Understanding the Connection Between Hypothyroidism and Atherosclerotic Heart Disease

As a physician, I often remind patients that the body functions as an interconnected system—what happens in one organ can quietly influence another. Nowhere is this more evident than in the relationship between your thyroid gland and your heart. While most people recognize that the thyroid controls metabolism, few realize that even mild thyroid dysfunction can have significant cardiovascular consequences.

Today, we’ll explore how hypothyroidism—an underactive thyroid—can increase your risk for atherosclerotic heart disease (ASHD), what mechanisms drive this connection, and what steps you can take to protect your cardiovascular health.

The Thyroid: A Master Regulator

The thyroid gland produces hormones—thyroxine (T4) and triiodothyronine (T3)—that regulate metabolism, growth, and cellular energy. These hormones influence nearly every tissue in the body, including the heart and blood vessels.

When the thyroid slows down, so does your metabolism. The heart beats less vigorously, blood vessels lose their elasticity, and cholesterol metabolism becomes sluggish. These changes collectively predispose a person to atherosclerosis—the progressive buildup of fatty plaques within arteries.

How Hypothyroidism Promotes Atherosclerosis

The connection between hypothyroidism and atherosclerotic heart disease is both biochemical and hemodynamic. Let’s examine the main pathways:

1. Dyslipidemia

Thyroid hormones are essential for the expression of LDL receptors in the liver, which help clear cholesterol from the blood. When thyroid hormone levels drop, LDL receptors decrease in number, leading to:

• Elevated total cholesterol

• Increased LDL cholesterol

• Elevated triglycerides

  
  

This lipid profile is highly atherogenic—meaning it promotes plaque buildup in the arteries. Even subclinical hypothyroidism (when TSH is mildly elevated but T4 is normal) can significantly elevate cholesterol levels.

2. Endothelial Dysfunction

The endothelium—the inner lining of blood vessels—depends on thyroid hormones to produce nitric oxide (NO), which helps arteries relax and maintain healthy tone. Low thyroid hormone levels cause endothelial stiffness, reduced NO availability, and enhanced oxidative stress—all precursors to plaque formation.

3. Increased Arterial Stiffness and Hypertension

Hypothyroidism leads to higher systemic vascular resistance, which increases diastolic blood pressure. The resulting vascular strain promotes remodeling of arterial walls, accelerating atherosclerosis.

4. Homocysteine and Inflammation

Low thyroid function is associated with elevated homocysteine levels and systemic inflammatory markers like C-reactive protein (CRP), both of which contribute to endothelial injury and plaque instability.

5. Altered Coagulation and Fibrinolysis

Hypothyroidism can tilt the balance toward hypercoagulability by increasing fibrinogen and factor VII while impairing fibrinolysis. This raises the risk of thrombotic events such as heart attack or stroke.

Clinical Evidence Supporting the Link

Numerous studies confirm the strong association between hypothyroidism and atherosclerotic cardiovascular disease:

• Patients with overt hypothyroidism exhibit higher coronary artery calcium scores and increased carotid intima-media thickness (CIMT)—both reliable markers of subclinical atherosclerosis.

• Subclinical hypothyroidism, once considered benign, has been shown to increase the risk of myocardial infarction and sudden cardiac death, particularly in women and older adults.

• Restoration of normal thyroid function through levothyroxine therapy can improve lipid profiles, lower CRP, and improve endothelial function—reducing long-term cardiovascular risk.

  
  

How Symptoms Overlap and Confuse the Picture

Many patients with hypothyroidism experience symptoms that mimic heart disease—fatigue, shortness of breath, cold intolerance, and weight gain. Because both conditions are common, it’s easy to miss the underlying thyroid problem until lab work reveals an elevated thyroid-stimulating hormone (TSH) level.

Conversely, patients with heart disease may develop secondary hypothyroidism due to chronic illness, medications such as amiodarone, or stress on the hypothalamic-pituitary-thyroid axis. This makes regular screening crucial, particularly for individuals with known cardiovascular disease or persistent lipid abnormalities.

