The Chickenpox Vaccine’s Unexpected Side Effect: Increased Incidence of Shingles by Jeffrey Dach MD

An unexpected finding after introduction of the live virus chickenpox vaccine in 1995 was the finding of increased Shingles incidence in children with prior natural infection. Because of this concern, the chickenpox vaccine was not recommended in the United Kingdom (England) from 1995 to 2003.

Chickenpox is caused by the Varicella-zoster virus (VZV), a herpes virus that causes two distinct illnesses. The first one is a primary infection in childhood called chickenpox (varicella). After primary infection, the virus hides in sensory nerves called the dorsal root ganglia. Later, if when cell-mediated immunity (CMI) weakens due to immunosuppression or aging, the virus can reactivate, travel along nerves, and cause herpes zoster (shingles), a painful, blistering rash. The rash is characteristic for its dermatome distribution, affecting a band of skin corresponding to the nerve distribution.

Varicella-Zoster Virus and Chickenpox: Overview

Clinical Features of Chickenpox Infection

Varicella-zoster virus (VZV) is a double-stranded DNA virus in the herpes virus family. It causes primary infection as chickenpox (varicella). After the initial illness resolves, the virus remains dormant (latent) for life in sensory nerve ganglia, particularly the dorsal root ganglia. It can later reactivate as herpes zoster (shingles). Humans are the only natural host, and the virus spreads mainly through respiratory droplets or direct contact with fluid from the skin blisters.

Typical Age Range and Clinical Features

Before the vaccine, chickenpox was almost universal in childhood—about 90% of cases occurred in children under age 15, with the highest rates in ages 1–4 and 5–9 years. Most people were infected by adolescence or early adulthood. While it can occur at any age, it is rarer and usually more severe in teens, adults, pregnant people, newborns, and those with weakened immune systems.

The incubation period averages 14–16 days (range 10–21 days).

In healthy children, the illness is often mild: a brief 1–2 day prodrome of low-grade fever (up to about 102°F), malaise, and fatigue precedes the rash. In adults, the prodrome tends to be more pronounced, sometimes with higher fever and more systemic symptoms.

The hallmark is an itchy, generalized rash that starts as red macules (flat spots), quickly becomes papules (raised bumps), then clear vesicles (“dew drops on a rose petal”) on an erythematous base, before turning pustular and crusting over. Lesions appear in successive crops, so different stages are present at once. The rash typically begins on the scalp, face, and trunk, spreading to the limbs, with the highest concentration on the trunk (centripetal distribution). Healthy children usually develop 250–500 lesions total. The entire course in uncomplicated cases lasts about 4–7 days, with fever and malaise resolving in 2–4 days.

Severity increases with age and immune status: adults often experience more intense symptoms and higher complication risks (e.g., bacterial skin infections, pneumonia, encephalitis).

In immunocompromised individuals, the disease can become disseminated, prolonged, or life-threatening.

Mortality and Burden (U.S. Data)

Pre-vaccine era (early 1990s)

Chickenpox caused an estimated 4 million cases annually, 10,500–13,500 hospitalizations, and 100–150 deaths each year. Fatality rates were low overall—about 1 per 100,000 cases in children ages 1–14, 6 per 100,000 in ages 15–19, and 21 per 100,000 in adults—but more than 90% of cases, roughly 70% of hospitalizations, and about half of deaths occurred in children. Most deaths happened in otherwise healthy individuals.

Post-vaccine era after routine vaccination began in 1995, with two-dose program from 2006:

The program dramatically reduced severe outcomes. Cases fell by more than 97%, hospitalizations by about 94%, and deaths by 97% or more in people under age 50 (with >99% decline in those under 20). Recent estimates show fewer than 150,000 cases, under 1,400 hospitalizations, and fewer than 30 deaths annually nationwide.

The age-adjusted mortality rate for varicella as the underlying cause dropped to 0.03 per million population (a 94% reduction from pre-vaccine levels).

