2q24 microdeletion syndrome is a rare genetic condition caused by a small missing piece on chromosome 2. People with 2q24 microdeletion syndrome often have developmental delay, learning differences, and low muscle tone. Some have epilepsy, feeding difficulties in infancy, or differences in growth and facial features. It is lifelong, and signs are usually noticed in infancy or early childhood, but not everyone will have the same experience. Care focuses on supportive therapies, seizure management if needed, and regular follow‑up, and many children make progress with early intervention.
Overview
2q24 microdeletion syndromeSymptoms
2q24 microdeletion syndrome often involves early seizures, low muscle tone, and developmental delay. Feeding problems, slow growth, and major speech and learning challenges are common. Some show distinctive facial features or hand‑foot differences, usually noticed in infancy or early childhood.
Outlook and prognosis
Many living with 2q24 microdeletion syndrome grow and learn at their own pace, with progress shaped by which genes are missing. Early therapies, seizure control, and tailored education often improve communication, mobility, and independence. Ongoing specialist care helps navigate changing needs over time.
Causes and risk factors
2q24 microdeletion syndrome results from a missing segment on chromosome 2, usually a new (de novo) change. Rarely, it’s inherited from a parent with a balanced chromosome rearrangement or mosaicism. No confirmed environmental or lifestyle risk factors are known.
Genetic influences
Genetics is central to 2q24 microdeletion syndrome: a small missing segment on chromosome 2 disrupts genes important for brain development and nerve signaling. The exact size and genes lost vary, so symptoms and severity differ widely. Most cases arise de novo, but parental testing guides recurrence risk.
Diagnosis
Doctors suspect 2q24 microdeletion syndrome based on clinical features such as early-onset seizures, developmental delays, and growth differences. The genetic diagnosis of 2q24 microdeletion syndrome is confirmed with chromosomal microarray or comparable genomic testing; imaging may support evaluation.
Treatment and drugs
Treatment for 2q24 microdeletion syndrome focuses on each person’s needs. Care often includes seizure management, feeding and growth support, physical/occupational/speech therapies, and educational plans; some need bracing or surgery for orthopedic issues. Regular cardiology, neurology, and developmental follow-up helps adjust care over time.
Symptoms
In 2q24 microdeletion syndrome, day-to-day differences often center on development, movement, and seizures. Parents or caregivers often first notice early features of 2q24 microdeletion syndrome such as delayed milestones or seizures in the first months of life. Features vary from person to person and can change over time. Some differences are present from birth, while others become clearer as a child grows.
Many babies have seizures that start in the newborn period or early infancy. Clinicians call this epilepsy, which means repeated seizures that need medical care. In 2q24 microdeletion syndrome, seizure type and timing can vary.
Rolling, sitting, standing, and first words often happen later than expected. Early on, this might look like a baby who needs more time to hold up their head or reach for toys. Many children with 2q24 microdeletion syndrome reach milestones later but continue to make progress.
Understanding may be stronger than speaking, and first words can come late. Some have a limited number of words or speech that is hard to understand. In 2q24 microdeletion syndrome, speech and language differences are common across childhood.
Babies can feel floppy when lifted and may tire quickly during play or feeding. In medical terms, this is hypotonia; in everyday life, it shows up as needing more support to sit or stand. This can improve gradually with growth.
How people usually first notice 2q24 microdeletion syndrome?
Families often first notice the first signs of 2q24 microdeletion syndrome in infancy, when a baby has low muscle tone (feels “floppy”), feeding difficulties, or delays in reaching early milestones like head control or sitting. Some babies develop seizures in the first months to years of life, which can prompt EEGs and genetic testing; doctors may also see distinctive facial features or subtle differences in hands and feet during exams. For many, how 2q24 microdeletion syndrome is first noticed is through a combination of developmental delay and early-onset seizures, leading clinicians to order chromosome microarray testing that identifies the missing piece of chromosome 2q24.
Types of 2q24 microdeletion syndrome
2q24 microdeletion syndrome can look different from one person to the next because the missing DNA segment can vary in size and in which genes it includes. This leads to a spectrum of features, from developmental delays and low muscle tone to epilepsy and differences in growth or speech. People may notice different sets of symptoms depending on their situation. Clinicians often describe variants of 2q24 microdeletion by the specific genes deleted, and these variants can shape the pattern and severity of symptoms over time, which helps explain the different types of 2q24 microdeletion syndrome seen in practice.
