In high school I started getting nauseating deja vu. Out of nowhere, the world suddenly seemed both unreal and hyperreal, like the clearest dream. I could remember everything before it happened, and then I could remember my entire life, all of human history, all of being. I got magnificent insights into philosophy, I could feel mortality in my bones and understood more than ever the importance of living a reflective and full life. Everything felt other-worldly and intense, and so beautiful. At the same time, I was gripped by horrible nausea and dread. An “unthinkable idea” was chasing my consciousness around my brain, and if I allowed myself to focus on it, something terrible would happen. Sometimes I had hallucinations, like having a dream while awake — I never thought they were real. It was always strange and abstract stuff, like my dog leading me through a rainforest or Friedrich Nietzsche trying to tell me how to live my life. And then within moments, everything went back to normal and I could hardly remember what had happened. For years I assumed this was ordinary deja vu, or maybe an existential crisis. I didn’t think much of it.
Then I began fainting. Episodes would start with the uncanny deja vu, but sometimes they got so powerful I’d fall unconscious. Doctors assured me, “This is OK, you probably have issues with low blood pressure – it’s nothing to worry about.” So I didn’t; after all, this was a reassuring misdiagnosis.
But the first six stressful months of graduate school brought more “fainting” than I had experienced in my life. Trying in vain to describe the deja vu to my boyfriend, I finally Googled it. Somebody else must get these, I thought. “Nausea at existence, being unto death, feeling of the sublime” – it can’t just be me and the existential philosophers.
My heart sank when I saw the results. It was page after page of epilepsy or brain tumor or neurological disorder. When I read the descriptions, I knew instantly this was it.
I saw a neurologist, was quickly diagnosed with temporal lobe epilepsy, and breathed a deep sigh of relief when my MRI revealed a tumorless brain. I learned that a seizure is a cascade of misfiring neurons. When this happens in my temporal lobe (my memory, emotion and spirituality centers), I get confused about reality and memory, I get intense and inexplicable feelings — and of course the spirituality aspect is the most obvious. All of this is called a “partial seizure.” Sometimes the cascade of misfiring neurons can spread from the temporal lobes into the rest of the brain, causing sudden loss of consciousness, which tends to look a lot like fainting. This is called a “generalized seizure” and they’re typically less common. Throughout history, partial seizures have been interpreted as spiritual awakenings or communications with God. With such bizarre and abstract warning signs, I’m not the only one who has gone a decade without realizing anything was wrong.
When I have seizures, dreams flood my consciousness. I feel sick but the world is illuminated; I feel as though some external force is showing me meaning, lifting me up. Eyes close, lips turn white, body falls.
I’ll get back up again, I always do. Epilepsy can be rough, and sometimes I wish I never had it. But I always reach a paradox — my seizures have been formative. Simulated or not, the philosophically profound moments have influenced my thoughts and experiences. I don’t think I would have followed the same path in life were it not for them. An Anna (that’s me!) without epilepsy isn’t Anna at all.
To be clear, even temporal lobe epilepsy is serious and requires treatment — as much as I’ve gained from seizures, they aren’t healthy and carry a risk of death. I take medication now, and seizures happen less frequently. It’s OK if they go away and never come back. I’ve taken all I need from them.
I wish it was more common knowledge that epilepsy isn’t only helmets and convulsions, seizures aren’t all strobe lights and unconsciousness — even doctors seem oblivious. Some seizures are radiant and horrific and unspeakably beautiful.
For me personally, this entails intermittent fasting and a cyclic approach of higher/lower carbs, plenty of protein and low/moderate fat. My main focus lies on high quality foods, with nutritious and satiating properties, and not discrimination towards a particular macronutrient.
I don’t believe there is any magic to be had when one is excluding fat or carbs from their diet. Both have their place. However, there are people that subscribe to a completely different set of opinions.
After watching the documentary Religulous
(melding of “religion” and “ridiculous) yesterday, it dawned upon me how much some religious fundamentalists have in common with certain nutritional fundamentalists. In recent years, I have seen the rise of one group in particular. I prefer to call them the low carb talibans.
When I am using the term ‘fundamentalist’ here, I am using it to characterize religious advocates that cling to a stubborn, entrenched position that defies reasoned argument or contradictory evidence – I am not talking about religious people in general, and I don’t have anything against them.
1. Religious fundamentalists believe in supernatural beings. Low carb talibans believe you can get fat without a positive energy balance, if you eat carbs.
Similar to the anti-fat proponents 15-20 years ago, we now have one group of people blaming one particular macronutrient as the sole reason for why people are getting fatter.
2. Religious fundamentalists base their beliefs on faith, not empirical evidence. Low carb talibans believe that dietary fat is unimportant for the development of obesity; the most jaded lot believe that you can eat an unlimited amount of fat, without weight gain, as long as carbs are excluded from the diet.
The ‘rationale’ behind this claim, is that the body can’t store fat without insulin (it can). Carbs equals insulin, and that means ditching carbs must mean no fat storage (wrong). They conveniently ignore that
a) eating protein produce insulin
b) fat stores itself with tremendous efficiency without insulin, due to a nifty little thing called acylation-stimulating protein (ASP).
3. Religious fundamentalists believe that forces of evil hide amongst us, trying to lead us into temptation and wrongdoing. Low carb talibans belive that carbs and insulin are to blame for obesity.
We live in an obesogenic environment; we lead sedentary lives and we are surrounded by easily obtainable foods with high energy density. High carb, high fat foods which taste great, and are extremely easy to overconsume. That people gain weight in such a setting is no great mystery, yet the low carbs talibans likes to make it out to be. It is the carbs specifically that made you fat, not that peanut butter jar you went through watching tv last night. Yes, that seems to make sense.
4. Religious fundamentalists believe there is only one way, and all other faiths are heretic. Low carb talibans tries to push their beliefs on others and will seldom accept alternative views.
More than one time, I have seen the talibans make the most ludicrous claims about their approach, often not accepting the fact that some people actually function better on a higher carb approach, and that people involved in anaerobic sports actually need them to perform better.
5. Religious fundamentalists do not accept current ideas of the creation of earth or human evolution, rather they make up their own stories of how we came to be here. Low carb talibans make up their theories regarding human metabolism.
