2026 Dyslipidemia Guideline: What Changed, What Matters, and How I Apply It

The 2026 ACC/AHA multisociety dyslipidemia guideline retires and replaces the 2018 blood cholesterol guideline. More importantly, it expands the conversation. It no longer focuses only on blood cholesterol. It addresses dyslipidemia more broadly, including elevated LDL-C, hypertriglyceridemia, and elevated lipoprotein(a), while keeping atherosclerotic cardiovascular risk reduction at the center.

As an endocrinologist, obesity medicine physician, clinical hypertension specialist, and lipid specialist, I find this shift both more biologically honest and more clinically useful. The new document still keeps statins at the foundation, yet it also pushes us to think earlier, measure better, personalize risk more carefully, and treat to clearer endpoints.

Why This Update Feels Bigger Than a Routine Revision

This guideline does more than add a few new medications. It changes the structure of lipid thinking. It emphasizes lifetime exposure to atherogenic particles, adopts a newer risk model for primary prevention, restores LDL-C and non-HDL-C treatment goals, gives apoB and Lp(a) more clinical weight, and uses coronary artery calcium more actively to guide treatment intensity. It also gives triglycerides a more organized and practical framework than most prior guidelines offered.

In practical terms, several themes stand out right away:

• Treat dyslipidemia earlier, because lifelong exposure matters.
• Use PREVENT instead of the older pooled cohort equations in most adults ages 30-79.
• Bring LDL-C and non-HDL-C goals back into routine care.
• Measure Lp(a) at least once in all adults.
• Use apoB when residual risk remains unclear.
• Let CAC guide not only whether to treat, but often how aggressively to treat.

Better Detection Starts Earlier

The new guideline clearly favors earlier recognition. It recommends lipid screening in adults beginning at age 19 and at least every 5 years thereafter, with more frequent testing when additional ASCVD risk factors are present. It also continues to support childhood screening, which matters because lifelong exposure begins long before the first event.

A few age cutoffs make this easier to remember:

• Adults should begin screening at age 19.
• Children ages 9-11 should be screened if not previously tested.
• In families with premature ASCVD, severe hypercholesterolemia, or FH, cascade screening can begin as early as age 2.

The measurement approach also improves. The guideline prefers the Martin/Hopkins equation or the Sampson/NIH equation over the older Friedewald formula for LDL-C estimation. It also recommends routine reporting of non-HDL-C and advises against routine advanced lipoprotein subclass testing for everyday risk assessment. In other words, it sharpens the standard lipid panel before it reaches for more exotic testing.

The Biggest Technical Change Is PREVENT

This is one of the most important updates. For adults ages 30-79 without ASCVD or subclinical atherosclerosis and with LDL-C 70-189 mg/dL, the guideline now recommends the PREVENT-ASCVD equations for 10-year risk estimation.

It categorizes 10-year risk as:

• Low if <3%.
• Borderline at 3–5%.
• Intermediate at 5–10%.
• High at 10% or above.

These categories now anchor much of the primary prevention framework.

The guideline notes that PREVENT was derived in about 3.3 million contemporary U.S. adults and externally validated in another similarly large cohort. It also generally produces 10-year risk estimates about 40% to 50% lower than the older pooled cohort equations for the same risk profile. That does not mean the guideline became softer. It means the risk calculator became more contemporary, while treatment thresholds shifted accordingly.

A useful way to think about the new system is the CPR model:

• Calculate risk with PREVENT.
• Personalize that estimate with factors PREVENT does not fully capture.
• Reclassify when CAC meaningfully changes the decision.

That sequence feels more realistic than pretending a calculator alone captures the full patient.

There is also a practical crosswalk between the old and new systems:

• Old PCE low risk under 5% roughly corresponds to PREVENT low risk under 3%.
• Old PCE borderline 5% to <7.5% roughly corresponds to PREVENT 3–5%.
• Old PCE intermediate 7.5% to <20% roughly corresponds to PREVENT 5–10%.
• Old PCE high risk 20% or above roughly corresponds to PREVENT ≥10%

Table 1: PREVENT Risk Categories and Practical Treatment Direction

Adapted from the 2026 dyslipidemia guideline framework.

Earlier Treatment Now Makes More Physiologic Sense

One of the strongest messages in this guideline is simple: prolonged exposure to atherogenic lipoproteins drives disease. That idea appears throughout the document. The writing committee repeatedly returns to duration of exposure, not just the number seen in the room today.

That is why the guideline now gives more attention to low 10-year risk adults who still carry meaningful long-term burden. In adults ages 30-59 with low 10-year risk, an LDL-C of 160-189 mg/dL or a 30-year ASCVD risk of 10% or more can justify moderate-intensity statin therapy, even when the short-term number looks modest.

The practical takeaway looks like this:

• Low 10-year risk with LDL-C <160 mg/dL and 30-year risk <10% favors health behavior counseling.
• Low 10-year risk with LDL-C 160-189 mg/dL can justify moderate-intensity statin therapy.
• Low 10-year risk with 30-year ASCVD risk 10% or above can also justify moderate-intensity statin therapy.
• Untreated LDL-C <70 mg/dL and non-HDL-C <100 mg/dL, without additional risk factors, makes primary prevention drug therapy unlikely to help.

This is an important philosophical shift. The guideline no longer waits so passively for short-term risk to become dramatic.

Treatment Goals Are Back, and That Matters

The 2018 cholesterol guideline emphasized statin intensity and percentage LDL-C reduction. The 2026 document keeps percentage reduction central, but it clearly restores LDL-C and non-HDL-C goals as part of routine decision-making. I think that helps clinicians and patients alike. Clear goals improve follow-up, adherence, and treatment adjustment.

In practical terms, the major goals look like this:

• Borderline or intermediate primary prevention, once statin therapy starts:
  • LDL-C <100 mg/dL
  • Non-HDL-C <130 mg/dL
• High-risk primary prevention:
  • LDL-C <70 mg/dL
  • Non-HDL-C <100 mg/dL
• Clinical ASCVD, not very high risk:
  • LDL-C <70 mg/dL
  • Non-HDL-C <100 mg/dL
• Clinical ASCVD, very high risk:
  • LDL-C <55 mg/dL
  • Non-HDL-C <85 mg/dL
• Severe hypercholesterolemia without ASCVD, heterozygous familial hypercholesterolemia (HeFH), subclinical disease, or added risk factors:
  • LDL-C <100 mg/dL
  • Non-HDL-C <130 mg/dL
• Severe hypercholesterolemia with HeFH, coronary calcification, or additional risk factors:
  • LDL-C <70 mg/dL
  • Non-HDL-C <100 mg/dL

The guideline still prioritizes percentage LDL-C reduction. It simply stops there less often. I think that is a welcome correction.

ApoB and Lp(a) Move Closer to the Center

The document gives apoB a more practical role than many clinicians have traditionally used. It does not replace LDL-C. Instead, it helps clarify residual atherogenic burden when LDL-C looks acceptable but the clinical picture still feels higher risk. This becomes especially relevant in ASCVD, Cardiovascular-Kidney-Metabolic (CKM) syndrome, type 2 diabetes, and elevated triglycerides.

The apoB message is straightforward:

• ApoB is reasonable in adults already on lipid-lowering therapy.
• It is especially useful in ASCVD, CKM syndrome, diabetes, and elevated TG.
• It helps guide further intensification once LDL-C and non-HDL-C goals are reached.

Lp(a) receives an even stronger recommendation. The guideline recommends measuring Lp(a) at least once in all adults for ASCVD risk assessment. That is a major shift in day-to-day practice.

The key thresholds are easier to navigate in this format:

• Elevated and risk-enhancing at 125 nmol/L, or 50 mg/dL.
• Associated with about a 1.4-fold higher ASCVD risk at that level.
• Approximately doubled ASCVD risk around 250 nmol/L, or 100 mg/dL.
• Even higher risk at very elevated levels, such as around 430 nmol/L, or 180 mg/dL.

The guideline also supports cascade testing of first-degree relatives when FH, premature ASCVD, or high Lp(a) is present. That matters because Lp(a) is largely genetic, remains relatively stable, and often goes unmeasured for years.

CAC Becomes More Actionable

The CAC section feels more usable than before. The document does not treat CAC as a simple yes or no test. It treats CAC as a risk and treatment-intensity tool. In intermediate-risk adults, and in selected borderline-risk adults, CAC can clarify whether to hold therapy, start therapy, or intensify further.

Here is the practical CAC framework:

• CAC = 0
  • Therapy may be deferred in selected patients.
  • This applies only when higher-risk conditions are absent.
  • Repeat CAC in 3-7 years can be reasonable.
• CAC 1–100 and <75th percentile, or mild incidental CAC
  • Moderate-intensity statin is reasonable.
  • Goal LDL-C <100 mg/dL.
  • Goal non-HDL-C <130 mg/dL.
• CAC 100–300, or 75th percentile or higher
  • Lipid-lowering therapy is recommended.
  • Target LDL-C <70 mg/dL.
  • Target non-HDL-C <100 mg/dL.
• CAC 300–1000
  • At least 50% LDL-C reduction is recommended.
  • Target LDL-C <70 mg/dL.
  • Target non-HDL-C <100 mg/dL.
  • Intensifying toward LDL-C <55 mg/dL can be reasonable.
• CAC ≥1000
  • Treat as an extremely high-risk phenotype.
  • Target LDL-C <55 mg/dL.
  • Target non-HDL-C <85 mg/dL.

This section also gives incidental CAC more clinical weight. If noncardiac CT identifies coronary calcification, the guideline wants that information to influence treatment decisions. In practice, that means we should stop ignoring calcium that is already sitting in front of us on another scan.

Table 2: LDL-C and Non-HDL-C Goals Across Major Clinical Settings

Condensed from major treatment targets in the 2026 guideline.

Statins Still Lead, but Combination Therapy Looks More Normal

None of this guideline weakens the role of statins. Statins remain the foundation of pharmacologic therapy in both primary and secondary prevention. That part did not change. What changed is the comfort with combination treatment when statins alone do not achieve the necessary reduction.

The add-on hierarchy looks more practical now:

• Ezetimibe often serves as the first add-on due to safety, tolerability, and accessibility.
• PCSK9 monoclonal antibodies (mAbs) provide major LDL-C lowering and event reduction in high-risk groups.
• Bempedoic acid offers another useful option, especially when statin-attributed side effects limit therapy.
• Inclisiran lowers LDL-C effectively and may suit patients who prefer less frequent dosing, although cardiovascular outcome trials remain pending.

The guideline also reinforces follow-up discipline. Clinicians should recheck a lipid profile 4-12 weeks after treatment initiation or dose change, then every 6-12 months thereafter to assess efficacy and adherence. That remains one of the simplest high-value steps in lipid care.

Severe Hypercholesterolemia Now Has Clearer Tiers

Adults with LDL-C 190 mg/dL or higher represent a very high lifetime-risk group. The document wants clinicians to exclude secondary causes, begin maximally tolerated statin therapy, and then intensify according to the patient’s broader phenotype rather than use one flat approach for everyone.

The major tiers now look like this:

• LDL-C ≥190 mg/dL without ASCVD, HeFH, subclinical disease, or added risk factors:
  • Goal LDL-C <100 mg/dL.
  • Goal non-HDL-C <130 mg/dL.
• LDL-C ≥190 mg/dL without ASCVD; but with HeFH, coronary calcification, or additional risk factors:
  • Goal LDL-C <70 mg/dL.
  • Goal non-HDL-C <100 mg/dL.
• LDL-C ≥190 mg/dL with clinical ASCVD:
  • Goal LDL-C <55 mg/dL.
  • Goal non-HDL-C <85 mg/dL.

The guideline also takes FH more seriously from a risk-estimation standpoint. Standard general-population risk calculators should not be used in HeFH, because they underestimate risk. CAC also does not de-risk FH. A CAC score of 0 should not justify statin deferral in FH.

Genetic testing also gets stronger support. In adults with possible, probable, or definite FH, panel-based testing can help identify those at highest risk and facilitate cascade screening. It can also prove useful in adults with severe hypercholesterolemia even before a classic FH label is fully established.

Diabetes Keeps Its Special Status, but the New Language Sharpens Treatment

The guideline continues to treat diabetes as a major primary prevention category. That is appropriate. Diabetes accelerates vascular risk, and the first event in diabetes often carries a heavier burden than many patients appreciate.

The recommendations become easier to scan in this format:

• Adults ages 40-75 with diabetes and no clinical ASCVD:
  • Moderate-intensity statin is indicated.
  • Aim for 30% to 49% LDL-C reduction.
  • Goal LDL-C <100 mg/dL.
  • Goal non-HDL-C <130 mg/dL.
• Adults ages 40-75 with diabetes plus multiple ASCVD risk factors:
  • High-intensity statin is reasonable.
  • Aim for at least 50% LDL-C reduction.
  • Goal LDL-C <70 mg/dL.
  • Goal non-HDL-C <100 mg/dL.
• Adults ages 20-39 with long-standing diabetes or microvascular complications:
  • Moderate-intensity statin may be reasonable.
• Adults with diabetes and statin-attributed side effects:
  • Ezetimibe, bempedoic acid, or a PCSK9 mAb can be used to lower LDL-C and reduce ASCVD risk.

The document also leaves room for icosapent ethyl in selected patients with diabetes who remain on statin therapy, have LDL-C below 100 mg/dL, and still carry fasting triglycerides of 150-499 mg/dL plus additional ASCVD risk features.

Secondary Prevention Grows More Aggressive

This is another major practical shift. The guideline recognizes that many adults with clinical ASCVD already belong in a very high-risk category. That drives the lower LDL-C and non-HDL-C goals and the greater use of combination therapy.

For secondary prevention, the structure now looks like this:

• Clinical ASCVD, not at very high risk:
  • High-intensity statin.
  • Goal LDL-C <70 mg/dL.
  • Goal non-HDL-C <100 mg/dL.
• Clinical ASCVD, very high risk:
  • High-intensity statin.
  • Goal LDL-C <55 mg/dL.
  • Goal non-HDL-C <85 mg/dL.
• If goals remain unmet:
  • Add ezetimibe and/or a PCSK9 mAb.
  • Add bempedoic acid when appropriate.
  • Use inclisiran selectively when dosing preference or access issues make it the better fit.

I also think an understated but important message sits here: the guideline does not support de-escalating treatment simply because LDL-C becomes very low. The document explicitly notes no signal suggesting that therapy should be backed down just because the achieved LDL-C falls into a very low range.

Triglycerides Finally Get the Structure They Deserve

The triglyceride section feels more disciplined than many clinicians are used to seeing. It keeps statins as the pharmacologic foundation for ASCVD risk reduction, but it also recognizes that very high triglycerides create a separate pancreatitis problem that requires different urgency and dietary precision.

The dietary framework becomes much easier to use when organized by range:

• Fasting TG 150–500 mg/dL:
  • Lower added sugar.
  • Reduce refined carbohydrates.
  • Reduce saturated fat.
  • Minimize alcohol.
• Fasting TG 500–1000 mg/dL:
  • Maintain the same carbohydrate and saturated fat restrictions.
  • Avoid alcohol entirely.
  • Individualize total fat restriction.
• Fasting TG ≥1000 mg/d
  • Use a very low-fat diet.
  • Sharply restrict refined carbohydrates.
  • Eliminate alcohol.
  • Eliminate added sugars.

The lifestyle message also deserves emphasis:

• Aim for 5% to 10% weight loss when overweight or obese.
• Perform at least 150 minutes per week of moderate-to-vigorous activity.
• Add upper and lower body resistance training 2 days per week.

The guideline also draws several practical lines:

• Dietary supplements are not recommended to lower LDL-C or TG.
• Fasting TG 1000 mg/dL or higher should trigger referral to a registered dietitian nutritionist.
• Adults with TG 150-999 mg/dL and CKM features can also benefit from RDN referral.
• In familial chylomicronemia syndrome with fasting TG 1000 mg/dL or higher, olezarsen is now recommended as an adjunct to diet to reduce TG and pancreatitis risk.

That is a meaningful expansion of triglyceride care.

Special Populations Receive More Explicit Attention

1. Chronic Kidney Disease (CKD)

The guideline makes CKD more visible in lipid decision-making. In adults ages 40-75 with CKD stage 3 or higher and LDL-C 70-189 mg/dL, moderate-intensity statin therapy, or moderate-intensity statin plus ezetimibe, is recommended. In adults with CKD stage 3 or higher plus clinical ASCVD, the guideline recommends high-intensity LDL-lowering therapy aimed at LDL-C <55 mg/dL and non-HDL-C <85 mg/dL.

2. Human Immunodeficiency Virus (HIV)

The document also becomes more explicit for people living with HIV. In adults ages 40-75 on stable antiretroviral therapy, statin therapy is recommended to reduce a first ASCVD event and to slow coronary atherosclerosis progression.

3. Older Adults

The older adult section reads thoughtfully. It avoids simplistic age cutoffs. The guideline says clinicians should weigh patient priorities, frailty, multimorbidity, polypharmacy, functional status, and life expectancy when deciding whether to start, continue, or discontinue lipid-lowering therapy. Age alone should not drive the decision.

It also allows a more restrained approach when appropriate:

• In adults older than 75 with adequate life expectancy, moderate-intensity statin initiation may be reasonable.
• If life expectancy is under 1 year, discontinuation may be reasonable.
• When uncertainty remains, CAC can help identify older adults with minimal or no calcification who are less likely to benefit from treatment.

4. Pregnancy and Lactation

This section also matters. For most lower-risk individuals planning pregnancy, the guideline advises stopping statin therapy 1-2 months before attempting conception, or as soon as pregnancy is discovered. At the same time, it allows more individualized thinking for pregnant patients with FH or established ASCVD when risk is high enough to justify continued therapy discussion.

The triglyceride guidance during pregnancy is especially practical:

• In severe gestational hypertriglyceridemia, fibrates after the first trimester may be reasonable.
• High-dose omega-3 ethyl esters may also be reasonable.
• Bile acid sequestrants remain reasonable for hypercholesterolemia in pregnancy when hypertriglyceridemia is not present.

5. Children and Adolescents

The pediatric section reinforces how early lipid biology begins. In children and adolescents with persistent LDL-C 160 mg/dL or higher and a phenotype consistent with FH, statin therapy can begin from age 8 if 3-6 months of lifestyle treatment do not lower LDL sufficiently. That reflects the guideline’s broader emphasis on cumulative exposure.

Frequently Asked Questions About the 2026 Dyslipidemia Guideline

1. What is the 2026 dyslipidemia guideline?

The 2026 dyslipidemia guideline is the new ACC/AHA multisociety update on cholesterol and lipid management. It replaces the 2018 blood cholesterol guideline and expands the focus to include LDL-C, triglycerides, lipoprotein(a), apoB, and coronary artery calcium.

2. Why did the cholesterol guideline change in 2026?

The guideline changed because cardiovascular prevention has evolved. Newer data support earlier treatment, more precise risk estimation, clearer LDL-C goals, broader use of Lp(a), and more structured triglyceride management.

3. What is the biggest change in the new cholesterol guideline?

One of the biggest changes is the shift from the older pooled cohort equations to the PREVENT-ASCVD equations for many adults in primary prevention. The guideline also brings back LDL-C and non-HDL-C treatment goals.

4. What is PREVENT in the new guideline?

PREVENT is the newer 10-year ASCVD risk calculator recommended for many adults ages 30–79 without known ASCVD or subclinical atherosclerosis. It helps guide statin decisions in a more contemporary way than older models.

5. How does PREVENT differ from older risk calculators?

PREVENT generally gives lower 10-year risk estimates than the older pooled cohort equations for the same patient profile. The guideline adjusts treatment thresholds accordingly, so this does not mean prevention becomes less aggressive.

6. What risk categories does PREVENT use?

The PREVENT system classifies risk as:

• Low if under 3%
• Borderline at 3–5%
• Intermediate at 5–10%
• High at 10% or above

7. Are LDL cholesterol goals back in the 2026 guideline?

Yes. The guideline clearly restores LDL-C and non-HDL-C goals while still keeping percentage LDL reduction important. This makes treatment easier to follow and adjust over time.

8. What LDL-C goal does the guideline use for high-risk patients?

In high-risk primary prevention, the guideline generally uses LDL-C below 70 mg/dL as a reasonable goal. In very high-risk ASCVD, it pushes lower, often aiming for LDL-C below 55 mg/dL.

9. Does the new guideline still recommend statins first?

Yes. Statins remain the foundation of treatment in both primary and secondary prevention. The difference is that the guideline now uses add-on therapies more comfortably when statins alone are not enough.

10. What other medications are used besides statins?

Depending on the clinical setting, the guideline discusses ezetimibe, PCSK9 monoclonal antibodies, bempedoic acid, inclisiran, and in selected triglyceride-related settings, icosapent ethyl or other targeted therapies.

11. What is lipoprotein(a), and why does it matter?

Lipoprotein(a), or Lp(a), is a genetically influenced lipoprotein that can increase cardiovascular risk. The new guideline gives it much more attention because many patients with high Lp(a) look “normal” on routine lipid testing.

12. Should everyone have Lp(a) measured?

The guideline recommends measuring Lp(a) at least once in all adults. That is one of the most important practical updates because elevated Lp(a) often goes undetected for years.

13. What level of Lp(a) is considered high?

The guideline treats Lp(a) of 125 nmol/L, or 50 mg/dL, as risk-enhancing. Higher levels carry progressively greater cardiovascular risk.

14. What is apoB, and when is it useful?

ApoB reflects the number of atherogenic lipoprotein particles. It can be especially helpful when LDL-C seems acceptable but the overall risk still appears higher than expected, especially in diabetes, elevated triglycerides, or established ASCVD.

15. What is CAC, and why is it important in the guideline?

CAC stands for coronary artery calcium. It measures calcified plaque in the coronary arteries and helps refine risk when the decision to start or intensify treatment is still uncertain.

16. If my CAC score is zero, does that mean I do not need treatment?

Not always. A CAC score of zero can support deferring treatment in selected patients, although not in every case. The full decision still depends on the overall risk profile, including factors like diabetes, familial hypercholesterolemia, and other risk enhancers.

17. Does the guideline say more about triglycerides now?

Yes. The 2026 guideline gives triglycerides a more structured framework, especially when levels are very high. It emphasizes diet, weight loss, alcohol reduction, activity, and referral to a dietitian in severe cases.

18. Are supplements recommended to lower cholesterol or triglycerides?

No. The guideline states that dietary supplements are not recommended for lowering LDL-C or triglycerides because evidence remains limited and inconsistent.

19. Does the guideline address diabetes and kidney disease separately?

Yes. The document gives more specific recommendations for diabetes, chronic kidney disease, HIV, pregnancy, older adults, and children. That makes the guideline more useful in real-world clinical care.

20. What is the main message patients should take from the 2026 guideline?

The main message is that cholesterol management has become more personalized, more preventive, and more proactive. The goal is not just to react to a high number, but to reduce long-term exposure to the particles that drive plaque and cardiovascular disease.

What I Think Matters Most in Everyday Practice

For me, this guideline succeeds because it feels more physiologic. It respects the fact that atherosclerosis reflects cumulative exposure, residual particle burden, inherited risk, and plaque biology, not just one LDL-C number measured once every few years.

It also makes daily practice easier. It gives cleaner risk categories, clearer goals, more structure around CAC, and more direct language around apoB, Lp(a), triglycerides, FH, CKD, HIV, pregnancy, and aging. It does not abandon statins. It simply stops pretending that statin monotherapy should solve every phenotype.

Final Thoughts

If I had to reduce the 2026 dyslipidemia guideline to a few core ideas, I would put it this way:

• Screen earlier.
• Measure more intelligently.
• Use PREVENT thoughtfully.
• Personalize with risk enhancers and CAC.
• Treat to clear goals.
• Intensify sooner when the phenotype warrants it.

That combination should help us do something medicine often struggles to do well: act early enough to change the long arc of disease, rather than simply reacting after plaque has already declared itself.

Dr. Tashko

For Personalized Lipid & Heart Prevention Care,
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References:

1. 2026 ACC/­AHA/­AACVPR/­ABC/­ACPM/­ADA/­AGS/­APhA/­ASPC/­NLA/­PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/­American Heart Association Joint Committee on Clinical Practice Guidelines. Journal of the American College of Cardiology. 2026. Blumenthal RS, Morris PB, Gaudino M, et al.
2. 2026 ACC/­AHA/­AACVPR/­ABC/­ACPM/­ADA/­AGS/­APhA/­ASPC/­NLA/­PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/­American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026. Writing Committee Members, Blumenthal RS, Morris PB, et al.

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About Dr. Gerti Tashko, MD

Dr. Gerti Tashko, MD, is an endocrinologist in Montgomery County, Maryland. He is uniquely quadruple board-certified in endocrinology, lipidology, hypertension, and obesity medicine. His practice delivers root-cause-focused metabolic and endocrine care, available virtually and in person. He uses advanced diagnostics, personalized nutrition, and preventive medicine to improve long-term health.