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Chronic Disease

Chronic Disease, Health Costs, Patient Care, Stanford News

Stanford Coordinated Care: A team approach to taming chronic illness

Stanford Coordinated Care: A team approach to taming chronic illness

team handsNearly two years ago, Stanford began an experiment in medical care, a novel way to bring down the extravagant costs of health care while improving people’s health and their experience with the system. If you ask Shelly Reynolds, RN, one of the first patients to benefit, she will tell you it’s been a wild success.

“They hold me accountable for my own health, which is great,” she told me for my recently published Inside Stanford Medicine story. “Physically and emotionally, I’m healthier than I was before.”

And the experiment is costing less, according to initial figures.

The experiment is called Stanford Coordinated Care, a clinic aimed at helping those who consume the lion’s share of health care dollars. These are patients with chronic illnesses, like diabetes or asthma, who often wind up in emergency rooms or in the hospital because their conditions aren’t being well-managed.

The clinic helps them gain control over their health through a personalized approach by a team of caregivers who are available day or night and who give them the tools and support to manage their conditions at home. It focuses on the patients’ goals and what is important to them.

“It’s easy to make a diagnosis of diabetes, but it can be hard for a person to manage day by day,” Ann Lindsay, MD, one of the clinic co-directors, commented. “We help patients in developing a plan. We support it, and we empower them along the way.”

The clinic is the brainchild of Arnold Milstein, MD, a professor of medicine at Stanford and nationally known health care innovator. He developed a model, called the “ambulatory caring ICU,” which was tested successfully in several major pilot sites around the country. He wanted to bring the model to Stanford and recruited the husband-and-wife team of Alan Glaseroff, MD, now a professor of medicine at Stanford, and Lindsay, who had led one of the sites in California’s Humboldt County.

The clinic now has more than 200 patients, all employees and their families at Stanford University and Stanford Hospital & Clinics. Glaseroff calculates that among the first 27 patients treated in the first six months of the clinic’s opening in May 2012, it saved about $420,000, a 39 percent decline in costs from the previous six months, when patients were receiving care elsewhere. He said the numbers are still small and that research is under way to determine if the model is effective in reducing costs, improving outcomes and promoting patient satisfaction.

Initial findings show patient satisfaction at 100 percent. Reynolds is a good example: Working with Lindsay, she has developed a plan to effectively manage her asthma and her back pain and keep her out of the emergency room. She no longer feels like “a number” in the health care system and says having support from Lindsay has made all the difference: “For the first time in a long time,” she told me, “I felt that someone was looking out for me, advocating for me. It was such a relief.”

Previously: Focusing on the whole person to treat chronic disease – and cut costs, At-home program aimed at helping patients with chronic illness and Innovative Stanford clinic to support chronic care patients
Photo (modified from original) by bibendum84

Chronic Disease, Public Health, Research

If your partner has Type 2 diabetes, you may also be at risk

couple_013014When assessing a patients’ risk of developing Type 2 diabetes, physicians may want to consider expanding their questions about family medical history and lifestyle to include if their spouse has been diagnosed with the disease. A study recently published in BMC Medicine found that partners of individuals with diabetes have a 26 percent increased risk of also developing the condition.

A post published today on Futurity explains the findings (subscription required): 

Researchers analyzed results from six selected studies that were conducted in different parts of the world and looked at key outcomes such as age, socioeconomic status, and the way in which diabetes was diagnosed in 75,498 couples.

Most of the studies used in the meta-analysis relied on health records, which may not always accurately record diabetes. Those that used direct blood testing suggested that diabetes risk doubles if your partner has diabetes. They found a strong correlation with pre-diabetes risk.

The study offers more evidence that the lifestyle choices of your friends and family, particularly in your household, influence your health habits. Researchers of the latest study say the findings could help doctors develop strategies to change patient’s health behaviors that involve both partners.

Previously: The scientific importance of social connections for your healthExamining how your friends influence your health and Can good friends help you live longer?
Photo by Bradley Gordon

Chronic Disease, Immunology, Research, Stanford News

Another piece of the pulmonary-hypertension puzzle gets plugged into place

Another piece of the pulmonary-hypertension puzzle gets plugged into place

puzzle piecePulmonary hypertension, a dangerous increase in the pressure of blood vessels in the lung, is one nasty disease, as I wrote in a Stanford Medicine article a few years ago. As many as three times as many women – many of them quite young – as men are diagnosed with the spontaneous form of PH (which can also arise from scleroderma or bad pharmaceuticals). While an increasing number of pharmaceutical treatments and advocacy groups have made the diagnosis more palatable, there is still no outright cure. Largely, this is because the molecular mechanisms of pulmonary hypertension have remained mysterious.