Diagnostic Clues and Laboratory Testing

When evaluating cardiovascular risk, thyroid function testing provides valuable insights. Key markers include:

• TSH: Elevated in primary hypothyroidism.

• Free T4 and Free T3: Low or low-normal levels confirm hormonal deficiency.

• Lipid profile: Elevated LDL and triglycerides, often with low HDL.

• Homocysteine and CRP: May be elevated in both hypothyroid and atherosclerotic patients.

  
  

Patients with unexplained hyperlipidemia or resistant hypertension should always be screened for hypothyroidism.

Management Strategies

1. Thyroid Hormone Replacement

Treatment with levothyroxine (synthetic T4) restores metabolic activity, reduces serum cholesterol, and improves cardiac output. For patients with pre-existing heart disease, replacement must be done gradually to avoid inducing arrhythmias or ischemia.

2. Lipid Management

Even with adequate thyroid control, some patients may continue to require statins, fibrates, or omega-3 supplements to achieve optimal lipid targets.

3. Lifestyle and Nutritional Support

• Adequate iodine, selenium, and zinc intake supports thyroid hormone synthesis and conversion.

• Regular aerobic exercise improves endothelial function and reduces both insulin resistance and LDL oxidation.

• A Mediterranean-style diet, rich in vegetables, olive oil, and lean protein, offers cardioprotective benefits.

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4. Periodic Monitoring

Once therapy begins, both TSH and lipid panels should be re-evaluated every 6–12 weeks until stable, then every 6–12 months. In patients with coronary artery disease, echocardiography and carotid ultrasound may help track disease progression or regression.

Why Early Detection Matters

The interplay between thyroid function and cardiovascular health is subtle but powerful. Identifying hypothyroidism early—before irreversible vascular damage occurs—can dramatically reduce your risk for heart attack and stroke.

A comprehensive evaluation of thyroid status should be considered part of routine cardiovascular risk assessment, especially if you have high cholesterol, hypertension, or a family history of heart disease.

At Stages of Life Medical Institute, we use integrated diagnostic panels to evaluate thyroid performance, lipid metabolism, and inflammatory markers simultaneously, ensuring no early warning signs go unnoticed.

Final Thoughts

Hypothyroidism is far more than a problem of low metabolism—it’s a quiet amplifier of vascular disease. By addressing thyroid imbalance, we not only restore energy and mental clarity but also protect the heart from atherosclerotic injury. Managing these conditions together yields the best outcomes for long-term vitality and longevity.

If you suspect that your thyroid may be contributing to your cardiovascular symptoms, schedule a comprehensive evaluation. Simple blood tests and thoughtful interpretation can make a lifesaving difference.

References

1. Duntas LH, Brenta G. The effect of thyroid disorders on lipid levels and metabolism. Med Clin North Am. 2012;96(2):269-281. doi:10.1016/j.mcna.2012.01.012

2. Klein I, Danzi S. Thyroid disease and the heart. Circulation. 2007;116(15):1725-1735. doi:10.1161/CIRCULATIONAHA.106.678326

3. Cappola AR, Ladenson PW. Hypothyroidism and atherosclerosis. J Clin Endocrinol Metab. 2003;88(6):2438-2444. doi:10.1210/jc.2003-030398

4. Razvi S, Jabbar A, Pingitore A, et al. Thyroid hormones and cardiovascular function and diseases. J Am Coll Cardiol. 2018;71(16):1781-1796. doi:10.1016/j.jacc.2018.02.045

5. Hak AE, Pols HA, Visser TJ, et al. Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction. Ann Intern Med. 2000;132(4):270-278. doi:10.7326/0003-4819-132-4-200002150-00004

6. Rodondi N, den Elzen WP, Bauer DC, et al. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA. 2010;304(12):1365-1374. doi:10.1001/jama.2010.1361

