SHOWING THE WAY: Suzanne Razaq (right) looks at her daughter Zara Cheek’s insulin pump and her glucose meter in Baltimore.
By Jonathan Pitts
As seven-year-old Zara Cheek packed her bags for her first sleep-away camp this summer, she found herself looking forward to more than just swimming, going on hikes and eating S’mores for two glorious weeks.
To her, the experience meant a chance to live like a normal kid for a while — and even, quite possibly, to help thousands of others afflicted with the illness that has shaped her life.
Zara, who lives in West Baltimore and started third grade this autumn, is one of about 2mn Americans who suffer from Type 1 diabetes, a chronic and potentially lethal disorder of the pancreas that leaves the body unable to make insulin or turn blood sugar into the energy it needs.
Though its causes are unknown, the implications of Type 1 diabetes are well established. Most who have it experience an acute onset, usually before age 30. Symptoms generally include weight loss, increased thirst and a need to urinate frequently. Sufferers must be given artificial insulin.
If left insufficiently treated, Type 1 diabetes can spark dangerous spikes or drops in blood-sugar level and, in the long term, complications as dire as heart failure and stroke.
Unlike Type 2 diabetes, which affects about 27mn Americans and can often be treated purely by diet and exercise, Type 1 diabetes is one of the world’s most taxing chronic illnesses to manage.
Diagnosed at age two, in 2008, Zara — an avid reader with a shock of sun-kindled blonde hair — has rarely been separated from the glucose sensor, digital monitor and electronic insulin pump she wears on her belt. Nor have her parents, Daniel Cheek and Suzanne Razaq, been free of the responsibility of monitoring that equipment 24 hours a day and adjusting it as a blizzard of factors evolve, from the amount of exercise Zara plans to take to the amount of stress she’s feeling.
“It’s an incredibly intense disease to handle, and unfortunately, it’s one that never lets up,” said Dr Robert Ratner, chief scientific and medical officer of the American Diabetes Association. This summer, Zara and her family finally got a chance to take a break.
Razaq, a real estate agent, was surfing the Internet late one night in July when she happened on a website that caught her eye. A Boston University biomedical engineer had spent years developing a system with all the functions of Zara’s equipment that, in effect, ran itself.
It had performed well in real-world settings, she read, and the engineer, Ed Damiano, was looking for child volunteers to test it in clinical trials at a summer camp in August.
Called a “bionic pancreas,” it included a glucose sensor, a display monitor and a pump that delivered insulin. What made it different was that Damiano had added a “brain” to the system.
Where caregivers must watch a patient’s levels, assess the changing conditions of a given day, estimate each dosage size and program the pump to deliver it, Damiano and his team had developed a mathematical algorithm by which a smartphone-sized computer could assess those changing factors, make every calculation on its own, then dispense the appropriate dose, all without the conscious intervention of the patient or caregiver.
Various researchers have been working on developing an artificial pancreas for years, Ratner said. Such a device, he added, ideally will function like “the pancreas Mother Nature made,” measuring the body’s needs, “squirting” insulin in just the right amount, then shutting off to prevent overdose. About 20 groups around the world are working on such a project.
While Damiano is still in the process of seeking FDA approval, Razaq said she learned his device is approaching that ideal. It still consists of three separate units, not one, but they’re about the size of the ones Zara already wears. It also takes glucose readings 288 times a day, tailors the dosage size each time, and delivers it, whether the patient is sleeping, going to class or dribbling a basketball.
The device does nothing to advance a cure — researchers say that outcome could be decades away — but it has the potential, Razaq said, to free sufferers and caregivers alike from having to think about Type 1 diabetes care every waking moment.
The previous summer, she learned, Damiano and fellow researchers, including a medical team from Massachusetts General Hospital, had run a two-week camp for adolescent Type 1 diabetes sufferers at Camp Clara Barton, a retreat and diabetes research centre in Oxford, Massachusetts. Attendees wore the device during normal camp activities.
The trial data suggested that the bionic pancreas keeps glucose levels significantly more stable than other available methods. “The results were good — much, much better than even we anticipated — and the kids seemed to have a great time,” said Damiano, whose paper on the project was published in the New England Journal of Medicine in June.
Razaq fired Damiano an e-mail to see if Zara could attend the next camp. She knew it was a long shot, as there was a sizable waiting list, but Zara happened to be one of the few 7-year-old applicants who fit the necessary medical profile and were willing to be away from home for two weeks. Within days, she was packing.
For 14 days in August, she lived like any other kid at camp — sleeping in tents, downing hot dogs, playing soccer — as the device did its work.
It was a time, she said, when she and the 11 other girls in the study didn’t have to count carbs, adjust dosing or make any preparations before exercise. No matter the stress she put on it, she said, the bionic pancreas made the necessary adjustments.
“I had an excellent time, and I never got homesick,” she recalled in her living room, flashing a multicoloured headband and bracelets she made at camp. “I can’t wait to go next year.”
Damiano, whose son, David, has Type 1 diabetes, has vowed to get the device to market by the time the young man goes off to college in 2017. He believes they’ll make the deadline. (Their next challenge: to meld the parts into a single unit a little bigger than a smartphone.)
Razaq is certainly hopeful. It wasn’t easy to let her daughter, now 8, go for two weeks, she said, but it was worth it. “If (the bionic pancreas) comes to market, Zara may be one of the early recipients,” she said.
“If it becomes the standard of care, she will have helped make history. But even if it doesn’t make it to market, Zara (has) experienced what it feels like to be a kid without diabetes.” — The Baltimore Sun/MCT
Is postpartum depression
a modern-day affliction?
Did prehistoric mothers suffer from postpartum depression?