Here’s a quick primer on how it works.
Dietary fat is stored easily as body fat without the presence of carbs or insulin.
Fat metabolism increase when fat intake is increased, but it is primarly dietary fats that are burned off, not fat stored in adipose tissue. For the latter to occur, energy balance needs to be negative. Energy can’t just disappear and an excess is stored*
When carbs are consumed, metabolism switches to glucose dependence; that is, while carbs do not get converted to fat**, they do inhibit fat metabolism to a point where dietary fats are more readily stored.
One can say that overconsuming dietary fat leads to fat storage through a direct mechanism, while overconsuming carbs leads to fat storage through an indirect mechanism, through blunting of fat metabolism/lipolysis. Either way you cut it, the key point is that energy balance is the main determinant for fat storage, or fat loss.
* carbs can only be converted to fat by a process called de novo lipogenesis (DNL). This metabolic pathway is very ineffective in humans and in studies it only comes into play during massive carbohydrate overfeeding. How come people still got fat from eating all those low fat foods back when low fat was the craze? Well, the body has the ability to upregulate key enzymes involved in the DNL pathway, making carb to fat conversion more efficient. And this occurs on high carb/low fat diets. So, there is no tricking the body from gaining weight during caloric excess by excluding fat or carbs from the diet.
** metabolism does increase a bit when energy consumption is increased; just a few percentages, nothing drastic (called ‘luxusconsumption’ or adaptve thermogenesis by some scientists). Ironically, this effect is greatest when the extra energy is provided from carbs, not fat.
Why low carb really works
I have extensive experience with all forms of low carb/ketogenic diets. I’ve done them all, the traditional standard ketogenic diet, the cyclical and the targeted ketogenic diet. I’ve come to the following conclusions:
1. There is a mild hunger blunting effect on ketogenic diets, which may help intially. This has to be weighed against the deprived feeling you get from not consuming carbs and the decrease in performance during weight training. This can be partially amended by doing a cyclical ketogenic diet (CKD) or a targeted ketogenic diet (TKD), where you either carb load through the weekend or consume carbs in conjunction with workouts.
2. Making the diet highly restrictive, in terms of completely cutting out one macronutrient, may help with adherance. It certainly takes away the hedonic aspect of eating.
Studies actually show that diets which allow ad libitum intake of protein and fat, usually leads to a spontaenous reduction of calorie intake. Cutting out carbs from the equation may be a sound approach for the average joe, who’s idea of carbs are in the form of cereal and white bread. IME, you’re less likely to binge on egg omelettes and ham, as opposed to chicken and pasta.
3. When people start eating low carb and lose weight, it is partially because they start eating more protein than on their past (failed) diet approaches. Protein leads to better satiety than any other macronutrient. There’s also the issue of being forced to make sound food choices overall, such as increasing veggie intake to make up most of your carb intake in order to stay below the threshold (max 50 g carbs/day usually).
4. And of course, there is also the insulin sensitivity/resistance factor to consider. Some people do in fact feel better on ketogenic/low carb diets, for physiological, not behavioral, reasons. No energy dips, hunger pangs and so forth. ***
*** However, as I see it, people have a tendency to draw the conclusion that they need to follow a low carb approach without having visited the middle road. I’ve had some clients that were convinced they could only do well on low carbs – and it turned out they did just as well, if not better, when I incorporated veggies, fruit and berries as their main carb source. The middle road, with a minimum of refined carbs, is very workable for most people that label themselves as ‘insulin resistant’.
It’s easy to think that it’s a bit of a scam. That if people with dyslexia worked harder, and really applied themselves, they could “get over it.” But that’s not the case.
Life is actually much more difficult for people with dyslexia. They have brilliant minds, but they’re hard to focus.
Dyslexia is a gift—the gift of being able to see things from lots of different points of view, all at once. But the gift comes with a curse, and the curse is that it’s hard to prioritize, or make sense of, all those perspectives.
People with dyslexia can be hard to live with, and hard to love, because their brains work so differently to ours. Even if you love someone with dyslexia, the day-to-day living with it can drive you insane. Because they can forget things, believe they’ve said or done things they haven’t, be incredibly messy and disorganized, and be less socially aware than other people.
Dyslexia is much more than just having difficulty reading, writing, and using numbers. They see the world in a completely different way, communicate differently, and have trouble organizing things.
Some people describe it as a lifestyle challenge, others as a lifestyle curse, because it affects almost all aspects of their lives.
2. They can seem weird.
Despite their high intelligence, and because they see so many different perspectives at once, they can appear incoherent in conversation. They can come out with strange ideas, and lack the ability to check if their thoughts are suitable for conversation. They can seem almost autistic because they’re often unaware of social rules.
3. They find details exhausting.
Because their brain is less efficient at processing letters and sounds, it has to work harder—much harder. So any time spent reading, using numbers, or focusing on details is really, really exhausting.
4. They function differently on different days.
Some days they seem to function better than others, and can appear to be improving. Other days, it’s like everything is getting worse. There’s no reason, and no pattern. It just is.
5. They are highly creative.
Their ability to view the world from all perspectives makes them highly creative. They can come up with wildly creative ideas, partly because they’re not constrained by the laws of physics, mathematical logic, or the impossible.
6. They see things that others don’t.
Like words moving on the page, or even off the page, and letters flipping about. You know how challenging it can be to read letters and numbers incaptcha? Imagine reading a whole book like that. Or reading a book through a magnifying lens that a child is holding, and moving about.
They can even see the word cat more than 40 different ways.
7. They get overwhelmed by what they see.
They see so many possibilities that their thoughts can become garbled and distorted. It’s hard to sort through all that information and work out what’s important or appropriate. Without the ability to filter, this special gift becomes a tragic, confusing, disability.
They can fully believe they’ve told you something, that they haven’t, or swear that you haven’t told them something that you have.
Often they express themselves in such a unique way that their message hasn’t come across coherently. And they may not realize that this aspect of their communication is part of their dyslexia.
10. They may not know they have dyslexia.
According to the Mayo Clinic, dyslexia can go undiagnosed for years, and may not be recognized until adulthood. This is one reason why it’s hard to calculate the number of people with dyslexia. And, unfortunately, people with undiagnosed dyslexia often label themselves as stupid or slow.