7. Taddei S, Caraccio N, Virdis A, et al. Impaired endothelium-dependent vasodilation in subclinical hypothyroidism: beneficial effect of levothyroxine therapy. J Clin Endocrinol Metab. 2003;88(8):3731-3737. doi:10.1210/jc.2003-030039

8. Pucci E, Chiovato L, Pinchera A. Thyroid and lipid metabolism. Int J Obes Relat Metab Disord. 2000;24(Suppl 2):S109-S112. doi:10.1038/sj.ijo.0801292

9. Razvi S, Shakoor A, Vanderpump M, et al. The influence of age on the relationship between subclinical hypothyroidism and ischemic heart disease: a meta-analysis. J Clin Endocrinol Metab. 2008;93(8):2998-3007. doi:10.1210/jc.2008-0167

10. Monzani F, Caraccio N, Kozakowa M, et al. Effect of levothyroxine replacement on lipid profile and intima-media thickness in subclinical hypothyroidism: a double-blind, placebo-controlled study. J Clin Endocrinol Metab. 2004;89(5):2099-2106. doi:10.1210/jc.2003-031669

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician

Bioidentical Hormone Replacement Therapy (BHRT): What it is, who benefits, and what the FDA says now

The skin is the first organ system to reflect the aging of the hormonal system. Wrinkles, sagging appear early.

If you’ve been struggling with hot flashes, night sweats, sleep disruption, brain fog, or painful intimacy, hormone changes are a likely driver. Bioidentical hormone replacement therapy (BHRT) uses hormones with the same molecular structure your body makes—most commonly 17β-estradiol, testosterone and micronized progesterone—to restore balance and relieve symptoms. Multiple national societies agree that appropriately prescribed hormone therapy is the most effective treatment for vasomotor symptoms and genitourinary syndrome of menopause, and it helps prevent bone loss and fractures. The optimal formulation, dose, and route are individualized—and that is precisely where a careful, physician-guided plan at Stages of Life Medical Institute can make a meaningful difference. PubMed+2LWW

Journals+2

The latest FDA context (2025)

In November 2025 the FDA moved to remove the long-standing boxed warning from labels of many estrogen-containing menopause therapies, reflecting contemporary evidence and encouraging individualized risk–benefit discussions. Professional societies, including ACOG, welcomed the change and simultaneously reiterated that compounded estrogen products are not backed by FDA for safety or efficacy. Separately, the FDA continues to emphasize that compounded drugs are not FDA-approved and that the agency does not have evidence they are safer or more effective than approved therapies. U.S. Food and Drug Administration+3AP News+3ACOG+3

Benefits patients actually feel

• Rapid symptom relief. Estradiol—especially transdermal—remains the most effective therapy for hot flashes and night sweats; many patients report better sleep and cognition once nocturnal symptoms abate. Micronized progesterone can improve sleep quality for some. PubMed

• Genitourinary health. Local vaginal estrogen (very low systemic absorption) improves dryness, dyspareunia, and recurrent UTI risk by restoring urogenital tissues. PubMed

• Bone protection. Standard-dose HT prevents bone loss and reduces fracture risk; timing, dose, and delivery route matter. PubMed

• Cardiometabolic nuance. Starting within 10 years of menopause and before age 60 is associated with a more favorable balance of benefits/risks; transdermal routes and lower doses may lower VTE and stroke risk compared with oral forms. Australasian Menopause Society

  
  

What about pellets and other compounded options?

I am not a fan of using Pellets to provide HRT. Your body needs the levels of these hormones to vary on a daily basis, and when you use pellet injection, the result is constant levels that are entirely unnatural. My preference is to use transdermal creams, applied on a daily basis, timed to correspond to the natural diurnal changes that the body requires.

