Published by
Stanford Medicine

Category

Chronic Disease

Chronic Disease, Health Costs, Infectious Disease, Research

Despite steep price tag, use of hepatitis C drug among prisoners could save money overall

Despite steep price tag, use of hepatitis C drug among prisoners could save money overall

pills-384846_640There’s nothing free about the revolution that’s shaking up hepatitis C treatment. A slew of newer drugs, including sofosbuvir, are nearly eliminating the virus with fewer side effects than the old standbys, pegylated interferon and ribavirin, which had limited effectiveness and caused fatigue, nausea and headaches. But at a cost of $7,000 a week, it seems obvious they are more expensive.

Not necessarily, however, says Jeremy Goldhaber-Fiebert, PhD. Working with colleagues including former Stanford graduate student Shan Liu, PhD, Goldhaber-Fiebert developed a model that examines the overall costs and benefits of treating hepatitis C with sofosbuvir rather than the traditional drugs in prisons. Prisoners are more likely than those in the general population to be infected with hepatitis C, a virus that attacks the liver, because it can be transmitted through intravenous drug use and unclean tattoos.

The researchers found that the high upfront cost saves money in later years by reducing the number of liver transplants and other more invasive treatments needed. In accordance with standard practices, this  study examined the overall societal cost without accounting for the source of the money. For example, the prison system’s are more likely to spend more money upfront, although savings might be recouped by Medicaid or other private insurers several decades later. From our release:

“Overall, sofosbuvir is cost-effective in this population, though its budgetary impact and affordability present appreciable challenges,” said Goldhaber-Fiebert,who is also a faculty member at Stanford’s Center for Health Policy/Center for Primary Care and Outcomes Research, which is part of the university’s Freeman Spogli Institute for International Studies.

Goldhaber-Fiebert called hepatitis C a “public health opportunity.”

“Though often not the focus of health-policy research, HCV-infected inmates are a population that may benefit particularly from a highly effective, short-duration treatment,” he said.

The research appears in this week’s Annals of Internal Medicine.

Previously: Fortune teller: Mice with ‘humanized’ livers predict HCV drug candidate’s behavior in humans, A primer on hepatitis C and For patients with advanced hepatitis C, benefits of new drugs outweigh costs
Photo by stevepb

Big data, Chronic Disease, Immunology, Research, Stanford News

Out of hiding: Found lurking in public databases, type-2 diabetes drug passes early test

Out of hiding: Found lurking in public databases, type-2 diabetes drug passes early test

lurking 3Way too often, promising-looking basic-research findings – intriguing drug candidates, for example – go swooshing down the memory hole, and you never hear anything about them again. So it’s nice when you see researchers following up on an upbeat early finding with work that moves a potential drug to the next peg in the development process. All the more so when the drug candidate targets a massively prevalent disorder.

Type 2 diabetes affects more than 370 million people worldwide, a mighty big number and a mighty big market for drug companies. (Unlike the much less common type 1-diabetes, where the body’s production of the hormone insulin falters and sugar builds up in the blood instead of being taken up by cells throughout the body, in type-2 diabetes insulin production may be fine but tissues become resistant to insulin.) But while numerous medications are available, none of them decisively halt progression, much less reverse the disease’s course.

About two-and-a-half years ago, Stanford data-mining maven Atul Butte, MD, PhD, combed huge publicly available databases, pooled results from numerous studies and, using big-data statistical methods, fished out a gene that had every possibility of being an important player in type 2 diabetes, but had been totally overlooked. (For more info, see this news release.) Called CD44,  this gene is especially active in fat tissue of insulin-resistant people and, Butte’s study showed, had a strong statistical connection to type-2 diabetes.

Butte’s study suggested that CD44′s link to type-2 diabetes was not just statistical but causal: In other words, manipulating the protein CD44 codes for might influence the course of the disease. By chance, that protein has already been much studied by immunologists for totally unrelated reasons. The serendipitous result is that a monoclonal antibody that binds to the protein and inhibits its action was already available.

So, Butte and his colleagues used that antibody in tests they performed on lab mice bioengineered to be extremely susceptible to type-2 diabetes, or what passes for it in a mouse. And, it turns out, the CD44-impairing antibody performed comparably to or better than two workhorse diabetes medications (metformin and pioglitazone) in countering several features of type 2 diabetes, including fatty liver, high blood sugar, weight gain and insulin resistance. The results appear in a study published today in the journal Diabetes.

