May 25, 2014
February 10, 2017
This is what it is (happened to me at 7 pm on 11 February 2017). It takes a minimum of eight weeks for a mallet finger to heal with splinting. WILL CHECK ON 11 APRIL 2017. At the end of this time the splint is worn for one to two weeks at night and whenever the finger might be at risk of injury. There may be slight loss of full straightening at the completion of treatment, and it may take several months to regain satisfactory function. Redness, swelling and tenderness of the skin on top of the end joint are common for three or four months after injury, but usually settle eventually.
Went to doc > emergency in Austin hostpital > x-ray and splint:
The fingertip should be held straight for 8-10weeks to allow the tendon to heal. This is followed by a period of night splinting and the use of Coban bandage during the day for 2 weeks.
Note – the finger must be kept dry.
The splint should be comfortable. If the finger is painful then the splint can be carefully removed and the back of the finger massaged with an alcohol swab to prevent ulcer formation. During this time the finger must be supported straight at all times. If the finger drops for even one second the treatment can fail. The splint is best reapplied with the assistance of another person.
After the splintage period the finger should be gently exercised. It is best to regain full bend of the finger over a period of 6-8 weeks rather than force the movement and end up rupturing the tendon again.
HOW TO WASH HAND WHILE SPLINTED AND ALSO CUT THE NAILS
ISSUES WITH STANDARD TREATMENT
December 28, 2016
Continuing from my post here.
This article: Survival of the fattest: Why we’re wrong about obesity
- 05 May 2014 by Samantha Murphy
Weight tells you far less about a person’s health than you might think (Image: Richard I’Anson/Getty) Can you be fat and fit? Everything we think we know about obesity may be wrong – sometimes it be could actually be good for you
In 2002, cardiologist Carl Lavie began to see a confusing trend. The people he was treating for heart failure were living longer if they were obese or overweight than if they were thin. How could that be right? Obesity is notoriously bad for your heart and every other part of your body.
In the US, obesity is one of the biggest causes of preventable deaths after smoking. Worldwide, it has been linked to chronic diseases like hypertension, stroke, heart disease and type-2 diabetes. Even so, the world keeps getting fatter, a trend that may mean we will all be obese by mid-century, propelling those of us in the West ever closer to the first drop in our life expectancy since 1800.
But how much of this is true? Lavie wasn’t the only one to notice some troubling inconsistencies in the seemingly simple story. Under fresh scrutiny, conventional wisdom about the obesity epidemic is beginning to unravel, prompting some medical professionals to call for changes to everything from public policy to healthcare training.
It is small wonder we have become so obsessed with our weight. Between 1980 and 2008, body mass index (BMI) – a measure of obesity that divides weight by height squared – rose all over the world. Obesity rates nearly doubled, rising most strikingly in the US. It wasn’t hard to see where it was all heading. In the title of a widely cited paper investigating the progression and cost of the US obesity epidemic, the authors asked: “will all Americans become overweight or obese?” Yes, they concluded: by about 2050.
So it came as a surprise when, in the early 2000s, epidemiologist Katherine Flegal began to see evidence that obesity rates had stopped rising. In study after study, Flegal, who works at the Centers for Disease Control (CDC) in Hyattsville, Maryland, found that instead of continuing relentlessly upwards, obesity rates had levelled off.
Not everyone was convinced, but this was no flash in the pan. Flegal and her team continued to replicate their research and, in a study released in 2012, they announced that the prevalence of obesity in the US has failed to increase in any significant way since at least 2008 (JAMA, vol 307, p 491). It appears to have flatlined around the 34 per cent mark in both adults and adolescents (see “Obesity plateau”). And this “obesity plateau” is not limited to the US: similar trends and even declines have been described in other developed countries over the past 10 to 15 years.
Because the research is still in the early stages, no one is sure what is causing the obesity plateau. But some competing theories are emerging. Researchers at the University of Jena in Germany point to small studies showing the success of better food and exercise programmes. Whatever the reason, the idea that obesity rates will rise unchecked seems to be in need of revision.
Where does that leave the 34 per cent of people still considered obese? In 2004, the CDC warned that obesity could soon be second only to smoking as a cause of preventable deaths. Of course, it won’t be the extra pounds that kill you. What supposedly shortens your life is the link between obesity and the development of a host of diseases including type 2 diabetes, heart disease, cancer and rheumatoid arthritis.