The varicella vaccine has prevented millions of cases and thousands of severe outcomes, making chickenpox rare in the U.S. today. (1-6)

The same virus that causes chickenpox also causes Shingles, or herpes zoster. After lying dormant for years or decades in the sensory nerve ganglia, the varicella-zoster virus (VZV) reactivates After a person recovers from chickenpox, the virus stays latent in these ganglia. Over time, as immunity naturally weakens (especially with age), the virus can travel along the nerve pathways to the skin, triggering a painful, localized rash. Shingles is not contagious in the same way chickenpox is. However, a person with active shingles can transmit the virus through direct contact with the rash fluid to someone who has never had chickenpox or the varicella vaccine—potentially causing chickenpox in that susceptible individual.

Who Gets Shingles and Why?

Anyone who has had chickenpox is at risk, and about 1 in 3 people in the United States will develop shingles at some point in their lifetime. The risk increases significantly after age 50 because cell-mediated immunity against VZV declines with age. Shingles is also much more common and severe in people with weakened immune systems, including those immunosupressed with cancer (especially blood cancers), organ transplants, or anyone taking immunosuppressive drugs such as corticosteroids. While children can get shingles, it is rare, and those who received the Chickenpox (varicella) vaccine have a lower risk than people who had natural chickenpox.

What Does Shingles Look and Feel Like?

Shingles often begins with a prodrome phase lasting a few days to a week or more. People may feel pain, burning, tingling, itching, or extreme sensitivity in a specific patch of skin, sometimes before any visible rash appears. Headache, fatigue, general malaise, or a mild fever can also occur. The classic sign is a unilateral (one-sided) rash that follows the path of one or two adjacent dermatomes (nerve distributions supplied by a single spinal nerve) and does not cross the midline of the body. The rash most commonly appears on the trunk (especially the chest or back) or face, though it can occur anywhere. It starts as red, flat spots (macules), quickly turns into raised bumps (papules), then forms fluid-filled blisters (vesicles), which may become pustular before drying and crusting over. New lesions can continue to appear for several days. The entire rash usually heals in 2 to 4 weeks, sometimes leaving scars or changes in skin color. Pain is often the dominant symptom, ranging from moderate to severe and described as burning, stabbing, electric-shock-like, or deep aching. In some cases (called zoster sine herpete), intense pain occurs without any rash.

Morbidity and Complications

Shingles can cause significant short and long-term problems. The most common and serious complication is post-herpetic neuralgia (PHN), persistent nerve pain that continues for 30 days or longer after the rash has healed. PHN affects about 10% to 18% of people with shingles, and the risk rises sharply with age.

Other complications include secondary bacterial skin infections, vision or hearing loss (especially when the rash involves the face or ear), encephalitis (brain inflammation), pneumonia, or disseminated (widespread) disease in immunocompromised patients. Roughly 1% to 4% of shingles cases lead to hospitalization, and about 30% of hospitalized patients have weakened immune systems. The condition often causes missed work, reduced quality of life, and chronic pain in those who develop PHN.

Mortality

Deaths from shingles are rare, fewer than 100 people die from it each year in the United States. Almost all fatalities occur in older adults or those with severely compromised immune systems. National data estimate the mortality rate at roughly 0.28 to 0.69 per 1 million population, with herpes zoster listed as the underlying cause in about 96 deaths annually.

Shingles Treatment

Antiviral medications are the cornerstone of treatment and work best when started within 72 hours of the rash appearing. The most commonly prescribed oral antivirals are:

Valacyclovir (often preferred due to easier dosing)

Famciclovir

Acyclovir

These drugs accelerate rash healing, reduce new lesion formation and viral shedding, and shorten the duration and severity of acute pain. Treatment decisions depend on the patient’s age, immune status, and overall health. Pain relief is a major focus. Options include over-the-counter pain relievers. Skin care helps prevent bacterial superinfection, and in severe cases (e.g., eye involvement or disseminated disease), hospitalization and intravenous antivirals may be required. Corticosteroids are sometimes used in select patients to reduce inflammation but are not standard for everyone.

