When is it good to accept suffering?

Accept? What?!?

That question sounds strange in a medical culture built, understandably, around relief. We want to reduce pain, treat disease, shorten recovery, and help people feel better. That is good work.

But the deeper question is not whether suffering is good in itself. Usually it is not. The better question is whether trying to avoid every form of suffering can quietly make us less honest, less resilient, and less able to love well.

Some suffering is needless and should be opposed. The suffering of untreated depression. The suffering of preventable disease. The suffering that comes from abuse, neglect, addiction, or medical error. We should not romanticize any of that.

But other forms of suffering seem woven into the structure of a meaningful life. There is the soreness of rehabilitation after surgery. The frustration of weight loss that makes it sustainable long term. The grief that comes with loving aging parents. The anxiety of waiting for an important biopsy result that signals the value of the result. The loneliness that can come with telling the truth when it costs you something. There is no mature life that avoids all of this.

Acceptance, in that sense, is not passive. It is not the same as giving up. It is closer to reality-based courage. It means recognizing that some discomfort is not a sign that something has gone wrong. Sometimes it is the price of healing. Sometimes it is the cost of love, meaning, and self-overcoming. Sometimes it is simply what it feels like to live truthfully in a fragile body in a finite world (Haque et al., 2026).

The art, both in medicine and in life, is learning to tell the difference between suffering that should be relieved and suffering that should be endured with patience, wisdom, and support.

A Clinical Pearl People Often Miss

A 56-year-old man once told me, with understandable satisfaction, that he had “fixed” his cholesterol. He had improved his diet, lost a little weight, and his latest LDL number looked better than it had the year before. What he had not really considered was time.

One of the most important things people miss about cholesterol is that risk is cumulative. Atherosclerosis does not care only about today’s LDL. It also reflects years of exposure. That is one reason modern lipid guidance emphasizes earlier and more sustained LDL lowering in people at meaningful risk. A better number this year is good news, but it does not fully erase the biological effects of a high number over the previous decade (Ference et al., 2017).

That does not mean every patient needs aggressive medication. It does mean cholesterol management is best understood as long-term risk reduction, not as a single lab result passed or failed.

Three Worthwhile Reads

How the Whole-Grain Trend Went Wrong by Trisha Pasricha.
Many whole-grain foods behave in the body much the same as the refined products they were meant to replace! A thoughtful corrective to simplistic nutrition labeling. The most useful point is not that whole grains are bad. It is that heavily processed “whole-grain” foods may not behave metabolically like the healthier foods many consumers imagine they are buying. (The Atlantic)

Lilly’s Weight-Loss Pill Wins U.S. Approval, Sets Up Next Battle With Rival Novo Nordisk by Leah Douglas and Christy Santhosh.
Worth reading because oral GLP-1 drugs may change the obesity conversation again, especially for patients who care as much about convenience and adherence as efficacy. Reuters reports that Lilly’s newly approved pill helped trial participants lose about 12% to 15% of body weight. (Reuters)

A Cancer Treatment That Does More Than Scientists Thought
Originally designed for cancer, CAR-T is now raising cautious hopes in some autoimmune diseases too. This piece is worth reading because it captures both the excitement and the restraint that frontier medicine requires when early promise begins to spill into entirely new areas of care. Published April 9, 2026. (The Atlantic)

One Final Thought

One mark of maturity is learning not to ask only, “How do I make this feeling go away?” Sometimes that is exactly the right question. But sometimes the better question is, “What is this burden asking of me?” More patience? Better judgment? More courage? More support? In health, as in the rest of life, wisdom often begins there.

Thank you for reading. This week’s theme is really about discernment: knowing which burdens should be treated, which risks should be reduced early, and which hard things are simply part of loving and living honestly.

If you know someone who might find this helpful, feel free to pass it along. Paid members are welcome to share questions or thoughts in the comments.

To your health,
-Dr. Haque

PS:

For a clear, evidence-based look at Zetia and statin intolerance, watch my new video here:

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References

Ference, B. A., Ginsberg, H. N., Graham, I., Ray, K. K., Packard, C. J., Bruckert, E., ... & Catapano, A. L. (2017). Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. European heart journal, 38(32), 2459-2472.

Haque, O. S., Wortham, J., Case, B. W., Cowden, R. G., Goodman, D., Lomas, T., ... & Vander Weele, T. J. (2026). Acceptance as a Response to Suffering: Insights from World Religious and Philosophical Traditions. Journal of Religion and Health, 1-25.

This newsletter is for educational and informational purposes only and should not be considered personal medical advice. Always consult your physician or a qualified healthcare professional before making changes to your medications, diet, supplements, exercise, or health routine. Reading this content does not create a physician–patient relationship with Dr. Haque.

I also walk through this step-by-step here (video):

What This Really Means

The best way to think about red light therapy for fibromyalgia is as a potentially useful adjunct, not a miracle treatment. A 2019 meta-analysis pooled 9 randomized trials involving 325 patients and found improvements versus placebo across pain, Fibromyalgia Impact Questionnaire scores, tender points, fatigue, stiffness, anxiety, and depression, although the underlying studies were small and methodologically mixed.

