Hearing Loss and Your Brain. Why Getting Hearing Aids Now Can Help Protect You From Dementia

As a practicing physician, over the past 40 years, or so, I have been asked a deceptively simple question: “Do I really need hearing aids yet?” My answer, more often than you might expect, is “yes.” Not only because hearing well restores confidence, relationships, and safety—but because untreated hearing loss is one of the strongest modifiable risk factors linked with cognitive decline and dementia. Modern evidence suggests that identifying and treating hearing loss earlier is a practical way to support long-term brain health. PubMed

What exactly is the link between hearing loss and dementia?

Over the last decade, several large population studies have shown that adults with untreated hearing loss have a higher risk of developing cognitive impairment and dementia than peers with normal hearing. The relationship is graded: the worse the hearing, the higher the risk. In a landmark prospective cohort from Johns Hopkins, every step from mild to moderate to severe hearing loss was associated with progressively greater dementia risk. JAMA Network+1

Why does this happen? There are three leading—complementary—mechanisms:

1. Cognitive load (“listening effort”) When hearing is impaired, your brain must reallocate resources to decode garbled sound. That chronic effort leaves fewer resources for memory and thinking, accelerating fatigue and reducing cognitive reserve.

2. Auditory deprivation and brain structure Reduced sensory input over years is associated with changes in brain structure and connectivity (especially in temporal and parietal regions). Recent longitudinal work tied hearing loss to smaller brain volumes and more white-matter abnormalities, with hearing-aid use appearing to mitigate some of these risks. JAMA Network

3. Social isolation and downstream health effects Hearing loss increases withdrawal, depression, and reduced physical activity—each independently linked with faster cognitive decline. The Lancet Commission identified hearing impairment as a major modifiable risk factor for dementia across the life course. The Lancet+1

Think of hearing as the brain’s daily workout. When the input is degraded, the brain works harder yet gets poorer “exercise.” Restoring clear input with hearing aids supports the neural networks that interpret speech and context, keeping them active and connected.

“But do hearing aids actually help my cognition?”

This is the crucial question—and we finally have randomized trial data. The ACHIEVE trial enrolled older adults with hearing loss and followed them for three years. Compared with a control group receiving health education, those randomized to a comprehensive hearing intervention (best-practice fitting of hearing aids plus counseling) experienced less cognitive decline—particularly among participants at higher baseline dementia risk (for example, older adults with cardiovascular risk burdens). These results align with years of observational studies showing that hearing-aid users tend to maintain better cognitive trajectories than non-users. AGs Journals+3The Lancet+3PubMed+3

Two nuances matter:

• Who benefits most? In ACHIEVE, protection against cognitive decline was most evident in the higher-risk subgroup (those with greater underlying risk based on age and comorbidities), suggesting that early adoption may be especially important for individuals with other dementia risks. The Lancet+1

• What to expect: Hearing aids are not a “cure for dementia,” and not every study shows the same magnitude of effect across all groups. But taken together, the evidence supports hearing care as a reasonable, actionable prevention strategy—with strong quality-of-life upside even beyond cognition. Health

  
  

How untreated hearing loss accelerates risk

Let’s translate data into everyday experience. Imagine two 70-year-old patients:

• Patient A strains to follow conversations, avoids restaurants, and “fills in the blanks” on television by guessing. Family notices more repetition (“What?”) and quiet withdrawal.

• Patient B uses well-fitted hearing aids and attends to maintenance (batteries/charging, cleaning, periodic adjustments). They stay socially active, engage in group exercise, and enjoy lectures and conversation.

• 
  

Both patients may have similar medical profiles, but Patient B is consistently stimulating auditory-language networks and minimizing isolation—two conditions associated with healthier long-term cognitive outcomes in observational data, reinforced by randomized evidence in higher-risk individuals. The Lancet+1

Early signs that deserve attention

Not all hearing loss announces itself. Look for:

• Needing captions even at normal volumes

• Trouble hearing in restaurants or meetings

• Family complaining you talk loudly or miss words

• Ringing in the ears (tinnitus)

• “I hear you, but I can’t understand you”

  
  

If these sound familiar, a professional audiologic evaluation is prudent. Objective testing goes far beyond the whispered-voice test and helps tailor precise amplification to your pattern of loss.

“I’m not ready for hearing aids.” Common barriers—and straight answers

“They’ll make me look old.”Contemporary devices are small, nearly invisible, and tech-forward—Bluetooth streaming, smartphone control, and rechargeable options. The greater “tell” of aging is repeatedly mishearing or withdrawing from conversation.

“I tried them and didn’t like them.”Adaption is a process. The auditory cortex needs time to re-learn crisp sound after years of muffled input. Best-practice fitting with real-ear measurement, follow-up fine-tuning, and communication strategies (placement at the dinner table, managing background noise) transform outcomes.

“They’re expensive.”Options exist across a spectrum—including over-the-counter (OTC) devices for mild to moderate loss. A medical-grade fitting is still ideal for most, but even OTC amplification can be a clinically meaningful first step. And when you weigh the cost of isolation, falls, medical errors, and caregiver stress, amplification is an investment in independence and brain health.

What the numbers say

• In a well-designed prospective study, each 10-dB increase in hearing loss was associated with a higher risk of incident dementia, with hazard ratios climbing from mild to severe loss. JAMA Network

• Large cohorts repeatedly show that people who use hearing aids experience slower cognitive decline than comparable adults who do not. PubMed+1

• The Lancet Commission ranks hearing loss among the top modifiable risk factors for dementia across the life course and recommends increasing access to hearing care (including hearing aids). The Lancet+1

• The ACHIEVE randomized trial indicates that a comprehensive hearing-care program can reduce cognitive decline over three years in older adults at elevated risk—evidence that targeted intervention matters. The Lancet

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Beyond cognition: whole-person benefits you’ll feel in weeks

• Safer mobility: Better environmental awareness reduces falls and improves driving safety.

• Medical accuracy: You’re less likely to mishear instructions or medication changes.

• Mood and relationships: Amplification relieves the chronic strain on spouses and families, reducing conflict and isolation.

• Energy: Many patients describe lower “listening fatigue,” improving resilience for exercise, hobbies, and social life.

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A practical plan to protect your brain

1. Get a baseline hearing test now.Adults over 55—earlier if you have noise exposure, diabetes, vascular risks, or a family history—benefit from audiometric screening. Repeat every 1–2 years.

2. Treat when ready—preferably sooner.If you have measurable loss that affects understanding (especially in noise), strongly consider hearing aids. Early adoption eases brain adaptation and supports social engagement.

3. Insist on best-practice fitting.Look for real-ear verification, device counseling, and structured follow-ups. These steps are not “nice-to-have”—they’re essential.

4. Address the full risk profile.Control blood pressure, lipids, and glucose; stay physically active; prioritize sleep; curb smoking; treat depression; and protect your vision—multi-domain prevention magnifies the benefit of hearing care. The Lancet

5. Lean into communication strategies.Face your conversation partner, reduce background noise when possible, and use assistive mics at restaurants or lectures. Pair your aids with your phone for calls and captions.

6. 
   

What if cognitive changes are already present?