Over the past 10 years, however, some of these links have been called into question as well. The most surprising of them is the one that always seemed the most intuitive: the relationship between obesity and heart disease. “Over a decade ago, I would have thought my heavy patient who just had a heart attack would have been worse off than my thin patient who just had a heart attack,” says Lavie, who is a cardiologist at the Ochsner Medical Center in New Orleans, Louisiana. “But it’s exactly the opposite.” Heart disease patients classified as lean had almost double the mortality rate of those ranked overweight and even obese.
Startled by his own anecdotal findings, Lavie began to dig into the literature. He found numerous large-scale studies that backed up his observations: some overweight patients with cardiovascular disease have better outcomes than their thinner counterparts. One of the largest, a 2012 study of 64,000 Swedish people with heart disease, found that obese or overweight participants had a reduced risk of dying compared with those of normal weight (European Heart Journal, vol 34, p 345). Underweight patients, meanwhile, upped their risk of death by a factor of three. In the paper, the authors went so far as to suggest that prescribing weight loss after diagnosis of heart disease might be a bad idea.
Heart conditions were far from being the only ailments where extra padding seemed to be an advantage. Equally surprising was the clear link between obesity and the fate of people with type 2 diabetes. Among others, a Northwestern University study of 2625 people recently diagnosed with type 2 diabetes found that normal-weight people were almost twice as likely to die over the period of the study as their overweight and even obese counterparts.
Next came rheumatoid arthritis and kidney disease. Over and over, the same pattern cropped up: people diagnosed with many medical killers fared better in the long run if they were overweight or even mildly obese than if their weight was normal. “Yes, this even remains true when researchers rule out weight loss attributable to other pre-existing illnesses such as cancer,” says Lavie. To be clear: becoming overweight is not a fitness goal – a sedentary lifestyle, poor diet and a BMI of 40 will not lead you to health. However, once you are overweight, it seems, being healthy is not synonymous with shedding pounds. Fatter people are more likely to survive many diseases. The phenomenon has been observed so often that it has earned the name “the obesity paradox”.
But how can flab be good for you in any way? One tentative theory doing the rounds is that body fat contains anti-inflammatory compounds and extra energy that can bolster the body’s defences against the ravages of disease. More specific experiments have pointed to the hormone leptin, which is stored in fat, suggesting that some extra fat may have protective effects for people with heart failure (Circulation Heart Failure, vol 2, p 676). People with more fat have access to these “extra reserves” stored within. In any case, the conflicting studies meant that, in 2005, even the CDC backed away from its earlier contention that obesity could be the leading cause of death after tobacco.
But last year, the plot thickened still further: could being overweight be healthier not just for sick people – but for all of us? In a meta-analysis that investigated the relationship between BMI and health in 2.88 million people, a CDC team led by Flegal – who had introduced the obesity plateau – showed that the relationship between health and weight was U-shaped rather than linear (see “Fat and fit”). That’s to say, being overweight or even mildly obese was associated with a lower risk of dying – from any cause – than being either underweight or extremely obese.
Flegal’s research started a firestorm of controversy. In a study of people with diabetes published last January, Deirdre Tobias of Harvard University found no similar benefits. When Tobias redid her analysis, focusing as Flegal had on death by any cause instead of diabetes, she found Flegal’s U-shaped curve. However, Tobias says taking out smokers changed the shape of the curve to a J. “There is no advantage for being overweight or obese,” she says, but her new curve does not clearly demonstrate the linear relationship between weight and health implied by BMI. Tobias’ group thinks the obesity paradox can be entirely chalked up to poor research methods. But can so many studies be so wrong? Or are the obesity plateau and the obesity paradox signs that it is time to abandon a metric whose inaccuracy verges on scandal?
The BMI system has been incorrectly used from the start (see “Why BMI?“). Its oft-cited flaws are almost too numerous to count.
First, whether applied to individuals or populations, BMI is a consistently unreliable indicator of actual fat. It fails to account for where fat is located on the body – according to several analyses, it is abdominal obesity, not total body fat, that truly predicts whether a person will develop cardiovascular problems or cancer. It also famously fails to distinguish between fat and muscle.