SCN-gene deletions
When the deletion includes SCN1A, SCN2A, or SCN3A, seizures often begin in infancy or early childhood and may be hard to control. Developmental delays and low muscle tone are common alongside epilepsy. Early symptoms of 2q24 microdeletion syndrome in this group can include feeding difficulty and poor weight gain.
Non-SCN deletions
If the deletion spares SCN genes but includes nearby genes, seizures are less likely or milder. Developmental and speech delays, coordination challenges, and learning differences tend to be more prominent. Muscle tone can be low in infancy with gradual motor progress over time.
Large 2q24 deletions
Bigger deletions spanning multiple genes usually bring broader effects, with more pronounced delays and a higher chance of epilepsy. Growth differences, distinctive facial features, and feeding trouble can be more noticeable. Medical needs may be more complex and require multiple specialists.
Small focal deletions
Smaller, more targeted deletions may cause subtler or more specific challenges. Some children walk and talk on time but have language, learning, or fine-motor differences. Seizures may be absent or start later, depending on which genes are affected.
What genetics can tell you about symptoms
Small deletions on chromosome 2q24 often remove genes that help brain cells signal, leading to seizures, low muscle tone, and developmental delays. When sodium channel genes like SCN1A, SCN2A, or SCN3A are missing, seizures can start early and be harder to control.
Causes and risk factors
In 2q24 microdeletion syndrome, the cause is a small missing piece of chromosome 2 in the 2q24 region. This usually arises as a new change before birth and is not due to anything parents did. It can rarely be inherited when a parent carries the same deletion, so genetic counseling can explain recurrence risk. Genes set the stage, but environment and lifestyle often decide how the story unfolds. Prenatal care, seizure control, nutrition, and early therapies do not cause or cure 2q24 microdeletion syndrome, but they can shape outcomes and prompt attention to early symptoms of 2q24 microdeletion syndrome.
Environmental and biological risk factors
Most cases of 2q24 microdeletion syndrome happen as new chromosome changes around conception. Being exposed to risks in your body or environment doesn’t mean illness is inevitable. A few biological and environmental factors may slightly raise the chance that a small piece of chromosome 2 is lost before or early in pregnancy. Below are the factors scientists consider when discussing risk.
Small, chance errors during egg or sperm formation can delete a tiny piece of chromosome 2. These events are not caused by actions or choices. Most cases of 2q24 microdeletion syndrome start this way.
Age-related changes in eggs and sperm can modestly raise the chance of new chromosome changes. Any effect appears small, and most pregnancies are unaffected.
Exposure of a parent’s reproductive organs to high levels of ionizing radiation can damage DNA and increase chromosomal breakage. Everyday background radiation and standard X-rays are far below these levels.
Very high radiation doses to the embryo in early pregnancy can increase the chance of chromosome segments being lost. Medical teams work to avoid or minimize such exposures.
Genetic risk factors
A tiny missing segment on chromosome 2 (the 2q24 region) is the core genetic change behind 2q24 microdeletion syndrome. Some risk factors are inherited through our genes. Most deletions happen as a new event in the egg or sperm, while a smaller number are passed down or stem from a parent’s chromosome rearrangement. Genetic testing is often pursued when early symptoms of 2q24 microdeletion syndrome prompt an evaluation, because it can also clarify family recurrence risk.
De novo deletion: Most cases arise as a one-time change during egg or sperm formation. Parents typically do not carry the deletion, so sibling risk is usually low.
Parent carries deletion: When a parent has the 2q24 microdeletion, it follows an autosomal dominant pattern. Each pregnancy then has a 50% chance of inheriting the deletion, because one changed copy is enough to cause the condition. Features can vary even within a family.
Balanced rearrangement: A parent with a balanced translocation or inversion involving 2q24 can pass on an unbalanced chromosome that includes the microdeletion. The chance depends on the exact rearrangement and is assessed by chromosome studies. Finding this in a parent changes recurrence counseling for 2q24 microdeletion syndrome.
Parental mosaicism: Rarely, a parent may have the deletion in a small fraction of egg or sperm cells but not in blood. This hidden mosaicism raises recurrence risk slightly after one affected child.
Size and genes: The health impact depends on how large the deletion is and which genes are missing. Loss of sodium channel genes such as SCN1A, SCN2A, or SCN3A is often linked to seizures and more complex needs. Smaller deletions that spare these genes may be associated with milder features.
Fragile region layout: Repeated DNA in the 2q24 area can misalign during cell division, making deletions more likely. This reflects the region’s architecture, not anything a parent did.
Variable expressivity: People with the same deletion can be affected differently. This is why features in 2q24 microdeletion syndrome may vary even among relatives. Severity does not always track perfectly with deletion size.
Lifestyle risk factors
Although 2q24 microdeletion syndrome is genetic and not caused by lifestyle, daily habits can shape symptom control and quality of life. Choices around sleep, activity, feeding, and routines can influence seizures, growth, comfort, and development. Below are examples of how lifestyle affects 2q24 microdeletion syndrome in day-to-day care.
Sleep loss and irregular schedules can increase seizure frequency and severity. Predictable routines and avoiding known personal triggers can support better control.
Inconsistent dosing or missed antiseizure medicines can lead to breakthrough seizures. Using timed routines and caregiver checklists helps maintain stable medication levels.
Irregular or fragmented sleep can worsen seizures, irritability, and daytime function. A consistent bedtime routine and calming environment can improve seizure control and learning.
Inadequate calories or unsafe food textures can worsen growth failure and aspiration risk. Structured feeding plans and texture modifications support growth and reduce respiratory complications.
Risk prevention
You can’t prevent 2q24 microdeletion syndrome itself because it’s a change in chromosome material that usually happens by chance, but you can lower the chance of complications and support healthier development. Prevention works best when combined with regular check-ups. For many families, this means planning ahead, spotting concerns early, and using practical steps to reduce seizures, infections, and feeding or mobility problems. A care plan tailored to your child’s needs helps everyday life run more smoothly.
A genetics professional can explain recurrence risk and whether a parent carries a balanced chromosome change. They can discuss options like preimplantation genetic testing and targeted prenatal testing in future pregnancies.
If a child has 2q24 microdeletion syndrome, parents may be offered blood testing to check for a silent (balanced) rearrangement. Finding one can guide reproductive choices and targeted testing in the next pregnancy.
Noticing early symptoms of 2q24 microdeletion syndrome, like feeding difficulty, developmental delays, or seizures, allows quicker referrals to specialists. Early support often reduces complications and improves day-to-day function.
Keep anti-seizure medications on schedule and know the seizure action plan. Rescue medication training for caregivers can shorten seizures and lower emergency visits.
Transmission
2q24 microdeletion syndrome is not contagious—you can’t catch it or spread it through contact. Most cases occur as a new change at conception, when a small piece of chromosome 2 (region q24) is missing, so parents usually do not carry it. If a parent does have the same deletion—or a chromosome rearrangement that can lead to it—it can be passed on in an autosomal dominant way, meaning each pregnancy has a 50% chance of inheriting the deletion. Because of this, genetic transmission of 2q24 microdeletion syndrome is uncommon overall but possible in some families; a genetics professional can explain how it is inherited and discuss testing and recurrence risk.
When to test your genes
2q24 microdeletion syndrome is genetic, so testing is most useful when there’s a family history, a prior child with the condition, or prenatal ultrasound findings like growth or limb differences. Consider testing if a child shows developmental delay, seizures, or atypical growth. Testing can confirm diagnosis, guide therapies, and inform future pregnancies.
Diagnosis
You might notice small changes in daily routines, like delayed milestones or seizures that start in infancy, leading a care team to look for an underlying cause. Getting a diagnosis is often a turning point toward answers and support. For 2q24 microdeletion syndrome, doctors typically combine a careful exam with genetic tests that can detect small missing segments of chromosome 2. The goal is to confirm the exact deletion and guide care for seizures, development, and growth.
Doctors look for a pattern of features such as low muscle tone, developmental delays, feeding challenges, and seizure history. A detailed family and health history can help connect these clues and decide which tests to order.
This is the first-line test for the genetic diagnosis of 2q24 microdeletion syndrome. It scans the whole genome for tiny missing pieces and can pinpoint the 2q24 region.
Targeted methods such as FISH, MLPA, or qPCR can confirm the exact size and boundaries of the deletion. This helps clarify which genes are involved and supports care planning.