Do not delay care. Even when memory complaints arise, improving hearing can enhance day-to-day function, reduce caregiver burden, and maintain independence. While no therapy can guarantee dementia prevention, hearing-care interventions are safe, scalable, and supported by growing evidence as part of comprehensive brain-health planning. The Lancet

References

1. Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020;396(10248):413-446. doi:10.1016/S0140-6736(20)30367-6 The Lancet+1

2. Lin FR, Metter EJ, O’Brien RJ, Resnick SM, Zonderman AB, Ferrucci L. Hearing loss and incident dementia. Arch Neurol. 2011;68(2):214-220. doi:10.1001/archneurol.2010.362 JAMA Network+1

3. Deal JA, Betz J, Yaffe K, et al. Hearing impairment and incident dementia and cognitive decline in older adults: the Health ABC Study. J Gerontol A Biol Sci Med Sci. 2017;72(5):703-709. doi:10.1093/gerona/glw069 PubMed

4. Maharani A, Dawes P, Nazroo J, Tampubolon G, Pendleton N. Longitudinal relationship between hearing aid use and cognitive function in older Americans. J Am Geriatr Soc. 2018;66(6):1130-1136. doi:10.1111/jgs.15363 PubMed+1

5. Lin FR, Pike JR, Albert MS, et al. Hearing intervention versus health education control to reduce cognitive decline in older adults with hearing loss (ACHIEVE): a randomized trial. Lancet. 2023;402(10397):1071-1081. doi:10.1016/S0140-6736(23)01406-X The Lancet+1

6. Liu K, Simmonds MB, Dillon H. Hearing intervention and cognitive decline: interpreting ACHIEVE. Lancet. 2024;403(10429):e56-e58. doi:10.1016/S0140-6736(24)00712-8 The Lancet

7. Gurgel RK, Ward PD, Schwartz S, Norton MC, Foster NL, Tschanz JT. Relationship of hearing loss and dementia: a prospective, population-based study. Otol Neurotol. 2014;35(5):775-781. doi:10.1097/MAO.0000000000000313 PubMed+1

8. Dawes P, Emsley R, Cruickshanks KJ, et al. Hearing-aid use and long-term health outcomes: hearing handicap, mental health, social engagement, cognitive function, physical health, and mortality. Int J Audiol. 2015;54(11):838-844. doi:10.3109/14992027.2015.1059503 PubMed

9. Amieva H, Ouvrard C, Giulioli C, Meillon C, Rullier L, Dartigues JF. Self-reported hearing loss, hearing aids, and cognitive decline in elderly adults: a 25-year study. J Am Geriatr Soc. 2015;63(10):2099-2104. doi:10.1111/jgs.13649 PubMed+1

10. Myrstad C, Moulsdale P, Engdahl B, et al. Hearing impairment and risk of dementia in the HUNT study. eClinicalMedicine. 2023;63:102198. doi:10.1016/j.eclinm.2023.102198 The Lancet

11. Livingston G, Huntley J, Sommerlad A, et al. The Lancet launches new guidance on dementia risk reduction (news release summarizing Commission findings). Alzheimer’s Disease International; 2020. Alzheimer's Disease International

12. Kolo FB, Zlatev A, Pase MP, et al. Hearing loss, brain structure, cognition, and dementia risk in the Framingham Study. JAMA Netw Open. 2025;8(11):exxxxxx. doi:10.1001/jamanetworkopen.2025.xxxxxx JAMA Network

13. Ray J, Popli G, Fell G. Association of cognition and age-related hearing impairment in the English Longitudinal Study of Ageing. JAMA Otolaryngol Head Neck Surg. 2018;144(10):876-882. doi:10.1001/jamaoto.2018.1656 JAMA Network

14. Dawes P, Cruickshanks KJ, Moore DR, et al. Hearing aids, social isolation, depression, and cognition in older UK adults. PLoS One. 2015;10(3):e0119616. doi:10.1371/journal.pone.0119616 PLOS

15. ACHIEVE Study Team. The ACHIEVE Study: design and key findings (public dissemination summary). achievestudy.org. Accessed November 10, 2025. Achieve Study

Bottom line for you

If you or someone you love is missing words, avoiding conversations, or turning up the TV, don’t wait for “it to get worse.” A straightforward hearing evaluation and timely, well-fitted hearing aids can restore daily clarity—and they’re a sensible, evidence-supported step for long-term brain health.

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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

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