11. They think in pictures instead of words.
Not surprisingly, they tend to be highly visual, think in pictures, and utilize visual aids to help them plan and organize their lives. Rather than using self-talk, their thought processes are more subliminal. Most people with dyslexia are not even aware that they do this.
12. They will always have dyslexia.
They can learn to read and spell, but they will always have dyslexia. To make life easier, a font and a dictionary specifically for people with dyslexia are on the way.
The font is designed to avoid confusion, and add clarity, while the dictionary will favor meaning over alphabetical order.
13. They use their brain differently.
People with dyslexia don’t use their brain the same way that most of us do. Their brain underutilizes the left hemisphere—the area required for reading—and the bridge of tissue between the two sides of the brain (the corpus callosum) doesn’t function in the same way. So, their brain doesn’t always direct information to the correct place for processing.
14. They get it from their family.
Dyslexia is inherited, and most people with dyslexia have an aunt or uncle, or a parent or grandparent with dyslexia. Scientists have discovered that the DCD2 appears to be a dyslexia gene.
15. They often have low self-esteem.
People with dyslexia are just as intelligent as the rest of us. And they’re fully aware that other people can read and write much more easily than they can. So they feel stupid compared to other people.
As Albert Einstein said:
“Everybody is a genius. But if you judge a fish by it’s ability to climb a tree, it will live it’s whole life thinking it’s stupid.”
16. They have different symptoms.
Dyslexia is a tricky thing, because no two people have the exact same symptoms. Some lose things, or have poor organization skills. Some are slow at reading or have poor comprehension. Some may have difficulty organizing ideas to write, or have difficulty processing auditory information. Some also have difficulty sequencing the days of the week, or months of the year.
17. They are full of contradictions.
They may be highly aware of their environment, but appear lost. They may recognize, or read, a word on one page but be unable to recognize it on the next. Their brains are often very fast, but they appear slow, because they’re filtering through all the possibilities that they see.
18. They have great strengths.
People with dyslexia are often very good at reading people, and have great people skills. They usually have fantastic memories, and rely on them. They’re often good at spoken language, and frequently spatially talented (think architects, engineers, artist and craftspeople). They are highly intelligent, and intuitive, with vivid imaginations.
19. They can be incredibly successful.
People with dyslexia can be incredibly successful, often because of their dyslexia.
Famous people with dyslexia include entertainers like Whoopi Goldberg, Jay Leno, Henry Winkler, Danny Glover and Cher. As well as artists like Leonardo da Vinci, Tommy Hilfiger, Andy Warhol and Pablo Picasso.
Carole Grieder and Baruj Benacerraf utilized their dyslexia to become Nobel prize-winning scientists. People with dyslexia also go on to be writers and journalists like Scott Adams (of Dilbert), Agatha Christie, F Scott Fitzgerald, and Fannie Flagg (the author of Fried Green Tomatoes at the Whistle Stop Café).
20. They can change the world.
People with dyslexia can, and have changed the world. People like George Washington, Richard Branson, Henry Ford and Stephen Spielberg have changed, and continue to change, the world we live in.
People with dyslexia are kind, creative, highly intelligent beings who are just as frustrated at their inabilities as you are. They just can’t take a break from the way their minds work.
Instead they rely on the people that love them to help them interpret the world, and to help them function in a world that’s not adjusted to their needs.
Yes, they can be frustrating to love at times, but they have incredible, unique, world-changing gifts.
I WAS prepared for the blood but the most shocking thing about watching brain surgery was seeing the surgical drapes being stapled to the patient’s face. But surgeon Peter Hutchinson dismisses my concern that the tiny holes might bother the patient when she wakes up: “That’s nothing compared with the massive hole we’re about to make in her head.”
I am at Addenbrooke’s Hospital in Cambridge, UK, to learn about craniectomy, a procedure that involves removing a large part of someone’s skull, to relieve the pressure inside. There are no official tallies but it’s thought that several hundred surgeries take place in the UK every year on people with head injuries or who have had a stroke. Once the brain is given room to swell, the pressure drops and the scalp is sewn back into place. The skull fragment can be stored in a freezer or kept sterile inside the patient’s abdomen for weeks or months before it is reattached.
The operation I’m witnessing is part of a randomised trial to compare the effectiveness of craniectomy with that of drugs alone to bring the pressure down. It will involve 400 people with head injuries, half of whom will get the surgery.
This is needed as craniectomy has a long and chequered history. Human remains suggest it was done with stone tools in Peru a thousand years ago, a practise known as trepanning, perhaps for similar reasons as today. As a modern surgical procedure, though, it has fallen in and out of favour over the last few decades. Whether you would be sent for surgery today depends on how safe your surgeon thinks it is.
There are concerns that while it may save people’s lives, it might make it more likely that someone will end up in avegetative state. The number of people in this state is rising in most Western countries, as more people survive serious injuries thanks to medical advances. But some are concerned that craniectomy is contributing.
The problem with the procedure is that such a brutal assault could be doing more harm than good. One risk is infection, caused by bacteria on the patient’s skin entering the wound. Hence the need to anchor the drapes so firmly in place to ensure the skin stays covered up.
Another risk is nicking a major blood vessel. I see how this fear affects the surgical team when I observe a second operation. The patient needs a circle of skull removed that overlies a major artery. The team members joke about how, if things go wrong, they will need to change their socks – because of the ensuing torrent of blood. The banter stops as they start to ease the skull away from the brain, gently severing recalcitrant tissue. With the skull removed, they step back to look at the blood vessel almost reverently, then delicately cover it with gauze.
The man’s brain throbs before our eyes with each beat of his heart. Hurt it, and he could awake unable to speak or move – or he might not wake at all.
Hutchinson has spent years planning this trial and convincing colleagues at other hospitals to take part. But he insists he doesn’t care what the outcome is, merely that we finally learn if we should use this controversial procedure. “I’m not passionate about the operation, I’m passionate about the trial,” he says. “We need answers.”