Off-Label Drugs: Cimetidine

Over the Counter (OTC) Cimetidine (Tagamet) is an H2-receptor antagonist primarily used for heartburn and ulcers, as an adjunctive treatment for shingles. Proposed mechanisms include immunomodulatory effects (e.g., blocking histamine-mediated immunosuppression to enhance cell-mediated immunity against VZV) and potential direct antiviral activity against herpesviruses. Early case reports from the 1980s suggested benefits such as faster pain relief, quicker resolution of the rash, and reduced duration of the acute phase (e.g., shortening active disease from an expected 35+ days to 10–17 days in some cases). A small prospective randomized trial reported faster pain reduction and skin healing with cimetidine compared to symptomatic treatment alone. Doses in these reports often ranged from 800–1200 mg/day (e.g., 400 mg three times daily or 200 mg three times daily plus 400 mg at bedtime), higher than typical heartburn doses. However, larger controlled trials (including a placebo-controlled study of 63 patients) failed to replicate earlier case reports and observational studies. For this reason, Cimetidine remains off-label use and is not usually included by mainstream medicine as a standard treatment for shingles.

The recombinant shingles vaccine (Shingrix) is highly effective at preventing shingles and its complications and is recommended for adults 50 and older (and certain younger immunocompromised individuals), but it is not used to treat active Shingles disease. (7-12)

Adverse Effects of the Live Virus Shingles Vaccine (Zostavax)

Since Zostavax is a live virus, it may cause disseminated viremia and death in immunosuppressed indiviuals. (21-22)

The Zostavax adverse effect, “Necrotizing Retinitis”, was reported at this link: Shingles Vaccine Eye Damage, courtesy of Matthews and Associates  2905 Sackett Street  Houston, Texas  77098 who write:

The shingles Zostovax vaccine Merck Pharmaceuticals has been marketing since 2006 now comes with a warning that it could cause eye damage. February 17, 2016, the FDA approved a label change to Merck’s Zostamax vaccine prescribing information. The change to the label added “Eye Disorders: necrotizing retinitis.” Merck consequently faces Shingles Vaccine Lawsuits over this dubious vaccine.Endquote.

Adverse Effects of Shingrix Vaccine Guillan-Bare Syndrome

Because of the adverse effects from the old live virus vaccine and greater efficacy of the new vaccine, in 2018, Zostavax was replaced by Shingrix, which does not contain a live virus. Unlike the Zostavax which contains live virus, the Shingrix combines an antigen, glycoprotein E, and an adjuvant system, AS01B.  Adverse side effects of the Shingrix Vaccine include an estimated 3 excess cases of Guillain-Barré Syndrome per million doses in adults aged 65+ (higher after the first dose in secondary analyses, but none after the second). As of March 24, 2021 the FDA added a Warning about Guillain-Barré Syndrome (GBS) included in the Prescribing Information for Shingrix.(13-16)

The Pre-Vaccine ERA

In the pre-vaccine era, almost every U.S. child caught wild-type chickenpox (varicella) , developing strong natural immunity. In 1995, the U.S. introduced universal vaccination using a live attenuated Oka-strain vaccine (initially one dose) to reduce childhood chickenpox (varicella) cases, hospitalizations, and rare severe outcomes. The program worked well and confirmed chickenpox cases fell dramatically.

Varicella Active Surveillance Project (VASP) in Antelope Valley, California

A 2003 Antelope Valley study by epidemiologist Gary Goldman revealed a potential trade-off. The widespread use of a varicella vaccine sharply reducing wild-type Varicella-Zoster Virus circulation. This eliminated a natural “exogenous boosting” process. This process had previously reinforced cell-mediated immunity (CMI) in adults and older children who’d had natural chickenpox, potentially delaying shingles reactivation.

What the Antelope Valley Data Showed

The Varicella Active Surveillance Project (VASP) in Antelope Valley, California (a community of ~300,000 people),was funded by the CDC. This surveillance project (VASP) actively tracked varicella/chickenpox and shingles cases by contacting schools, daycares, and providers, with lab confirmation when possible.

By 2002, verified varicella cases dropped 85% (from 2,934 in 1995 to 412). Vaccine effectiveness, however, declined over time: from 95.7% (95% CI: 82.7–98.9%) in 1999 to 73.9% (95% CI: 57.9–83.8%) in 2001.

Shingles patterns stood out. Goldman’s 2003 analysis from 2000–2001 found an adjusted shingles/herpes zoster incidence of 307 per 100,000 person-years in children under 10 yrs. This is far above historical pre-vaccine estimates for that age group (typically 50–100 per 100,000).

However the vaccinated children had very low rates: an unadjusted 9.5 per 100,000 person-years (~22 cases per 100,000 doses), indicating the weakened Oka virus strain in the vaccine rarely reactivates.