Most exciting of all: In targeting CD44, the monoclonal antibody was working quite differently from any of the established drugs used for type-2 diabetes.

These are still early results, which will have to be replicated and – one hopes – improved on, first in other animal studies and finally in a long stretch of clinical trials before any drug aimed at CD44 can join the pantheon of type-2 diabetes medications. In any case, for a number of reasons the monoclonal antibody Butte’s team pitted against CD44 is far from perfect for clinical purposes. But refining initial “prototypes” is standard operating procedure for drug developers. So here’s hoping a star is born.

Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Nature/nurture study of type-2 diabetes risk unearths carrots as potential risk reducers and Mining medical discoveries from a mountain of ones and zeroes
Photo by Dan-Scape.co.uk

Chronic Disease, Pediatrics, Public Health, Stanford News

Diabetes self-management program helps at-risk teens and their families make healthier choices

Diabetes self-management program helps at-risk teens and their families make healthier choices

Diabetes_coaches_classThe prevalence of Type 2 diabetes among Americans ages 12 to 19 has grown from nine percent to 23 percent in less than a decade. In an effort to reduce U.S. adolescents’ diabetes risk, researchers at Stanford developed a school-based program where medical residents train healthy at-risk teens to be self-management coaches for family members diagnosed with Type 2 diabetes.

Researchers tested the initiative, called the Stanford Youth Diabetes Coaches Program, over the course of a year at three Bay Area high-schools serving primarily ethnic minority youth of low socioeconomic status. The study involved 97 adolescents – 49 student coaches and 48 non-participant students. Student coaches participated in an eight-week training course that was taught by family medicine residents and modeled after the Stanford University Diabetes Self-Management Program for adults. All participants completed pre- and post-study questionnaires and a select group of student coaches and family members gave in-depth interviews.

The program emphasized communication skills, problem solving and setting achievable goals using action plans. Beyond providing basic diabetes knowledge, the program also included guidance on nutrition, healthy meal planning, physical activity, weight management and stress management and on developing relationships with health-care providers. Student-coaches engaged with their family members during weekly 30-minute sessions where they shared information about topics they learned in class, discussed their relatives’ experiences and goals and helped them make an action plan for the week. In discussing their findings, study authors’ wrote:

The results of the study indicate that the Stanford Youth Diabetes Coaches Program increases knowledge and psychosocial assets of participant youth … Youth participants also reported positive changes in their own lives as the coached family members, and family members emphasized the importance of student coaches’ role in encouraging healthy behaviors. Additionally youth participants reported high program satisfaction.

These results substantiate current work suggesting that school-based programs benefit adolescents and that children have potential to support the self-management of family members with diabetes. Evidence strongly suggests that school-based programs hold promise to improve the health of at-risk adolescents.

“This study really speaks to the question of: How do you engage teens about their health?,” said first author Liana Gefter, MD, a research associate in Stanford’s Center for Research and Education in Family and Community Medicine. “The effectiveness of the program is rooted in the idea of empowering students to be a leader in a setting where they are traditionally only told what to do. A lot of the students really had a transformation during the eight-week course. Our findings demonstrated that after only eight weeks, compared to non-participants, students had significant increases in self-worth and belonging – assets that have been shown to be necessary precursors for adopting healthy behaviors. In this way, we believe the program could lay the foundation for sustainable health improvement.”

During interviews with researchers, student coaches and diabetes patients said the program inspired them to improve their diet and increase their regular physical activity. Additionally, they noted that the program strengthened their relationships with each other, and students reported their appreciation for having a physician come into their classroom.

In light of the program’s success, Gefter and colleagues Nancy Morioka-Douglas MD, MPH; Eunice Rodriguez, MPH, DrPH, and Lisa Rosas, MPH, PhD, are working to expand the program to underserved schools at other sites in California and around the country. Pilots are currently underway, or will begin, at campuses in Delaware, Georgia, Washington, Ohio and Michigan.