But recent work has strongly implicated inflammation in pushing predisposed tissues over the edge into the diseased state. And this week, a Journal of Experimental Medicine study led by PH specialist Marlene Rabinovitch, MD, and her colleagues at Stanford’s PH-focused Vera Moulton Wall Center plunks a potentially pivotal piece of the puzzle into place. Rabinovitch and her associates showed that levels of a pro-inflammatory growth factor usually designated by the acronym GM-CSF (if you really must know, it’s “granulocyte-macrophage colony stimulating factor”) rise substantially when a cell-surface receptor with a heavyweight acronym of its own, BMPR2 (for “bone morphogenic protein receptor”) isn’t functioning properly. That can be due to mutations in the gene that codes for the receptor (as occurs in familial versions of PH), to various environmental causes, or the interaction of the two.

Elevated GM-CSF levels in pulmonary tissue work like a siren to call various hot-tempered inflammatory cells to the vasculature of the lung, resulting in thickened vessel walls and commensurately narrowed blood vessels. Conversely, by finding ways to compensate for BMPR2 under-performance, perhaps researchers will be able to develop therapeutics that keep GM-CSF levels within safe limits, modifying the course of incipient PH or even arresting it.

Several million actual and potential sufferers await that Big If with bated breath.

Previously: Researchers reverse pulmonary hypertension in rats by blocking inflammation-producing pathway, New arterial insights portend potential treatments for life-threatening diseases, and Man receives life-saving transplant thanks to health-care reform and a truck
Photo by ePublicist

Chronic Disease, Technology

A rare-disease patient turns to the Internet for comfort, confidence in managing her condition

woman_computerOverall there are 7,000 rare diseases affecting more than 25 million Americans, according to the National Institutes of Health. But since fewer than 200,000 people are diagnosed with any one specific rare disease, patients often feel isolated in their struggle to manage their condition.

In a recent Atlantic piece, rare disease patient Simona Supekar explains how her diagnosis of idiopathic angioedema and chronic urticaria prompted her to turn to the Internet to cope with the condition. In doing so, she found the comfort of a support network and confidence to be her own health-care advocate. She writes:

It’s this small group of people online, hailing from right here in Los Angeles to as far as England, South Africa, Nigeria, and beyond, who’ve been able to help me cope with the anvils that angioedema throws at you. People I’ll likely never meet.

Besides support, I’ve gained valuable treatment insights from them, too. The nature of this condition—that it’s idiopathic—means that doctors really don’t know how to treat it or what causes it.

But my fellow sufferers have taught me that I do have some control over this. I learned about natural remedies like nettle tea and quercetin, a bioflavonoid derived from fruits. I learned about foods that were high in histamine and salicylates and read the latest peer-reviewed articles about angioedema they shared. I learned about how simply hydrating could lessen the swelling and hives. How Reiki and acupuncture could help with the panic attacks that were now accompanying my bouts of throat swelling. How it was possible to manage this disease on antihistamines alone, as opposed to the heavy steroids I was taking.

But most of all, despite how little anyone knows about this disease and how seemingly rare it is—only about 1 in 1,000 have it—I learned that I am not alone.

Previously: Developing a Google-like search system to improve diagnosis, treatment of pediatric brain disorders, Parent details practical ways to get care and support for your child’s rare disease, When do you tell a potential partner about your rare illness? and Broken: A poem about coming to grips with chronic disease
Photo by Pascal Marmanis

Aging, Chronic Disease, Health and Fitness, Men's Health, Research, Women's Health

More evidence that prolonged inactivity may shorten life span, increase risk of chronic disease

More evidence that prolonged inactivity may shorten life span, increase risk of chronic disease

sitting_deskIf you have a lengthy daily commute, spend hours at a desk clacking on the computer, or sit for a prolonged period for other reasons, a pair of recent studies may have you leaping to your feet.

The first study, conducted by researchers at Cornell University, examined the effects of sitting for a long period of time each day over a 12-year period. Results showed that individuals who were inactive for more than 11 hours had a 12 percent higher mortality rate than those who sat for four hours or less. And don’t think you’re not at risk because you occasionally hit the gym. Cornell researcher Rebecca Seguin, PhD, explained in a Futurity post:

The assumption has been that if you’re fit and physically active, that will protect you, even if you spend a huge amount of time sitting each day… In fact, in doing so you are far less protected from negative health effects of being sedentary than you realize.

