Using Ultrasound to Prevent Stroke: A Patient's Guide

Table of Contents

• Key Points
• Why This Research Matters
• Measuring Atherosclerosis: IMT vs. Plaque Burden
• Total Plaque Area (TPA): A Powerful Predictor of Risk
• A New Approach: Treating Arteries Instead of Risk Factors
• Unexplained Atherosclerosis and the Gut Microbiome
• 3D Ultrasound: Plaque Volume and Vessel Wall Volume
• Identifying Dangerous Plaques: Echolucency, Ulceration, and Plaque Texture
• Transcranial Doppler: Listening to Blood Flow in the Brain
• What This Means for Patients
• Study Limitations
• Recommendations for Patients
• Frequently Asked Questions
• Source Information

Key Points

• Carotid plaque burden, measured by ultrasound, predicts heart attack and stroke risk better than intima-media thickness.
• In a single-center study, a plaque-guided 'treating arteries' approach was associated with an over 80% reduction in 2-year stroke and heart attack risk.
• Gut microbiome metabolites such as TMAO and p-cresyl sulfate were higher in patients with unexplained atherosclerosis in a study of over 3,000 patients.
• Transcranial Doppler can detect microemboli; patients with two or more in one hour had a 15.6% one-year stroke risk versus 1% without.
• Most asymptomatic carotid stenosis patients do better with intensive medical therapy; TCD embolus detection helps identify the minority who might benefit from intervention.

Why This Research Matters

Stroke is a leading cause of death and disability worldwide, and its burden is growing as populations age. This review article, written by Prof. J. David Spence of the Stroke Prevention & Atherosclerosis Research Centre at Western University, explains how ultrasound—a safe, radiation-free imaging technique—can be used to prevent stroke in several important ways.

The review highlights that ultrasound is not just a diagnostic tool. It can guide treatment decisions, identify which patients are at highest risk, help researchers discover new risk factors, and even serve as a target for therapy. The author argues that these methods should be used more widely to reduce the growing burden of stroke in aging populations.

Measuring Atherosclerosis: IMT vs. Plaque Burden

Atherosclerosis is the buildup of fatty plaque inside arteries. For decades, doctors measured something called intima-media thickness (IMT)—the thickness of the inner two layers of the artery wall—as an early sign of "preclinical atherosclerosis" (atherosclerosis that hasn't yet caused symptoms). However, this review makes a strong case that this widespread practice is based on a misunderstanding.

According to the author, IMT as measured by the Mannheim consensus does not represent true atherosclerosis. Instead, it is a biologically, pathologically, and genetically distinct phenotype (a different physical trait with different underlying causes). Studies that report IMT predicting risk are actually those that combine plaque thickness with IMT—and those studies should not call their measurement "IMT" because they mix together patients with plaque and patients without plaque.

Plaque thickness itself does predict risk, but the evidence shows that measuring the total plaque burden (the overall amount of plaque) is far more useful. Key differences highlighted in the review:

• Plaque area is a much stronger predictor of risk than IMT
• Plaque burden measured by ultrasound is highly correlated with coronary calcium scores (another heart risk test) and is just as predictive of risk—but ultrasound is less costly and does not require radiation
• Progression of IMT does not predict risk, whereas progression of plaque area and 3-dimensional (3D) plaque volume does predict cardiovascular risk

Total Plaque Area (TPA): A Powerful Predictor of Risk

Total plaque area (TPA) is measured by tracing the outline of a plaque in a longitudinal (lengthwise) ultrasound image, in the plane where the plaque is biggest. All plaques seen on both sides of the neck, between the collarbone and the angle of the jaw, are measured, and the sum of all plaque areas gives the TPA.

The measurement is surprisingly easy to perform. It can be taught to any experienced ultrasound technologist, takes only a short time, and is very reliable: the intraclass correlation (a measure of test-retest reliability) for repeat measurement is 0.94, which is considered excellent. The method was invented in 1986 by Maria DiCicco RVT at the author's laboratory, and was first used in a study of the effects of psychological stress on atherosclerosis.