More recent whole-body photobiomodulation trials have also reported improvements in pain and quality of life after about 4 weeks of treatment. At the same time, fibromyalgia guidelines still place exercise, education, and broader nonpharmacologic care at the center of treatment, which is why I think of light therapy as a way to widen the window for recovery rather than replace the fundamentals.

My Clinical Framework on Light-Based Adjuncts for Fibromyalgia

1. Start with the bottleneck. I ask what is most disabling right now: pain, post-exertional flare, nonrestorative sleep, or fear of movement. Fibromyalgia treatment works better when the main barrier is identified early.

2. Use light therapy when pain is blocking re-entry into activity. The most clinically interesting patient is not the one already doing well with exercise, but the person whose pain is still too high to restart walking, stretching, or strengthening.

3. Judge it by function, not novelty. I would track whether the patient can move more, flare less, or wake slightly more restored over 2 to 4 weeks. Immediate “feels good” impressions are less useful than a functional trend.

4. Do not let it become passive care. If a treatment lowers symptoms but never gets translated into better pacing, sleep habits, and graduated movement, the long-term value is usually limited.

What I’d Do If This Were Me or My Family

I would consider a time-limited trial of clinic-grade photobiomodulation if fibromyalgia pain were preventing normal movement and if standard approaches had only partly helped. I would be much less eager to spend heavily on a consumer device up front, because the better evidence so far comes from supervised clinical protocols with repeated sessions over several weeks, not from home gadgets marketed directly to patients.

Key Numbers That Matter

• 9 randomized trials and 325 patients were included in the 2019 meta-analysis.

• 4 weeks of treatment is a common duration in newer whole-body trials.

• 12 sessions, often given 3 times per week, is a common whole-body protocol.

• 660 nm and 850 nm are among the most commonly studied wavelengths in newer whole-body systems.

• Exercise remains the only strong therapy-based recommendation in the EULAR guideline framework.

Biggest Mistake I See Patients Make

Treating red light therapy as if it should replace the rest of fibromyalgia care. The better question is not “Did my pain score dip after treatment?” but “Did this help me move, sleep, and function a little better over the next several weeks?”

Who This Applies To (and Who It Doesn’t)

Applies to:

• People with fibromyalgia whose pain or fatigue is preventing them from re-entering exercise or physical therapy.

• People who want a non-drug option added to a broader plan, not substituted for one.

• People who can assess progress by function, not only by how they feel during a session.

May not apply to:

• People expecting a one-session fix or a stand-alone cure.

• People ready to spend large amounts on consumer devices when the stronger evidence base comes from supervised, protocol-driven treatment.

A Test Worth Discussing With Your Doctor

A sleep study may be worth discussing if you have loud snoring, witnessed apneas, prominent daytime sleepiness, or severe nonrestorative sleep. In fibromyalgia, untreated sleep apnea can overlap with and amplify fatigue, pain sensitivity, and cognitive fog, so sometimes the most useful next step is not another supplement or gadget, but identifying a treatable sleep disorder.

If You Only Remember One Thing, Remember This

Red light therapy is most promising as a bridge that may help some people with fibromyalgia regain function, not as a cure by itself.

My Take / My Bias

I am generally favorable toward low-risk treatments when the claims are modest and the evidence is directionally encouraging. I am much less favorable when a decent adjunct gets marketed as a breakthrough. In fibromyalgia, I trust treatments more when they help patients re-enter life, not when they simply create another expensive ritual around pain.

If you’d like to see how I walk through this step-by-step:

Fibromyalgia is a condition in which patients are often forced to sort through too much false hope and too little thoughtful guidance, so I hope this helped clarify where red light therapy may genuinely fit.

If you know someone who might find this useful, feel free to pass it along. Paid members are also welcome to leave questions or comments below.

To your health,
-Dr. Haque

P.S. What I’m Reading This Week

New US cholesterol guideline recommends earlier screening and statin treatment
A recent news piece highlights a new U.S. cholesterol guideline that pushes clinicians to start earlier, individualize more, and pay closer attention to lifetime cardiovascular risk.
Why it matters: Prevention is slowly shifting away from waiting for late disease and toward identifying risk sooner, which is exactly where medicine is often most effective.

Lilly reports trial results for retatrutide in diabetes
STAT recently covered late-stage trial results suggesting that retatrutide produced meaningful reductions in both HbA1c and body weight in people with diabetes.
Why it matters: The obesity and metabolic-treatment landscape is moving quickly, and the practical question is no longer whether these drugs matter, but how to compare efficacy, tolerability, cost, and long-term strategy.

MASALA Study Suggests Earlier Cardiovascular Vigilance Needed for People With South Asian Ancestry
MASALA Study-related findings suggesting earlier and more tailored cardiovascular vigilance may be warranted in South Asian populations.
Why it matters: Good prevention increasingly depends on understanding that risk is not distributed evenly across ancestry populations, and that “average-risk” thinking can miss real disease, especially when BMI is the focus.