This familiar critique – that BMI cannot differentiate between Arnold Schwarzenegger and the Michelin Man – is often dismissed. After all, not many people who have an obese BMI look like Arnold Schwarzenegger. But the dismissal masks a subtler point: in many cases a person classified by BMI as overweight or “grade 1” obese (adjacent to the overweight range) may be metabolically healthier than their normal-weight counterpart simply as a result of better fitness. According to the standard BMI categories, however, this person is indistinguishable from a severely obese person with minimal fitness.
Worse, when an overweight person gains muscle, they change their health for the better but often change their BMI for the worse. Occasionally this even bumps them into the “obese” category. And this category is wildly over-inclusive, encompassing any BMI over 30, which conflates a range of weights that stretches, in theory, to infinity. Flegal, for one, thinks this is the confounding factor in many of the studies. In her 2013 findings, she says, she saw major differences in health between people classified as “grade 1” obese and people whose BMI was closer to 40. “Grade 2 to 3 obesity was significantly associated with excess mortality but grade 1 obesity was not,” she says. Most studies that rely on BMI, however, rarely make the distinction. Healthcare providers tend to ignore it as well.
This is why BMI consistently fails to account for healthy obese people and unhealthy thin people, two groups that keep turning up in new research. For example, in a 2013 study of 43,000 people that investigated the link between obesity and cardiovascular disease, 46 per cent of the obese population were found to be metabolically healthy, having none of the high blood pressure, high cholesterol and insulin resistance normally associated with obesity. This “healthy obese” group had the same chance of dying from cardiovascular disease or cancer as their normal-weight counterparts who were also metabolically healthy (European Heart Journal, vol 34, p 389). Based on the size of their 25-year study, the authors speculate that this state of being metabolically healthy but obese is common in the general population. Alongside the steadily growing body of work describing the obesity paradox, this reveals that BMI doesn’t even necessarily work as a proxy for the general health of a population.
“Weight is the wrong thing to be paying attention to,” says Linda Bacon, a nutritionist at the University of California, Davis. Lavie agrees. “There’s just not that much evidence that you’re gaining a lot by losing weight,” he says. So for anyone between 18.5 and 35 on the BMI chart, he says the key is physical fitness, not weight loss. “If I’m sitting with a mildly obese patient who just had a heart attack, they can actually have a good prognosis, or even a better prognosis than a thin person, if we can get them to become more physically fit,” he says. Bacon and Lavie are far from the only ones coming to this conclusion.
No size fits all
This represents a paradigm shift for cardiologists, who have tended to recommend weight loss to anyone whose BMI is above normal. It is a controversial position. After all, one concern raised frequently about Flegal’s work is that it could undermine policies to curb obesity rates. If everyone starts to think of higher weights as normal, parents might no longer understand that their overweight children have a weight problem, England’s chief medical officer recently told New Scientist.
However, research is beginning to show that the focus on BMI may not be helping. In a study published in February, researchers from the Johns Hopkins School of Medicine in Baltimore, Maryland, found that patients who felt their doctor judged them for their weight were more likely to attempt weight loss, though not more likely to succeed.
Indeed, the fixation on BMI could be causing actual harm, discouraging overweight and obese people from seeing their doctors in the first place. A team of researchers from Columbia University in New York identified weight-related barriers such as fear, modesty, insensitivity and lack of facilities, all of which were discouraging obese women from going for potentially life-saving mammograms and smear tests (Obesity, vol 20, p 1611).
The deeper question may be – why is anyone still using BMI? At least five alternatives have been proposed, ranging from a subtler mathematical formula to a waist-to-height system that better reflects actual risk of disease. At this point, however, no public health agencies have any plans to switch to another measure. Part of the problem is that BMI is alone in offering the official cut-offs that are so useful in making easy assessments.
To minimise the damage, in the shorter term, many recommend that doctors use BMI with more care. For young people, for example, classic BMI metrics appear to be relevant, but for the elderly in particular, Lavie thinks the BMI guidelines are misguided; research is accumulating to show that obesity in this population is associated with a lower, not higher, risk of death. Likewise, BMI does not apply equally to all races, and should be different for the genders – as the NIH understood in its original version of the guidelines (see “Why BMI?“). And under some circumstances, people with certain diseases including cancer and HIV might even consider gaining weight beyond the recommendations set by BMI.