The original vaccine (Zostavax) used a live attenuated virus. Zostavax has been largely replaced in 2018 by the newer recombinant vaccine Shingrix (which does not contain live virus or the Oka strain). Remember, Zostavax was the original shingles vaccine, FDA approved in 1995 using the weakened live virus.

Children Under 10 with Natural Chickenpox/Varicella Infection

In his 2005 paper, Goldman focused on children under 10 with documented previous natural (wild-type) chickenpox/varicella infection. In these children, cell mediated immunity is boosted by occasional repeated exposure to the circulating wild type virus, thus preventing shingles outbreaks.

The cumulative true incidence of shingles in this group was 223 per 100,000 person-years (95% CI: 180–273). Accounting for under-reporting via capture-recapture (estimated at ~50%), the adjusted rate neared 446 per 100,000 person-years, comparable to levels historically seen in older adults. Remember, Shingles pre-vaccine estimates for that age group (typically 50–100 per 100,000) not 446 in the post vaccine era in this subgroup of children with prior natural chickenpox infection. These findings suggested that, in the subgroup still harboring wild-type latent virus, reduced community exposure to Varicella Zoster Virus caused the cell mediated immunity (CMI) to wane and raised shingles risk earlier in life.

The Exogenous Boosting Explanation

Goldman attributed this phenomenon to “Exogenous Boosting”. Before vaccination, children with active chickenpox regularly exposed adults (who’d already had chickenpox) to wild-type chckenpox (VZV). These low-level exposures stimulated memory T cells, bolstering cell mediated immunity (CMI) and postponing reactivation. With vaccination slashing wild-type circulation by over 80%, this natural reinforcement disappeared for millions carrying latent wild-type virus. Cell mediated immunity (CMI) declined faster, tipping the balance toward earlier shingles.

The very low shingles rate among vaccinated children aligns with this: the attenuated Oka strain seems less prone to strong latency or aggressive reactivation. The increased burden appeared mainly in those children with prior natural infection.

Public Discussion and Policy Context

Goldman’s work has sparked broader debate on vaccine policy and long-term viral ecology. In a circulated video (below), Robert F. Kennedy Jr. referenced the Antelope Valley findings, stating that when the CDC considered mandating the chickenpox vaccine, Goldman’s California study showed mass vaccination “stops chickenpox, but causes shingles epidemics later on; which is 20x deadlier.” He contrasted U.S. policy with Europe’s (noting the British NHS at the time avoided routine childhood vaccination partly due to shingles concerns) and stressed evaluating long-term implications beyond preventing one disease.

RFK JR – Many don’t realize, the Chickenpox Vaccine Causes shingles Epidemics

“When the CDC was thinking about mandating the chickenpox vaccine for your children, they did a study.

The person they hired to do that study was a scientist named Gary Goldman, who did a long-term… pic.twitter.com/WZ4x9QLoea

— healthbot (@thehealthb0t) March 19, 2026

The “20x deadlier” phrasing likely draws from discussions around Goldman’s analyses and related commentary, where chickenpox in adults carries significantly higher risks of severe outcomes (including hospitalization and death) than in children, sometimes estimated at 10–25 times greater mortality risk depending on age and context.

Pre-vaccine U.S. data showed around 100 to 150 annual varicella deaths (many in children), while shingles deaths (mostly in older or immunocompromised adults) remain low but involve greater morbidity in reactivated cases. Real-world U.S. surveillance has not shown a sustained population-wide shingles “epidemic,” though early localized data raised valid questions about shifted epidemiology.

What This Means for Virology and Public Health

Goldman’s observations highlight an ecological trade-off with latent viruses. Blocking primary chickenpox infection with a vaccine eliminates circulating virus thus reducing community acquired cell mediated immunity. Responses included the U.S. adding a second dose in 2006 and approving recombinant Shingrix for adults. The United Kingdom (England) avoided routine childhood vaccination due to loss of community acquired immunity boosting effects, however in 2006, they renewed the vaccine program after reviewing long-term data showing no major sustained shingles rise. In the UK, they now recommend a two-dose program as of 2026.