Patty Duke, best known as Helen Keller in the 1962 film The Miracle Worker, has died at the age of 69. After surviving the dark side of child stardom, Duke sat down with PEOPLE in 1999 to open up about her battle with manic depression and reveal how she turned her life around. Read the profile below:
It’s feeding time at the 40-acre northern Idaho farm that actress Patty Duke calls home. Clad in faded overalls and work boots, Duke ignores three donkeys braying for their breakfast in favor of Tommy, her pet tortoise, to whom she proffers a banana. But while Duke tries to coax Tommy out of his shell, Brother, her chocolate Labrador, chomps the banana in Duke’s hand. “That’s not the way it’s supposed to be,” says Duke, laughing. “But then,” she adds, “things often don’t turn out the way you plan.”
In Duke’s case, that has to be the understatement of the year. As perhaps the most celebrated child star of her generation, she wowed Broadway theatergoers at age 12 in her stunning debut as the blind and deaf Helen Keller in 1959’s The Miracle Worker. Who would have guessed that Duke, who went on to play perky all-American teen Patty Lane and her demure Scottish cousin Cathy on TV’s The Patty Duke Show (1963-66), would grow up to be hooked on tranquilizers and later diagnosed as a manic-depressive? Nor could anyone have imagined that the mercurial starlet who at 18 tied the knot with a TV director nearly twice her age – the first of four marriages – would end up devotedly married to a retired Army drill sergeant.
“I lucked out and found goodness personified,” says Duke, 52, of her husband, Michael Pearce, 44. She is sitting on the living room rug of the spacious four-bedroom farmhouse they share with their son Kevin, 10. “Mike’s selfless, and he has humor and remarkable strength” – traits his wife seems to share. Since moving to Idaho nine years ago – and getting fewer acting roles – “a certain amount of ego has gone by the wayside,” says the three-time Emmy winner. “Here, I clean the toilets, shop at the grocery store and visit the pawn shop with Kevin for Beanie Babies. And I love it.”
Of course, she still loves acting too and last November flew to Montreal to shoot a TV movie sequel – airing April 27 on CBS – with her old Patty Duke Show family. Among those who turned up were William Schallert, now 76, who played her dad, Martin; Jean Byron, 73 (mom Natalie), Paul O’Keefe, 48 (kid brother Ross) and Eddie Applegate, 63 (then boyfriend – now ex-husband – Richard). Duke had long resisted the idea of a sequel. “I pooh-poohed the show for many years. It wasn’t sophisticated or classy,” she says. “But as I got close to 50, it became important to touch base with those people again.” Says Schallert of Duke: “She’s much more together and mature. She’s raised two kids [and five stepchildren], and she’s a grandmother. I can’t get over that.”
Nor can she. “One of the reasons I survived as well as I did,” she says, “was my genetics. My mother and father both had very tough lives, and boy, were they survivors.”
Anna Marie Duke – Patty’s given name – was just six years old when her mother, Frances, a restaurant cashier who suffered bouts of depression, kicked her alcoholic husband, John, a cabbie and handyman, out of the family’s bedbug-infested New York City walkup. Though Duke would see him – usually at his favorite bar– only a few times before his death in 1963, “I worshipped my father,” she says today.
At seven, Anna Marie met the couple who would become her surrogate parents. John and Ethel Ross were managers who specialized in child actors, including her older brother Ray. (Ray eventually lost interest and is now, at 57, a payroll consultant; sister Carol, 58, is a financial aid counselor.) When the Rosses asked Frances if they could take on her younger daughter as a client, she agreed. Soon they had taken over the girl’s life, “everything from what I wore to when I slept to what I ate,” says Duke. When she was eight, she recalls, Ethel announced: “We’re gonna change your name. Anna Marie is dead. You’re Patty now.”
As Patty Duke, she began to build an acting resume – in TV ads, daytime soaps, bit parts on live dramas – more than 50 shows by the time she was 12. At that point, with her mother’s consent, Duke moved into the Rosses’ apartment. There, she began training for her biggest role. “I remember John Ross teaching her how to walk blind and look blind for a year before the audition for The Miracle Worker,” Ray Duke says. She wound up beating out 100 other girls, and on opening night she, Anne Bancroft (who played teacher Annie Sullivan) and their castmates received 13 curtain calls. “She was fantastic in the role,” says Patricia Neal, who played Helen Keller’s mother. “She just worked from the heart. She was an actress, pure and simple.”
But success carried a price. The Rosses curtailed their protégée’s visits with her mother and close friends. In fact, concerned that the chronically depressed Frances would embarrass Patty, they even kept her from attending the 1963 ceremony at which her daughter won a Best Supporting Actress Oscar for the film version of The Miracle Worker.
There were limits to Patty’s submissiveness. On two occasions, says Duke, John and Ethel each tried to fondle her in bed. “My response both times was to vomit,” she says. The abuse ended.
Their spell over her was broken only after Patty, 17, fell for Harry Falk, 31, an assistant director on The Patty Duke Show, which was then produced in New York City. Seeking to quash their romance, the Rosses got the sitcom moved to Los Angeles. A furious Duke left the Rosses and moved into her own L.A. apartment, then got them barred from the set. John died in 1970, Ethel eight years later. “I forgive them for the bad,” Duke says today, “and have come to acknowledge that if I love this life I have – and I do – then certainly they are responsible for it in a large part.”
Duke and Falk wed in November 1965, just shy of her 19th birthday. But, she says, “I didn’t know how to be an adult. I had no preparation.” Nor did either of them know how to handle her increasingly manic mood swings. Their side effects were disastrous: She briefly became anorexic – dropping at one point to a skeletal 76 pounds. Duke also began drinking heavily and taking Valium – on which she overdosed, she estimates, eight times. “They were cries for help,” she insists.
Falk twice persuaded her to go to a psychiatric hospital, but both stays were short-lived. The couple divorced in 1967. Three years later, Duke, then 23, embarked on an affair with the 17-year-old Desi Arnaz Jr., whose mother, Lucille Ball, demanded that he end it. But they continued to see each other, off and on, for several months. In June 1970, Duke, in a manic state, impulsively wed Michael Tell, a rock promoter who had been subletting her apartment. Their 13-day marriage, never consummated, was annulled. Just prior to their union, Duke had discovered she was pregnant. Afterward she deduced that the father of her baby was actor John Astin (formerly of TV’s The Addams Family), with whom she had been secretly trysting.