While this study focused on postmenopausal women, additional research from Kansas State University shows that the health risks of being sedentary affect both both genders. The study analyzed data on nearly 200,000 men and women ages 45 to 106 taken from a large Australian study of health and aging. The research showed that both exercising and reducing sitting time were key to improving health. MedicalXPress reports:

Even standing throughout the day—instead of sitting for hours at a time—can improve  and quality of life while reducing the risk for  such as , diabetes, heart disease, stroke, breast cancer and colon cancer, among others.

Sitting for prolonged periods of time—with little muscular contraction occurring—shuts off a molecule called lipoprotein lipase, or LPL, [Sara Rosenkranz, PhD,] said. Lipoprotein lipase helps to take in fat or triglycerides and use it for energy.

“We’re basically telling our bodies to shut down the processes that help to stimulate metabolism throughout the day and that is not good,”  [Rosenkranz] said. “Just by breaking up your , we can actually upregulate that process in the body.”

Previously: Exercise is valuable in preventing sedentary deathIs standing healthier than sitting?How sedentary behavior affects your health and Stanford hosts conference on the science of sedentary behavior 
Photo by Danny Choo

Autoimmune Disease, Chronic Disease, Dermatology

My two-decade battle with psoriasis

My two-decade battle with psoriasis

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often rare diseases share their unique stories; the latest comes from Alisha Bridges.

Psoriasis has affected every aspect and transition of life that I’ve encountered thus far. I’ve had the itchy, flaky, non-contagious autoimmune disease since I was 7 years old; I’m now 26. As I approach the 20-year anniversary of encountering the disease, I think of how my treatment has evolved, and as I reflect on the differences in treatment between then and now, it’s a Catch-22 in some ways.

It all started after a bad case of chicken pox. My scars weren’t healing correctly. They looked crusty and inflamed. After more than 90 percent of my body remained covered with this mysterious rash, my grandmother decided it was time for me to see the doctor, who diagnosed me with psoriasis. The positive side was that I had Medicaid as insurance, and it covered any and everything I needed. But unfortunately, due to my age, there weren’t many treatment options. From the age of seven to 19, I was prescribed an array of topical treatments and UVA light treatment, none of which were really effective in ridding me of psoriasis. The treatments just kept it at bay.

Once I went to college, treatment became more challenging. First, I went out of state for college, so the only time I could get treatment was when I came home for winter vacation. This particular treatment required me to stay in the hospital for three weeks, which was basically my entire winter break. Once I realized a treatment twice a year wasn’t going to be effective, my family attempted to find me a doctor near my school. The only caveat then was that Medicaid is state-to-state; therefore I was removed from hometown Michigan Medicaid and required to apply for Alabama Medicaid where I attended school. I wasn’t approved for Alabama Medicaid, though, which caused me to go essentially without insurance, aside from the simple coverage the school offered for emergencies.

After a few years of being in school without any insurance, I finally landed a job with coverage and started my routine doctor visits. This time I had more options. As a child I couldn’t consider biologic injections and oral medications, but as a working adult these options became available to me. The flip side was and remains that the medicine is harder to get because of high deductibles and regulations by insurance. I’ve also found that it’s harder to maintain insurance due to life situations such as layoffs or career changes.

There are vast differences between having this disease as a child through adulthood, yet there are a few similarities that I experienced in both phases of life. Doctors have fought to get me treatment no matter what age. As a teenager with severe psoriasis, doctors attempted to get me approved for Enbrel, which has only been authorized for adults over 18. I’ve even had doctors battle the insurance company to gain approval and decrease the cost of various medicines.

Though there have been many things that have changed there is one aspect of psoriasis that is too often neglected. From childhood until now there have been no coping strategies offered to me when dealing with this disease. Out of the approximately ten doctors I’ve seen in regards to my psoriasis, not one inquired on how the condition affected me psychologically. Although this disease appears to be a battle from the outside, the mental anguish faced as a psoriasis patient is life-altering and can even be virtually paralyzing. Patients need to know that there are other people in the world with this disease, and that there are resources outside of medicine to help them cope. Coping strategies are just as important as treatment. Although I have found organizations such as the National Psoriasis Foundation to help manage this disease, it wasn’t because of professional recommendation. I found them on my own at the age of 24.

I can only fathom how having support would have enhanced the overall quality of life for me if a doctor would have made me aware of these organizations at the age of seven. Although I have struggled to find a successful treatment, knowing that there’s support for the mental aspect of psoriasis will give me peace until a cure is found.

Now, psoriasis does not define me - I define it.