Previously: Sugar intake, diabetes and kids: Q&A with a pediatric obesity expert, Have you voted in the Healthy Living Innovation Awards?, Diabetes prevention program trains youth in chronic disease self-management and Stanford Diabetes Coaches Class selected as 2011 Healthy Living Innovation Awards finalist
Photo by Stanford Youth Diabetes Coaches Program

Big data, Chronic Disease, Clinical Trials, Health and Fitness, Public Health

Stanford to launch Wellness Living Laboratory

Stanford to launch Wellness Living Laboratory

1200px-Female_joggers_on_foggy_Morro_Strand_State_BeachIf you’re the kind of person who wears a heart monitor while jogging, tracks your sleep with an app or meditates to lengthen your lifespan, then a new Stanford project, called WELL, just might be for you.

WELL, which stands for the Wellness Living Laboratory hasn’t started quite yet — it will launch in 2015 — but when it does, it will unleash a variety of cutting-edge tools in an effort to define health.

Health seems like a no-brainer, but it is more than the absence of disease, says John Ioannidis , MD, DSc, the head of the Stanford Prevention Research Center. Ioannidis wants to find out how people can be “more healthy than healthy.”

To do that, he secured $10 million and laid out plans for the project. WELL plans to enroll thousands of volunteers — who Ioannidis calls “citizen scientists” — in two initial locations: Santa Clara County, Calif., and China, with plans to expand to other sites in the future.

Participants may be able to select which health factors to track and to report much of their information remotely and digitally, although some in-person visits may be required. Participants will also have the opportunity to enroll in a variety of clinical trials to test various interventions, such as nutrition counseling or smoking cessation programs.

The program will focus on wellness, rather than diseases, with the hypothesis that promoting wellness thwarts diseases, Ioannidis said.

Volunteers who would rather not provide health information will also have the opportunity to benefit from access to a program-wide social networking effort that will spread news of successful practices, he said. “This outer sphere could reach out to tens of millions of people,” Ioannidis told me.  Stay tuned to learn how to sign up.

The $10 million came as an unrestricted gift to Stanford University from Amway’s Nutrilite Health Institute Wellness Fund.

Previously: Medicine X explores the relationship between mental and physical health, Stanford partnering with Google [x] and Duke to better understand the human body, New Stanford center aims to promote research excellence and Teens these days smoking less but engaging in other risky behaviors
Photo by: Mike Baird

Chronic Disease, Medical Education, Medicine X, Mental Health, Parenting, Stanford News

Medicine X explores the relationship between mental and physical health: “I don’t usually talk about this”

Medicine X explores the relationship between mental and physical health: "I don’t usually talk about this"

standing o at MedX - smallThis year, Medicine X examined the relationship between physical and emotional well-being with three breakout panels. Psychologists and ePatients came together in two of the sessions to discuss depression in chronic illness and coping through online communities, as well as the topic of mental health and the whole person.

The conversations centered on five themes: how the uncertainty, fear and overall stress of living with a chronic illness, or being a caregiver, can lead to depression and anxiety; why patients’ desire to be empowered can prevent them from seeking help; why eliminating the stigma associated with mental health conditions is so important; the need to better integrate the training of future doctors and mental-health professionals; and ways patients can identify that they may need mental health services and how to find them.

Ann Becker-Schutte, PhD, a Kansas City-based psychologist who participated in both panels, told the audience, “Living with any of these illnesses, whether it’s rare or well-known, requires a lot of work. There is a burden of gilt, fear and shame that are all rolled into one. It’s not unusual for anyone facing these conditions to get tired and just say ‘I’m done’.”

Sarah Kucharski, a Medicine X ePatient advisor diagnosed with depression, anxiety and fibromuscular dysplasia, gave the audience insight into how depression can take over – explaining that she was shocked to learn during a therapy session that a recent string of major life events (getting married, having bypass surgery and buying a house) had elevated her score on the Holmes and Rahe Stress Scale to roughly 500. “I had no ideas that such things had a rating or that they could be cumulative,” she said. “As a result, I try to be more cognizant and slow down.”

Other ePatients spoke candidly and courageously about some for their darkest moments, with many saying it was challenging to discuss their experiences with depression and anxiety outside their inner circles. ”I don’t usually talk about this,” said Hugo Campos, an ePatient with an implantable cardiac defibrillator in his chest. “This will be particularly difficult to admit in public.”