They agreed to keep their affair a secret until after their son Sean was born and Astin was divorced. At their 1972 nuptials, 17-month-old Sean (now 28 and an actor) cried out, “Daddy.” Soon after the 1973 birth of Sean’s brother Mackenzie (now 26 and also an actor), John’s sons, David, Allen and Tom, moved in with them.
With five rambunctious boys, the Astin household was hardly the Brady Bunch. “It was terrible,” Duke says of those years. “I was a truly loving mom, but I didn’t have the tools to do the job.” As in the past, she would retreat to the bedroom and her tranquilizers. Once, in a manic rage, she threw her Oscar across the room, shattering it.
In 1982 a psychiatrist diagnosed her manic depression and prescribed lithium to control her mood swings. “It saved my life and it gave me life,” says Duke. “Prior to that, I wasn’t able to make any long-term decisions.” Astin, 16 years older, had been a father figure. In 1984 he became a Buddhist whose fervor to convert his family alienated his wife. “We had gone as far as we could,” she says. They divorced in 1985.
Later that year, Duke went to Fort Benning, Ga., to shoot A Time to Triumph, a TV movie about a housewife turned Army helicopter pilot. There she met Sgt. Michael Pearce, who had been assigned to toughen up the actress he nicknamed Private Pyle. “She looked like a tomato, in her green suit and red hat [on] the obstacle course,” he recalls. But the then-married but separated sergeant and his divorced trainee soon found themselves smitten. Following his divorce, they wed in 1986, and Duke became an enthusiastic stepmother to his daughters Raelene, then 10, and Charlene, 8. Kevin was adopted in 1988.
In Pearce’s native Idaho, Duke’s survival skills were tested anew. Her mother, who had moved in with the family a few years earlier, died in 1992. Then, last April, Raelene, 22, drowned when the car she was driving skidded into a river near the farm. The tragedy “drew our family closer together,” says Duke, “but there isn’t a day that goes by that some part of you isn’t anguished.”
Still, life on the farm goes on. “Anna’s back door is always open,” says her friend Liese Thompson, 40, a bank officer, “and the coffee is hot.” Sipping some now, Duke muses, “I’ve taken a lot of detours, kind of like a myopic homing pigeon, but I’ve finally made it. With my marriage and my children, and with those strangers who come up to me in the supermarket. When they say, ‘I love you,’ I think they mean it. And I get to say it back.”
Every spring, major breast cancer charities like Susan G. Komen and the Avon Foundation encourage people to raise money by walking. Each year, multiple organizations put on hundreds of walks, raising tens of millions of dollars. Since the 1980s, they’ve argued that these efforts are key to ending a devastating disease. About their three-day event, Komen proclaims: “This isn’t just a walk. It’s the journey to the end of breast cancer.”
As executive director of the national Breast Cancer Action organization, I’ve seen these walks become larger, shinier and more closely tied to their corporate sponsors. That bloat is bad for supporters and those with cancer alike.
Here’s why: The cost of putting on breast cancer walks today, especially multi-day walks, can be extravagant. And many of the best-known breast cancer charities don’t report how much their walks cost or raise, so it’s impossible to find out how much money really goes to breast cancer programs. These figuresshould be easy to find, especially as some walks require people to raise thousands of dollars to participate.
For example, based on their news releases, the Avon Foundation raised about $34 million from their two-day walks last year. They gave about $18 million in grants to breast cancer organizations. That means 47 percent of the money raised by walk participants wasn’t publicly accounted for. If all that money is going toward putting on the walks themselves, participants and donors deserve that information so they can decide whether that’s the way they want to spend their time, money and energy.
Even when money does go to breast cancer organizations, it’s unclear what the funds are being used for. The very name of the Susan G. Komen Race for the Cure® Series suggests that the money raised from these walks will go to research to find a cure. But Komen’s own website states that only 25 percent of the money raised goes toward “research and training grants.” And even that category doesn’t reveal how much money is going to research alone or the type of research that’s being funded. The other 75 percent goes to “breast cancer health education and breast cancer screening and treatment programs,” a nebulous category that could include everything from pink ribbons to poster campaigns.
Participants at the 2010 Avon Walk for Breast Cancer San Francisco, as seen in the documentary “Pink Ribbons Inc.” (Lea Pool)
Getting answers to where the money goes is critical, because we haven’t made nearly enough progress dealing with the disease’s mortality rate. Today, 250,000 women in the U.S. are diagnosed with breast cancer annually. More than 40,000 women die of the disease each year, a number that has hardly declined in 25 years.
And essential research is severely underfunded. We’re still not devoting enough resources to studying metastatic, or advanced breast cancer — so fewer women die of the disease — or to understanding the environmental links to breast cancer, which would prevent women from getting breast cancer in the first place.
The Internet of Things (IoT) has the potential to solve our biggest global challenges and bring people everywhere a better quality of life.
While we’re on the topic of environmental toxins, one of the most galling aspects of walks for breast cancer is how many of the corporations which produce toxins also sponsor walks and runs for breast cancer and get great PR in the process. We call this pinkwashing, a term we coined in 2002 to describe a company or organization that claims to care about breast cancer while at the same time making or promoting products that increase a woman’s risk of the disease.
As pinkwashing becomes more and more pervasive, people need to be asking whether a breast cancer walk should be sponsored by a corporation that increases our breast cancer risk. Susan G. Komen promotes and takes money from Ford for its Race for the Cure® Series despite the links between auto exhaust and breast cancer. The American Cancer Society does the same with Chevrolet at its “Making Strides Against Breast Cancer” walks. Perhaps the most hypocritical pinkwashing offender is Avon, the multibillion-dollar cosmetics corporation behind the Avon Foundation. While the corporation gains brand loyalty by hosting walks in its name, it also uses chemicals in its makeup that are linked to an increased risk of breast cancer and may eveninterfere with breast cancer treatment.