Alisha Bridges is the creator of, where she blogs about life with psoriasis. She’s a community ambassador and volunteer for the National Psoriasis Foundation.

Chronic Disease, Parenting, Patient Care

Parent details practical ways to get care and support for your child’s rare disease

Parent details practical ways to get care and support for your child's rare disease

holding hands with child_560Since rare diseases are inherently uncommon, researchers have few opportunities to learn about them. As Marcela De Vivo explained earlier this month on the National Organization for Rare Disorders (NORD) blog, this can make it hard for people with such disorders to get the care the need.

In her post, Vivo describes the challenges she faced as a mother of a child with a rare disease. But the bulk of her story is crafted to help other parents in similar situations. Think of it as a frank, how-to guide that details the practical ways that parents can overcome the challenges of caring for a child with an uncommon medical condition.

Among the actions she recommends in her post:

  • Become a part of an online community (such as NORD), where you can get information on your child’s disease.
  • Be relentless when trying possible treatments for your child’s condition – if the first (or second or third) treatment is unsuccessful, keep trying.
  • Share what you learn about the treatments your child tries with other parents and with your doctors.

Even if you don’t have a child, this post is an enlightening and helpful read.

Holly MacCormick is a writing intern in the medical school’s Office of Communication & Public Affairs. She is a graduate student in ecology and evolutionary biology at University of California-Santa Cruz.

Previously: The day my doctor thanked meLessons from five million patient and caregiver posts, When do you tell a potential partner about your rare illness?When you say nothing at all: Living with an invisible illness and New search engine designed to help physicians and the public in diagnosing rare diseases
Photo by stephanski

Chronic Disease, Genetics, Neuroscience, Research, Stanford News

Drug found effective in two mouse models of Huntington’s disease

Drug found effective in two mouse models of Huntington's disease

Woody GuthriePerhaps the most famous name associated with Huntington’s disease is that of populist folk singer Woody Guthrie, who died of it at age 52 in 1967. Guthrie’s mom had died of it, too, when Woody was a teenager. So, it’s believed, did his mom’s dad. Two of Woody’s children by his first wife, Mary, died at age 41 of Huntington’s. (In 1968, his second wife, Marjorie, founded the Huntington’s Disease Society of America.)

A person first diagnosed with Huntington’s disease, an ultimately lethal genetic neurodegenerative disorder characterized by jerky movement as well as cognitive and psychiatric problems, can on average expect to live another 20 years – but not without heartache. There are drugs to alleviate some symptoms of Huntington’s, which most often manifests in the fourth and fifth decades of life, but none that delay its onset or slow its progression.

Work by Stanford neuroscientist Frank Longo, MD, PhD, may change that. As described in a study just published in The Journal of Neuroscience, Longo and his colleagues have shown that a drug that mimics some aspects of a key brain protein was able to reduce degeneration and movement deficits associated with Huntington’s disease in two different mouse models of the disorder. The findings add to a growing body of evidence that protecting or boosting neurotrophins — bulky proteinaceous molecules that support the survival and function of nerve cells — may slow the progression of Huntington’s disease and other neurodegenerative conditions.

Longo’s team used a compound called LM22A-4, unearthed by Longo a couple of years ago in a computer search in collaboration with University of California-San Francisco neurologist Steven Massa, MD, PhD. LM22A-4 is a small molecule with less than 1/70 the bulk of the particular protein it mimics: brain-derived neurotrophic factor or BDNF, which has been studied in depth by many researchers and is known to be critical during the development of the nervous system and involved in important brain functions including memory and learning.

But unlike BDNF, LM22A-4 binds to and activates only one of two major cell-surface receptors for BDNF found in nerve cells. That’s a good thing, because the receptor LM22A-4 activates is associated with BDNF’s long-known ability to foster the survival of newborn nerve cells, while the receptor it doesn’t activate has been shown to respond to BDNF stimulation by inducing the death of nerve cells. This is helpful, perhaps, during early development when the brain needs to prune redundant nerve circuitry produced in a series of growth spurts, but it’s presumably going to be counterproductive in the treatment of a neuron-destroying disorder like Huntington’s.

Longo’s group examined the effects of LM22A-4 treatment in mice that were predisposed to develop symptoms of Huntington’s disease rapidly (within weeks) or gradually (within months). LM22A-4 treatment reduced the accumulation of abnormal proteins in the striatum and cortex — brain regions affected in Huntington’s disease. Motor behaviors (downward climbing and grip strength) also improved in the mice that received daily LM22A-4 treatments.

LM22A-4 has also shown promise in the treatment of stroke and other brain conditions. Because it was already commercially available when Longo and his colleagues’ computer stumbled on it, it also promises to be relatively cheap – kind of a “folk drug” – should any of its potential applications pan out. That would make Woody proud.

Previously: Newly identified protein helps explain how exercise boosts brain healthStanford neuroscientists uncover potential drug treatment for stroke and Stanford neuroscientist discusses the coming dementia epidemic
Photo courtesy of the Library of Congress

Chronic Disease, Mental Health, Neuroscience, Research, Science, Stanford News

Star-shaped cells nab new starring role in sculpting brain circuits

Star-shaped cells nab new starring role in sculpting brain circuits

starfishA healthy person’s brain has thousands, or maybe millions, of times as many synapses – contact points that relay signals from one nerve cell, or neuron, to the next – as there are stars in the Milky Way. In a blog entry not so long ago, I wrote:

In a sense, “you” are your synapses. They’re the defining features of the brain circuits that fire up or chill out to generate every thought that passes through your mind and every flicker of emotion or glimmer of recollection you experience. You wouldn’t want to leave home without them. Some of us get no choice. Massive synapse loss accompanies neurodegenerative diseases from Alzheimer’s to Parkinson’s to multiple sclerosis.

In a paradigm-shifting discovery just published in Nature, Stanford researchers found that a common but mysterious class of non-neuronal brain cells, called astrocytes because of their star-like shape, actively refine nerve-cell circuits throughout life by selectively eliminating synapses. much as a sculptor chisels away excess bits of rock to create an artwork.

Astrocytes, which account for between one-third and half of all the cells in our brains, belong to a general category of brain cells collectively called “glia,” from the Greek term for glue. That’s because until not long ago, neuroscientists (note the bias in that term) figured that these seemingly passive cells weren’t much more than packing peanuts for the “really cool” cells, neurons, that hog the lion’s share of attention.

Neurons, which compose merely 10 percent of all the cells in a healthy human brain, are so celebrated they’ve lent their name to brain science: neurology. But a team led by pioneering Stanford gliologist (I made that term up) Ben Barres, MD, PhD, has shown in the new study that astrocytes play a starring role in sculpting the very synaptic connections that are central to consciousness, cognition, motion and emotion.

As I once noted:

[Barres] – who trained as a practicing neurologist before circling back for his PhD – couldn’t help noticing, in autopsies, that the brains of people with “neurological” disorders invariably showed obvious signs of glial disarray. So he resolved to devote his career to the study of glial cells…

Thus began a decades-long efforts to unveil the manifold functions of astrocytes and their glial comrades-in-arms (described in detail in this Stanford Medicine article).  Barres and his colleagues have already shown that astrocytes in particular (there are two other glial cell types) play a critical role in determining exactly where and when new synapses are generated. With the finding that astrocytes also single out outmoded or downright counterproductive synapses and gobble them up, it’s increasingly certain that substantial remodeling of brain circuits takes place in the adult brain and that astrocytes are master sculptors of its constantly evolving synaptic architecture. This holds huge implications, according to my press release on the new study:

The findings also raise the question of whether deficits and excesses in this astrocytic function could underlie, respectively, the loss of this remodeling capacity in old age or the wholesale destruction of synapses that erupts in neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease.

Previously: Protein known for initiating immune response may set our brains up for neurodegenerative disorders, Unsung brain-cell population implicated in variety of autism and Brain imaging, and the ‘image management’ cells that make it possible
Photo by Ed Bierman

Chronic Disease, Stanford News

Preventing pre-diabetes from turning into diabetes

Preventing pre-diabetes from turning into diabetes

Stanford’s BeWell has posted a helpful piece with information on pre-diabetes and how monitoring your fasting blood glucose level can help you stay healthy. Additionally, the piece offers tips – including losing weight and increasing physical activity – on how to keep the condition from progressing into type-2 diabetes.

Why is now the time to start paying attention? The piece explains:

It is estimated that 79 million adults aged 20 and older have pre-diabetes and 25.8 million Americans have diabetes — 8.3% of the U.S. population.

The number of people diagnosed with diabetes each year has risen from 1.5 million in 1958 to 18.8 million in 2010, an increase of epidemic proportions.

What’s more:

Diabetes is the seventh leading cause of death listed on U.S. death certificates. The overall risk for death among people with diabetes is about double that of people without diabetes.

Previously: The exercise pill: A better prescription than drugs for patients with heart problems? and More than three-quarters of Americans projected to be overweight, obese by 2020

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