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Scholarly References on Photobiomodulation for Fibromyalgia

1. Yeh, S.-W., Hong, C.-H., Shih, M.-C., Tam, K.-W., Huang, Y.-H., & Kuan, Y.-C. (2019). Low-level laser therapy for fibromyalgia: A systematic review and meta-analysis. Pain Physician, 22(3), 241-254.

2. Navarro-Ledesma, S., Carroll, J., Burton, P., & González-Muñoz, A. (2023). Short-term effects of whole-body photobiomodulation on pain, quality of life and psychological factors in a population suffering from fibromyalgia: A triple-blinded randomised clinical trial. Pain and Therapy, 12(1), 225-239.

3. Navarro-Ledesma, S., Carroll, J. D., González-Muñoz, A., & Burton, P. (2024). Outcomes of whole-body photobiomodulation on pain, quality of life, leisure physical activity, pain catastrophizing, kinesiophobia, and self-efficacy: A prospective randomized triple-blinded clinical trial with 6 months of follow-up. Frontiers in Neuroscience, 18, Article 1264821.

4. Fitzmaurice, B. C., Heneghan, N. R., Rayen, A. T. A., Grenfell, R. L., & Soundy, A. A. (2023). Whole-body photobiomodulation therapy for fibromyalgia: A feasibility trial. Behavioral Sciences, 13(9), Article 717.

5. Macfarlane, G. J., Kronisch, C., Dean, L. E., Atzeni, F., Häuser, W., Fluß, E., Choy, E., Kosek, E., Amris, K., Branco, J., Dincer, F., Leino-Arjas, P., Longley, K., McCarthy, G. M., Makri, S., Perrot, S., Sarzi-Puttini, P., Taylor, A., & Jones, G. T. (2017). EULAR revised recommendations for the management of fibromyalgia. Annals of the Rheumatic Diseases, 76(2), 318-328.

With oral semaglutide, the real question is not whether it works. It is whether it fits your body, your mornings, and your long-term routine well enough to keep working.

I also walk through this step-by-step here (video):

What This Really Means

Oral semaglutide is not a much weaker imitation of the injection. It can produce substantial weight loss, and the newly approved Wegovy tablet has shown meaningful benefit both for weight reduction and for cardiovascular risk reduction.

But the pill is less forgiving. It must be taken on an empty stomach, with only a small amount of water, and then followed by a wait before food, coffee, or other oral medications. That means the real dividing line is often not needle aversion. It is adherence architecture.

My Clinical Framework on Choosing Oral vs Injectable GLP-1

1. Start with the routine, not the preference.
   If someone has a stable morning routine, the pill may be a strong option. If mornings are chaotic, weekly injection often wins even for people who dislike needles.

2. Match the formulation to the real goal.
   If the goal is meaningful weight loss and avoiding injections, oral semaglutide is now a legitimate option. If the goal is maximum average weight loss, tirzepatide still has the edge in trial data.

3. Audit the medication list before prescribing.
   This matters more than many patients realize. The oral formulation delays gastric emptying and can affect other oral drugs. Levothyroxine is the clearest example, with increased exposure seen in interaction studies.

4. Prepare for the first six to eight weeks.
   Early nausea, vomiting, diarrhea, and constipation are common reasons people conclude a medication is “not for them” before the body has had a fair chance to adapt. A prevention plan often matters as much as the prescription.

What I’d Do If This Were Me or My Family

If this were me, I would be less impressed by the fact that the drug is a pill and more interested in whether I could reliably take it correctly for years. I would also look closely at why I wanted it.

If I cared most about avoiding injections, the pill would be attractive. If I cared most about maximizing weight loss or minimizing daily friction, I would lean injectable. And if I were on morning medications like levothyroxine, I would slow down and think carefully before assuming the pill was the simpler choice.

Key Numbers That Matter

• Oral Wegovy tablet: about 13.6% mean weight loss at 64 weeks in the treatment policy analysis.

• Injectable semaglutide 2.4 mg: about 14.9% mean weight loss at 68 weeks in STEP 1.

• Oral semaglutide 50 mg in OASIS 1: about 15.1% mean weight loss at 68 weeks.

• Tirzepatide in SURMOUNT-1: roughly 16.0% to 22.5% mean weight loss at 72 weeks, depending on dose.

• SOUL trial: oral semaglutide was associated with a 14% relative reduction in major cardiovascular events in high-risk patients with type 2 diabetes.

Biggest Mistake I See Patients Make

The biggest mistake is choosing the pill because it feels more convenient, without asking whether their mornings are structured enough to make it work, and they are ready for GI side effects. With oral semaglutide, convenience is only real if the dosing ritual is realistic for your actual life.

Who This Applies To (and Who It Doesn’t)

Applies to:

• Adults with obesity, or overweight plus a weight-related condition, who want a non-injectable GLP-1 option.

• People with consistent mornings who can reliably separate the pill from breakfast, coffee, and other oral medications.

• Patients who value meaningful weight loss but do not necessarily need the single strongest average effect available.

May not apply to:

• People with chaotic mornings, frequent travel disruptions, or many time-sensitive morning medications.