Conclusion: Overall, the two varicella vaccines have been effective in preventing chickenpox and its complications. The first, Zostavax is a live virus. The more effective second vaccine, Shingrix, is a glycoprotein adjuvant system without the live virus. Dr. Goldman’s 2003 Antelope Valley surveillance study revealed a biological cost. Namely, the loss of community exogenous boosting may accelerate shingles risk in children with natural prior infection. This remains an important lesson in viral latency, herd immunity, and the nuances of interfering with nature. This lesson is still discussed in the medical literature.(17-20)

Articles with related interest:

Shingles Vaccine for Recurrent Herpes SImplex

Herpes Simplex Natural Treatments

The failure of global Polio Eradication

What is More Worrisome, Measles or the Measles Vaccine?

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Header Image: Varicella. Verwerving en rechten
Credit line: Aankoop met steun van de Mondriaan Stichting, het Prins Bernhard Cultuurfonds, het VSBfonds, het Paul Huf Fonds/Rijksmuseum Fonds en het Egbert Kunstfonds
Verwerving: aankoop 2001 Copyright: Publiek domein
Date ca. 1870 – in of voor 1881 Source http://hdl.handle.net/10934/RM0001.COLLECT.600732 Author Rijksmuseum. Coutesy of Wikimedia Commons.

References:

1) Centers for Disease Control and Prevention. Clinical Overview of Chickenpox (Varicella). https://www.cdc.gov/chickenpox/hcp/clinical-overview/index.html

2) Centers for Disease Control and Prevention. Chapter 22: Varicella. In: Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book). https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html

3) Centers for Disease Control and Prevention. Impact of U.S. Chickenpox Vaccination Program. https://www.cdc.gov/chickenpox/vaccination-impact/index.html

4) Leung J, Harpaz R. Trends in varicella mortality in the United States, 1990–2011. Vaccine. 2015. https://pubmed.ncbi.nlm.nih.gov/25714052/ (Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC4514403/)

5) Leung J, Marin M. Update on trends in varicella mortality during the varicella vaccine era—United States, 1990–2016. Human Vaccines & Immunotherapeutics. 2018. https://pubmed.ncbi.nlm.nih.gov/29939802/ (Full text: https://pmc.ncbi.nlm.nih.gov/articles/PMC6284515/)

6) Marin M, et al. Decline in Severe Varicella Disease During the United States Varicella Vaccination Program: 1990–2019. Journal of Infectious Diseases. 2022. https://academic.oup.com/jid/article/226/Supplement_4/S407/6764826

7) Centers for Disease Control and Prevention. Clinical Overview of Shingles (Herpes Zoster). Updated June 27, 2024. https://www.cdc.gov/shingles/hcp/clinical-overview/index.html

8) Centers for Disease Control and Prevention. Shingles Facts and Stats. Updated April 12, 2024. https://www.cdc.gov/shingles/data-research/index.html Miller A, Harel D, Laor A, Lahat N.

9) Cimetidine as an immunomodulator in the treatment of herpes zoster. *Journal of Neuroimmunology*. 1989;22(1):69-76. doi:10.1016/0165-5728(89)90011-8. https://pubmed.ncbi.nlm.nih.gov/2521868/

10) Hayne ST, Mercer JB. Herpes zoster: treatment with cimetidine. *Canadian Medical Association Journal*. 1983;129(12):1284-1285. https://pmc.ncbi.nlm.nih.gov/articles/PMC1875716/

11) van der Spuy S, Levy DW, Levin W. Cimetidine in the treatment of herpesvirus infections. *South African Medical Journal*. 1980;58(3):112-116. https://pubmed.ncbi.nlm.nih.gov/6250237/ Banerjee AK, Levy DW.

12) Cimetidine in the treatment of herpes zoster. *Journal of the Royal College of Physicians of London*. 1985;19(2):97-99. (PDF available via: https://jeffreydachmd.com/wp-content/uploads/2015/06/Cimetidine-in-the-treatment-of-herpes-zoster-Levy-D-W-J-Royal-College-Physicians-London-1985.pdf)

13) FDA Safety Communication. Published March 24, 2021.
https://www.fda.gov/vaccines-blood-biologics/safety-availability-biologics/fda-requires-warning-about-guillain-barre-syndrome-gbs-be-included-prescribing-information-shingrix

14) Shingrix Package Insert (Highlights of Prescribing Information)
SHINGRIX (Zoster Vaccine Recombinant, Adjuvanted) suspension for intramuscular injection. Initial U.S. Approval: 2017. Revised: March 2021 (with subsequent minor updates; the GBS warning in section 5.2 remains as added in 2021).