Others wonder whether health concerns are truly at the heart of the obesity panic. “We live in a society that condones fat shaming,” says Abigail Saguy, a sociologist at the University of California in Los Angeles. “There remains a kind of social acceptance for this type of judgment, a lack of empathy.” Saguy notes that she has seen no evidence that discrimination, stigma and shaming is motivating in terms of weight loss. “It has no positive effects,” she says. The real public health epidemic, she suggests, is discrimination against the overweight and obese: “less social acceptance of weight-based discrimination and shaming could potentially save lives.” This article appeared in print under the headline “Flabbergasted”
So where did we get the idea that general health and BMI are closely linked? The system was developed by a Belgian statistician in 1832, more out of academic curiosity about what constitutes the “normal” person than interest in obesity.
In the 1940s, life insurance companies adapted it as an easy way to determine policy risk. In 1985, it was adopted by the US National Institutes of Health (NIH), and then in 1995 by the World Health Organisation, to estimate obesity in large populations.
Even these guidelines have not been written in stone. In 1998 the NIH pushed the definition of obesity to 30 from 27 and added a new category – overweight – instantly classifying millions of previously “fit” Americans as fat. It also consolidated previously different guidelines for men and women.
No one ever suggested that it should be a proxy for a single individual’s health – its inventor warned explicitly against doing so.
But that is exactly how we use it today: anyone whose statistics stray outside the normal BMI range is advised to lose weight. Context-free online BMI calculators proliferate. There is good reason to rethink this approach (see main story).
Samantha Murphy is a journalist based in Lancaster, Pennsylvania
October 21, 2016
October 12, 2016
How to ensure seeds germinate: https://www.growveg.com.au/guides/5-gardening-hacks-for-seed-sowing-success/
Monthly guide: http://www.gardenate.com/
MY PLANTING PLAN:
May 9, 2016
With real fat (not processed), the body quickly gets the “full” signal, and that’s probably what holds the key to its success in weight reduction. One is unlikely to get that sensation with sugar.
Human body is designed to burn fat, not to live off a ready-made fuel (sugar).
So, eating fat – and cutting out almost all sugar – would (a) help the body reach satiation quickly, (b) force the body to burn fat in order to operate.
Fat is also critically necessary for skin cells and almost all enzymes.
I’m becoming increasingly convinced that ghee/ lard were good things, not bad. Bad science persuaded us that traditional foods (which never made anyone obese) were bad for us.
Instead, they ignored the massive surge in the supply of sugar and processed carbohydrates (which are similar to sugar in their effect) in the modern human diet.
In this case, correlation (increase in sugar/ processed carbos correlated with obsesity) is causation.
Sugar basically **stopped** us from burning fat. No wonder everyone became fatter and fatter. It led to a vicious cycle.
The only way out is to get into a virtuous cycle: eat fat so you feel satiated quickly, then let the body burn stored fat.
Indians are the world’s BIGGEST consumer of sugar. Indian sweets are laden with sugar. Nothing else comes even remotely close. This explains the alarmingly high rate of death from heart attacks among Indians.
“India has become the world’s biggest sugar consumer today, consuming one-third more sugar than the entire E.U. and 60 per cent more than China!” [Source]
Now, the question is finding fat. Butter/ ghee are obvious sources; but also animal fat.
A wide range of animal fats available here. Animal fat is really expensive – around 20 times the price of vegetable fat.
Further, there is an Allowrie brand.
THE SCIENCE BEHIND THE DANGERS OF SUGAR (AND HARMLESSNESS OF FAT)
THE BIG FIGHT AMONG HEALTH PRACTITIONERS IS NOW ON. I THINK FAT HAS WON THE DAY. SUGAR HAS LOST.
“My patients don’t lose weight or improve their health by cutting fats or calories. “The proof being that obesity levels are higher than they have ever been and show no chance of reducing. “A new approach is needed – a return to 18th century values, drawn up before modern interference with basic principles occurred.” [Source]
John S. Yudkin’s book, published 40 years ago, has been found to be correct: “Pure, White and Deadly: The new facts about the sugar you eat as a cause of heart disease, diabetes and other killers”. [Download]
I had mysteriously put on weight over the years, despite eating very little fatty foods (definitely no butter, very few eggs, almost no oil, and slicing away all animal fat before cooking).
However, I didn’t make a fetish of my low fat preference and so it did not destroy my metabolism. I have continued to have normal blood pressure and no diabetes.
A couple of weeks ago, persuaded by the **logic** of physiology, that fat is good (in moderation, of course) and sugar/ carbohydrate is bad (again, only in excess), I’ve slightly increased the fat and protein ratio in my food (a bit of butter, one more slice of bacon each week – buying only fatty bacon; more lentils, e.g. rajma – which have both carbohydrates and proteins), cut down carbohydrate share (cut down almost all ice cream and dessert and rice/roti), and increased the share of vegetables and fruits.
The switch is very small and modest. I’m not dieting (I never diet, by which I mean cutting down overall food intake) but I’m beginning to experience a tiny bit of weight reduction already.
I’m persuaded that carbohydrates should be minimised. Vegetarians should consume pure ghee. Parathas are bad not because of the ghee/oil, but because of the wheat. Replacing rotis/ naans/ parathas with lentils (cooked in a lot of pure ghee) will be a great way to keep weight in check, even as the body is able to build new muscle and cell walls.
May 5, 2016
It has now been conclusively proven that Nexium and other proton pump inhibitors (e.g. Prilosec) dramatically increase the following health risks:
- kidney failure: “It is very reasonable to assume that PPIs themselves can cause chronic kidney disease,” said Dr. Pradeep Arora, a nephrologist and associate professor at the SUNY Buffalo School of Medicine and Biomedical Science in Buffalo, N.Y. [Source]. Further: “People who use proton pump inhibitors (PPIs) have a 20 percent to 50 percent higher risk of chronic kidney disease compared with nonusers, said lead author Dr. Morgan Grams, an assistant professor of epidemiology at Johns Hopkins University in Baltimore. The study was published Jan. 11 in JAMA Internal Medicine.” [Source]
- premature death: People taking a PPI also had nearly twice the risk of dying prematurely [Source]
- bone fractures and infections of C. difficile and pneumonia: “they’ve been tied to other health problems such as bone fractures and infections of C. difficile and pneumonia” [Source] Clostridium difficile bacteria can cause life-threatening colitis. people taking proton pump inhibitors were almost three times more likely to have a C-difficile infection than non-users. he risk of pneumonia was 89% higher for those using proton pump inhibitors and 63% higher for those using H2-receptor antagonists.[Source].
- liver toxicity: [Source]
- All kinds of other problems: “PPI users were more likely to have health problems, such as obesity, high blood pressure and heart problems” [Source]
- Depletion of magnesium: “The medications can cause magnesium levels to decline in the body, and a lack of this important mineral could damage the kidneys” [Source]
- Depletion of calcium: Due to reduced acid, it becomes harder to absorb calcium.
See also: CNN: Popular medications linked to higher risk of kidney failure
THE MORE NEXIUM YOU TAKE THE HIGHER THE RISK
twice-daily use was associated with a 46 percent increased risk of chronic kidney disease, versus a 15 percent increased risk in those taking one daily dose. [Source]
Nexium & Prilosec Lawsuit
There is a lawsuit going on: https://www.levinlaw.com/prilosec-nexium-lawsuit-lawyer-side-effects-recall-help
ALTERNATIVES: WHAT CAN BE DONE?
This article argues that prilosec/omeprazole should be taken, but these are effectively the same drug. That’s no solution.
Natural alternatives: at Livestrong |
1) Take as little of Nexium as possible.
If you do have to take Nexium, take magnesium supplements.
2) Try H2 blockers: Pepcid, Tagamet or Zantac.
“These types of studies, these big data studies, can sometimes suggest a signal that something’s going on, but I don’t know if they prove it,” DeVault said. Grams said the study authors tried to address that concern by comparing PPI users to people using another heartburn medication called H2 blockers. Both patient groups tended to be equally unhealthy, but PPI users had a 39 percent higher risk of chronic kidney disease, the researchers said. [Source]
“Doctors also might opt to prescribe an H2 blocker like Pepcid, Tagamet or Zantac. “To me, this is a cheaper, safer alternative that might work as well with some patients,” Swaminath said.” [Source]
BUT NOTE, H2 RECEPTOR BLOCKERS AREN’T SAFE, EITHER
In 2000, the histamine H-2 receptor blocker, Propulsid, was taken off the market due to associated cardiac deaths. [Source] (I was initially prescribed Propulsid for many years)
Both proton pump inhibitors and the histamine H-2 blocking drugs can raise the risk of hip fractures by 44% if taken for longer than a year because, when you block acid production, you make it more difficult for the body to absorb calcium. [Source]
3) Try Dexsilant
“medications do not fix anything, they allow the underlying problem to continue uncorrected and actually accelerate” [Source: see note by Jodi-Hummingbird here]
1) The usual advice
Give up: coffee, cigarettes, carbonated beverages, food additives, artificial foods
Test for: candida, HPylori, parasites, food allergies, bacteria, gluten sensitivity, lactose sensitivty, leaky gut syndrome
Try: chewing more times, raising head of bed, smaller meals, digestive enzymes, DGL, aloe, wait 3 hours before lying down, probiotics, food elimination diet [Source]
2) Try apple cider vinegar
– for a short period of time.
3) Try to wean off Nexium
This youtube video provides some thoughts.
4) eat frequent small meals throughout the day instead of the usual three large meals.
5) vegetable juices include carrot, spinach, beet, cucumber, parsley, celery, cabbage and potato
6) Reduce carbohydrates
This was very persuasive (from around 4.5 minutes)
Ini particular, white flour seems to be a culprit [See review by Frog Man here] – bread?
May 1, 2016
February 25, 2016
These are good articles:
January 31, 2016
your body does not get stronger when you are training, but rather when you are resting and recovering from your training. [Source]
Recovery from sore muscles after climbing stairs/ mountains
stretching prior to warming up and getting your blood flowing and muscles loose is not a good idea. The exception to this would be stretching in the day following a workout to loosen sore and tight muscles. [Source]
Continued high-intensity exercise (with no rest), however, will cause lactic acid levels to skyrocket and muscular failure to occur in less than three minutes.
Detailed description of the kinds of fatigue
Climbing stairs/ hills is a FAR MORE STRENUOUS exercise than walking/ running
stair climbing works multiple muscles in your bottom half, including your calves, glutes, hips, hamstrings and quadriceps. Walking, jogging or running also uses your legs, but it focuses more on toning muscles and strengthening the heart. Although climbing stairs also works your heart, it uses your legs more strenuously and hence tends to build more muscle.
Stair climbing provides a triple workout because it strengthens your heart, your leg muscles and even your bones. Because your legs bear a load — your body weight — while working vigorously, your leg muscles pull against your leg bones. In response, according to a web page on the University of Arizona’s website, your bones strengthen and become denser. Accordingly, stair-climbing not only makes your legs stronger, it also helps prevent osteoporosis. Stair-climbing provides aerobic exercise as well as strength training — in other words, it raises your heart rate and increases endurance. [Source]
Exercises to prepare for climbing
Which muscles are used in climbing
Hip extension is a major component in walking up stairs. You have two primary hip extension muscles — your gluteus maximus and your hamstrings, both located on the rear of your hip/thigh. As these muscles contract, they drive your femur or thigh bone backward to provide forward and upward momentum.
Climbing stairs requires active knee extension. Higher stair will require you to bend your knees more deeply and the greater the amount of knee flexion, the greater the involvement of your knee extensor muscles — the quadriceps. Your quadriceps are located on the front of your thigh, originating near your hip and terminating just below your knee. These are the muscles that can feel tired and hot as you climb a long flight of stairs.
As you climb stairs, you must swing your leg from an extended position and into a flexed position in preparation for another stride. This is the job of your iliacus, psoas major and psoas minor. Collectively these muscles are called iliopsoas and are located on the front of your hip. In addition to extending your knee, one of the quadriceps, rectus femoris, also flexes your hips as your swing your leg forward and up onto the next step.
Extending your ankle, correctly called plantarflexion, is the job of your calf muscles — specifically soleus, gastrocnemius and tibialis posterior. These muscles work to keep your ankle braced as your climb the stairs so that the energy produced by your leg muscles is not wasted. They also provide assistance as they extend your ankle which results in a strong push off from the balls of your feet.
The degree of involvement of your calf muscles in stair climbing depends on how much you push off the balls of your feet. If you climb the stairs using a flat footed technique, there will be relatively little in the way of calf muscle work. If, however, you actively push off your toes, for example when running up stairs two at a time, your calf muscles will have to work much harder.
November 24, 2015
Scientists now think that being overweight can protect your health (By the time a person is in their 70s, the statistically optimal BMI is around 26, or solidly in the “overweight” category.)
See this: Value of BMI as health measure queried