A standard chromosome picture can identify large deletions but often misses small microdeletions at 2q24. It may be used alongside more sensitive tests rather than on its own.
Stages of 2q24 microdeletion syndrome
2q24 microdeletion syndrome does not have defined progression stages. It’s a genetic change present from birth, and while features can shift with age—such as seizures changing over time or learning needs evolving—the course varies widely rather than following set steps. Different tests may be suggested to help confirm what’s causing the symptoms, including a chromosomal microarray or targeted genetic testing. Early symptoms of 2q24 microdeletion syndrome are often picked up through routine developmental checks and neurological assessment, and ongoing care typically monitors growth, development, and seizure control with regular visits and, when needed, brainwave (EEG) tests.
Outlook and prognosis
Looking at the long-term picture can be helpful. For many people with 2q24 microdeletion syndrome, the day-to-day outlook centers on managing seizures, developmental delays, and learning differences. Early care can make a real difference, especially when seizures are brought under control and therapies start early. Many people find that symptoms change over time—seizures may lessen or shift in type, while communication and motor skills can improve with consistent support.
Doctors call this the prognosis—a medical word for likely outcomes. Life expectancy is often near typical when seizures are well managed and there are no severe heart, breathing, or feeding complications; the main mortality risk comes from uncontrolled epilepsy, including rare events like status epilepticus or sudden unexpected death in epilepsy (SUDEP). Some children have milder developmental impacts and walk and talk with support, while others need ongoing assistance with mobility, communication, and daily activities. Early symptoms of 2q24 microdeletion syndrome can include difficult-to-control seizures in infancy and low muscle tone; with the right team, many families see steadier progress in school-age years and adolescence.
The future may look uncertain now, but many living with 2q24 microdeletion syndrome build skills over time and enjoy a good quality of life with tailored education, therapy, and seizure safety planning. Talk with your doctor about what your personal outlook might look like, including seizure control goals and ways to reduce risks like SUDEP.
Long-term effects
2q24 microdeletion syndrome can lead to ongoing neurologic and developmental challenges that change with age. Long-term effects vary widely, depending in part on the size of the deletion and which genes are involved. While early symptoms of 2q24 microdeletion syndrome often appear in infancy, the long-term picture usually centers on seizures, development, communication, and growth. Research in adults is still limited, but available reports suggest many continue to make gradual gains alongside persistent differences.
Persistent epilepsy is common when sodium channel genes in this region are affected. Seizures may lessen or change with age, but can remain lifelong. Severity ranges from well-controlled to difficult-to-control.
Intellectual disability typically ranges from mild to severe. Learning needs are usually lifelong, with uneven strengths and weaknesses. Some achieve functional academic skills.
Expressive speech is often more affected than understanding. Many use few words or short phrases, with progress over years. Communication remains limited for some into adulthood.
Low muscle tone and coordination challenges can persist. Milestones like walking may come late, with a clumsy or unsteady gait. Fine motor skills can remain limited.
How is it to live with 2q24 microdeletion syndrome?
Daily life with 2q24 microdeletion syndrome often revolves around supporting communication, movement, and learning at a pace that fits the child’s strengths. Many families notice delays in speech and motor skills, low muscle tone, and sometimes seizures, which can make schedules more structured around therapies, medical visits, and medication routines. School and community activities are very possible with the right supports—speech, occupational, and physical therapy; individualized education plans; and seizure safety plans—though progress may come in smaller, steady steps. For parents, siblings, and caregivers, it can be both demanding and deeply rewarding, and building a reliable care team and leaning on support networks can make the day-to-day feel more manageable and hopeful.
Treatment and drugs
Treatment for 2q24 microdeletion syndrome focuses on easing symptoms and supporting development, since there is no single medicine that fixes the underlying genetic change. Care often includes early therapies such as physiotherapy for low muscle tone and motor delays, speech and feeding therapy, and educational support; many children also benefit from occupational therapy to build daily living skills. Seizures are common in 2q24 microdeletion syndrome and are usually managed with anti-seizure medicines, with a neurologist adjusting the dose to balance seizure control and side effects; rescue medicines may be prescribed for prolonged events. Heart, gut, vision, or hearing issues—when present—are treated by the relevant specialists, and nutrition support may include high-calorie feeds or a temporary feeding tube if growth is affected. Supportive care can make a real difference in how you feel day to day, and regular follow-up with a coordinated team helps update the plan as needs change over time.