In 1995, the research team began measuring TPA routinely in their vascular prevention clinics. By 2002, they had strong evidence that TPA predicted cardiovascular risk among patients referred for prevention. The findings were striking:

• By quartile (quarter) of plaque area, the 5-year risk of stroke, heart attack (myocardial infarction), or vascular death was 5.6%, 10.7%, 13.9%, and 19.5%—from the lowest to the highest quartile
• These results were adjusted (statistically corrected) for age, sex, blood pressure, serum cholesterol, smoking (pack-years), diabetes, plasma total homocysteine, and treatment of blood pressure and cholesterol
• In other words, TPA was a much stronger predictor of risk than traditional risk scores such as the Framingham risk score

The review also revealed important patterns in how plaque behaves over time. Plaque progression (worsening) occurred in half of the patients despite usual therapy, and patients whose plaque progressed had twice the risk of those whose plaque was stable or regressed (shrank). Regression occurred in only 25% of patients. This meant that "usual therapy" was failing half of the patients—a sobering realization that led to a new approach to vascular prevention.

A New Approach: Treating Arteries Instead of Risk Factors

In 2003, the research team implemented a fundamentally different approach to vascular prevention. Instead of being satisfied with reaching target levels of risk factors like blood pressure and LDL cholesterol (LDL-C), the new target of therapy was to stop plaque progression or achieve plaque regression. In other words: "Treating arteries instead of treating risk factors."

The results were dramatic. By 2010, the proportion of patients with plaque regression versus progression had reversed. Now only about a quarter of patients had plaque progression, and about half had regression. Additional benefits followed:

• The percentage of patients with microemboli (tiny blood clots detected by transcranial Doppler, discussed later) declined from 12.6% to 3.7% of patients
• The rate of carotid plaque progression declined significantly
• The 2-year risk of stroke and heart attack declined by more than 80%

One of the most practical advantages of this approach is that plaque responds quickly enough to guide treatment. Even plaque area changes within 3 months—the review includes an example of a 64-year-old patient whose plaque area grew from 20 mm² to 28 mm² after stopping a statin (rosuvastatin) and taking only ezetimibe, then regressed to 19 mm² over 13 weeks after restarting rosuvastatin 5 mg daily with ezetimibe 10 mg daily and CoQ10 200 mg daily to prevent muscle pain.

The author emphasizes the core philosophy with a memorable analogy: "Treating arteries without measuring plaque would be like treating hypertension without measuring blood pressure."

Unexplained Atherosclerosis and the Gut Microbiome

After treating more than 4,000 patients with this plaque-guided approach, the team noticed something important: some patients had atherosclerosis that could not be explained by traditional risk factors. These patients had "unexplained atherosclerosis" and were extraordinarily resistant to even intensive medical therapy.

Surprisingly, neither baseline levels of LDL-C ("bad cholesterol") nor changes in LDL-C over a year predicted whether plaque would progress or regress. Even among patients with LDL-C below 1 mmol/L (19 mg/dL)—an extremely low level—half still had plaque progression. (These were the patients being treated most intensively, which explains why they had the lowest cholesterol.) Two factors that did predict resistance to therapy were age and kidney (renal) function.

This observation pointed toward a new hypothesis: metabolic toxins that the kidneys normally clear from the body might account for a large proportion of "unexplained atherosclerosis." Patients with kidney failure are known to have extremely high cardiovascular risk. They also have high blood levels of several potentially harmful substances:

• Total homocysteine (an amino acid linked to heart and stroke risk)
• Asymmetric dimethylarginine (ADMA, which blocks nitric oxide, a molecule that relaxes blood vessels)
• Thiocyanate (a potent factor that increases oxidative stress, which damages cells)
• Toxic metabolites produced by the intestinal microbiome (gut bacteria) from dietary precursors such as carnitine (found in red meat) and phosphatidylcholine (found in egg yolk)

In 2016, the team estimated that plasma total homocysteine only accounted for about 20% of the effect of kidney impairment on atherosclerosis. They hypothesized that toxic metabolites of the intestinal microbiome might account for a greater proportion.

In 2018, they reported a breakthrough finding. Among a clinic population of 3,056 patients, they identified the 5% extremes: patients with "unexplained atherosclerosis" (much more plaque than predicted by traditional risk factors) and "protected" patients (much less plaque than expected despite high levels of traditional risk factors). Key results:

• Plasma levels of trimethylamine N-oxide (TMAO), p-cresyl sulfate, and two other gut-derived metabolites were significantly higher in patients with unexplained atherosclerosis than in patients whose atherosclerosis was explained by traditional risk factors
• These same metabolites were significantly lower in "protected" patients who had little or no plaque despite high risk factor levels
• In linear regression analysis, both TMAO and p-cresyl sulfate were significant predictors of plaque burden

Specific metabolite results (see Figure 3 in the original article):

• TMAO: P=0.005 (statistically significant)
• P-cresyl sulfate: P=0.0001 (highly significant)
• P-cresyl glucuronide: P=0.0001 (highly significant)
• Phenylacetyl glutamine: P=0.0001 (highly significant)
• Hippuric acid: P=0.14 (not significant)
• Indoxyl sulfate: P=0.08 (borderline, not significant)
• Phenyl sulfate: P=0.35 (not significant)

For context, a P value below 0.05 means there is less than a 5% probability that the result occurred by random chance. A P value of 0.0001 means there is only a 0.01% chance the finding was due to luck.

This research opens an exciting new frontier: modifying the diet to change the gut microbiome could potentially reduce atherosclerosis risk in ways that go beyond traditional cholesterol-lowering treatments.

3D Ultrasound: Plaque Volume and Vessel Wall Volume

While 2D plaque area measurements (TPA) are useful, researchers have also developed 3D ultrasound methods to measure total plaque volume (TPV) and vessel wall volume (VWV). These methods, developed by Fenster and colleagues, use manual segmentation (tracing) of cross-sectional slices of plaques.

The review acknowledges that these measurements have practical challenges. They are tedious to perform, about a third of people cannot master them (some are too perfectionist and cannot make boundary decisions; others are too careless), and it takes several months of training to become certified to do the measurements reliably.

However, measuring change in 3D plaque volume is the most efficient way to assess how well a therapy is working on atherosclerosis. Here's why:

• IMT changes by only about 1.5 mm per year, and the spatial resolution of carotid ultrasound is about 3 mm—so it is not possible to measure IMT change within an individual in a clinically meaningful time frame
• Consensus sample sizes for IMT studies of anti-atherosclerotic therapies are about 300 patients per group, followed for 2 years
• Coronary plaque studies using intravascular ultrasound (IVUS) need about 200 patients per group followed for 2 years
• Carotid plaques are focal (localized), so they can change in 3 dimensions: length, thickness, and circumferential extent. They also grow along the vessel in the direction of blood flow 2.4 times faster than they thicken

This means 3D plaque volume requires far smaller sample sizes and shorter study durations. In one study of patients with asymptomatic carotid stenosis (ACS), significant plaque volume reduction was seen with atorvastatin compared to placebo in only 3 months, using only 17 patients on placebo and 21 on atorvastatin. Specifically:

• Placebo group: plaque volume progressed by 16.81 ± 74.10 mm³
• Atorvastatin group: plaque volume regressed by −90.25 ± 85.12 mm³
• The difference was highly statistically significant (P<0.0001)

For patients who don't yet have carotid plaque, 3D ultrasound measurement of vessel wall volume (VWV) is superior to IMT because the dynamic range is much greater and the ability to detect change over time is far better. In a dietary study, blood pressure reduction with weight loss was strongly associated with reduced VWV over 2 years in a relatively small study of only 140 participants.

Identifying Dangerous Plaques: Echolucency, Ulceration, and Plaque Texture

In patients with asymptomatic carotid stenosis (ACS)—meaning narrowing of the neck arteries that hasn't yet caused a stroke—the risk of stroke is now lower with intensive medical therapy than with either stenting or surgery (endarterectomy). This makes it critically important to identify the few patients (perhaps 10–15%) who could still benefit from intervention. Ultrasound helps identify these high-risk patients by detecting specific "vulnerable" plaque features.

Echolucency and Juxtaluminal Black Plaque Area

Echolucent plaques appear dark on ultrasound, meaning they are soft and fat-rich rather than dense and calcified. Of particular concern is the juxtaluminal black plaque area (JBA)—a dark area right next to the artery opening, which may represent thrombus (blood clot) and predicts a higher risk of stroke.

Nicolaides and colleagues studied 324 patients with 50–99% carotid stenosis. They found that a gray scale median (GSM) of ≤15 (very dark plaque) and JBA ≥8 mm² were independent predictors of the presence of hemispheric symptoms (symptoms related to one side of the brain). This model identified a high-risk group with an odds ratio of 6.7 (95% confidence interval, 4.08–10.91; P<0.001)—meaning these patients were nearly 7 times more likely to have symptoms.