• Patients whose main priority is the highest average weight loss seen in current obesity trials.

A Test Worth Discussing With Your Doctor

Hemoglobin A1c. Even in people focused mainly on weight, this can clarify whether the conversation is really about obesity treatment alone, or about obesity plus insulin resistance or diabetes risk. That matters, because the expected metabolic upside may change how much daily hassle is worth tolerating.

If You Only Remember One Thing, Remember This

• The best GLP-1 is not the one that sounds easiest. It is the one you can take correctly and consistently for the long haul.

My Take / My Bias

My bias is that long-term adherence deserves more respect than novelty. In medicine, people often over-focus on headline efficacy and under-focus on the daily mechanics that determine whether a treatment survives real life. I am generally enthusiastic about oral semaglutide, but only when the patient’s routine is sturdy enough to support it. Otherwise, the “simpler” option can quietly become the less effective one.

If you’d like to see how I walk through this step-by-step:

A Final Thought

Thank you for reading. I think this topic matters because many treatment decisions are made too quickly, especially when a new pill seems to remove an old barrier. Sometimes it does. Sometimes it simply replaces one barrier with another.

If you know someone trying to decide between an oral and injectable GLP-1, feel free to pass this along.

Paid subscribers are also welcome to reply in the comments with questions or reflections.

To your health,
-Dr. Haque

P.S.

What I’m Reading This Week

Psychotropic medication use and bone loss in men: longitudinal study
This study suggests that in men, SSRI and anticonvulsant use were associated with greater bone loss at the spine and hip, especially in non-obese men.
Why it matters: It is a useful reminder that medication risk assessment should include bone health, not just mood symptoms and short-term tolerability.

Use of Coronary Artery Calcium Scoring in Individuals With Elevated Lipoprotein(a): A Multicohort Study
This paper examines how coronary calcium (CAC) scoring may refine risk assessment in people with elevated Lp(a), a group that often creates uncertainty in the clinic.
Why it matters: Lp(a) can tell you who may carry inherited risk, but CAC may help clarify how much atherosclerosis is already present now.

Childhood Oral Health is Associated with the Incidence of Cardiovascular Disease in Adulthood
This large Danish cohort study linked poor childhood oral health, including dental caries and gingivitis, with higher adult rates of ischemic heart disease, myocardial infarction, and ischemic stroke.
Why it matters: It adds to the broader case that oral health is not cosmetic. It may be one window into lifelong inflammatory and cardiovascular risk.

Scholarly References on Oral GLP-1 Medications

Wharton, S., Lingvay, I., Bogdanski, P., do Vale, R. D., Jacob, S., Karlsson, T., Shaji, C., Rubino, D., & OASIS 4 Study Group. (2025). Oral semaglutide at a dose of 25 mg in adults with overweight or obesity. The New England Journal of Medicine, 393(11), 1077–1087.

Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., & Kushner, R. F. (2021). Once-weekly semaglutide in adults with overweight or obesity. The New England Journal of Medicine, 384(11), 989–1002.

Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., Kiyosue, A., Zhang, S., Liu, B., Bunck, M. C., & Stefanski, A. (2022). Tirzepatide once weekly for the treatment of obesity. The New England Journal of Medicine, 387(3), 205–216.

McGuire, D. K., Marx, N., Mulvagh, S. L., Deanfield, J. E., Inzucchi, S. E., Pop-Busui, R., Buse, J. B., McMurray, J. J. V., Mann, J. F. E., Husain, M., Idorn, T., Leiter, L. A., Lewis, E. F., Ponikowski, P., Pratley, R. E., Rosenstock, J., & SOUL Study Group. (2025). Oral semaglutide and cardiovascular outcomes in high-risk type 2 diabetes. The New England Journal of Medicine, 392(20), 2001–2012.

Pratley, R., Amod, A., Hoff, S. T., Kadowaki, T., Lingvay, I., Nauck, M., Pedersen, K. B., Saugstrup, T., & Meier, J. J. (2019). Oral semaglutide versus subcutaneous liraglutide and placebo in type 2 diabetes (PIONEER 4): A randomised, double-blind, phase 3a trial. The Lancet, 394(10192), 39–50.

Novo Nordisk. (2026). Rybelsus (semaglutide) tablets, for oral use: Prescribing information. DailyMed. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=27f15fac-7d98-4114-a2ec-92494a91da98

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This newsletter is for educational and informational purposes only and should not be considered personal medical advice. Always consult your physician or a qualified healthcare professional before making changes to your medications, diet, supplements, exercise, or health routine. Reading this content does not create a physician–patient relationship with Dr. Haque.

That does not always mean you are doing something wrong. Often, it means the real driver is not diet at all, but something deeper in the way your body is processing cholesterol.

[I also walk through this step-by-step here (video)]

What This Really Means

Many people are told, directly or indirectly, that high LDL mainly reflects poor food choices. That is only part of the story. LDL is shaped not just by what you eat, but by how your liver clears cholesterol, how your hormones regulate metabolism, whether insulin resistance is developing, whether kidney disease is present, and even whether the lab was drawn during a period of rapid weight loss. Untreated hypothyroidism can reduce LDL receptor activity and worsen clearance, nephrotic syndrome can raise LDL through both overproduction and reduced catabolism, and normal pregnancy and menopause can both shift lipids in predictable ways.

My Clinical Framework on Secondary Causes of High LDL

1. Ask whether the number fits the person.
   If someone is eating reasonably well and the LDL still seems out of proportion, I start thinking about secondary causes before assuming nonadherence.

2. Look upstream metabolically.
   A fasting insulin can sometimes reveal insulin resistance before A1C becomes clearly abnormal. That matters because insulin resistance often shifts lipoproteins in a more atherogenic (artery clogging) direction even before diabetes is diagnosed.

3. Check whether timing is distorting the result.
   During major weight loss, cholesterol can temporarily rise as adipose cholesterol is mobilized. In practice, I am more cautious interpreting LDL while weight is still moving.

4. Audit the medication list carefully.
   Glucocorticoids can worsen lipid profiles, and thiazide diuretics can sometimes raise LDL and triglycerides, especially at higher doses. Some psychiatric medications raise risk more indirectly through weight gain and insulin resistance than through a direct LDL effect.

What I’d Do If This Were Me or My Family

I would not assume I had simply failed at diet. I would want one careful step back before taking one aggressive step forward.

For myself or someone I love, I would want to know whether the number reflects thyroid disease, kidney protein loss, insulin resistance, menopause, medication effects, or a transient state like recent illness or active weight loss. The uncertainty matters because the right next step is not always “more restriction.” Sometimes it is better timing, better testing, or better clinical context.

Key Numbers That Matter

• Pregnancy: LDL often rises about 30 to 50% in normal pregnancy.

• Postmenopause: Early postmenopausal women have about 2.1 times the odds of LDL-C at least 130 mg/dL versus premenopausal women.

• Prednisolone: Clinical studies associate it with higher LDL and total cholesterol than hydrocortisone replacement.

• Hydrochlorothiazide: Higher doses can cause a temporary rise in LDL and triglycerides.

Biggest Mistake I See Patients Make

The biggest mistake is treating LDL as a moral scorecard.

Once people think the number is simply a verdict on discipline, they often miss the more useful question: what is the body doing that explains this result? That mindset shift is often where better care begins.

Who This Applies To (and Who It Doesn’t)

Applies to:

• People with persistently high LDL despite a fairly thoughtful diet

• Patients with central weight gain, prediabetes, diabetes, or suspected insulin resistance

• Women who notice a change during pregnancy, perimenopause, or after menopause

May not apply to:

• People with clearly established familial hypercholesterolemia, where the main issue is inherited LDL clearance impairment

• Situations where LDL is already well controlled and the question is primarily treatment maintenance

A Test Worth Discussing With Your Doctor

Fasting insulin!

It is not the right test for every situation, but it can sometimes reveal an earlier metabolic problem than A1C or fasting glucose alone. In the person whose LDL seems strangely high for the lifestyle, that added context can be surprisingly useful.

If You Only Remember One Thing, Remember This

High LDL is a clue, not a complete explanation.

My Take / My Bias

My bias is toward interpretation before escalation. If the number and the story do not match, I usually think the next job is to understand the physiology more clearly, not just intensify blame or treatment reflexively. LDL matters, but context matters too.

If you’d like to see how I walk through this step-by-step:

Closing

Thank you for reading. High LDL can be discouraging precisely because it looks simple on paper and often is not simple in the body. If this clarified the issue for you, or for someone you care about, feel free to pass it along.

Paid subscribers are always welcome to leave thoughtful questions or comments below.

To your health,
-Dr. Haque

P.S. What I’m Reading This Week

Glucagon-like peptide-1 receptor agonists and risk of substance use disorders among US veterans with type 2 diabetes.
A new BMJ cohort study examined whether GLP-1 receptor agonists were associated with lower risks of substance use disorders among U.S. veterans with type 2 diabetes.
Why it matters: It is an intriguing example of how drugs developed for metabolism may have effects that reach into behavior and addiction medicine, though this was observational research and not proof of causation.

Development of the Weight and Emotions Scale (WES).
This paper describes a new patient-reported outcome measure designed to assess the emotional impact of obesity more rigorously in research and clinical studies.
Why it matters: Good obesity care is not only about pounds or A1C. Better measurement of emotional burden may improve how trials and clinicians understand the lived experience of obesity.

The New York Times report on electronic fetal monitoring and C-sections.
The article examines how continuous electronic fetal monitoring may contribute to unnecessary C-sections despite decades of concern about limited benefit in low-risk labor.
Why it matters: It is a powerful reminder that a test can become deeply embedded in practice for legal, financial, or cultural reasons even when the clinical value is less clear than many assume.

Scholarly References on Persistent High LDL

1. Primary Clinical Guidelines

Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., Anderson, T. S., Bittner, V. A., ... & Wilkins, J. T. 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, S0735-1097.

Virani, S. S., Morris, P. B., Agarwala, A., Ballantyne, C. M., Birtcher, K. K., Kris-Etherton, P. M., ... & Stone, N. J. (2021). 2021 ACC expert consensus decision pathway on the management of ASCVD risk reduction in patients with persistent hypertriglyceridemia: a report of the American College of Cardiology Solution Set Oversight Committee. Journal of the American College of Cardiology, 78(9), 960-993.

Grundy, S. M., Stone, N. J., Bailey, A. L., Beam, C., Birtcher, K. K., Belanger, M. J., ... & Yeboah, J. (2019). 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology, 73(24), e285-e350.

2. Endocrine & Metabolic Drivers

Hypothyroidism: Rizos, C. V., Elisaf, M. S., & Liberopoulos, E. N. (2011). Effects of thyroid dysfunction on lipid profile. The Open Cardiovascular Medicine Journal, 5, 76–84.

Insulin Resistance & Particle Size: Lamarche, B., Tchernof, A., Moorjani, S., Cantin, B., Dagenais, G. R., Lupien, P. J., & Després, J. P. (1997). Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Circulation, 95(1), 69-75.

3. Renal & Hepatic Causes

Chronic Kidney Disease: Vaziri, N. D. (2006). Dyslipidemia of chronic renal failure: The nature, mechanisms, and potential consequences. American Journal of Physiology-Renal Physiology, 290(2), F262-F272.

Biliary Obstruction (Lipoprotein X): Heimerl, S., Boettcher, A., Kaul, H., & Liebisch, G. (2016). Lipid profiling of lipoprotein X: implications for dyslipidemia in cholestasis. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 1861(8), 681-687.

4. Dietary & Weight Dynamics

The Weight Loss Paradox: Phinney, S. D., Tang, A. B., Waggoner, C. R., Tezanos-Pinto, R. G., & Davis, P. A. (1991). The transient hypercholesterolemia of major weight loss. The American journal of clinical nutrition, 53(6), 1404-1410.

Lean Mass Hyper-Responders (Keto): Norwitz, N. G., Feldman, D., Soto-Mota, A., Kalayjian, T., & Ludwig, D. S. (2022). Elevated LDL cholesterol with a carbohydrate-restricted diet: evidence for a “lean mass hyper-responder” phenotype. Current Developments in Nutrition, 6(1), nzab144.

5. Physiological Transitions

Pregnancy: Piechota, W., & Staszewski, A. (1992). Reference ranges of lipids and apolipoproteins in pregnancy. European Journal of Obstetrics & Gynecology and Reproductive Biology, 45(1), 27-35.

Menopause: Matthews, K. A., Crawford, S. L., Chae, C. U., Everson-Rose, S. A., Sowers, M. F., Sternfeld, B., & Sutton-Tyrrell, K. (2009). Are changes in cardiovascular disease risk factors in midlife women due to aging or the menopausal transition? Journal of the American College of Cardiology, 54(25), 2366-2373.

6. Iatrogenic (Medication-Induced)

Antipsychotics: Meyer, J. M., Davis, V. G., Goff, D. C., McEvoy, J. P., Nasrallah, H. A., Johannesen, J. K., & Lieberman, J. A. (2008). Change in metabolic syndrome parameters with antipsychotic treatment in the CATIE Schizophrenia Trial: Baseline associations with antipsychotic use. Schizophrenia Research, 101(1-3), 273-286.

Glucocorticoids: Quinkler, M., Ekman, B., Marelli, C., Uddin, S., & Zelissen, P. (2017). Prednisolone is associated with a worse lipid profile than hydrocortisone in patients with adrenal insufficiency. Endocrine, 6, 1-8.

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This newsletter is for educational and informational purposes only and should not be considered personal medical advice. Always consult your physician or a qualified healthcare professional before making changes to your medications, diet, supplements, exercise, or health routine. Reading this content does not create a physician–patient relationship with Dr. Haque.

Why the Fat You Can’t Pinch Matters

Many people worry about the number on the scale, but the most dangerous fat in the body is often the fat you cannot see or pinch. Visceral fat—the fat stored deep around the organs, the fat contributing to the “beer belly”—behaves very differently from the fat under the skin. It acts like an endocrine organ, releasing inflammatory signals that influence the heart, liver, pancreas, and even the immune system.

This is a question I’m often asked by patients: if visceral fat is so dangerous, what actually reduces it?

Many people assume the answer is simply “do crunches” or “lose weight,” but the biology is more nuanced than that. You may know someone who has struggled with metabolic health despite not appearing overweight, which is part of why visceral fat has become such an important topic in modern medicine.

When researchers study interventions that reduce visceral fat, a pattern emerges. No single intervention works in isolation. Instead, the evidence consistently points toward a coordinated approach involving metabolic signaling, nutrition, physical activity, sleep, and in some cases, medications. Understanding how these pieces fit together is what allows patients to make meaningful progress rather than chasing one new health trend after another.

Key Takeaways

• Visceral fat is metabolically active tissue linked to inflammation, fatty liver disease, diabetes, and cardiovascular disease.