15) Key excerpt from section 5.2 Guillain-Barré Syndrome: “In a postmarketing observational study, an increased risk of Guillain-Barré syndrome was observed during the 42 days following vaccination with SHINGRIX… The primary analysis… found an increased risk of GBS during the 42 days following vaccination with SHINGRIX, with an estimated 3 excess cases of GBS per million doses administered to adults aged 65 years or older.”

16) Goud R, et al. Risk of Guillain-Barré Syndrome Following Recombinant Zoster Vaccination in Medicare Beneficiaries. *JAMA Internal Medicine*. 2021;181(12):1623-1630. doi:10.1001/jamainternmed.2021.6222.
https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2785607

17) Goldman GS. (2003). Incidence of herpes zoster among children and adolescents in a community with moderate varicella vaccination coverage. *Vaccine*, 21(27–30), 4243–4249. https://doi.org/10.1016/s0264-410x(03)00459-6
[PubMed abstract](https://pubmed.ncbi.nlm.nih.gov/14505905/)

18) Goldman GS. (2005). Universal varicella vaccination: efficacy trends and effect on herpes zoster. *International Journal of Toxicology*, 24(4), 205–213. https://doi.org/10.1080/10915810591000659
[PubMed abstract](https://pubmed.ncbi.nlm.nih.gov/16126614/)

19) Kennedy, R. F., Jr. (2026). Statement on chickenpox vaccine and shingles epidemics [Video clip]. Circulated via X @thehealthb0t, March 19. https://x.com/thehealthb0t/status/2034480030516932963

20) UK Joint Committee on Vaccination and Immunisation (JCVI). (2023). JCVI recommends chickenpox vaccine in childhood immunisation programme. https://www.gov.uk/government/news/jcvi-recommends-chickenpox-vaccine-in-childhood-immunisation-programme

21) Alexander KE, Tong PL, Varma R, Macartney KK. Live zoster vaccination in an immunocompromised patient leading to death secondary to disseminated varicella zoster virus infection. Vaccine. 2018 Jul 5;36(29):3890-3892. doi:10.1016/j.vaccine.2018.05.078. Epub 2018 May 25. PMID: 29807711.
URL: https://pubmed.ncbi.nlm.nih.gov/29807711/ (Abstract; full text available via ScienceDirect or institutional access: https://www.sciencedirect.com/science/article/abs/pii/S0264410X18307448) This report describes a patient with chronic lymphocytic leukemia (an immunocompromising condition) who received Zostavax despite no documented history of primary varicella infection. The patient developed disseminated VZV infection complicated by meningoencephalitis, leading to cardiac arrest and death on day 10 of hospitalization. The case highlights the dangers of administering a high-titer live vaccine to immunocompromised individuals where contraindications are common.Case Report 2

22) Costa E, Buxton J, Brown J, Temple B, Bryant P, Thursky K. Fatal disseminated varicella zoster infection following zoster vaccination in an immunocompromised patient. BMJ Case Reports. 2016;2016:bcr2015212688. doi:10.1136/bcr-2015-212688. PMID: 27154989. PMCID: PMC4885517.
URL: https://casereports.bmj.com/content/2016/bcr-2015-212688 (Full open-access text available; also via PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC4885517/) This case involves a 79-year-old man with chronic lymphocytic leukemia who presented with fever and a widespread vesicular rash approximately one month after receiving the shingles vaccine (Zostavax). He had not been on active immunosuppression for six months prior but had underlying CLL. He developed disseminated varicella zoster infection leading to multiorgan failure (respiratory failure and other complications), and died on day 25 of hospitalization. The authors note this as one of the first reported deaths following zoster vaccination, emphasizing the risk in patients with hematologic malignancies even if not actively immunosuppressed at the time.These cases contributed to heightened awareness of Zostavax contraindications in immunocompromised populations, which played a role in its eventual discontinuation in the U.S. in favor of the non-live recombinant vaccine Shingrix.

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Published on March 19th, 2026 by Jeffrey Dach MD