The sea of pink cheeriness also covers up what it’s like to live with the disease. In their marketing materials and featured attendees, mainstream breast cancer charities seem to suggest that overcoming a breast cancer diagnosis is as simple as getting an annual mammogram, thinking positively and fighting hard. These messages, and the festive atmosphere of the walks, hide the devastating, complex reality of the disease. There is no cure for metastatic breast cancer; suggesting that breast cancer is something you can “beat” if you just do the right things is both cruel and inaccurate. Komen says their Race for the Cure® “honors women who have lost their battle with the disease.” Saying women “lost a battle” implies they didn’t “fight” hard enough to win.
As Lisa Boncheck Adams, a prolific writer who died of metastatic breast cancer last year, wrote: “I felt the Komen organization was putting a happy face on breast cancer, and not paying attention to the often-unpleasant realities of life as a survivor (including recurrence).”
Of course, there is nothing wrong with a physical challenge, spending time together remembering a loved one, or connecting with people who have a similar experience. But those walking and running to have an impact on the breast cancer epidemic deserve better from major breast cancer charities.
We deserve organizations that are accountable, transparent and using their power to make a real difference in the lives of women with the disease. We need to do our part by holding them accountable and asking these important questions. If you can’t get the answer, or the answer is unsatisfactory to you, I encourage you to give directly to an organization doing work you believe is important.
This Spring, join me in pushing these big-name charities putting on breast cancer walks truly make a meaningful difference in the lives of women living with and at risk of breast cancer.
This article originally appeared on Spectrum on May 23, 2016.
The mutations that men accumulate in their sperm as they age don’t account for most of their increased risk of having a child with autism, reports astudy published Monday in Nature Genetics. Instead, the researchers suggest, men who carry risk factors for the condition simply tend to have children late in life.
Several large epidemiological studies from the past decade suggest that the older a man is when he has a child, the more likely he is to have a child with autism or schizophrenia. For example, one study reported that men aged 50 years and older are twice as likely as men under age 30 to have a child with autism. At the same time, sequencing studies suggest that each year a man ages, he passes an estimated two more de novo, or spontaneous, mutations to children he sires.
Many scientists assumed these two phenomena were linked. “People have put two and two together and said that the extra mutations explain the increased risk in the children,” says lead investigator Jacob Gratten, a research fellow in neurogenetics and statistical genomics at the University of Queensland in Brisbane, Australia.
Gratten and his colleagues used mathematical models to determine whether this assumption holds up. The models incorporate published estimates of how de novo mutation rates in the general population change with paternal age, theprevalence of autism and schizophrenia in the general population, as well as the conditions’ heritability and effects on fertility.
The findings suggest that de novo mutations in sperm account for, at most, 20 percent of the increased autism and schizophrenia risk associated with the father’s advanced age. “The small number of additional mutations in children with older fathers can’t really explain the increase in risk that we see,” Gratten says.
The findings are convincing and based on reasonable assumptions, say other experts. “This paper does a good job on the theoretical components,” says Mark Daly, associate professor of medicine at Harvard University, who was not involved in the work. “[It] indicates that there may be other more substantial contributors to the paternal age effect.”
Gratten and his colleagues built four mathematical models that each predict autism risk in the children of older fathers for different combinations of risk factors. The researchers looked for combinations that could account for the 20 percent increased risk for men who are 35 to 39 years old, relative to men a decade younger, a figure reported in several large epidemiological studies.
All four models assume that the risk of autism in the general population is 1 percent and that men who are 35 to 39 years old transmit 20 more mutations to their children than do men in their mid-to-late 20s. The four models differ in how strongly they assume de novo mutations contribute to autism risk, as well as whether the de novo mutations act alone or in combination with other variants.
For example, the scenario the researchers say is most realistic assumes that de novo mutations account for about 20 percent of autism risk and inherited variants account for at least half and that people with autism have 35 percent as many children as those in the general population. In this situation, a father’s age-related mutations account for only about 10 percent of the increase in autism risk due to paternal age.
“It’s quite clear from this that it’s very difficult to get close to [accounting for] the paternal age effect without some very, very extreme ideas about how these de novo mutations contribute to autism,” says Stephan Sanders, assistant professor of psychiatry at the University of California, San Francisco, who was not involved in the work.
Genetic epidemiologist Elise Robinson says she has come up with a similar estimate for the role of de novo mutations in the paternal age effect through a preliminary, unpublished analysis of genome sequences from more than 2,000 families. “What they predict through their models is pretty much what we see empirically,” says Robinson, instructor in medicine at Harvard University, who was not involved in the new study.
Gratten and his colleagues developed a fifth model to test an alternate explanation for the paternal age effect: that men with a high genetic risk for autism—and who show autism traits—tend not to have children until they are older.
The researchers found that a man’s genetic risk for autism would only need to be weakly linked to a delay in fatherhood to account for more than half of the paternal age effect. Even so, the researchers say that autism-like traits are not likely to be the whole story.
“We don’t think that this alternative mechanism, which is really just a hypothesis, accounts for all the risk on its own,” Gratten says. “Probably de novo mutations contribute, and this mechanism may also contribute, and many others may as well.”
Still, this alternative hypothesis “makes sense for autism and seems quite likely for schizophrenia too,” says Bernie Devlin, professor of psychiatry at the University of Pittsburgh, who was not involved in the work. That’s because de novo mutations are believed to contribute to only a small fraction of risk for either condition. For autism, de novo mutations are thought to account for about 3 percent of risk.
To find a link between autism traits and delayed fatherhood, studies would need to include more than 100,000 men of various ages and genetic backgrounds, the researchers estimate. Studies with such sample sizes do not yet exist but may be available soon, Gratten says. “What we’re really doing is putting forward a hypothesis, which we hope will inspire people to follow up as the available datasets get to the size that we think we need.”
Probiotic supplements may have clinical and metabolic benefits for patients with rheumatoid arthritis (RA), according to a study published in the International Journal of Rheumatic Diseases.
After 8 weeks of taking probiotics, patients with RA showed improvement in Disease Activity Score of 28 joints (DAS-28), serum insulin levels, homeostatic model assessment-B cell function (HOMA-B), and serum high-sensitivity C-reactive protein (hs-CRP) concentrations.