• In most studies, visceral fat reduction closely tracks overall weight loss, so claims of “spot-reducing” visceral fat should be treated skeptically.

• Certain medications—particularly GLP-1 receptor agonists and related therapies—can significantly reduce visceral fat by promoting sustained weight loss and metabolic changes.

• Exercise has a disproportionate effect on visceral fat, especially when aerobic training is combined with resistance training.

• Lifestyle signals such as sleep quality, stress regulation, and circadian alignment influence where the body stores fat, not just how much fat is stored.

Additional Clinical Pearl: Visceral Fat as a Hormonal Organ

One of the most underappreciated aspects of visceral fat is that it behaves less like passive storage tissue and more like an active endocrine organ. Visceral adipose tissue secretes inflammatory cytokines and adipokines that influence insulin sensitivity, vascular health, and liver metabolism.

Clinically, this helps explain why two individuals with the same body weight can have very different metabolic risk profiles. A patient with relatively low visceral fat but higher subcutaneous fat may have normal metabolic markers, while someone with central visceral accumulation may develop fatty liver disease, insulin resistance, or cardiovascular disease even at moderate body weight.

This concept also helps clinicians interpret imaging findings such as epicardial fat around the heart or increased visceral adiposity on CT or MRI scans. These findings are not merely cosmetic—they represent a metabolically active environment that contributes to systemic inflammation.

For patients, the implication is important: interventions that improve metabolic signaling—sleep, exercise, stress regulation, and sustained weight loss—often have outsized effects on visceral fat compared with superficial fat stores.

My Personal Framework I Use When Applying This Information To My Own Health (or a Loved One’s Health)

When thinking about visceral fat for my own health or the health of someone close to me, I try to avoid the common trap of focusing on a single intervention. Instead, I think about the problem in terms of three biological signals that determine whether visceral fat accumulates or recedes.

First, I ask whether the body is receiving signals to store fat. Chronic sleep deprivation, elevated stress hormones, and repeated insulin spikes from highly refined foods all push metabolism toward fat storage. If those signals remain unchanged, even the best exercise program or medication will have limited impact.

Second, I think about the fuel supply. A sustained calorie surplus—particularly from high glycemic foods—creates repeated insulin elevations that favor visceral fat deposition. Improving dietary quality, increasing fiber intake, and aligning meals with circadian rhythms can gradually shift that metabolic environment.

Finally, I consider the mobilization signal. Physical activity—especially aerobic training combined with resistance work—creates the metabolic demand that allows stored fat to be used as fuel.

What is striking about the research is that these factors interact. Better sleep can reduce appetite the next day. Exercise improves insulin sensitivity. Stress management alters cortisol signaling that influences fat distribution. None of these variables operates in isolation, which is why the most effective approaches tend to address several of them simultaneously.

In practice, I try to think less about dramatic changes and more about sustainable signals that the body receives day after day.

Closing

From the complaints I hear from patients, and my own struggle, I believe visceral fat is one of the hardest problems to reverse. If you found these ideas useful, and you know someone who might find them helpful as well, feel free to pass this along.

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And as always, thoughtful questions or reflections are welcome in the comments, especially from readers who are exploring these ideas in their own lives.

For those who are interested in seeing the biological mechanisms and clinical studies discussed in greater detail, I’ve also included a video exploration of this topic below.

Full Scholarly References on Visceral Fat and Metabolic Health

Agência FAPESP. (2025). Study points out that a synthetic molecule helps reduce visceral fat and improve sleep.

Baylor Scott & White Health. (2024). Cortisol belly: How stress can impact your weight (and what you can do about it).

Chawla, S., Tessarolo Silva, F., Amaral Medeiros, S., & Mekary, R. A. (2020). The effect of low-fat and low-carbohydrate diets on weight loss and lipid levels: A systematic review and meta-analysis. Nutrients, 12(12), 3774.

Coskun, T., Wu, Q., Schloot, N. C., Haupt, A., Milicevic, Z., Khouli, C., & Harris, C. (2025). Effects of retatrutide on body composition in people with type 2 diabetes: A substudy of a phase 2, double-blind, parallel-group, placebo-controlled, randomised trial. The Lancet Diabetes & Endocrinology.

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Eli Lilly and Company. (2025). Lilly’s triple agonist, retatrutide, delivered weight loss of up to an average of 71.2 lbs along with substantial relief from osteoarthritis pain in first successful Phase 3 trial.

Ghosal, S., Sinha, B., Ghosal, A., & Sarkar, S. (2025). Comparative efficacy of lifestyle and GLP-1RA-based interventions for visceral adipose tissue reduction: Meta-analysis of 36 randomised controlled trials. Obesity Abstracts, 5(P1).

Heimann, A. S., Singh, P., Ferro, E. S., Greenway, F., & Krongrad, A. (2025). Pep19: A novel approach for reducing visceral fat and improving sleep quality in obese adults—results from an early-stage clinical trial. Diabetes/Metabolism Research and Reviews, 41(5), e70056.

