Cholesterol-ester transfer protein deficiency is a rare genetic condition that leads to very high HDL cholesterol. Many people with cholesterol-ester transfer protein deficiency have no symptoms and feel well. It is lifelong and is usually noticed on routine blood tests in adulthood. Most people live a normal lifespan, and the outlook is generally good. Treatment focuses on managing overall heart risk with lifestyle and sometimes medications, and doctors describe this as targeting blood pressure, LDL cholesterol, diabetes risk, and smoking.
Overview
Cholesterol-ester transfer protein deficiencySymptoms
Most people with cholesterol-ester transfer protein (CETP) deficiency feel well. The main signs are very high HDL (“good”) cholesterol on a routine blood test, sometimes with larger HDL particles. Day-to-day health and physical exam are typically normal.
Outlook and prognosis
Most people with cholesterol-ester transfer protein (CETP) deficiency have very high HDL (“good”) cholesterol and feel well, with a normal life expectancy. Heart risk varies: some benefit from higher HDL, while others have mixed lipid patterns. Regular lipid checks and heart‑healthy habits help guide personalized care.
Causes and risk factors
Cholesterol-ester transfer protein deficiency stems from CETP gene variants, usually autosomal recessive or occasionally new. Risk rises with family history, consanguinity, and some East Asian ancestry; lifestyle doesn’t cause it, though diet or medicines can influence lipid tests.
Genetic influences
Genetics are central in cholesteryl ester transfer protein (CETP) deficiency, which is caused by inherited changes in the CETP gene. Variants usually raise HDL (“good”) cholesterol and can alter LDL levels. Effects on heart disease risk vary by specific mutation and background.
Diagnosis
Doctors suspect it after a routine lipid panel shows markedly high HDL cholesterol. Confirmation uses specialized lipid testing for CETP activity or protein and genetic tests; this approach supports the genetic diagnosis of Cholesterol-ester transfer protein deficiency.
Treatment and drugs
Treatment for cholesterol-ester transfer protein (CETP) deficiency focuses on overall heart health and individualized risk. Many people need no specific drug; care may include lifestyle steps, periodic lipid checks, and managing blood pressure, diabetes, and smoking. If medication is needed, clinicians tailor choices—often statins or other lipid-lowering therapies—based on your full cholesterol pattern and cardiovascular risk.
Symptoms
Many people with Cholesterol-ester transfer protein deficiency (often called CETP deficiency) feel completely well, and most daily activities are unaffected. In medical terms, this is very high HDL cholesterol; in everyday life, it shows up most often as an unexpected lab result. The early features of cholesterol-ester transfer protein deficiency are usually found on a routine cholesterol test rather than by how you feel. Physical signs are uncommon, and heart disease risk depends on your overall profile, not just an HDL number.
Most people with CETP deficiency do not feel different or unwell. It’s commonly picked up during a standard cholesterol check rather than because of noticeable changes.
HDL (the “good” cholesterol) can be very high, often above 90–120 mg/dL (2.3–3.1 mmol/L). Some have values even higher, yet feel completely fine.
The HDL particles are often bigger than usual, which changes how cholesterol is carried in the blood. This is something labs can see on advanced lipid tests, not something you can feel.
LDL cholesterol and triglycerides may be in typical ranges or slightly shifted. Your overall lipid pattern can differ from one person to another.
How people usually first notice Cholesterol-ester transfer protein deficiency?
Many first learn about cholesterol-ester transfer protein (CETP) deficiency after a routine blood test shows very high HDL cholesterol, sometimes far above typical ranges, despite feeling well. Doctors may first suspect it when a lipid panel in adolescence or adulthood looks unusual—HDL is markedly elevated, LDL may be normal or low, and there’s no clear lifestyle reason—prompting genetic testing in some cases. In families with known CETP variants, the first signs of CETP deficiency can be noticed through cascade screening, where relatives get lipid tests and some show the same striking HDL pattern.
Types of Cholesterol-ester transfer protein deficiency
Cholesterol-ester transfer protein deficiency is a genetic condition with a few well-recognized variants that differ in how much CETP function is reduced and how HDL (“good”) cholesterol behaves. The main differences come from which CETP gene change is present and whether someone has one or two copies. People may notice different sets of symptoms depending on their situation. In practice, most people feel well, but lab results—especially very high HDL cholesterol—vary by variant, and triglycerides can differ too; understanding the types of CETP deficiency can help make sense of lab patterns when discussing types of CONDITION with your clinician.
Complete deficiency
This variant comes from having two copies of a loss-of-function change in the CETP gene. HDL cholesterol is usually extremely high, CETP activity is nearly absent, and triglycerides are often average to slightly low. Most people feel fine and only learn about it through unusual lipid test results.
Partial deficiency
This variant usually occurs when only one CETP gene copy is affected. HDL cholesterol is high but typically not as extreme as in complete deficiency, and CETP activity is reduced but not absent. Triglycerides are often normal, and symptoms are uncommon.
Common missense variant
Certain CETP changes (such as D442G in East Asian populations or I405V in diverse groups) reduce CETP function to varying degrees. HDL levels can be moderately to very high depending on the specific change and whether one or two copies are present. Clinical effects are usually mild and picked up on routine lipid panels.
Null mutations
These rare variants completely disrupt CETP production or function. People with two null alleles tend to have the highest HDL levels and undetectable CETP activity, while one null allele produces a partial deficiency pattern. Cardiovascular risk impact remains uncertain, so management focuses on the overall risk profile rather than the variant alone.
What genetics can tell you about symptoms
People with CETP deficiency often have very high HDL (“good”) cholesterol and sometimes experience no symptoms, while a few may notice early corneal clouding or fat deposits under the skin. Specific CETP gene variants reduce or disable the protein, slowing cholesterol exchange between lipoproteins and raising HDL levels.
Causes and risk factors
Cholesterol-ester transfer protein deficiency is usually caused by inherited changes in the CETP gene. The main risk factor for cholesterol-ester transfer protein deficiency is a family history of the same gene change. It is more common in some East Asian populations. Doctors distinguish between risk factors you can change and those you can’t. Diet, exercise, alcohol, certain medicines, and thyroid or liver problems can shift cholesterol levels and may change how the condition appears on blood tests.
Environmental and biological risk factors
For cholesterol-ester transfer protein (CETP) deficiency, the chance that a child is born with it mainly reflects biological events at or before conception. Some biological risks are written in our genes, others arise through environment. Most everyday environmental exposures have not been shown to cause CETP deficiency, and any known environmental influences tend to have very small effects. Below are environmental and body-based factors that may increase the likelihood of CETP deficiency at birth.
Fathers in their late 40s or beyond have a slightly higher rate of new DNA changes in sperm. This can very rarely lead to conditions present from birth, including CETP deficiency. The absolute chance remains low for any single pregnancy.
Radiation to the pelvis or certain chemotherapy before conception can damage egg or sperm DNA. Clinicians often recommend waiting a period after treatment before trying to conceive to help lower this small risk. Any added chance for this condition is considered minimal.
Occupational or accidental exposure of parents to high levels of ionizing radiation can raise mutation rates in reproductive cells. Such exposures are uncommon and tightly regulated in the EU and US. Any effect on risk appears very small.
Common exposures like typical background radiation, household products, or urban air pollution have not been shown to cause this condition. Current research has not found a consistent link.
Genetic risk factors
When discussing the genetic causes of cholesterol-ester transfer protein deficiency, the focus is on changes in the CETP gene that reduce or block the protein’s function. Some people inherit two harmful variants and develop full deficiency, while others carry one variant and have milder effects or normal health. Risk is not destiny—it varies widely between individuals.
CETP gene variants: Pathogenic changes in the CETP gene reduce or stop the protein’s activity. This is the primary genetic driver of cholesterol-ester transfer protein deficiency. Different variants can lead to different degrees of enzyme loss.
Autosomal recessive pattern: Most affected people inherit two disease‑causing CETP variants, one from each parent. Each child of two carriers has a 25% chance to be affected. Parents are usually healthy carriers.
Heterozygous carriers: People with one CETP variant often have partially reduced CETP activity and higher HDL cholesterol. Many carriers have no symptoms and may be identified only on blood tests. Effects can vary by variant.
Compound heterozygosity: Having two different harmful CETP variants can cause full deficiency. The specific pair can shape how high HDL levels rise and whether features are noticed.
Founder variants: Certain CETP changes are more common in some groups, such as people of Japanese or East Asian ancestry. These variants raise the chance of inherited CETP deficiency within those families and communities. Distribution varies across regions.
Variant severity: Some variants sharply lower or abolish CETP function, while others reduce it only partly. The severity of the change helps predict how much CETP activity is lost. Lab measurements of CETP activity can reflect this.
Family history: Having close relatives with the condition or very high HDL levels increases the chance of carrying CETP variants. This is especially relevant in families from groups with known founder changes. Patterns in a family can suggest who may be a carrier.
Modifier genes: Variants in other lipid‑related genes can influence HDL levels and clinical features in CETP deficiency. This helps explain why two people with the same CETP change can look different in blood tests.
Lifestyle risk factors
Cholesterol-ester transfer protein deficiency is a genetic condition; lifestyle habits do not cause it, but they can shape lipid balance and long-term heart risk. Choices that lower triglyceride-rich and apoB-containing particles may matter most, because very high HDL in this condition may be less protective than expected. This overview explains how lifestyle affects Cholesterol-ester transfer protein deficiency.
Emphasizing unsaturated fats, vegetables, legumes, and whole grains can lower apoB and triglyceride-rich lipoproteins that drive plaque risk. In CETP deficiency, reducing these particles may offset the uncertain protection from very high HDL.
Sugary drinks and refined starches raise triglycerides and remnant cholesterol. In CETP deficiency, extra triglyceride-rich particles can strain reverse cholesterol transport despite high HDL levels.
High intake of butter, fatty red meats, and full‑fat dairy can increase apoB-containing lipoproteins. Lowering saturated fat helps reduce particles most linked to atherosclerosis when HDL is unusually high but may be less functional.
Regular aerobic and resistance exercise lowers triglycerides and apoB while enhancing HDL function and cholesterol efflux. In CETP deficiency, improving HDL quality and reducing remnant particles may better protect arteries.
Risk prevention
Cholesterol-ester transfer protein deficiency is inherited, so you can’t prevent the condition itself, but you can lower long-term heart and blood vessel risks. Screening and early detection of cholesterol-ester transfer protein deficiency usually happen through a lipid panel that shows very high HDL cholesterol. Your care plan focuses on heart-healthy routines, regular check-ups, and managing other risks like high blood pressure, diabetes, and smoking. Knowing your risks can guide which preventive steps matter most.
Get periodic blood tests to track HDL, LDL, and triglycerides. This helps your clinician spot changes early and tailor care to this condition.
Choose plenty of vegetables, fruit, whole grains, beans, fish, and unsalted nuts. This supports artery health even if HDL is very high with CETP deficiency.
Aim for at least 150 minutes a week of moderate activity, like brisk walking or cycling. Movement improves overall heart health and helps other risks like blood pressure and blood sugar.
Quitting smoking lowers inflammation and artery damage. This is important because very high HDL from CETP deficiency doesn’t always offset smoking-related harm.
Transmission
Cholesterol-ester transfer protein deficiency is a genetic condition, not an infection—you can’t catch it or spread it through touch, the air, sex, blood exposure, or breastfeeding. If you’re wondering how Cholesterol-ester transfer protein deficiency is inherited, it usually follows an autosomal recessive pattern: when both parents carry one changed CETP gene, each pregnancy has a 25% chance of a child with the condition, a 50% chance of a carrier, and a 25% chance of neither. Carriers generally feel well; many have higher HDL (“good”) cholesterol but not the full condition.
When to test your genes
Consider genetic testing if you have extremely high HDL cholesterol, a strong family history of unusual lipid patterns or early heart disease, or unexplained results on standard lipid panels. Testing can clarify whether CETP deficiency is present and guide tailored care, including how to interpret HDL levels and choose therapies. Discuss timing with your clinician if planning pregnancy or starting new lipid-lowering medications.
Diagnosis
Many people with cholesterol-ester transfer protein (CETP) deficiency feel completely well, and the first hint is often an unusually high HDL result on a routine blood test. For some, routine check-ups reveal the first clues. Because this is a genetic condition, diagnosis usually starts with a pattern seen on lab work and is confirmed with targeted tests. In some cases, the genetic diagnosis of cholesterol-ester transfer protein deficiency helps explain very high HDL levels and guides testing for relatives.
Doctors look for very high HDL cholesterol, often above 2.6 mmol/L (100 mg/dL), with normal or low triglycerides. LDL cholesterol may be normal or low. This pattern raises suspicion for CETP deficiency.
A specialized blood test can measure CETP activity. Markedly reduced or absent activity supports the diagnosis. These tests are run in select laboratories.
Targeted testing looks for changes in the CETP gene. Finding a disease-causing variant confirms the diagnosis. Your provider may suggest testing relatives if a clear variant is found.
Doctors check for reasons HDL can be high, such as certain medications, heavy alcohol use, thyroid or liver problems. Simple blood tests and a medication review help exclude these. This step prevents a missed non-genetic explanation.
Stages of Cholesterol-ester transfer protein deficiency
Cholesterol-ester transfer protein deficiency does not have defined progression stages. There are usually no early symptoms of cholesterol-ester transfer protein deficiency; most people feel well, and it’s typically noticed on a routine lipid test showing very high HDL cholesterol. Different tests may be suggested to help confirm the cause and assess heart risk, such as repeat fasting lipids and, in some cases, genetic testing.
Outlook and prognosis
Looking ahead can feel daunting, but most people with cholesterol-ester transfer protein deficiency (often shortened to CETP deficiency) live normal lifespans without serious complications. In medical terms, the long-term outlook is often shaped by both genetics and lifestyle. Many living with CETP deficiency only learn about it after a routine lipid panel shows very high HDL cholesterol, sometimes with slightly higher triglycerides, and they feel well. Mortality does not appear increased based on current data; large population studies have not linked CETP deficiency itself to early death.
That said, the outlook is not the same for everyone, but the pattern most often seen is stable health with careful cardiovascular monitoring. A few people may still develop heart disease from other risk factors like smoking, high blood pressure, diabetes, or a strong family history. Early symptoms of CETP deficiency are usually absent, so the “prognosis” largely depends on the broader heart-risk picture rather than the gene change alone. For most, keeping blood pressure, blood sugar, and triglycerides in range matters more than the HDL number being very high.
Over time, most people with CETP deficiency do well when they follow standard heart‑healthy habits and keep up with checkups. Doctors call this the prognosis—a medical word for likely outcomes. If you’ve had a heart event already, your care team may tailor treatment and avoid medicines that interact with your unique lipid pattern. Talk with your doctor about what your personal outlook might look like.
Long-term effects
Cholesteryl ester transfer protein (CETP) deficiency is a rare inherited condition where HDL (“good”) cholesterol stays very high over a lifetime. Long-term effects vary widely, and many people have no day-to-day health concerns. Research on heart disease risk shows mixed results, so the long-term outlook depends on the specific gene change and other risk factors.
HDL cholesterol often remains markedly elevated, with larger HDL particles. For most, this trait is stable over decades.
High HDL in CETP deficiency does not always lower heart attack risk. Studies report neutral or sometimes higher risk depending on the variant and overall risk profile.
LDL cholesterol may be normal or low, and triglycerides are usually in the normal range. These laboratory features tend to persist over time.
Many living with CETP deficiency feel well and have no specific complaints. Early symptoms of CETP deficiency are often absent, and the condition is usually found on routine blood tests.
How is it to live with Cholesterol-ester transfer protein deficiency?
Living with cholesterol-ester transfer protein (CETP) deficiency often means feeling well and never knowing you have it; many people are identified only through routine blood tests showing very high HDL (“good”) cholesterol. Day to day, there are usually no symptoms to manage, no special diet required beyond heart‑healthy choices, and no activity limitations. The main impact is practical: making sure your healthcare team interprets your lipid panel in context, since high HDL from CETP deficiency doesn’t always translate into extra cardiovascular protection and can complicate treatment decisions. Family members may have questions if it runs in the family, but sharing accurate information—that it’s typically benign—can ease worries while encouraging everyone to keep up with standard heart‑health habits.
Treatment and drugs
Treatment for cholesterol-ester transfer protein deficiency (often called CETP deficiency) depends on whether it’s causing health problems, which for many people it doesn’t. Most people with CETP deficiency are found to have very high HDL (“good”) cholesterol but feel well, so care often focuses on regular checkups, heart risk assessment, and healthy habits like not smoking, staying active, and eating a balanced diet. There’s no specific medicine required to “correct” CETP deficiency itself, and standard cholesterol drugs are used only if overall heart risk, LDL (“bad”) cholesterol, triglycerides, or other factors call for it. Doctors sometimes recommend a combination of lifestyle changes and drugs when other cholesterol numbers are high or when there’s a strong family or personal history of early heart disease. If you’re unsure how CETP deficiency affects your risk, ask your doctor about the best starting point for you.
Non-drug treatment
People with cholesterol-ester transfer protein deficiency often have very high HDL cholesterol but may still need to protect their heart and blood vessels. Non-drug treatments often lay the foundation for long-term health, whether or not medicines are used later. There are often no early symptoms of cholesterol-ester transfer protein deficiency, so everyday choices that lower overall cardiovascular risk still matter.
Center meals on vegetables, fruits, legumes, whole grains, nuts, and olive oil, with fish or lean poultry for protein. This pattern helps lower LDL and triglycerides and supports blood pressure.
Aim for moderate aerobic activity most days, plus muscle-strengthening a couple of times weekly. Movement improves cholesterol handling and keeps blood vessels flexible.
If you live with excess weight, even a 5–10% loss can improve blood pressure, blood sugar, and triglycerides. Small, steady changes in eating and activity usually work best.
Quitting tobacco quickly benefits blood vessels and reduces inflammation. This matters in cholesterol-ester transfer protein deficiency because high HDL alone does not fully protect the heart.
Your genes may have an impact on how drugs work for you
Medicines that lower LDL or raise HDL can work differently in people with cholesterol-ester transfer protein (CETP) deficiency because gene changes alter how cholesterol moves between lipoproteins. Genetic testing and careful lipid monitoring help clinicians choose doses and drug types that fit your biology.
Pharmacological treatments
Many people with cholesterol-ester transfer protein (CETP) deficiency don’t need medication, because HDL is already high and LDL is often lower than average. Treatment, when used, focuses on overall heart risk—especially lowering LDL cholesterol and treating high triglycerides if they’re present. First-line medications are those doctors usually try first, based on strong evidence for lowering heart risk. There are often no early symptoms of cholesterol-ester transfer protein deficiency, so decisions hinge on lab results and your personal risk profile.
Atorvastatin or rosuvastatin lower LDL cholesterol and reduce heart risk. They are the usual first step if LDL or overall risk is high in CETP deficiency. Muscle aches can occur, but lowering the dose or switching often helps.
Ezetimibe blocks cholesterol absorption in the gut to further lower LDL. It’s often added if a statin alone isn’t enough in CETP deficiency. It’s generally well tolerated.
Alirocumab or evolocumab are injections that markedly reduce LDL. They’re considered when LDL remains high despite pills or when risk is very high in CETP deficiency. Injections are usually every 2–4 weeks.
This pill lowers LDL by working in the liver, not in muscle. It can be helpful if statins aren’t tolerated or don’t reach goal in CETP deficiency. It may slightly raise uric acid in some people.
Genetic influences
In most cases, cholesterol-ester transfer protein (CETP) deficiency traces back to changes in the CETP gene that are passed down through families. People who inherit a nonworking change in both copies of this gene usually have a more pronounced deficiency; this pattern is called autosomal recessive. Those with one changed copy are carriers. A “carrier” means you have the gene change but may not show symptoms. Different CETP gene changes can either shut the protein off or just weaken it, so cholesterol results can look quite different from person to person. Family history of very high HDL cholesterol can be a clue, and genetic testing can confirm whether a CETP variant is present. Not everyone with CETP deficiency shares the same heart disease risk, but knowing the genetic cause can help tailor monitoring and care for you and your family.
Is Cholesterol-ester transfer protein deficiency genetic?
Genetics are central in cholesteryl ester transfer protein (CETP) deficiency, which is caused by inherited changes in the CETP gene. Variants usually raise HDL (“good”) cholesterol and can alter LDL levels. Effects on heart disease risk vary by specific mutation and background.
Pharmacogenetics—how genetics influence drug effects
For people living with cholesterol-ester transfer protein (CETP) deficiency, treatment usually centers on lowering LDL (“bad”) cholesterol and overall heart risk rather than trying to raise HDL. Genes can influence how quickly you process certain statins, which can change the risk of muscle side effects and may guide which drug and dose is safest. If statins cause problems or aren’t enough, options like ezetimibe or PCSK9 inhibitors are less affected by drug‑metabolizing genes and can be used on their own or together with a statin. Very high HDL from CETP deficiency doesn’t automatically protect against heart disease, so care plans still focus on your personal risk, family history, and other health conditions. Genetic testing isn’t required for treatment of cholesterol-ester transfer protein deficiency, but it can sometimes help predict statin side effects or refine drug choice, especially if you’ve had trouble with statins in the past.
Interactions with other conditions
Because it changes how cholesterol particles move, cholesterol-ester transfer protein deficiency can interact with heart and metabolic conditions. In people with existing coronary artery disease or diabetes, very high HDL from CETP deficiency doesn’t always act the way we expect, and overall heart risk may still depend on LDL, blood pressure, inflammation, and kidney health. If familial hypercholesterolemia or severe high triglycerides are also present, CETP deficiency may shift the numbers on a lipid panel but does not remove the need to manage those higher-risk conditions. There are often no early symptoms of cholesterol-ester transfer protein deficiency, so these interactions usually show up through blood tests or in how your care team estimates cardiovascular risk over time. Some medicines can play into this picture: statins and PCSK9 inhibitors remain helpful for lowering LDL when needed, while drugs that block CETP offer little added benefit if CETP is already low. Talk with your doctor about how your conditions may influence each other.
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
Throughout history, people have described families in which several relatives had unusually low “bad” cholesterol but seemed otherwise well. A grandparent might have lived into their 90s with few heart issues, while children and grandchildren shared strikingly high “good” cholesterol on routine blood tests. These patterns prompted questions long before the underlying cause was known.
From early theories to modern research, the story of cholesterol-ester transfer protein deficiency has unfolded step by step. First described in the medical literature as an unexpected mismatch between very high HDL cholesterol and low LDL cholesterol, it was initially spotted in clusters within certain communities. Doctors noted that people with these results often felt fine and had no obvious symptoms. At the time, no one knew whether this was protective, harmful, or simply a neutral quirk of cholesterol handling.
As medical science evolved, researchers linked these lab patterns to changes in a single protein that helps shuttle cholesterol between particles in the blood. The protein’s job acts a bit like a traffic coordinator, helping move cholesterol esters from HDL to other lipoproteins. When this protein is missing or works poorly, HDL can build up and LDL can fall. Advances in genetics in the late 20th century identified changes in the CETP gene as the cause, confirming that cholesterol-ester transfer protein deficiency is inherited.
Over time, descriptions became more precise. Scientists recognized partial and complete forms, which helped explain why not everyone with CETP deficiency looks the same on blood tests. Early reports called it rare, but population studies later found certain variants to be more common in some regions, especially parts of East Asia. This widened the historical picture from isolated case reports to broader community patterns.
In recent decades, knowledge has built on a long tradition of observation. The condition, once a laboratory curiosity, influenced the development of drugs that block CETP, aiming to raise HDL and improve heart outcomes. Trials showed that simply boosting HDL numbers is not always enough, reshaping how clinicians think about cholesterol biology. Despite evolving definitions, the historical thread remains clear: careful observation of families led to the discovery of a genetic change, which then guided both research and treatment strategies.
Today, the history of cholesterol-ester transfer protein deficiency continues to inform care. Knowing how it was recognized—first through family stories and unusual lab results, and later through gene studies—helps explain why someone may have lifelong high HDL without clear symptoms. It also reminds us that lab numbers tell only part of the story, and that understanding a condition’s past can improve the conversations and decisions people have with their care team now.