On the other hand, Pellets are a compounded delivery system (not FDA-approved) implanted subcutaneously. Because the dose cannot be adjusted or removed easily and quality can vary, professional guidance cautions against routine pellet use—particularly for testosterone in women—when FDA-approved alternatives exist. Reported adverse effects (e.g., mood changes, acne, abnormal bleeding) appear more frequent with pellets than with approved products in some observational datasets. ACOG+1

How Stages of Life approaches BHRT

1. Evidence-guided evaluation. We start with a detailed history, risk assessment, and labs only when they’ll change management.

2. Prefer FDA-approved bioidentical options (estradiol, micronized progesterone) tailored to your goals, risk profile, and preferences (patch, gel, ring, oral, or local therapy). The ObG Project

3. Thoughtful monitoring. We track symptom response, side effects, and dose—not just lab numbers—to keep you squarely in the therapeutic sweet spot.

4. Compounding only when indicated. If an allergy, intolerance, or unique dose/form is required, we use reputable compounding partners and counsel transparently on benefits and limits. The FDA and multiple societies note that evidence for routine compounded BHRT is limited. U.S. Food and Drug Administration+1

   
   

Safety, risks, and personalization

Hormone therapy isn’t for everyone. Contraindications and relative risks must be weighed (e.g., prior estrogen-sensitive cancer, active thromboembolic disease, uncontrolled hypertension). For most healthy, symptomatic women within 10 years of menopause onset and under 60, the benefits often outweigh risks when therapy is individualized. The 2025 label update underscores the importance of nuanced, patient-specific decisions rather than blanket fear from outdated warnings. Australasian Menopause Society+1

Bottom line

Bioidentical hormone therapy—using FDA-approved formulations whenever possible—can safely and powerfully improve quality of life, intimacy, sleep, and bone health when matched to the right patient, at the right dose and route, with competent follow-up. If you’re ready to feel like yourself again, the Stages of Life team will meet you where you are and guide you forward, step by step.

References

1. Faubion SS, et al. The 2022 hormone therapy position statement of The North American Menopause Society. Menopause. 2022;29(7):767-794. doi:10.1097/GME.0000000000002028. PubMed

2. The Menopause Society. 2022 Hormone Therapy Position Statement—Press and summary materials. 2022. The Menopause Society+1

3. FDA. Menopause—Are compounded “bioidentical hormones” safer or more effective? Updated Dec 14, 2023. U.S. Food and Drug Administration

4. FDA. Compounding and the FDA: Questions and Answers. Updated Sept 16, 2025. U.S. Food and Drug Administration

5. FDA Expert Panel on Menopause and Hormone Replacement Therapy (public meeting). July 17, 2025. U.S. Food and Drug Administration

6. Associated Press. FDA removes boxed warning from hormone-based menopause drugs. Nov 2025. AP News

7. ACOG. President says label change on estrogen will increase access to hormone therapy. Nov 2025. ACOG

8. ACOG Clinical Consensus No. 6: Compounded bioidentical menopausal hormone therapy. Obstet Gynecol. 2023. (and web version). ACOG+1

9. Stuenkel CA, et al. Compounded bioidentical hormone therapy. Climacteric. 2021;24(4):389-397. PubMed

10. National Academies of Sciences, Engineering, and Medicine. The Clinical Utility of Compounded Bioidentical Hormone Therapy. Washington, DC: NAP; 2020. doi:10.17226/25791. National Academies Press

11. Endocrine Society. Position Statement: Compounded “Bioidentical” Hormone Therapy. 2019. Endocrine Society+1

12. Alabama Board of Medical Examiners summary of ACOG Clinical Consensus (2023). Alabama Medical Board

13. The OB-G Project. NAMS HT Position Statement summary and FDA-approved formulations list (2022–2024). The ObG Project+1

14. Contemporary OB/GYN. Safety and efficacy of non-FDA-approved menopause therapies (pellet adverse effects summary). 2023. Contemporary OB/GYN

15. Let’s Talk Menopause. NAMS 2022 HT highlights for patients (benefit/risk framing). 2022.

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David S. Klein, MD FACA FACPM

David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician

The Link Between Fructose Beverages and Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) has become a common health concern worldwide, affecting millions of people regardless of age or lifestyle. One surprising contributor to this condition is the consumption of beverages high in fructose. Understanding how fructose-containing drinks impact liver health can help people make better dietary choices and reduce their risk of developing NAFLD.

Tasty, surely. Toxic to your liver? In subtle yet deadly ways

What is Non-Alcoholic Fatty Liver Disease?

NAFLD occurs when excess fat builds up in the liver cells without significant alcohol consumption. This fat accumulation can lead to inflammation, liver damage, and in severe cases, cirrhosis or liver failure. NAFLD is often linked to obesity, insulin resistance, and metabolic syndrome, but diet plays a crucial role in its development.

Why Fructose in Beverages Matters

Fructose is a type of sugar naturally found in fruits, but it is also added to many processed foods and drinks in the form of high-fructose corn syrup (HFCS) or other sweeteners. Beverages like sodas, fruit juices, energy drinks, and sweetened teas often contain high levels of fructose.

Unlike glucose, which is metabolized by many cells in the body, fructose is primarily processed in the liver. When consumed in large amounts, fructose overloads the liver’s metabolic pathways, leading to fat production and storage.

How Fructose Leads to Fatty Liver

When fructose enters the liver, it undergoes a process called fructolysis. This process bypasses the normal regulatory steps that control glucose metabolism, causing the liver to convert excess fructose into fat through a pathway called de novo lipogenesis.

This fat can accumulate inside liver cells, causing the liver to enlarge and become fatty. Over time, this fat buildup can trigger inflammation and scarring, which are hallmarks of NAFLD.

Key mechanisms include:

• Increased fat synthesis: Fructose stimulates enzymes that produce fatty acids in the liver.

  
  

• Reduced fat breakdown: Fructose impairs the liver’s ability to burn fat for energy.

  
  

• Insulin resistance: High fructose intake can worsen insulin resistance, which further promotes fat storage in the liver.

  
  

The Role of Fructose Beverages in Daily Diets

Many people consume fructose-containing beverages regularly without realizing the impact on their liver health. For example:

• A 12-ounce can of soda can contain up to 40 grams of sugar, mostly fructose.

  
  

• Sweetened fruit juices often have similar or higher sugar content than sodas.

  
  

• Energy drinks and flavored teas add hidden sources of fructose.

  
  

Regular consumption of these drinks can lead to chronic fructose overload, increasing the risk of NAFLD even in people who do not drink alcohol.

Evidence from Research

Studies have shown a clear link between high fructose intake and fatty liver development. For instance, a 2013 study published in the Journal of Hepatology found that people who consumed more than one sugary beverage per day had a significantly higher risk of developing NAFLD.

Animal studies also demonstrate that diets high in fructose cause liver fat accumulation and inflammation. These findings support the idea that reducing fructose intake, especially from beverages, can help prevent or reverse fatty liver disease.

It It is not just the alcohol that kills the liver. The sugar in the beverage may be causing even more damage!

Practical Tips to Reduce Fructose Beverage Intake

Reducing consumption of fructose-containing drinks can protect liver health. Here are some practical steps:

• Choose water or unsweetened beverages: Replace sodas and sweetened juices with plain water, herbal teas, or sparkling water without added sugar.

  
  

• Read labels carefully: Check for high-fructose corn syrup or other sweeteners in drinks before buying.

  
  

• Limit fruit juice intake: Even 100% fruit juices can be high in fructose; consume in moderation.

  
  

• Prepare homemade drinks: Make your own flavored water with slices of lemon, cucumber, or berries to avoid added sugars.

  
  

Other Lifestyle Factors to Support Liver Health

While cutting back on fructose beverages is important, other habits also help reduce NAFLD risk:

• Maintain a healthy weight through balanced diet and regular exercise.

  
  

• Avoid excessive alcohol consumption.

  
  

• Manage blood sugar levels and insulin resistance.

  
  

• Get regular medical checkups to monitor liver function.

  
  

Understanding the connection between fructose-containing beverages and fatty liver disease empowers people to make informed choices. By reducing sugary drink intake and adopting healthier habits, it is possible to protect the liver and improve overall health.

SUMMARY

1. Metabolic Mechanism

Sweetened drinks are typically rich in fructose, often as high-fructose corn syrup or sucrose. Unlike glucose, fructose is metabolized almost exclusively in the liver, where it bypasses normal glycolytic regulation. This leads to:

• Rapid conversion of fructose to triglycerides via de novo lipogenesis (DNL).

• Increased hepatic fat accumulation, promoting steatosis.

• Insulin resistance, which amplifies hepatic lipid synthesis and impairs fat oxidation.

• Increased production of uric acid, contributing to mitochondrial oxidative stress and hepatic inflammation.

2. Clinical and Epidemiological Evidence

Multiple observational and interventional studies link high intake of sugary drinks with both prevalence and severity of NAFLD:

• Cross-sectional studies show that individuals consuming ≥1 SSB per day have significantly higher liver fat content on imaging.

• Longitudinal data (e.g., from the Framingham Heart Study and NHANES cohorts) indicate a dose-dependent risk—greater consumption leads to higher incidence of NAFLD, independent of body mass index.

• Interventional trials demonstrate that reducing fructose-laden beverages can decrease liver fat within weeks, even without major weight loss.

3. Pathophysiologic Sequelae

Chronic hepatic fat accumulation from fructose overload promotes:

• Inflammation and oxidative stress, leading to non-alcoholic steatohepatitis (NASH).

• Fibrosis progression, eventually risking cirrhosis or hepatocellular carcinoma.

• Systemic metabolic consequences—dyslipidemia, insulin resistance, and elevated cardiovascular risk.

4. Clinical and Preventive Implications

• Dietary counseling for NAFLD should explicitly restrict sugary beverages, not merely overall calorie intake.

• Replacing SSBs with water, unsweetened tea, coffee, or naturally flavored sparkling water can markedly reduce hepatic lipid burden.

• Even “natural” sweeteners (e.g., fruit juices, agave) contain high fructose loads and are not benign.

REFERENCES

1. Abdelmalek MF, Suzuki A, Guy C, et al. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. J Hepatol. 2010;53(2):372-379. doi:10.1016/j.jhep.2010.03.014

2. Ma J, Fox CS, Jacques PF, et al. Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts. J Hepatol. 2015;63(4):934-942. doi:10.1016/j.jhep.2015.05.020

3. Stanhope KL, Havel PJ. Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. J Hepatol. 2008;48(6):993-1007. doi:10.1016/j.jhep.2008.03.008

4. Ouyang X, Cirillo P, Sautin Y, et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol. 2008;48(6):993-999. doi:10.1016/j.jhep.2008.03.019

5. Schwarz JM, Noworolski SM, Wen MJ, et al. Effect of a high-fructose weight-maintaining diet on lipogenesis and liver fat in humans. Gastroenterology. 2015;149(2):382-393. doi:10.1053/j.gastro.2015.04.016

6. Malik VS, Hu FB. Sugar-sweetened beverages and cardiometabolic health: an update of the evidence. Nutrients. 2019;11(8):1840. doi:10.3390/nu11081840

7. Vos MB, Lavine JE, Chalasani N, et al. Clinical research challenges in nonalcoholic fatty liver disease: end points and clinical trial design. Hepatology. 2017;65(5):1557-1565. doi:10.1002/hep.29076

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David S. Klein, MD, FACA, FACPM

1917 Boothe Circle, Suite 171

Longwood, Florida 32750

Tel: 407-679-3337

Fax: 407-678-7246

www.suffernomore.com

---

David S. Klein, MD Functional Medicine Physician