The study included 60 patients with RA aged 35 to 70 years. Each participant was randomized to receive probiotic capsules (n=30) or placebo (n=30). Participants in the probiotic group received a once-daily capsule for 8 weeks that contained 3 probiotic strains: Lactobacillus acidophilus (2 × 109 colony-forming units [CFU]/g), Lactobacillus casei (2 x 109 CFU/g), and Bifidobacterium bifidum (2 x 109 CFU/g). Participants in the placebo group received capsules filled with cellulose once-daily for 8 weeks. The researchers took fasting blood samples from participants at the beginning and end of the study period.
Compared with the placebo group, participants in the probiotic group showed improvements in DAS-28 (-0.3 ± 0.4 vs. -0.1 ± 0.4). Participants in the probiotic group also had significant decreases in serum insulin levels (-2.0 ± 4.3 vs. +0.5 ± 4.9 μIU/mL), HOMA-B (-7.5 ± 18.0 vs. +4.3 ± 25.0) and serum hs-CRP concentrations (-6.66 ± 2.56 vs. +3.07 ± 5.53 mg/L) compared with placebo.
Zamani B, Golkar HR, Farshbaf S, et al. Clinical and metabolic response to probiotic supplementation in patients with rheumatoid arthritis: a randomized, double-blind, placebo-controlled trial. Int J Rheum Dis. Published online May 2, 2016. doi:10.1111/1756-185X.12888.
1. First things first, the phrase “double-jointed” is inaccurate — it actually has to do with loose ligaments.
The medical term is hypermobility or laxity (looseness) of the joint, which means the joint can move beyond a normal range of motion, says Dr. Jonathan Vigdorchik, professor of orthopedic surgery at NYU Langone Medical Center.
Three things determine a joint’s range of motion: bone stability (how the joint sockets fit together), ligaments and tendons (the connective tissue wrapping around the joint to hold it in place), and the surrounding muscles (that keep your joint aligned when you move).
Hypermobility can be associated with a range of medical conditions (more on some of those in a sec) or it can just be something random that your body does occasionally. It’s usually caused by loose ligaments and tendons that don’t properly connect the joint, says Dr. Jennifer Hand, medical geneticist and dermatologist at the Mayo Clinic. That looseness can be from a defect in connective tissue, or from repeated extension and contortion of the body in a way that stretches the ligaments.
2. It’s totally normal to have a hypermobile joint here and there, especially in the hands.
Having a bendy finger or two is super common since the hand is full of joints and ligaments. Something like that, or a random backwards-bending elbow, is called localized hypermobility, meaning it’s specific to one joint. This happens when specific ligaments happen to be loose or the bone is abnormal, says Vigdorchik.
You might also develop hypermobile joints from putting unique stress on them at young age when those bones are still forming (like a baseball pitcher’s throwing shoulder) or if an injury causes them to heal in a weird way.
3. But some people have generalized joint hypermobility, which means they’re bendy and “double-jointed” all over.
Generalized hypermobility means that many joints in the body can move beyond the normal range of motion due to an overall looseness in ligaments. Exactly which and how many major joints are affected — the hips, shoulders, or knees — and the severity of associated joint problems varies by person, Vigdorchik says.
“A lot of people with generalized hypermobility don’t even notice until they’re adults and they start to have joint pain,” he says. It’s more common in women than men, says Hand, but doctors don’t have enough research to explain why gender is such a big factor.
4. A doctor can actually diagnose this with special flexibility tests.
Ehler-Danlos National Foundation / Via ednf.org
You don’t need to see a doctor if you are hypermobile, but if you’ve had dislocations and joint pain or you’re super bendy and just want to know what’s up, you can see a doctor to test for it. They’ll perform series of tests to assess the mobility of the joints on a 9-point scale called the Beighton score.
“You get one point for each pinky finger, elbow, knee, shoulder, etc.,” Vigorchik says. Basically, it’s an easy way for doctors to diagnose hypermobility without genetic testing for a related disorder. You have to score at least a 5 to have generalized hypermobility, says Hand, but from there, the looseness of your joints is on a spectrum and can range from moderate to severe.
5. In some cases, having flexible joints all over can be a symptom of a more serious genetic disorder that affects the connective tissue.
US-D, MedPix Medical Image Database, Wikimedia Commons / Via commons.wikimedia.org
When generalized hypermobility comes with a lot of other symptoms, it’s usually associated with the following:
–Ehlers-Danlos syndrome (EDS)
–Postural orthostatic tachycardia syndrome (POTS)
People with EDS or Marfans can experience a range of other serious symptoms because these disorders cause a defect in all the connective tissue in the body, which includes not only the ligaments around joints but also the blood vessels, aorta, eyes, internal organs, and skin. So along with bendy joints, people can have fatal and disabling symptoms like aortic rupture or cataracts. POTS is an autonomic disorder also seen in hypermobile patients, says Vigdorchik, and it affects pulse and blood pressure, so patients often feel light-headed and fatigued. These definitely aren’t the only disorders to be associated with hypermobility, but they’re a few of the most common ones.
6. Ehlers-Danlos syndrome, one of the most common causes of severe hypermobility, can range from mild to fatal.
Veronica Foale CC BY-NC-ND / Via Flickr: sleeplessnights
EDS is actually a group of disorders caused by a defect in collagen, a connective tissue that supports your joints, skin, blood vessels, and other organs. There are six different subtypes, and most (but not all) include hypermobility.
“People with EDS tend to have the hypermobility but also chronic pain, a history of sprains and dislocations, skin elasticity [pictured above], scars and bruising, bowel problems, and blood vessel ruptures depending on their subtype,” says Hand. And there’s a lot of variation in the subtypes. One subtype, “hypermobility type,” can just make you super bendy with minor joint pain, while another can cause serious issues like aneurysms. Fortunately, there’s genetic testing that can determine which type of EDS you have.
7. But you can also just be a super-hypermobile, bendy person.
Technically it’s called benign joint hypermobility syndrome, but recently doctors havere-classified it under Ehlers-Danlos hypermobility type, since they are so similar.