Non-drug treatment
Daily life with 2q24 microdeletion syndrome often involves supporting movement, communication, learning, and safety at home and school. Alongside medicines, non-drug therapies can strengthen skills, reduce frustration, and help families feel more confident day to day. The goal is to build abilities step by step and prevent complications where possible. Plans are tailored, since needs vary widely across ages and between children and adults.
Coordinated services in infancy or toddler years can boost motor, language, and social skills. Getting help soon after early symptoms of 2q24 microdeletion syndrome appear may improve long‑term progress.
Targeted exercises can build strength, balance, and coordination. Therapists also teach safe ways to move and play to prevent falls.
Practice with dressing, feeding, and hand skills helps everyday independence. Therapists may suggest adaptive tools to make tasks simpler and less tiring.
Support focuses on understanding, speaking, and social communication. Augmentative and alternative communication, like pictures or devices, can give a reliable voice when speech is limited.
Your genes may have an impact on how drugs work for you
Medicines for seizures, behavior, or sleep in 2q24 microdeletion syndrome can work differently because missing genes may change how brain cells signal and how the body processes drugs. Genetic testing and careful dose titration help clinicians choose safer, more effective options.
Pharmacological treatments
Medicines for 2q24 microdeletion syndrome focus on controlling seizures and easing day‑to‑day issues like sleep trouble, stiffness, reflux, and constipation. Not everyone responds to the same medication in the same way. There’s no single “best seizure medication for 2q24 microdeletion syndrome”; choices depend on the seizure type, age, and which genes are affected. When the deletion includes SCN1A, some sodium‑channel–blocking drugs can make seizures worse, so doctors often favor broad‑spectrum options first.
A broad‑spectrum anti‑seizure medicine that can help with generalized and focal seizures in 2q24 microdeletion syndrome. Regular blood tests check liver function and platelets.
Often effective across many seizure types and easy to combine with other drugs. Mood or irritability changes can occur, so behavior monitoring helps.
A benzodiazepine commonly added when seizures remain frequent. It can reduce clusters but may cause sleepiness or drooling.
Useful as add‑on therapy for difficult seizures. Possible effects include decreased appetite, tingling in fingers, or kidney stones, so good hydration is important.
Genetic influences
Genetically, this condition usually comes from a tiny missing segment on chromosome 2 (region 2q24) that removes sodium channel genes that help control electrical signals in the brain and nerves. In 2q24 microdeletion syndrome, the exact size and position of the missing piece—and which genes are lost—strongly influence how the condition shows up from person to person. Even with the same gene change, people can have very different features and degrees of impact. Parents often ask whether 2q24 microdeletion syndrome is inherited; most cases arise as a new change in the child and are not passed down from either parent. If a parent does carry the same deletion, each pregnancy has a 50% chance to inherit it; in rare families, a hidden chromosome change or mosaicism in a parent can slightly raise the chance even if standard blood-based genetic testing is normal. Genetic testing such as a chromosome microarray can usually detect the 2q24 deletion, and meeting with a genetic counselor can help explain results and discuss recurrence risks.
Is 2q24 microdeletion syndrome genetic?
Genetics is central to 2q24 microdeletion syndrome: a small missing segment on chromosome 2 disrupts genes important for brain development and nerve signaling. The exact size and genes lost vary, so symptoms and severity differ widely. Most cases arise de novo, but parental testing guides recurrence risk.
Pharmacogenetics—how genetics influence drug effects
In 2q24 microdeletion syndrome, which genes are missing can shape how well seizure medicines work and which side effects show up. When the deleted region includes sodium channel genes, the brain’s electrical balance changes, so medicines that block those channels may be less helpful or even aggravate seizures. If the loss includes SCN1A, care teams often steer away from sodium‑channel–blocking drugs like carbamazepine or lamotrigine and lean toward GABA‑boosting options such as valproate or clobazam.
Differences in common drug‑processing genes can also change dosing and side‑effect risk with medicines used for epilepsy; for some, drugs like clobazam or phenytoin last longer in the body and need careful titration, and in certain ancestries a specific marker can flag higher risk of severe skin reactions with carbamazepine. Alongside medical history and seizure pattern, genetic testing can help guide which anti‑seizure medicines to try first. There’s no single “best” plan, so your neurology team will adjust over time, especially when choosing seizure medications for 2q24 microdeletion syndrome.