Jennifer Hahn-Holbrook, a psychology professor at Chapman University, in Orange, California, has been researching whether the condition can be considered a so-called disease of modern civilisation such as obesity and type 2 diabetes.
Hahn-Holbrook and Martie Haselton of UCLA wrote a paper examining the connection between postpartum depression rates and lifestyle factors that differ significantly from earlier eras.
They note that hunter-gatherer women breastfed for several years, had consistent exposure to vitamin D through sunshine and lived among extended family. Additionally, they would have exercised more and eaten diets rich in omega-3 fatty acids from wild organ meat, both of which have been linked to lower rates of depression.
Hahn-Holbrook also recently gave birth to her first child and is on maternity leave from Chapman. “My question is: Is this a normal state of human affairs?” she said. “Because it is so devastating to mothers and babies, it just didn’t make sense to me that we were built this way and that 1 in 5 mothers were going to experience a debilitating illness at a time when we needed to be on our A game.”
The exact causes of postpartum depression are unknown, but medical experts note that changes in hormone levels may influence mood. Changes in work and relationships, a reduction in leisure time and freedom, lack of sleep, and worries about motherhood may also play a role.
In addition to typical depressive symptoms, postpartum depression may include feeling numb or disconnected from the baby; having scary or negative thoughts, including fear of harming the baby; and feeling guilty about not being a good mother, according to the Centers for Disease Control and Prevention.
Postpartum depression varies from the so-called baby blues, which commonly include mood swings and teariness but don’t last longer than two weeks.
Hahn-Holbrook said postpartum depression rates vary around the world, suggesting that societal factors play a role. For instance, breastfeeding rates are much lower than they were for most of human history, with roughly 20% of American mothers never trying it. The paper notes that prehistoric fossils indicate that infants were weaned between ages two and four.
Hahn-Holbrook runs a breastfeeding research lab where she’s found that breastfeeding mothers experience less stress than other women. Additionally, other studies have shown that nursing mothers are less likely to be depressed. “I think evolution built in some mental health effects,” she said. “By not doing that, I think some women aren’t getting their postpartum stress buffer.”
Lack of communal support is also a big challenge for many new mothers, which could be contributing to depression rates, she said. “Somebody to hold the baby while you take a shower is the difference between sanity or not,” she said. “I live 1,000 miles away from my nearest blood relative, and it is not easy. We’re what we call co-operative breeders. Human children are the most labour-intensive mammals.”
The paper also explores vitamin D, which has anti-inflammatory properties. Some studies have linked deficiency to depression.— By Courtney Perkes, The Orange County Register, MCT
Antidepressants rapidly alter
brain architecture, study finds
A single dose of a popular class of psychiatric drug used to treat depression can alter the brain’s architecture within hours, even though most patients usually don’t report improvement for weeks, a new study suggests.
More than 1 in 10 adults in the US use these drugs, which adjust the availability of a chemical transmitter in the brain, serotonin, by blocking the way it is reabsorbed. The so-called Selective Serotonin Reuptake Inhibitors, or SSRIs, include Prozac, Lexapro, Celexa, Effexor, Paxil and Zoloft.
The findings could be a first step toward figuring out whether a relatively simple brain scan might one day help psychiatrists distinguish between those who respond to such drugs and those who don’t, an area of mystery and controversy in depression treatment.
Researchers at the Max Planck Institute in Leipzig, Germany, used a magnetic resonance imaging machine to compare connections in the grey matter of those who took SSRIs and those who did not. They were particularly interested in what goes on when the brain is doing nothing in particular.
“We just tell them to let their minds wander and not think of anything particularly dramatic or upsetting,” said neuroscientist Dr Julia Sacher, a co-author of the study published online in the journal Current Biology.
They created 3-D maps of connections that “matter” to grey matter: interdependence, not just anatomical connection. They relied on a discovery in the late 1990s that low-frequency brain signalling during relative inactivity, such as daydreaming, is a good indicator of functional connectivity.
When more serotonin was available, this resting state functional connectivity decreased on a broad scale, the study found. This finding was not particularly surprising — other studies have shown a similar effect in brain regions strongly associated with mood regulation.
But there was a twofold shock: Some areas of the brain appeared to buck the trend and become more interdependent. And all the changes were evident only three hours after the single dosage.
“It was interesting to see two patterns that seemed to go in the opposite direction,” Sacher said. “What was really surprising was that the entire brain would light up after only three hours. We didn’t expect that.”
Most people who use antidepressants don’t report any discernible change in mood for at least two weeks, said Sacher, who also is a psychiatrist.
The rapid connectivity shifts noted by the study might therefore be precursors to longer-term changes, perhaps starting with remodelling of synapses, the microscopic gaps where chemical neurotransmitters such as serotonin flood across to an adjacent brain cell, the study suggests. But this type of brain scanning can’t pick up changes at such a scale, so the hypothesis will have to be tested other ways, Sacher added.
More research also will be needed to explain why the functional connectivity of the cerebellum and thalamus apparently increased. The cerebellum, or “little brain” is a relatively primitive structure that processes signals from the spinal cord, relaying them to the thalamus and on up to the cortex. Many of those pathways are regulated by serotonin.
Although the cerebellum is associated mostly with such basic functions as motor control and co-ordination, there are hints that it plays a role in higher cognitive tasks, perhaps by changing the way the thalamus relays signals to the cortex.
Although many open hypotheses remain to be explored, the brain maps produced by the study advance the effort to identify a brain “fingerprint” for those who might respond to SSRI therapy, researchers said.
Study subjects did not have diagnoses of depression, so researchers will need to generate similar maps among those diagnosed with depression, and re-map them during and after depressive episodes, as well as after treatment, Sacher said. Comparisons might then show whether a certain initial architecture predicts treatment success. — By Geoffrey Mohan/Los Angeles Times, MCT