Hypermobility syndrome (for short) is diagnosed when, in addition to generalized hypermobility, people have discomfort, joint injuries, or pain for more than 12 weeks and genetic disorders have been ruled out. It’s a spectrum disorder, says Vigdorchik, so it ranges from mild to severe joint extensibility and musculoskeletal symptoms. “Some people are just really good at yoga and contortion acts — and it doesn’t hurt them, because they’re on the end of spectrum with few other symptoms,” Vigdorchik says.
8. With severe hypermobility, activities like walking and exercising can cause serious injury.
Youtube user exwrestlter125 / Via youtube.com
When bigger joints like the shoulder socket or hips and knees move around a lot, it can become super uncomfortable to do normal things like walking and carrying objects. For example, if a hypermobile person runs, the kneecaps can slide back and forth and grind down on the cartilage because the ligaments in the knees are too loose to keep the kneecap joint in its groove, Vigdorchik says.
It’s common to have tears, sprains, dislocations, and overuse injuries from severe hypermobility. These can require anything from simple physical therapy and rest to surgeries like hip replacements. Many patients with EDS struggle with chronic pain and disabilities because of recurring injuries.
9. And it can actually be annoying and painful to be able to dislocate your joints.
mdumont10 / Wikimedia commons / Via commons.wikimedia.org
GE Malone / Wikicommons / Viacommons.wikimedia.org
A lot of hypermobile people can easily dislocate their joints and pop them back in place. If the joint is super loose and dislocations happen regularly, it might not hurt much, but it can also be just as painful as a dislocation is for anyone without hypermobility.
“A hypermobile person’s shoulder joint can dislocate from just reaching your arms behind your back to fasten a bra,” Vigdorchik says. So in many cases, it’s unintentional and pretty annoying. Not all joints can be easily popped back into place, so it can actually wind up costing you a ton in trips to the ER for a doctor to relocate and align your joints.
10. So those “party tricks” can hurt you.
imgur.com / Via reddit.com
If you’re born super bendy, it might seem fun to wow people with crazy party tricks and weird contortion acts. In many cases of hypermobility, these tricks can be harmless and actually give people an advantage in things like gymnastics or ballet, Vigdorchik says. But since the joint is already unstable, over time these weird movements can stress the ligaments and tissues and cause painful injuries. So even if your hypermobility isn’t severe, if you’ve had any pain or joint problems, it’s smart to avoid this.
The experts warn against doing any weird joint tricks if you have a serious form of EDS or Marfans, because it’s more likely to result in injury. “It also really depends on the person and the limits of their body, but it’s always better to be cautious,” Hand says.
11. If you do end up injuring yourself or just dislocate often, you might want to try physical therapy.
Instagram: @businessinsider / Via instagram.com
People often notice their symptoms after exercising, Vigdorchik says, because they get injured due to the lack of stability in the joints. But hypermobile people shouldn’t be discouraged from exercise — they just might need to meet with a physical therapist and take extra steps to avoid further problems.
The experts say that you can somewhat overcome loose ligaments by doing specific isometric exercises to strengthen the muscles around the joint to keep it super stable — especially in the knees and hips. Even hypermobile-friendly exercises like yoga can put joints under stress, so it’s important to focus on strength training and knowing your limits, Vigdorchik says.
12. There is no cure for severe hypermobility or EDS, but treatment includes pain management and surgery.
Purestock via Thinkstock / Via thinkstockphotos.com
“Besides monitoring any possible heart or eye issues, treatment is usually anti-inflammatory pain meds, ice and compression, bed rest, and that’s about it, because the real cause is an incurable genetic problem,” says Vigdorchik. The experts do warn against muscle relaxers (which make the joint less stable) and opioids (because they’re addictive).
Some people need surgeries to alter the bone and create joint stability, Vigdorchik says, especially after injuries like hip dysplasia (a painful misalignment of the hip joint) or knee dislocation. Otherwise, many patients explore different holistic and therapeutic options for the chronic pain. The prognosis for someone with severe hypermobility varies by person, but unless it affects the blood vessels, it’s a manageable and non–life threatening condition.
13. It’s not uncommon for these painful physical symptoms to affect mental health.
unspokenwords.tumblr.com / Via instagram.com
“I think many hypermobile patients suffer from anxiety and depression because they go through years of pain and hundreds of doctors with no answer — I’ve even seen people who’ve had multiple invasive surgeries for the wrong thing, which was later diagnosed as EDS,” says Vigdorchik.
The experts explain it’s an easily overlooked and misunderstood condition because there’s still a lot of research to be done and hypermobility occurs on such a wide spectrum, varying greatly by the individual. And even though a diagnosis does bring relief to patients, Vigdorchik says, many have trouble coping with the fact that it’s a chronic illness with no cure. That being said, knowing your diagnosis can help you to understand your symptoms better so you can manage them properly to get healthy and happy again.
14. So if you need to talk to someone, there are support groups and online communities that can help.
Instagram: @zebrasurvivors / Via instagram.com
The hypermobile, EDS, and Marfans syndrome communities have formed many online spaces to provide education, resources, and support for affected people and their families. Popular resources include the Ehlers-Danlos National Foundation andEhlers-Danlos Syndrome Today Advocates. You can also find support on Instagram and Tumblr, where people with hypermobility disorders (who call themselves “zebras” or “zebra warriors”) share their experiences and connect with each other.
“The most important thing is that patients with severe hypermobility or EDS suffering from chronic pain and other symptoms know it’s not in their head and there are a lot of people out there just like them,” Vigdorchik says.
15. Doctors are still working hard to understand more about these disorders and increase awareness.
Instagram: @_dysautonomiahumor / Via instagram.com
There’s a big lack of understanding and awareness of what these disorders mean to people, says Vigdorchik, but this will change with more research and awareness efforts. Supposedly, the first case of hypermobility was described in 400 BCE by Hippocrates — so we’ve been trying to figure this thing out for a long time. The definition and classification of Ehlers-Danlos syndrome has changed so much over the last few decades as doctors have learned about the underlying genetics and different subtypes.
So, if you can move way too many joints and frequently experience joint pain or dislocation, you might want to get tested just in case to avoid any potential injury. And if you’re just hypermobile with no other symptoms, enjoy being super flexible (carefully, please).
And PS: Puppies can have hypermobility and EDS too!