed pinched nerves from inflammation at the base of his spinal cord. The cause was not clear. The doctor gave him steroids for the inflammation but warned that it could be a sign of something much more serious, possibly even fatal. The inflammation subsided, luckily, but it left Bruno unable to work out, much less teach his spin classes. He skipped the MS ride in September for the first time since 2004. Inevitably, his weight started creeping back up again. By the end of the summer, he’d gained back 60 pounds. And some of the diabetes symptoms had returned. “My legs feel like they’re filled with sand at times, the extreme thirst and hunger is back, it’s hard to breathe, I have weakness and back pain,” he told me in November. “The intense exercise I had been doing has helped me through this fight so far, but I can feel it fading as more time goes by. I’m frightened, depressed, and just not doing well at all.” Then he had another setback, and he wound up spending six days in the hospital with heart issues—atrial fibrillation, related to the enlarged heart he’d acquired from all those years when he was heavy. Ironically, a-fib is also known to be a side effect of long-term, intense exercise, particularly in middle-aged (or older) men. The last time we spoke, in December, Bruno had been placed on more medication, to thin his blood and prevent clotting, and on beta-blockers, to try and regularize his heartbeat. Still, he was determined to make it through his spin class that Saturday, and he surprised himself by riding hard for an hour and 10 minutes. “Everyone welcomed me back with open arms,” he says. “It was awesome.” It’s been nearly nine years since Phil Bruno shambled into Beth Sanborn’s spin class. “I love telling people the Phil story,” she says. “Just imagine how he must have felt walking into the gym, not even a spin class. I know people who are only 50 pounds overweight, and they think they have to lose weight before setting foot in the gym.” Since that time, Bruno has lost nearly 250 pounds, and while he’s gained some of it back, he insists that all that cycling has continued to help him, continued to protect him, even as he has backslid a little. Could his health problems be a kind of delayed-reaction result of having been so overweight for so long? That’s not how he chooses to see it. He thinks it would have been worse if he hadn’t walked into Gold’s that day. As he put it recently: “The bright spot in all this craziness is that my working out over the years has saved my life.” Scientist Bente Pedersen, who helped discover the existence of myokines, would agree. She argues that the most dangerous issue that Bruno and people like him face is not being heavy per se but being sedentary. In papers she defines a “diseasome” of inactivity, a collection of nasty health consequences stemming from lack of exercise—independent of an individual’s body weight. “It’s much better to be fit and fat,” she says, “than skinny and lazy.” Bill Gifford wrote about the Lance Armstrong Foundation in February 2012

Yes, I'm thinking of sclerophyll areas. The only native vegetation that was left in the worst areas were established trees, though some small saplings battle to make it through the lantana to light.

Impacts of plant invasions become less robust over time Nov 20, 2013 by Julie Cohen This photo shows the African invader Melinis minutiflora in Hawaii Volcanoes National Park when first studied (left) and 20 years later. Credit: UCSB Among the most impressive ecological findings of the past 25 years is the ability of invasive plants to radically change ecosystem function. Yet few if any studies have examined whether ecosystem impacts of invasions persist over time, and what that means for plant communities and ecosystem restoration. UC Santa Barbara's Carla D'Antonio, Schuyler Professor of Environmental Studies, has conducted one of the only long-term studies of plant invader impacts that spans two decades. Returning to the same grass-invaded field sites in Hawaii Volcanoes National Park that she used in her 1990-1995 studies, D'Antonio, along with postdoctoral scholar Stephanie Yelenik, gathered new data that shed light on mechanisms regulating exotic plant dominance and community change through invasion. The findings are published online today in Nature. "We were able to take advantage of detailed studies I and others had conducted in the 1990s. We permanently marked sites we had set up and were able to go back and gain insight into how plant invasions changed over time without management," said D'Antonio, who also is a professor in the Department of Ecology, Evolution and Marine Biology. "Such studies are important because managers have little money to control invasive species or to study how impacts might change without management." "Non-native plants can have very large impacts on ecosystem functioning—including altering groundwater, soil salinity or pH and pollination syndromes," said lead author Yelenik, who earned her doctorate from UCSB's Department of Ecology, Evolution and Marine Biology and now works for the U.S. Geological Survey's Pacific Island Ecosystems Research Center on the island of Hawaii. When D'Antonio and Yelenik revisited the study sites, they noticed that the invasive exotic perennial grasses (primarily an African invader called Melinis minutiflora) were dying, so they decided to repeat measures of nutrient cycling and plant community change. They found that the grasses' self-reinforcing effects on soil nutrients had disappeared and the percentage of invader coverage had declined. Data showed that in the past 17 years, nitrogen mineralization rates at the sites dominated by the exotic grasses declined by half, returning them to pre-invasion levels. Nitrogen mineralization is the process by which organic nitrogen is converted to plant-available inorganic forms. "Measuring mineralization the way we do is extremely time-consuming and expensive, so we did it in snapshots of time (mid-1990s versus 2010-2012)," Yelenik explained. "This is less than ideal because differences between the two study periods could be due to differences in rainfall." To eliminate rainfall as a factor, the researchers examined long-term rainfall data for the region to determine if a relationship exists between nitrogen mineralization and rainfall during the study years. The data showed that rainfall during the two study periods was similar. In addition, rainfall did not correlate with differences in mineralization between time points. A mineralization assay in the lab, where moisture was kept constant, showed similar patterns to the researchers' most recent field data, gathered in 2011 and 2012. Taken together, these results suggest that nitrogen mineralization variations between the 1990s and recent years were not due to differences in rainfall. While the study demonstrates that ecosystem impacts and feedbacks shift over time, it also indicates that this may not necessarily help native species' recovery. Yelenik and D'Antonio conducted a large outplanting experiment to test how a suite of native and exotic woody species responded to shifting ecosystem impacts. They added nitrogen fertilizer to mimic earlier stages of Melinis invasion and reduced Melinis competition to mimic patches during late invasion. Similar responses occurred in five of the seven outplanted species: Growth rates and survivorship increased due to reduced competition from the exotic grasses as well as nitrogen additions. This indicates that the changing impacts of the grass over time do not alter the seedlings' ability to grow in the ecosystem. Two nitrogen-fixing trees were exceptions: the native Hawaiian tree Acacia koa and the exotic tree Morella faya (from the Canary Islands but invading Hawaii today). These species did much better in later Melinis invasion conditions, and Morella faya did particularly well. "The non-native Morella faya did a lot better for various reasons, but primarily because it has a faster growth rate," Yelenik said. "Plus in our sites it is bird-dispersed, which means it gets around and is, in fact, moving into the sites at a frightening rate. By contrast, the native Acacia did reasonably well in the experiment, but it just does not have as robust a growth rate as Morella. It is a very slow disperser and sparse in the region so we are not seeing it entering the sites on its own." An important lesson here is that even if plant invasions can slow down on their own given enough time, native species may need further assistance in order to make a comeback, the researchers said. Other invaders may be poised to take advantage of reduced competition from the original invader. "Knowing the mechanisms of how and why invasions alter ecosystems is insightful for predicting what will happen, but without further management we may not get native species back," Yelenik said. "When we see non-native species dying back and getting patchy, that may be the time to plant native species. It might turn out to be the most cost-effective way to get an ecosystem back to a more desirable state."

Nice to see you've got a crest out of some of those seedlings interbeing.

I would wait until they're a little older. Being crowded won't kill them, just slow them down. Transplanting now is far riskier.

You weren't half kidding when you said those seedlings were crowded, hostilis!

One day, when I have space, I will get into aquaponics

Good point.

That is awesome! Great work Stillman.