Markus and colleagues reported that the combination of echolucency with microemboli detected on transcranial Doppler was associated with a marked increase in stroke risk.

Ulceration

Plaque ulceration—a crater or break in the surface of the plaque—is another dangerous feature. The North American Symptomatic Carotid Endarterectomy (NASCET) Study first showed that plaque ulceration detected by angiography predicted a higher risk of stroke. However, angiograms only show the inside of the artery lumen. The best way to assess carotid ulceration is actually 3D ultrasound, which can see the plaque surface in detail.

In 2011, the author's team reported findings from patients with ulcers visible on 3D ultrasound:

• Patients with 3 or more ulcers in either or both carotid arteries had a risk very similar to that of patients with microemboli on transcranial Doppler
• 4% of patients had ≥3 ulcers, 6% had microemboli, and 10% had either microemboli or ≥3 ulcers
• Patients with 3 or more ulcers in either carotid were more likely to have a stroke or death within 3 years (18% vs. 2%; P=0.03), regardless of which side the ulcers were found on
• The 3-year risk of stroke or death was 20% with microemboli vs. 2% without (P<0.003)
• The annual rate of ipsilateral stroke (stroke on the same side as the carotid disease) was 0.8%

In 2014, the team assessed ulcer volume as a predictor of cardiovascular risk among 349 patients followed for 5 years. Patients with total ulcer volume ≥5 mm³ had a significantly higher risk of stroke, transient ischemic attack (TIA, a "mini-stroke"), or death (P=0.009), and also of stroke/TIA/death/heart attack/revascularization (P=0.017).

Plaque Texture

An emerging field is the analysis of plaque texture using complex mathematical analysis of radiofrequency signals from carotid ultrasound. While these analyses are difficult to conceptualize as mathematical constructs, they provide information on how pixel intensities are distributed within plaques, yielding "texture parameters" such as coarseness or contrast.

These measures have already shown promise:

• They can differentiate between symptomatic and asymptomatic patients
• They were superior to assessment of plaque shape
• They predicted events better than a combination of a history of prior events and plaque features such as plaque area and gray scale median

In a 2014 study, the author's team evaluated 298 patients with carotid atherosclerosis using 3D ultrasound at baseline and after 1 year. They measured carotid plaque volume and 376 measures of plaque texture. Patients were followed for up to 5 years (median follow-up 3.12 years, range 0.77–4.66 years) for heart attack, TIA, and stroke.

The results showed that changes in texture and total plaque volume combined provided the best predictor of vascular events. In multivariate Cox regression:

• Changes in plaque texture: median hazard ratio 1.4 (P<0.001)—meaning each unit increase in texture change raised risk by 40%
• Total plaque volume: median hazard ratio 1.5 per 100 mm³ (P<0.001)—meaning each 100 mm³ increase in plaque volume raised risk by 50%
• The Framingham risk score was not a significant predictor in this model

Transcranial Doppler: Listening to Blood Flow in the Brain

Transcranial Doppler (TCD) is an ultrasound technique that measures blood flow in the brain's blood vessels. It serves several important functions in stroke prevention.

Embolus Detection

Detection of microemboli (tiny particles or clots traveling in the bloodstream) is perhaps the best-validated way to identify which patients with asymptomatic carotid stenosis (ACS) are at high risk of stroke. In 2005, the author's team reported a study of 319 patients with ACS:

• 10% had two or more microemboli detected in one hour of monitoring
• Their 1-year risk of stroke was 15.6%, compared to only 1% among patients without microemboli

This very clearly distinguishes which patients with ACS could benefit from intervention. Patients with microemboli could benefit from procedures like carotid endarterectomy (surgical removal of plaque) or stenting, which carry a periprocedural risk of stroke or death of about 3–4%. Patients without microemboli would be better treated with intensive medical therapy alone.

In 2010, a study of 468 patients (199 enrolled before 2003 and 269 after 2003) confirmed that intensive medical therapy reduced the percentage of patients with microemboli, as described earlier (from 12.6% to 3.7%).

Patent Foramen Ovale (PFO) Detection

A patent foramen ovale (PFO) is a small opening between the upper chambers of the heart that fails to close after birth. In some people, this "hole in the heart" allows blood clots to pass from the right side of the heart to the left side, where they can travel to the brain and cause a stroke. This is called paradoxical embolism.