Interactions with other conditions
Colds, stomach bugs, or any illness with fever can interact with 2q24 microdeletion syndrome by making seizures more likely or more intense, and dehydration may add to that risk. Early symptoms of 2q24 microdeletion syndrome often include seizures that flare with fevers from everyday infections, so prompt fever control and hydration matter. Doctors call it a “comorbidity” when two conditions occur together, and many living with 2q24 microdeletion syndrome also have autism features, attention difficulties, sleep problems, or feeding and reflux issues that can compound seizures, growth, and learning. Because the deletion often affects sodium‑channel genes, some antiseizure medicines that block these channels may worsen seizures; this also means medicines for other illnesses that lower the seizure threshold can have outsized effects and should be reviewed carefully. Breathing problems such as recurrent chest infections or sleep apnea can aggravate nighttime seizures and daytime fatigue, while significant reflux or swallowing challenges can raise the risk of aspiration during illnesses. It helps to coordinate care so treatments for infections, stomach issues, or behavior symptoms are chosen with seizure safety in mind and adjusted as needs change.
How genes can cause diseases
Humans have more than 20,000 genes, each carrying out one or a few specific functions in the body. One gene instructs the body to digest lactose from milk, another tells the body how to build strong bones and another prevents the body's cells from beginning to multiply uncontrollably and developing into cancer. As all of these genes combined are the building instructions for our body, a defect in one of these genes can have severe health consequences.
Through decades of genetic research, we know the genetic code of any healthy/functional human gene. We have also identified that in certain positions on a gene, some individuals may have a different genetic letter from the one you have. We call these hotspots "Genetic Variations" or "Variants" in short. In many cases, studies have been able to show that having the genetic letter "G" in the position makes you healthy, but having the letter "A" in the same position disrupts the gene function and causes a disease. Genopedia allows you to view these variants in genes and summarizes all that we know from scientific research, which genetic letters (Genotype) have good or bad consequences on your health or on your traits.
History
Families and communities once noticed patterns of babies who were unusually fussy, prone to early seizures, and later showed delays in walking or talking. Notes from clinic logs and family letters described long nights, frequent hospital visits, and children who developed more slowly than their peers. These early accounts focused on what could be seen and felt, without a clear reason why it was happening.
First described in the medical literature as clusters of symptoms—infant-onset seizures, low muscle tone, and developmental delay—the condition later gained clarity as chromosome testing improved. In the late 20th century, doctors began using high‑resolution chromosome studies to look for tiny missing pieces of DNA. As these tools sharpened, a consistent missing segment on the long arm of chromosome 2 emerged in some children with these features. This became known as 2q24 microdeletion syndrome.
From early theories to modern research, the story of 2q24 microdeletion syndrome reflects how technology reshaped diagnosis. Basic karyotypes rarely saw it; array-based tests and, later, genome-wide methods could. With each step, more children and adults were identified, including people with milder signs who might previously have gone undiagnosed. Researchers also noticed that the deleted region often includes genes that act like electrical channels in brain cells, helping explain why seizures were so common.
Once considered rare, now recognized as part of a spectrum, 2q24 microdeletion syndrome showed wide variation. Some newborns had hard‑to‑control seizures in the first weeks of life; others developed seizures later or not at all. Feeding issues, growth differences, and speech delays appeared in different combinations. These patterns helped clinicians refine care—anticipating early symptoms of 2q24 microdeletion syndrome such as seizures or feeding challenges—and guided families toward early therapies.
Advances in genetics also clarified inheritance. While many cases happen as new (de novo) changes, a few families were found to carry balanced changes that could increase the chance of a child having the deletion. This improved counseling and allowed relatives to make informed choices. At the same time, long-term follow-up studies began documenting school progress, mobility, and seizure outcomes into adolescence and adulthood, shifting focus from just diagnosis to lifelong support.
In recent decades, knowledge has built on a long tradition of observation. Clinicians now link the location and size of the missing segment with certain features, though predictions are never exact. Support networks and registries have grown, connecting families across countries and speeding research. Today, the history of 2q24 microdeletion syndrome is still being written, as better testing and coordinated care continue to refine what we know and how best to help people living with it.