Hewell, K. D., Vaschillo, E. G., & Vaschillo, B. (2011). Stress and abdominal fat: Preliminary evidence of moderation by the cortisol awakening response in Hispanic peripubertal girls. Journal of Behavioral Medicine.

Iannetta, D., et al. (2024). Zone 2 intensity: A critical comparison of individual variability in different submaximal exercise intensity boundaries. Frontiers in Physiology.

Jayedi, A., Soltani, S., Zargar, M. S., Khan, T. A., & Shab-Bidar, S. (2020). Abdominal visceral adipose tissue and all-cause mortality: A systematic review. Frontiers in Endocrinology.

Kelley, G. A., Kelley, K. S., & Pate, R. R. (2016). The effect of diet or exercise on visceral adipose tissue in overweight youth. Childhood Obesity.

Li, C., et al. (2022). GLP-1 RAs and SGLT-2 inhibitors for insulin resistance in nonalcoholic fatty liver disease: A network meta-analysis. Journal of Clinical Medicine.

Lopez, P., et al. (2025). Comparing exercise modalities during caloric restriction: A systematic review and network meta-analysis on body composition. Frontiers in Nutrition.

Pramyothin, P., et al. (2024). Impact of diet intervention on visceral adipose tissue and hepatic fat in patients with obesity and type 2 diabetes: A randomized controlled trial. Scientific Reports.

Rao, G. H., Powell-Wiley, T. M., Ancheta, I., & Hairston, K. (2019). The impact of exercise and pharmacological interventions on visceral adiposity: A meta-analysis and systematic review. Mayo Clinic Proceedings.

Rynders, C. A., Thomas, E. A., Zaman, A., Pan, Z., Catenacci, V. A., & Melanson, E. L. (2019). Effectiveness of intermittent fasting and time-restricted feeding compared to continuous energy restriction for weight loss. Nutrients, 11(10), 2442.

Society of Chile for Obesity (SOCHOB). (2026). Efficacy of weight-lowering agents on fat distribution: A systematic review and network meta-analysis of randomized controlled trials.

Su, L., Fu, J., Sun, S., Zhao, G., & Cheng, W. (2019). Effects of high-intensity interval and moderate-intensity continuous training on body composition in overweight and obese adults: A systematic review and meta-analysis. PLOS ONE, 14(1), e0210292.

Sun, W., et al. (2025). Effects of sodium-glucose co-transporter-2 inhibitors on body composition in patients with type 2 diabetes: A systematic review and meta-analysis. Journal of Diabetes.

Tasali, E., Wroblewski, K., Kahn, E., Kilkus, J., & Schoeller, D. A. (2022). Effect of sleep extension on objectively assessed energy intake among adults with overweight in real-life settings: A randomized clinical trial. JAMA Internal Medicine, 182(4), 365–374.

Verheggen, R. J., Maessen, M. F., Green, D. J., Hermus, A. R., Hopman, M. T., & Thijssen, D. H. (2016). An exercise program to reduce abdominal visceral and subcutaneous fat in adults with overweight and obesity: A systematic review and meta-analysis of randomized controlled trials. Obesity Reviews.

Viana, R. B., Naves, J. P. A., Coswig, V. S., De Lira, C. A. B., Steele, J., Fisher, J. P., & Gentil, P. (2019). Effect of high-intensity interval training vs. moderate-intensity continuous training on fat loss and cardiorespiratory fitness in the young and middle-aged: A systematic review and meta-analysis. International Journal of Environmental Research and Public Health, 16(23), 4840.

Vissers, D., Hens, W., Taeymans, J., Baeyens, J. P., Poortmans, J., & Van Gaal, L. (2013). The effect of exercise intervention dosage on reducing visceral adipose tissue: a systematic review and meta-analysis of randomized controlled trials. Mayo Clinic Proceedings, 88(7), 712–721.

Weill Cornell Medicine. (2025, May 11). Head-to-head trial compares weight loss drugs.

Wewege, M., van den Berg, R., Ward, R. E., & Keech, A. (2017). The effects of high-intensity interval training vs. moderate-intensity continuous training on body composition in overweight and obese adults: A systematic review and meta-analysis. Obesity Reviews, 18(6), 635–646.

Xu, F., et al. (2023). The effects of GLP-1 receptor agonists on visceral fat and liver fat content in adults with and without diabetes: A systematic review and meta-analysis. Frontiers in Pharmacology.

Zelniker, T. A., & Braunwald, E. (2020). How do SGLT2 inhibitors and GLP-1 receptor agonists reduce cardiovascular outcomes? Arteriosclerosis, Thrombosis, and Vascular Biology, 40(2), 269–278.

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Zhang, Y., et al. (2025). SGLT2 inhibitors reduce epicardial adipose tissue more than GLP-1 agonists or exercise interventions in patients with type 2 diabetes mellitus and/or obesity: A systematic review and network meta-analysis. Diabetes, Obesity and Metabolism.

**

This newsletter is for educational and informational purposes only and should not be considered personal medical advice. Always consult your physician or a qualified healthcare professional before making changes to your medications, diet, supplements, exercise, or health routine. Reading this content does not create a physician–patient relationship with Dr. Haque.

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