Campos opened up about the severe depression he encountered during the month following a procedure to implant into his chest a cardiac defibrillator, which shocks the heart to control life-threatening arrhythmias and prevent sudden cardiac arrest. Since the device was implanted preventatively, he felt that by having the surgery he had somehow failed himself and continued to be unsure if the device was necessary. There was also anxiety and fear about the device spontaneously shocking him. He turned to his online community to learn how to cope with these feelings. “I felt I would be better of speaking with my peers online, rather than a professional who did not have an implantable device and didn’t know what I was going through,” he explained.

Scott Strange, who was diagnosed with Type 1 diabetes in 1970 and also struggles with chronic depression, also turned to the Internet for support. “My journey to acceptance started when I found my online community. Until I found them, I never really faced it.”

Strange talked about growing up with the knowledge that not properly monitoring his glucose and insulin levels could be fatal. He also addressed the shame and exhaustion that results from “busting your rear end and trying to do everything your doctor says” and not seeing an improvement in your health.

While some turned to their patient communities online, others turned to someone outside of their social networks. When the demands of being a caregiver began to overwhelm Erin Moore, the mother of a four-year-old son with cystic fibrosis (CF) and three other children, she opted not to discuss it with someone well-versed with her situation. “Initially I sought help outside of the CF community because I was aware of how many people rely on me for my strength and I didn’t want to admit a weakness.”

Continue Reading »

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

Can Alzheimer’s damage to the brain be repaired?

Can Alzheimer's damage to the brain be repaired?

repair jobIn my recent Stanford Medicine article about Alzheimer’s research, called “Rethinking Alzheimer’s,” I chronicled a variety of new approaches by Stanford scientists to nipping Alzheimer’s in the bud by discovering what’s gone wrong at the molecular level long before more obvious symptoms of the disorder emerge.

But Stanford neuroscientist Frank Longo, MD, PhD, a practicing clinician as well as a researcher, has another concern. In my article, I quoted him as saying:

Even if we could stop new Alzheimer’s cases in their tracks, there will always be patients walking in who already have severe symptoms. And I don’t think they should be forgotten.

A study by Longo and his colleagues, which just went into print in the Journal of Alzheimer’s Disease, addresses this concern. Longo has pioneered the development of small-molecule drugs that might be able to restore nerve cells frayed by conditions such as Alzheimer’s.

Nerve cells in distress can often be saved from going down the tubes if they get the right medicine. Fortunately, the brain (like many other organs in the body) makes a number of its own medicines, including ones called growth factors. Unfortunately, these growth factors are so huge that they won’t easily cross the blood-brain barrier. So, the medical/scientific establishment can’t simply synthesize them, stick them into an artery in a patient’s arm and let them migrate to the site of brain injury or degeneration and repair the damage. Plus, growth factors can affect damaged nerve cells in multiple ways, and not always benign ones.

The Longo group’s study showed that – in mice, at least -  a growth-factor-mimicking small-molecule drug (at the moment, alluded to merely by the unromantic alphanumeric LM11A-31) could counteract a number of key Alzheimer degenerative mechanisms, notably the loss of all-important contacts (called synapses) via which nerve cells transmit signals to one another.

Synapses are the soldier joints that wire together the brain’s nerve circuitry. In response to our experience, synapses are constantly springing forth, enlarging and strengthening, diminishing and weakening, and disappearing.They are crucial to memory, thought, learning and daydreaming, not to mention emotion and, for that matter, motion. So their massive loss — which in the case of Alzheimer’s disease is a defining feature – is devastating.

In addition to repairing nerve-cells, the compound also appeared to exert a calming effect on angry astrocytes and  microglia, two additional kinds of cells in the brain that, when angered, can produce inflammation and tissue damage in that organ. Perhaps most promising of all, LM11A-31 appeared to help the mice remember where things are and what nasty things to avoid.

Previously: Stanford’s brightest lights reveal new insights into early underpinnings of Alzheimer’s, Stanford neuroscientist discusses the coming dementia epidemic and Drug found effective in two mouse models of Huntington’s disease
Photo by Bruce Turner

Autoimmune Disease, Chronic Disease, Health and Fitness, Research, Technology

Video game accessory may help multiple sclerosis patients reduce falls, boost brain connections

Wii_balance_boardNintendo’s Wii Balance Board has helped get people off the couch and moving as they play aerobic video games like Super Hula Hoop or Dance Dance Revolution. Now a study published this week in Radiology shows that the video game console’s balance board may help reduce multiple sclerosis (MS) patients’ risk of falls by rewiring their brains.