TCD saline studies (also called bubble studies) are used to detect PFO. During this test, a small amount of saline with tiny bubbles is injected into a vein while the doctor uses TCD to listen for those bubbles crossing to the brain. This technique is actually more sensitive than trans-esophageal echocardiography (TEE) for detecting PFO, and the size of the right-to-left shunt (RLS) as assessed by TCD is more predictive of recurrent stroke than merely detecting a PFO.

The review notes an important clinical challenge: even among patients with cryptogenic stroke (stroke of unknown cause), approximately half of PFOs are incidental—meaning they are not the cause of the stroke. Therefore, before recommending percutaneous closure of a PFO (a procedure to plug the hole), doctors need ways to identify patients who are likely to benefit.

Clinical clues that a PFO may have caused a stroke (paradoxical embolism) include:

• Prolonged sitting (which increases the risk of blood clots in the legs)
• Shortness of breath (dyspnea) at the onset of stroke
• Low oxygen (pO₂) and carbon dioxide (pCO₂) levels at the time of stroke
• Previous history of deep vein thrombosis (DVT), pulmonary embolism, or varicose veins
• History of sleep apnea
• Waking up with stroke symptoms (possibly related to sleep apnea)

The author explains that a paradoxical embolus is essentially a pulmonary embolus (blood clot in the lungs) that "turned left through a PFO instead of turning right to go into the pulmonary artery." This is why the clinical clues overlap so much with those of pulmonary embolism.

What This Means for Patients

This research has several direct implications for patients concerned about stroke risk:

1. Plaque measurement matters more than cholesterol numbers alone. Two patients with identical cholesterol levels can have very different plaque burdens—and the plaque burden is what determines risk. Asking your doctor about carotid plaque measurement (TPA) can provide a more personalized picture of your risk.
2. Treatment can be guided by plaque response. If your plaque is progressing despite treatment, it may be time to intensify therapy or consider additional factors. If your plaque is regressing, you'll know your treatment is working.
3. Gut health may affect stroke risk. The finding that gut microbiome metabolites like TMAO are linked to unexplained atherosclerosis suggests that diet could play a role in stroke prevention beyond traditional risk factors. However, more research is needed before specific dietary recommendations can be made.
4. Not everyone with carotid stenosis needs surgery. With modern intensive medical therapy, most patients with asymptomatic carotid stenosis are safer with medication than with stenting or surgery. Tests like TCD embolus detection help identify the 10–15% who might benefit from intervention.
5. PFO closure decisions should be individualized. If you've had a stroke and have a PFO, the presence of additional clues (like DVT history or sleep apnea) can help determine whether the PFO was the culprit or just an incidental finding.

Study Limitations

This article is a narrative review, not a single clinical trial. It draws on multiple studies conducted over several decades, largely from one research center. Some specific limitations worth noting:

• Many of the key findings come from a single center (Western University's Stroke Prevention & Atherosclerosis Research Centre) and may not apply equally in all settings
• The "treating arteries" approach was implemented without a randomized controlled trial; the >80% risk reduction was observed by comparing patients before and after 2003, which could be influenced by other changes in care over time
• The microbiome findings, while statistically significant, are observational and do not prove that TMAO or p-cresyl sulfate cause atherosclerosis—only that they are associated with it
• 3D plaque volume measurement is technically challenging and requires extensive training; about a third of people cannot master it
• The plaque texture analysis is an emerging field that is mathematically complex and not yet widely available in clinical practice
• The PFO section was cut short in the original text, so some details of that discussion are not included here

Recommendations for Patients

Based on this research, here are practical steps patients can discuss with their healthcare providers:

1. Ask about carotid plaque measurement. If you have risk factors for stroke or heart disease, ask whether a carotid ultrasound to measure plaque area (TPA) would be useful—even if a standard carotid ultrasound was normal. Plaque burden is a stronger predictor than IMT.
2. If you have carotid stenosis, ask about TCD monitoring. Microembolus detection can tell you whether you're in the 10% of patients with a 15.6% 1-year stroke risk (who may need intervention) or the 90% with a 1% risk (who are better treated with medication).
3. If you've had a cryptogenic stroke and have a PFO, ask whether TCD saline studies would help. The size of the right-to-left shunt, along with clinical clues like DVT history or sleep apnea, can guide whether PFO closure is worth considering.
4. Follow up with repeat plaque measurements. Carotid plaque changes over months, not years. Regular monitoring can tell you whether your treatment is actually working.
5. Don't rely solely on cholesterol levels. Even patients with very low LDL-C can have plaque progression. If your plaque is progressing despite "good" cholesterol numbers, talk to your doctor about additional strategies.
6. Consider the gut-heart connection. While specific dietary recommendations await more research, limiting excess red meat (a source of carnitine) and being mindful of dietary patterns that support a healthy gut microbiome are reasonable steps.

The author's closing message is clear: ultrasound methods for stroke prevention are underutilized. With the burden of stroke increasing in aging populations, wider adoption of these techniques could meaningfully reduce the toll of this devastating disease.

Frequently Asked Questions

Why is measuring plaque burden better than measuring intima-media thickness (IMT)?

Plaque area is a much stronger predictor of heart attack and stroke risk than IMT. In a 2002 study, 5-year risk rose from 5.6% to 19.5% across increasing plaque-area quartiles, even after adjusting for cholesterol, blood pressure, and smoking. IMT, as measured by the Mannheim consensus, does not represent true atherosclerosis.

What is total plaque area (TPA) and how is it measured?

Total plaque area is the sum of all carotid plaque areas, measured by tracing each plaque in a lengthwise ultrasound image. Plaques between the collarbone and the jaw on both sides are included. It is reliable (intraclass correlation 0.94), quick to perform, and was first used in 1986. Higher TPA predicts higher cardiovascular risk.

What does 'treating arteries instead of risk factors' mean?

Instead of only targeting blood pressure and LDL cholesterol numbers, doctors use repeat plaque measurements to guide therapy. The goal is to stop plaque progression or achieve regression. At one center, this approach reversed the proportion of patients with progression versus regression, and the 2-year risk of stroke and heart attack fell by more than 80% compared with prior treatment.

Can gut microbiome metabolites explain unexplained atherosclerosis?

In a 2016–2018 study of over 3,000 clinic patients, those with unexplained atherosclerosis (more plaque than expected) had higher blood levels of gut-derived metabolites like TMAO and p-cresyl sulfate. These metabolites were lower in patients with less plaque than expected. This suggests diet and gut bacteria may influence stroke risk beyond traditional factors, but causality isn't proven.

How does transcranial Doppler (TCD) help prevent stroke?

TCD uses ultrasound to detect microemboli—tiny blood clots traveling to the brain. In a 2005 study of 319 patients with asymptomatic carotid stenosis, those with two or more microemboli in one hour had a 15.6% one-year stroke risk, versus 1% in those without. This helps identify which patients might need surgery or stenting instead of just medication.

If I have asymptomatic carotid stenosis, do I need surgery?

Most patients with asymptomatic carotid stenosis are safer with intensive medical therapy than with stenting or surgery. Only about 10–15% might benefit from intervention. Tests such as TCD for microemboli or ultrasound for three or more plaque ulcers can identify higher-risk patients, who may then consider procedures, which carry a periprocedural stroke or death risk of about 3–4%.

How can I know if a PFO caused my stroke?

A patent foramen ovale (PFO) is an opening in the heart that can let clots cross to the brain. But half of PFOs in cryptogenic stroke are incidental. TCD saline (bubble) studies help detect PFOs, and the shunt size is more predictive than just presence. Clinical clues like deep vein thrombosis, sleep apnea, or prolonged sitting suggest the PFO was the cause.

Source Information

Original article title: Spence 2020 Uses of ultrasound in stroke prevention

Author: Prof. J. David Spence, CM, MD, FRCPC, FAHA

Affiliation: Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, Western University, London, ON, Canada

Journal: Cardiovascular Diagnosis and Therapy, Vol 10, No 4, August 2020, pages 955–964

Publication details: Review Article on Advanced Imaging in The Diagnosis of Cardiovascular Diseases. Submitted Oct 22, 2019; accepted Dec 09, 2019. doi: 10.21037/cdt.2019.12.12

Note: This patient-friendly article is based on peer-reviewed research. It is intended for informational purposes and does not replace professional medical advice. Always consult your healthcare provider about your specific medical situation.