In a small study, researchers used an MRI technique called diffusion tensor imaging to analyze changes in the brain of MS patients that used the Wii Balance Board while playing video games for 30-40 minutes a day five days a week.

According to a recent Forbes post:

MRI scans in the MS patients in the study demonstrated significant growth of nerve tracts which are integral in movement as well as balance. It turns out that the changes seen on MRI correlated with improvements in balance as measured by an assessment technique called posturography.

These brain changes in MS patients are likely a manifestation of neural plasticity, or the ability of the brain to adapt and form new connections throughout life, said lead author Luca Prosperini, M.D., Ph.D., from Sapienza University in Rome, Italy.

”The most important finding in this study is that a task-oriented and repetitive training aimed at managing a specific symptom is highly effective and induces brain plasticity.”

“More specifically, the improvements promoted by the Wii balance board can reduce the risk of accidental falls in patients with MS, thereby reducing the risk of fall-related comorbidities like trauma and fractures,”

 added Prosperini.

Researchers cautioned that the improvements in balance did not persist after patients stopped playing the video games, suggesting that patients will need to continue their training in order benefit from the intervention.

Previously: Study analyzes video game-related injuries and Comparing the Wii Fit board to a clinical force platform
Photo by Joachim S. Müller

Behavioral Science, Chronic Disease, Neuroscience, Pain, Research, Stanford News

Obscure brain chemical indicted in chronic-pain-induced “Why bother?” syndrome

Obscure brain chemical indicted in chronic-pain-induced "Why bother?" syndrome

why botherChronic pain, meaning pain that persists for months and months or even longer (sometimes continuing well past the time when the pain-causing injury has healed), is among the most abundant of all medical afflictions in the developed world. Estimates of the number of people with this condition in the United States alone range from 70 million to 116 million adults – in other words, as much as half the country’s adult population!

No picnic in and of itself, chronic pain piles insult on injury. It differs from a short-term episode of pain not only in its duration, but also in triggering in sufferers a kind of psychic exhaustion best described by the rhetorical question, “Why bother?”

In a new study in Science, a team led by Stanford neuroscientist Rob Malenka, MD, PhD, has identified a particular nerve-cell circuit in the brain that may explain this loss of motivation that chronic pain all too often induces. Using lab mice as test subjects, they showed that mice enduring unremitting pain lost their willingness to perform work in pursuit of normally desirable goals, just as people in chronic pain frequently do.

It wasn’t that these animals weren’t perfectly capable of carrying out the tasks they’d been trained to do, the researchers showed. Nor was it that they lost their taste for the food pellets which with they were rewarded for successful performance – if you just gave them the food, they ate every bit as much as normal mice did. But they just weren’t willing to work very hard to get it. Their murine morale was shot.

Chalk it up to the action of a mysterious substance used in the brain for god-knows-what. In our release describing the study, I explained:

Galanin is a short signaling-protein snippet secreted by certain cells in various places in the brain. While its presence in the brain has been known for a good 60 years or so, galanin’s role is not well-defined and probably differs widely in different brain structures. There have been hints, though, that galanin activity might play a role in pain. For example, it’s been previously shown in animal models that galanin levels in the brain increase with the persistence of pain.

In a surprising and promising development, the team also found that when they blocked galanin’s action in a particular brain circuit, the mice, while still in as much pain as before, were once again willing to work hard for their supper.

Surprising, because galanin is a mighty obscure brain chemical, and because its role in destroying motivation turns out to be so intimate and specific. Promising, because the discovery suggests that a drug that can inhibit galanin’s activity in just the implicated brain circuit, without messing up whatever this mystery molecule’s more upbeat functions in the brain might be, could someday succeed in bringing back that drive to accomplish things that people in chronic pain all too often lose.

Previously: “Love hormone” may mediate wider range of relationships than previously thought, Revealed: the brain’s molecular mechanism behind why we get the blues, Better than the real thing: How drugs hot-wire our brain’s reward circuitry and Stanford researchers address the complexity of chronic pain
Photo by Doug Waldron

Aging, Chronic Disease, Public Health, Research

How multiple chronic conditions are affecting older Americans’ life expectancy

old_coupleOne in four adults in the United States has two or more chronic conditions, according to the latest data from the Centers for Disease Control and Prevention. And, findings published in the August issue of Medical Care show that the burden of multiple chronic diseases could explain why life expectancy increases among elderly Americans are slowing.

In the study (subscription required), researchers at Johns Hopkins Bloomberg School of Public Health analyzed a nationally representative sample of 1.4 million Medicare beneficiaries. According to a release:

The analysis found that, on average, a 75-year-old American woman with no chronic conditions will live 17.3 additional years (that’s to more than 92 years old). But a 75-year-old woman with five chronic conditions will only live, on average, to the age of 87, and a 75-year-old woman with 10 or more chronic conditions will only live to the age of 80. Women continue to live longer than men, while white people live longer than black people.

It’s not just how many diseases you have, but also what disease that matters. At 67, an individual with heart disease is estimated to live an additional 21.2 years on average, while someone diagnosed with Alzheimer’s disease is only expected to live 12 additional years.

On average, life expectancy is reduced by 1.8 years with each additional chronic condition, the researchers found. But while the first disease shaves off just a fraction of a year off life expectancy for older people, the impact grows as the diseases add up.

Previously: Americans are living longer, but are we healthier in our golden years?, Longevity gene tied to nerve stem cell regeneration, say Stanford researchers, Study shows regular physical activity, even modest amounts, can add years to your life and TED Talk with Laura Carstensen shows older adults have an edge on happiness
Photo by Marcel Oosterwijk

Chronic Disease, Research, Science, Stanford News, Technology

Stanford team develops nanotech-based microchip to diagnose Type 1 diabetes

Stanford team develops nanotech-based microchip to diagnose Type 1 diabetes

Dr. Brian Feldman?s M.D. hold a computer chip that he develop that will benefit diabetic patients at the Stanford School of Medicine,  on Thursday, July 4, 2014.  ( Norbert von der Groeben/ Stanford School of Medicine )

Years ago, when patients showed up at the doctor with excessive thirst, frequent urination and unexplained weight loss – in other words, the classic symptoms of diabetes mellitus – diagnosing them was usually just a matter of checking for high blood sugar. Yes, they needed to be treated for the correct form of the disease, but the two main types were found in different populations. So, in most cases, no lab test was needed to figure out whether someone had Type 1 or Type 2 diabetes; demographic factors were enough to make the distinction.

Of late, there’s been much more cross-over between the two groups. To treat patients correctly, it’s important to diagnose the right form of diabetes, but there’s a problem: The only test that does so is expensive, cumbersome and available only in hospitals.

So it’s great news that Stanford scientists are developing a new Type 1 diabetes test, described in a paper published online this week in Nature Medicine. The new nanotechnology-based microchip, which researcher Brian Feldman, MD, PhD, holds in the photo above, tests patients’ blood for the auto-antibodies that cause Type 1 diabetes. The new test is cheap, portable, and uses much less blood than the older diagnostic test. Unlike the old test, it requires no radioactive reagents and is simple enough to use in low-tech settings.

The test uses a nanotech enhancement (specifically, nano-sized islands of gold; hence the golden glow of the chip that Feldman is holding) to help detect auto-antibodies. In addition to diagnosing new patients, this technology will also enable better research into how Type 1 diabetes develops, as our press release explains:

…[P]eople who are at risk of developing Type 1 diabetes, such patients’ close relatives, also may benefit from the test because it will allow doctors to quickly and cheaply track their auto-antibody levels before they show symptoms. Because it is so inexpensive, the test may also allow the first broad screening for diabetes auto-antibodies in the population at large.

“The auto-antibodies truly are a crystal ball,” Feldman said. “Even if you don’t have [Type 1] diabetes yet, if you have one auto-antibody linked to diabetes in your blood, you are at significant risk; with multiple auto-antibodies, it’s more than 90 percent risk.”

Feldman’s team has started a biotech company to further develop the test and is seeking FDA approval for the new method. In addition, Stanford University and the researchers have filed a patent for the new technique.

Previously: A simple blood test may unearth the earliest signs of heart transplant rejection, Stanford microbiologist’s secret sauce for disease detection and One family’s story on caring for their children with type 1 diabetes
Photo by Norbert von der Groeben

Stanford Medicine Resources: