




On the Cover: BCMS physicians continue to advocate for “The Family of Medicine.” At the 2025 TexMed conference in San Antonio, Jayesh “Jay” Shah, MD, the newly installed 160th TMA President, is joined by William W. “Bill” Hinchey, MD, who was the last BCMS physician to serve as TMA President in 2007-2008.
TMA Presidents from BCMS Present-Jay Shah, MD, and Past-Bill Hinchey, MD in this issue
Erythematosus By Pendleton Wickersham, MD
Cystic Fibrosis in Adulthood: Recognizing a lifelong
You Need to be Involved with CASA By David Siegel, MD,
Phillip W. Voltz, Jr,
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John Shepherd, MD, President
Lyssa Ochoa, MD, Vice President
Jennifer R. Rushton, MD, President-Elect
Lubna Naeem, MD, Treasurer
Lauren Tarbox, MD, Secretary
Ezequiel “Zeke” Silva, III, MD, Immediate Past President
Woodson “Scott” Jones, Member
John Lim, MD, Member
Sumeru “Sam” G. Mehta, MD, Member
M. “Hamed” Reza Mizani, MD, Member
Priti Mody-Bailey, MD, Member
Dan Powell, MD, Member
Saqib Z. Syed, MD, Member
Nancy Vacca, MD, Member
Col Joseph J. Hudak, MD, MMAS, Military Representative
Jayesh Shah, MD, TMA Board of Trustees Representative
John Pham, DO, UIW Medical School Representative
Robert Leverence, MD, UT Health Medical School Representative
Cynthia Cantu, DO, UT Health Medical School Representative
Lori Kels, MD, UIW Medical School Representative
Ronald Rodriguez, MD, UT Health Medical School Representative
Alice Gong, MD, Board of Ethics Representative
Melody Newsom, BCMS CEO/Executive Director
George F. “Rick” Evans, Jr., General Counsel
Melody Newsom, CEO/Executive Director
Brissa Vela, Chief Membership & Development Officer
Yvonne Nino, Controller
Betty Fernandez, BCVI Director of Operations
Phil Hornbeak, Auto Program Director
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Jacob Hernandez, Advocacy and Public Health Specialist
Jennifer C. Seger MD, Chair
Timothy C. Hlavinka, MD, Member
John Robert Holcomb, MD, Member
Soma S. S. Jyothula, MD, Member
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Adam Ratner, MD, Member
John Joseph Seidenfeld, MD, Member
Amith Skandhan, MD, Member
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Louis Doucette, Consultant
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Trisha Doucette, Editor
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By John Shepherd, MD, President, Bexar County Medical Society
As President of the Bexar County Medical Society, I had the distinct honor of witnessing our community’s leadership shine at this year’s Texas Medical Association (TMA) conference TexMed, held right here in our hometown of San Antonio. This vibrant gathering brought the Family of Medicine from across the state together, and I’m proud to share that five of our own Bexar County leaders — including myself — played prominent roles in shaping conversations, guiding policy, and representing our region with excellence. Together, our contributions showcased the depth of expertise and unwavering commitment that define our medical society.
As I opened the House of Delegates, I had the privilege of welcoming attendees to San Antonio — a city rich in history and known for the iconic phrase, “Remember the Alamo.” But I reminded them that what truly sets the Alamo City apart is our dedicated physician community and our proud legacy as the home of military medicine. It was also a meaningful moment for me personally, marking the close of my term as TEXPAC Candidate Evaluation Chair and the beginning of a new chapter as the incoming TEXPAC Chair.
Dr. Zeke Silva, immediate Past President of BCMS, helped kick off the conference by highlighting the long and distinguished history of organized medicine in Bexar County and Texas. Of particular note was the Bexar County Medical Society Alliance, founded two years before both the statewide TMA Alliance and the ratification of the 19th Amendment granting women the right to vote. Zeke has served with distinction as Chair of the TMA Council on Legislation, dedicating his year to tirelessly advocating for physicians and the practice of medicine. A steady and respected presence in both Texas House and Senate hearings, his calm, thoughtful testimony has helped preserve the integrity of our profession and protect physicians’ ability to care for their patients.
Dr. David Henkes, a pathologist and passionate advocate, received the TMA Distinguished Service Award — TMA’s highest honor. For over 25 years, David has represented Texas as part of the AMA delegation, many of those as chair. Under his leadership, Texas secured delegate seats on nearly every AMA council, placed three members on the AMA Board of Trustees, and saw Dr. Susan Bailey elected AMA president. One of his most impactful accomplishments was the formation of the “Big Five” coalition — Texas, California, Florida, New York and Pennsylvania — which elevated Medicare physician payment as a national priority and led to the “Fix Medicare Now” campaign. David has mentored countless physicians at the county, state and national levels. In his remarks to the House of Delegates, he humbly expressed gratitude to even be mentioned alongside past recipients, whom he called the “legends of medicine.” He also gave heartfelt thanks to his wife, Danielle, and children, Nichole and Daniel, for their unwavering support throughout his career.
Bexar County was also well-represented at the highest levels of leadership with Jenny Shepherd completing her term as TMA Alliance President and Dr. Jayesh Shah stepping into his new role as TMA President. Both have long histories of service to organized medicine and physician families, having held leadership roles at the county, state and national levels.
Jenny Shepherd wore many hats over the past year — serving alongside me on the TEXPAC Executive Board and Candidate Evaluation Committee, co-chairing the TMA Foundation Gala, leading First Tuesdays at the Capitol, and serving as President of the TMA Alliance. In her outgoing address to the House of Delegates, she reflected on the Alliance’s many accomplishments, united by her powerful theme, “The Power of One.” She reminded us that one voice, one action and one person can make a meaningful difference. Her focus was twofold: preparing the Alliance for the future and broadening participation in advocacy. She led an overhaul of the bylaws, introduced new mission and vision statements, and developed the Alliance’s first-ever strategic plan. Her efforts to make advocacy accessible resulted in a record number of first-time attendees at First Tuesdays. Though her term has ended, Jenny isn’t slowing down — you’ll likely find her alongside TEXPAC Director Brianna Menard, taking her advocacy education program, “The Party of Medicine,” on the road across Texas.
Dr. Jayesh Shah, who practices hyperbaric medicine and wound care, took the stage to be installed as the 160th President of the Texas Medical Association. In the 172-year history of the organization, Jay is the first Indian American to hold this prestigious position — a milestone that reflects his personal dedication. A longtime advocate for reducing administrative burdens and restoring the joy of practicing medicine, Jay spoke with clarity and conviction about the mounting pressures that are driving physicians away from the profession they love. In his inaugural address, he painted a vivid picture of the current landscape, where doctors are often overwhelmed by red tape, insurance obstacles and regulatory demands that take time away from patient care. His presidential theme, “Let Doctors Be Doctors,” is both a rallying cry and a strategic focus for the year ahead — one that aims to empower physicians, reduce unnecessary barriers, and re-center the patient-physician relationship at the heart of healthcare. Jay’s leadership promises to bring thoughtful, solutions-driven advocacy to the forefront during his term, and we are proud to have another Bexar County physician serving in such a prominent statewide role.
As if the accomplishments of these leaders weren’t enough, TexMed concluded with a spectacular finale — the TMA Foundation Gala. Jenny and I, along with Dr. Zeke and Erika Silva, had the honor of serving as co-chairs for this year’s event, which embraced an adventurous theme and proved to be another record breaker. The energy in the room was electric, and the generosity on display was truly inspiring.
Beyond the celebration, the purpose behind the gala couldn’t be more meaningful. The funds raised play a vital role in supporting the TMA Foundation’s mission to improve the health of all Texans. Through programs like “Hard Hats for Little Heads,” which provides bicycle helmets to children, and “Texas BookShare,” which puts books into the hands of underserved children, the Foundation ensures that our outreach reaches far beyond the walls of any exam room. The gala also helps fund scholarships for future physicians and provides grants for innovative, community-serving health projects across the state. It was deeply fulfilling to see the medical community come together in such a joyful and impactful way — giving back, lifting others, and celebrating the power of medicine to heal not just individuals, but entire communities.
TexMed 2025 was more than just a conference — it was a powerful reminder of what’s possible when passionate, committed leaders come together to serve a greater cause. From shaping policy and mentoring the next generation, to breaking barriers and giving back to our communities, Bexar County’s presence was felt at every level. I left the weekend inspired — not only by the achievements of my fellow leaders, but by the collective strength of our medical family. As we look ahead, let us carry that momentum forward, continuing to lead with purpose, advocate with courage, and work together to ensure a healthier future for all Texans.
John Shepherd, MD, 2025 President of the Bexar County Medical Society and TEXPAC Chair, has been an active advocate for the Family of Medicine at the Texas State Capitol and has held several “Party of Medicine” events, introducing physicians on how to get involved with legislation that affects medical issues. He has been Chief of Surgery at Christus Santa Rosa Children’s Hospital and a past member of the Board of Directors of Tejas Anesthesia. Dr. Shepherd is currently a Pediatric Anesthesiologist with University Medical Associates, and serves on the BCMS Legislative Committee and the Bexar Delegation to TMA.
By Victoria Kohler-Webb
Viva Fiesta! Viva Bexar County Medical Society Alliance! BCMSA combined both of those amazing traditions as we gathered for our most beautiful and enduring Alliance calendar fixture — our Past President’s Luncheon. We welcomed our members to this deeply meaningful chance to celebrate our special bond of friendship and highlight the value of our connections.
Wearing our Fiesta Finest, we found ourselves discussing why our Alliance is important to us all and what it means to be a member. As you undoubtedly know, we define our Alliance role in three ways: Community Outreach, Legislative Advocacy and Strengthening the Medical Community. All three roles come together for today’s Alliance member in an ever-changing world as we advocate for the physician, their business model and livelihood, and their family. However, the glue that holds us together is the bond of friendship and that was apparent during the luncheon as evidenced by the loud volume and frequent laughter as we enjoyed being in each other’s company.
Consider for a moment our BCMSA legacy of leadership — after all, that is what our Past President’s Luncheon is about. We proudly boast 108 Past Presidents since our inception! Presidents who give
their time freely to this unpaid corporate position to organize and manage a large budget (and a larger group of volunteers), to serve their community, and to support all Bexar County physicians and families.
What a great honor it is for Bexar County to claim the current Texas Medical Association Alliance President, Jenny Shepherd, as our own! Three BCMSA Past Presidents have been elected as TMAA President — a lot for one Alliance and a clear demonstration of the quality of our local leaders and members.
We hope you enjoy these pictures of your BCMSA Past Presidents and members in their Fiesta best! Thank you to all of you reading who have served this amazing organization as President — your tradition of strong leadership and community service has kept us vibrant!
Victoria Kohler-Webb, BBA, MS Marketing Statistics, is the BCMSA immediate Past President, served as 2024-2025 TMAA Board Secretary and currently serves as Membership Liaison. She and Ben, an ENT/Head & Neck Surgeon, are proud Aggies and parents to Luke, 16, and four rescue dogs.
By Eliot Young, MD, FAAFP, CAQ-SM
Sports-related concussion (SRC) affects millions of athletes every year and is increasingly becoming a topic of interest and concern for active individuals, parents and medical providers alike. While many of these injuries spontaneously resolve, some patients may experience prolonged effects. As such, they can be disruptive to work, school, social life and relationships. Medical providers should be aware of the typical signs and symptoms to avoid delayed diagnosis. The diagnosis and management should be individualized, as each injury is unique in its presentation and recovery.
SRCs are considered a form of mild traumatic brain injury occurring during exercise or sports, which is “caused by a direct blow to the head, neck or body resulting in an impulsive force being transmitted to the brain.”16 It is estimated that 3.8 million concussions occur annually in sport and recreation at all ages in the U.S.,7 of which nearly 50% occur in those 18 years of age and younger. In fact, by the age of 16, 20% of children will have experienced a traumatic brain injury.22
There seems to be a higher risk of concussion in girls within comparable sports (soccer, basketball), though the reason for this is unknown. The sports with the highest rates of concussion are boys’ football and girls’ soccer, followed by boys’ lacrosse, boys’ ice hockey, boys’ wrestling and girls’ lacrosse.7
The diagnosis of concussion should consist of a detailed history and a focused examination involving neurologic, vestibular, cervical and oculomotor components.
History should be obtained from the patient as well as a close observer, if possible, to fill in memory gaps if necessary. Loss of consciousness is infrequent in SRC, while the most common symptoms include dizziness, headache, “feeling in a fog” and balance problems. Most symptoms will be apparent immediately or within a few minutes, though occasionally they can be delayed up to 72 hours.14 Once concussion is suspected, the person should be removed immediately from any potential secondary insult (e.g., an athlete should be removed from further sport that day). In Texas, UIL rules mandate this approach and use the slogan “when in doubt, sit them out.”19
“Red flag” symptoms, if present, should prompt transport to an emergency room. These include seizure activity, midline neck tenderness, prolonged loss of consciousness >1-minute, focal neurologic deficit, abnormal pupillary exam, vomiting or deteriorating neurological exam.6
There are multiple screening tools and apps that can guide the evaluation and management of suspected concussion. Screening tools such as the BESS (Balance Error Scoring System), King-Devick test and the SCAT (Sport Concussion Assessment tool) have undergone validation and modification over time.10 The SCAT6 is the most recent
iteration of a tool developed by the Concussion in Sport Group, an international body that has convened multiple times over the last two decades to review, update, and summarize the evidence and practice surrounding concussion.16 This tool is a very robust but lengthy examination and may be difficult to perform in a clinical setting with limited time. To improve efficient clinical evaluation, Leddy et. al. detailed an exam that helps the clinician conduct a brief but directed examination in the office setting.12 If there is still a question, computerized neurocognitive tests (e.g., ImPACT, Cogstate), exercise testing14 or formal neuropsychological evaluation may help confirm the diagnosis.
As management of concussion has evolved, the practice of placing concussed patients in a dark room (“cocooning”) has been replaced with early controlled activity and light exercise to tolerance. Recent studies have shown that light exercise and reduction of screen time (not elimination) within 48 hours of concussion can facilitate recovery, while sleep disturbances can prolong symptoms.13 In fact, longer daytime sleep in adolescents in the week following a concussion led to a lower likelihood of symptom resolution in one study.20
Most experts recommend modified activity, adequate nutrition and sleep hygiene, and serial evaluations with symptom scores/physical exam findings to help guide recovery. The 2022 Amsterdam International Consensus on Concussion in Sport published several tools for clinicians to aid monitoring of concussion, including the sport concussion office assessment tool (SCOAT6) and one for children aged 7-12 (Child SCOAT6).16 Although the typical SRC will resolve within weeks, up to one-third of pediatric patients may experience symptoms beyond four weeks.22
Once symptoms are beginning to resolve, the focus of the patient will typically shift to return to activities or return to play. For adolescents, children and young adults, there should be emphasis on “return to learn” (RTL) before return to play. Recent studies indicate that early gradual physical and cognitive activity shortens the time to RTL. Academic support may be helpful in this setting, and the clinician can support this with a school note that recommends temporary academic modifications.17 Likewise, the return to sport (RTS) should be gradual and follow a 5-step graded return, from relative rest to full contact.17 The Texas Education code (Section 38.157c) requires supervision of a return-to-play protocol for all student athletes and uses the example protocol provided by the Concussion in Sport Group.7
Since the Berlin Consensus conference in 2016, there has been a sharp increase in studies using advanced neuroimaging, blood biomarkers, genetic testing and newer technologies to diagnose concussion and follow recovery. While some of these are promising and have potential to improve the care of concussion, at present the body of evidence is judged to be SORT level B (inconsistent or limited-quality patient-oriented evidence).18
In addition, the prevention of concussion has been targeted as a focus of study. There have been quality studies showing the reduction of concussion by implementation of rule changes and policies in youth sports, use of mouth guards (specifically in ice hockey) and neuromuscular warm-up programs.5 However, due to the anatomy of the brain suspended inside the cranium, other external devices don’t often make a
significant difference in concussion reduction. The exception may be the well-fitted helmet, with padding over the zygoma/mandible, in American football. Several studies have reported a reduced rate or severity of concussions with these, and more studies are needed.8 Although there have been well-publicized examples of professional athletes wearing the Guardian cap device over the helmet, to date the evidence is lacking to show real-world concussion reduction in high school football.8
• Sport-related concussion is prevalent in all sports, and under-diagnosed.
• Prompt diagnosis improves outcomes, so the clinician should be familiar with diagnostic tools available.
• When in doubt, sit them out.
• Early, controlled physical activity and less daytime sleeping reduce prolonged post-concussion symptoms.
• Serial examinations are important in determining progress or in identifying deterioration.
• Most SRCs will resolve within four weeks.
• Return-to-learn should be facilitated with measures to reduce symptoms in the learning environment.
• Return-to-play strategies should follow the recommended 5-step graded process of progressive intensity and coordination.
• Future tools may include biomarkers and advanced imaging, but are not yet advanced enough to be useful in the clinical setting.
References:
1. Broglio, S.P., Register-Mihalik, J.K., Guskiewicz, K.M., Leddy, J.J., Merriman, A., Valovich McLeod, T.C. National Athletic Trainers’ Association Bridge Statement: Management of Sport-Related Concussion. J Athl Train. 2024 Mar 1;59(3):225242. doi: 10.4085/1062-6050-0046.22. PMID: 38530653; PMCID: PMC10976337
2. Conti, F., McCue, J.J., DiTuro, P., Galpin, A.J., Wood, T.R. Mitigating Traumatic Brain Injury: A Narrative Review of Supplementation and Dietary Protocols. Nutrients. 2024 Jul 26;16(15):2430. doi: 10.3390/nu16152430. PMID: 39125311; PMCID: PMC11314487
3. Cuff, S., Maki, A., Feiss, R., Young, J., Shi, J., Hautmann, A., Yang, J. Risk factors for prolonged recovery from concussion in young patients. Br J Sports Med. 2022 Dec;56(23):1345-1352. doi: 10.1136/bjsports-2022-105598. Epub 2022 Sep 14. PMID: 36104148
4. De Luigi, A.J., Bell, K.R., Bramhall, J.P., Choe, M., Dec, K., Finnoff, J.T., Halstead, M., Herring, S.A., Matuszak, J., Raksin, P.B., Swanson, J., Millett, C. Consensus statement: An evidence-based review of exercise, rehabilitation, rest, and return to activity protocols for the treatment of concussion and mild traumatic brain injury. PM R. 2023 Dec;15(12):1605-1642. doi: 10.1002/ pmrj.13070. Epub 2023 Nov 14. PMID: 37794736
5. Eliason, P.H., Galarneau, J.M., Kolstad, A.T., Pankow, M.P., West, S.W., Bailey, S., Miutz, L., Black, A.M., Broglio, S.P., Davis, G.A., Hagel, B.E., Smirl, J.D., Stokes, K.A., Takagi, M., Tucker, R., Webborn, N., Zemek, R., Hayden, A., Schneider, K.J., Emery, C.A. Prevention strategies and modifiable risk factors for sport-related concussions and head impacts: a systematic review and meta-analysis. Br J Sports Med. 2023 Jun;57(12):749-761. doi: 10.1136/bjsports-2022-106656. PMID: 37316182
6. Gregory, A., Poddar, S. Diagnosis and Sideline Management of Sport-Related Concussion. Clin Sports Med. 2021 Jan;40(1):5363. doi: 10.1016/j.csm.2020.08.011. PMID: 33187613
7. Halstead, M.E., Walter, K.D., Moffatt, K.; COUNCIL ON SPORTS MEDICINE AND FITNESS. Sport-Related Concussion in Children and Adolescents. Pediatrics. 2018 Dec;142(6):e20183074. doi: 10.1542/peds.2018-3074. Epub 2018 Nov 12. PMID: 30420472
8. Hammer, E., Mosiman, S., Joachim, M.R., Taylor, E., Cordum, A., Brooks, M.A., McGuine, T. The association between Guardian Cap use during practices and sport-related concussion risk in high school American football players. Br J Sports Med. 2025 Feb 6;59(4):257-262. doi: 10.1136/bjsports-2024-108945. PMID: 39875183
9. Jones, J.C., O’Brien, M.J. Medical Therapies for Concussion. Clin Sports Med. 2021 Jan;40(1):123-131. doi: 10.1016/j. csm.2020.08.005. PMID: 33187603
10. Kaufman, M.W., Su, C.A., Trivedi, N.N., Lee, M.K., Nelson, G.B., Cupp, S.A., Voos, J.E. The Current Status of Concussion Assessment Scales: A Critical Analysis Review. JBJS Rev. 2021 Jun 8;9(6). doi: 10.2106/JBJS.RVW.20.00108. PMID: 34101673
11. Kriz, P.K., MacDonald, J.P. Outpatient Management of Sport-Related Concussion, Return to Learn, Return to Play. Clin Sports Med. 2021 Jan;40(1):65-79. doi: 10.1016/j. csm.2020.08.015. PMID: 33187614
12. Leddy, J., Lesh, K., Haider, M.N., Czuczman, N., Baker, J.G., Miecznikowski, J., Willer, B. Derivation of a Focused, Brief Concussion Physical Examination for Adolescents With Sport-Related Concussion. Clin J Sport Med. 2021 Jan;31(1):7-14. doi: 10.1097/JSM.0000000000000686. PMID: 30418219; PMCID: PMC6488454
13. Leddy, J.J., Burma, J.S., Toomey, C.M., Hayden, A., Davis, G.A., Babl, F.E., Gagnon, I., Giza, C.C., Kurowski, B.G., Silverberg, N.D., Willer, B., Ronksley, P.E., Schneider, K.J. Rest and exercise early after sport-related concussion: a systematic review and meta-analysis. Br J Sports Med. 2023 Jun;57(12):762-770. doi: 10.1136/bjsports-2022-106676. PMID: 37316185
14. Leddy, J.J. Sport-Related Concussion. N Engl J Med. 2025 Jan 30;392(5):483-493. doi: 10.1056/NEJMcp2400691. PMID: 39879594
15. Makdissi, M., Critchley, M.L., Cantu, R.C., Caron, J.G., Davis, G.A., Echemendia, R.J., Fremont, P., Hayden, K.A., Herring,
S.A., Hinds, S.R., Jordan, B., Kemp, S., McNamee, M., Maddocks, D., Nagahiro, S., Patricios, J., Putukian, M., Turner, M., Sick, S., Schneider, K.J. When should an athlete retire or discontinue participating in contact or collision sports following sport-related concussion? A systematic review. Br J Sports Med. 2023 Jun;57(12):822-830. doi: 10.1136/bjsports-2023-106815. PMID: 37316181
16. Patricios, J.S., Schneider, K.J., Dvorak, J., Ahmed, O.H., Blauwet, C., Cantu, R.C., Davis, G.A., Echemendia, R.J., Makdissi, M., McNamee, M., Broglio, S., Emery, C.A., Feddermann-Demont, N., Fuller, G.W., Giza, C.C., Guskiewicz, K.M., Hainline, B., Iverson, G.L., Kutcher, J.S., Leddy, J.J., Maddocks, D., Manley, G., McCrea, M., Purcell, L.K., Putukian, M., Sato, H., Tuominen, M.P., Turner, M., Yeates, K.O., Herring, S.A., Meeuwisse, W. Consensus statement on concussion in sport: the 6th International Conference on Concussion in Sport-Amsterdam, October 2022. Br J Sports Med. 2023 Jun;57(11):695-711. doi: 10.1136/ bjsports-2023-106898. PMID: 37316210
17. Putukian, M., Purcell, L., Schneider, K.J., Black, A.M., Burma, J.S., Chandran, A., Boltz, A., Master, C.L., Register-Mihalik, J.K., Anderson, V., Davis, G.A., Fremont, P., Leddy, J.J., Maddocks, D., Premji, Z., Ronksley, P.E., Herring, S., Broglio, S. Clinical recovery from concussion-return to school and sport: a systematic review and meta-analysis. Br J Sports Med. 2023 Jun;57(12):798809. doi: 10.1136/bjsports-2022-106682. PMID: 37316183
18. Tabor, J.B., Brett, B.L., Nelson, L., Meier, T., Penner, L.C., Mayer, A.R., Echemendia, R.J., McAllister, T., Meehan, W.P. 3rd, Patricios, J., Makdissi, M., Bressan, S., Davis, G.A., Premji, Z., Schneider, K.J., Zetterberg, H., McCrea, M. Role of biomarkers and emerging technologies in defining and assessing neurobiological recovery after sport-related concussion: a systematic review. Br J Sports Med. 2023 Jun;57(12):789-797. doi: 10.1136/ bjsports-2022-106680. PMID: 37316184
19. University Interscholastic League: Health and Safety/Concussions and Concussion Management Protocol Requirements and Information. Available at: https://www.uiltexas.org/health/concussions, (accessed April 22, 2025)
20. VonDeylen, O., Alshaikh, E., Wheeler, K., Recker, R., Malerba, P., Valasek, A., Yeates, K.O., Yang, J. Sleep quantity and quality during the first week postinjury and time to symptom resolution in youth with concussion. Br J Sports Med. 2025 Feb 26:bjsports-2024-109058. doi: 10.1136/bjsports-2024-109058. Epub ahead of print. PMID: 40011013
21. Wilson, J.C., Patsimas, T., Cohen, K., Putukian, M. Considerations for Athlete Retirement After Sport-Related Concussion. Clin Sports Med. 2021 Jan;40(1):187-197. doi: 10.1016/j. csm.2020.08.008. PMID: 33187608
22. Zimmerman, S.D., Vernau, B.T., Meehan, W.P. 3rd, Master, C.L. Sports-Related Concussions and the Pediatric Patient. Clin Sports Med. 2021 Jan;40(1):147-158. doi: 10.1016/j. csm.2020.08.010. PMID: 33187605
Eliot Young, MD, FAAFP, CAQ-SM, is a physician/owner at Sports Medicine Associates of San Antonio. He is an AOA graduate from the University of Texas Medical School at San Antonio in 1993, and did his Family Medicine residency at Madigan Army Medical Center in Tacoma, Washington. He has been in academic medicine since 1996, and completed a Sports Medicine fellowship in 2006. He has been a team physician for high school and collegiate athletes, USA basketball, USA skiing, the San Antonio Missions, San Antonio Rampage, San Antonio Silver Stars (WNBA), San Antonio Football Club and the San Antonio Spurs. He is the director of the TIGMER Sports Medicine Fellowship and local medical director for the San Antonio Marathon and Valero Texas Open. Dr. Young is a member of the Bexar County Medical Society.
By Arush Shekar
Mild cognitive impairment (MCI) and dementia are broad clinical diagnoses that encompass a wide array of underlying neurodegenerative and non-neurodegenerative causes, with Alzheimer’s disease (AD) being the most common underlying cause. Dementia occurs in more than one in 10 people over the age of 65, affects one in three people over the age of 85, and is the most expensive chronic disease in the U.S. Significant breakthroughs have recently occurred in dementia clinical care, including identifying potentially modifiable risk/protective factors, biomarkers to guide precision diagnosis and management, and the first disease modifying treatments for AD.
In Bexar County, dementia affects over 33,000 residents, reflecting roughly 13% of the county’s population over age 65. The burden of the disease extends to those that care for them, with Texas having over 1.4 million unpaid caregivers for patients with dementia. South Texas has among the highest prevalence of dementia in the U.S., particularly among Hispanic adults, and prior studies have suggested that Hispanic adults have a higher risk of developing dementia. As a result of population growth, demographics and aging, San Antonio is anticipated to have a rapidly rising prevalence of dementia, creating a need for increased awareness, early detection and access to resources.
MCI and dementia are clinical syndromes characterized by a gradual progressive decline in cognition from an individual’s baseline, which can be noticed by the individual, a family member and/or a clinical provider. The diagnosis is supported by objective impairment on cognitive testing. MCI is diagnosed when the individual has preserved independence in daily functioning and activities, while dementia is diagnosed when the individual now requires assistance in performing activities needed to live independently. The syndromes are most frequently caused by underlying neurodegenerative diseases. These are diseases that cause chronic, progressive loss of neurons, most commonly due to the accumulation and spread of abnormal proteins in the brain. Most patients have multiple co-pathologies that contribute to their clinical symptoms.
AD is the most common cause of dementia, responsible for over 60% of cases. The hallmark brain pathology is extracellular amyloid beta peptide plaques and intracellular aggregates of hyperphosphorylated tau protein called neurofibrillary tangles. Early clinical signs may include difficulty in short-term memory, orientation to time, executive function (planning, organization, problem-solving, complex tasks), visuospatial function (getting lost) and word-finding tasks. There are often early neuropsychiatric symptoms including irritability, depression, anxiety and/or apathy. There is a growing list of risk/protective factors, with potentially modifiable factors including vascular disease, hearing/ vision loss, social isolation, physical inactivity and tobacco/alcohol use. Recent advancements in biomarkers for amyloid and tau have rapidly changed the field, prompting new proposals for biology-based diagnosis of AD using new PET, cerebrospinal fluid and/or plasma biomarkers of
amyloid and tau, which are now available for clinical practice in specialty clinics. There is a wide variability in biomarker assay performance, which providers should consider when ordering biomarkers. Cognitively supportive therapies include acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine) and NMDA receptor antagonists (memantine). Two novel anti-amyloid monoclonal antibody therapies, lecanemab and donanemab, have now been FDA approved as treatments for biomarker-confirmed early-stage AD. These monoclonal antibodies bind to amyloid beta plaques and clear them from the brain. These therapies have been shown to significantly slow decline, but not to reverse symptoms or stop decline. Benefits appear to be greater early in the disease course. Patients require close monitoring for side effects (e.g., amyloid-related imaging abnormalities).
Vascular dementia refers to dementia primarily caused by cerebrovascular disease, and it is the second most common cause of dementia. Vascular dementia can present as a gradual or stepwise decline in cognitive function, and the most common symptoms include difficulty with executive functions, memory retrieval (improves with cue), and irritability. Vascular dementia is estimated to contribute to up to 50% of all dementias and often co-exists with other causes. Management focuses on optimizing cardiovascular health, and acetylcholinesterase inhibitors are often used for cognitive support.
Dementia with Lewy Bodies (DLB) is the third most common form of dementia, caused by the abnormal buildup and spread of Lewy bodies, which are aggregations of alpha-synuclein proteins. The disease is marked by fluctuations in cognition, visual hallucinations, parkinsonism and REM sleep behavior disorder. Cognitive symptoms include a progressive decline in visuospatial, attention and executive function skills. While clinical diagnosis is the mainstay, novel biomarkers are now available to test for alpha-synuclein via skin biopsy and cerebrospinal fluid testing. Acetylcholinesterase inhibitors have been shown to improve cognition in DLB (often more effective than in AD).
Frontotemporal Dementia (FTD) is a heterogenous group of clinical syndromes and underlying brain pathologies that cause progressive degeneration in the frontal and/or temporal lobes of the brain, with associated changes in behavior, personality, language and executive function. FTD is responsible for about 3% of dementia over the age of 65, but over 10% of dementia under the age of 65. The disease is highly heritable, with an autosomal dominant inheritance pattern seen in up to a quarter of all patients with FTD. One clinical syndrome is behavioral variant FTD (bvFTD), manifesting with early and prominent changes in personality including disinhibition, apathy, hyperorality and compulsive behaviors. Primary progressive aphasia is another syndrome characterized by early and prominent loss of language skills. Nonpharmacologic interventions and care support are mainstays of treatment, and there is active ongoing research to identify biomarkers and treatments.
Chronic Traumatic Encephalopathy (CTE) is a rare progressive neurodegenerative disease caused by the accumulation and spread of
tau proteins in the brain. CTE is associated with a history of substantial repeated head impacts, including concussions. It is most commonly associated with athletes in contact sports (like football, boxing and hockey), military veterans, rodeo participants and others exposed to repetitive head trauma. Symptoms include personality changes and impulsivity (“neurobehavioral dysregulation”), executive dysfunction, memory impairment, neuropsychiatric symptoms and/or motor abnormalities. CTE symptoms typically appear years or even decades after repetitive brain trauma and worsen over time. Treatment is primarily supportive care and symptom management, and biomarkers and treatments are also an active area of research.
For the initial workup of a patient who presents with new cognitive or behavioral concerns, the history is the most important component. Providers should ask about when the symptoms first began, symptoms displayed, symptom progression and current functional status. Family members’ accounts of symptom progression are also important, and often there are different perspectives. The bedside exam should include a brief cognitive screening tool (such as MMSE or MOCA). Labs should assess for possible metabolic and infectious disease contributors (complete blood count, comprehensive metabolic panel, B12, thyroid disease, often ruling out HIV, syphilis or other risk factors). Structural brain imaging (MRI brain without contrast) should be obtained to assess for neurodegeneration and other contributing factors. Patients can be counseled on strategies to optimize brain health and reduce modifiable risk factors for cognitive decline, and cognitive supportive therapies offered when appropriate.
The specialist evaluation includes a more detailed history and examination, in-depth neuropsychological testing and review of structural brain imaging. Depending on the clinical diagnosis and evaluation, genetic and biomarker testing for AD (blood, cerebrospinal fluid and/or PET) and/or DLB (skin biopsy, cerebrospinal fluid, dopamine transporter imaging) may be offered. Patients with AD who are potentially eligible for antiamyloid therapies (e.g., MCI/early dementia, MMSE >22, AD biomarker positive, minimal bleeding risk factors) will undergo an eligibility evaluation and discussion regarding therapies. Patients to consider referring to a specialty or sub-specialty clinic include those with challenging or atypical diagnoses (such as DLB, CTE), challenges in management, or those interested in biomarker testing, antiamyloid therapies and/or research opportunities.
Dementia is a life-long illness, deeply affecting both patients and their caregivers. Those who care for a loved one with dementia are susceptible to caregiver burnout, a state of mental exhaustion that presents alongside depressive symptoms. Patients and their families should be made aware of local and national resources that can help them navigate the challenges of this illness and support them through the disease journey.
At the national level, patients and families can be referred to, among others:
• Alzheimer’s Association: https://www.alz.org
• Lewy Body Dementia Association: https://www.lbda.org
• Family Caregiver Support: https://www.caregiver.org
• National Aphasia Association: https://aphasia.org
• The Association for Frontotemporal Degeneration: https://www. theaftd.org/
• Concussion Legacy Foundation: https://concussionfoundation.org/
There are also several local resources for Bexar County residents:
• Multidisciplinary specialty clinical care: Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases at UT Health San Antonio; 210-450-9960; https://biggsinstitute.org/
• Research opportunities (including AD, vascular, DLB, FTD, CTE): Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases, primary site for only NIA-designated Alzheimer’s Disease Research Center in Texas; 210-450-9742 (Research Navigator); https://biggsinstitute.org/research/
• Caring for the Caregiver Program: A UT Health San Antonio program that supports caregivers of those with dementia through education, resources, peer support, and wellness activities, like Memory Cafes, social opportunities and activities for families affected by dementia; 210-567-5831; https://utcaregivers.org/
• Local Support Groups: Several disease-specific support groups for patients and their families can be found in Bexar County; https:// biggsinstitute.org/patient-care/supportgroups
Finally, there are several online resources that can be given to patients and their families:
• Communicating with a loved one with dementia: https://memory. ucsf.edu/caregiving-support/tips#Communication
• Five ways to say sorry (Teepa Snow): https://www.youtube.com/ watch?v=vasnp81x63E
• Responding to new behaviors in dementia: https://www.amazon.com/Coping-Behavior-Change-Dementia-Caregivers/ dp/0692385444
• Book Guide to Caring with Patients with Dementia (The 36-Hour Day): https://www.amazon.com/36-Hour-Day-Alzheimer-Disease-Dementias/dp/1421441713/
References:
1. https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/ trc2.70033
2. https://news.uthscsa.edu/san-antonio-has-a-new-designation-dementia-friendly-city/
3. https://www.ncbi.nlm.nih.gov/books/NBK536956/
4. https://pmc.ncbi.nlm.nih.gov/articles/PMC6153625/
5. https://medicine.washu.edu/news/highly-accurate-blood-test-diagnoses-alzheimers-disease-measures-extent-of-dementia/
6. https://pubmed.ncbi.nlm.nih.gov/23390181/
7. https://pubmed.ncbi.nlm.nih.gov/19535999/
8. https://pubmed.ncbi.nlm.nih.gov/26052687/
9. https://pubmed.ncbi.nlm.nih.gov/33704781/
10. https://pmc.ncbi.nlm.nih.gov/articles/PMC4062551/
Arush Shekar is a fourth-year medical student at the Long School of Medicine at the University of Texas Health Science Center of San Antonio (UTHSCSA). He completed his undergraduate education at Rice University in 2020, where he received a Bachelor of Arts in Neuroscience. He will begin Neurology residency at UTHSCSA in 2025.
By Gregory Michael Tomlinson, OMS-II, and Ramaswamy Sharma, MS, PhD
The United States Cost of Dementia Project, in its inaugural statement, estimated an overall cost of $781 billion this year, with the number of new dementia cases expected to double over the next few decades as those born between 1946 to 1964 (the baby boom generation) cross 80 years of age and above. Dementia is an umbrella term for a range of symptoms that includes loss of memory, problem-solving abilities and language difficulty, among others. Alzheimer’s disease is the most common cause of dementia; Lewy body dementia (LBD), vascular dementia and frontotemporal dementia are other primary causes of dementia. Approximately 20% to 30% of patients with dementia suffer from LBD.
LBD has been further classified as dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD) based on clinical criteria. In DLB, dementia precedes or occurs within a year of disorders of movement. In PDD, a patient diagnosed with Parkinson’s disease (PD) begins to develop dementia symptoms a year or more after the original diagnosis. However, since many clinical features of Parkinson’s disease and DLB are similar, new classification systems are being proposed to appropriately diagnose and identify patients for new clinical trials.
Symptoms vary from patient to patient and with time; these include progressive dementia with or without memory loss, unpredictable fluctuation in cognition, visual hallucinations, delusions and Parkinson-
ism-like symptoms such as bradykinesia, shuffling gait and tremor. Sleep disturbances are associated with LBD; rapid eye movement behavior disorder (RBD), in which people act out their dreams, is more severe in patients with LBD. Depression may also occur. Since symptoms of LBD overlap with other neurological disorders, it is difficult to diagnose. The diagnostic criteria for probable LBD include dementia with progressive cognitive decline (tested using the Mini-Mental Status Exam) along with two additional features such as fluctuating cognition, recurrent visual hallucinations, or spontaneous motor manifestations of Parkinsonism. Other “suggestive” features include RBD, neuroleptic sensitivity, orthostatic hypertension, or imaging showing low dopamine transporter activity in the basal ganglia.
LBD is characterized by the presence of Lewy bodies and Lewy neurites, abnormal cytoplasmic aggregates consisting primarily of misfolded alpha-synuclein and ubiquitin, which disrupt neuronal function and trigger cell death. Alpha-synuclein is expressed primarily in the brain, mostly within neuronal presynaptic axon terminals, wherein it attenuates neurotransmitter release. In LBD, alpha-synuclein forms aggregates of insoluble fibrils that impair the function of microtubules, mitochondria, proteasomes and lysosomes, and interferes with calcium signaling and synapses, resulting in acetylcholine deficiency and, consequently, visual hallucinations.
Delusions may occur as muscarinic M1 receptors are elevated. The location of these aggregates relates the underlying pathophysiology to clinical presentation. Aggregates within neurons of the brainstem and cerebral cortex are responsible for the impairment of cognition, thought and language resulting in early dementia and therefore, DLB; aggregates that only occur within neurons of the brainstem lead initially to a diagnosis of Parkinson’s disease and then PDD as Lewy bodies form in the cerebral cortex and lead to dementia.
The prognosis for LBD patients is poor, with patients typically living for only five to seven years after diagnosis. Delays in diagnosis or misdiagnosis, especially in the absence of visual hallucinations, are major contributing factors and so are a lack of targeted therapies. Current interventions focus on managing the symptoms, such as using cholinesterase inhibitors for cognitive symptoms, carbidopa-levodopa for movement symptoms, antipsychotics such as pimavanserin for hallucinations, melatonin for RBD, and selective serotonin reuptake inhibitors (SSRIs) for sleep disorders.
While therapeutics that reverse disease progression or remove Lewy bodies are not available, a few medications currently in clinical trials show promise. For example, the exploratory phase 2 SHIMMER clinical trial, based on Cognition Therapeutic’s CT1812, which works by antagonizing sigma 2 receptor (S2R) that regulates cellular damage, just reached its end point of safety and reliability. Data from the study also showed a reduction in neuropsychiatric symptoms by 82% and a decrease in cognitive decline by 91%. Another pharmaceutical in clinical trials is CervoMed’s neflamapimod, which inhibits a mitogen-activated protein kinase, p38 alpha, involved in mediating inflammation and consequent loss of basal forebrain cholinergic neurons (BFCN). Neflamapimod has been shown to improve synaptic vesicle function and neurotransmitter release resulting in improved cognitive performance. In March 2025, reports following 16 weeks of the extension phase of the phase 2b RewinD-LB clinical trial indicated that neflamapimod significantly benefited DLB patients in terms of cognitive changes and in decreasing the incidence of falls. Several other therapies for dementia and cognitive impairment are in various stages of clinical trials such as Aptinyx’s NYX-458 and Athira Pharma’s ATH-1017.
LBD remains a complex neurodegenerative condition, but ongoing research offers hope for better treatment options. While there is still a long way to go, each step forward brings us closer to a better quality of life for those living with LBD.
References:
1. Ciccone, I. (2025, March 13). Neflamapimod shows promising phase 2B extension data in dementia with lewy bodies. Neurology Live. https://www.neurologylive.com/view/ neflamapimod-shows-promising-phase-2b-extension-data-dementia-lewy-bodies
2. ClinicalTrials.gov. (n.d.) RewinD-LB - Clinical Study of Neflamapimod in Patients with Dementia with Lewy Bodies. https://clinicaltrials.gov/study/NCT05869669
3. ClinicalTrials.gov. (n.d.). Study to Evaluate the Safety, Tolerability and Efficacy of CT1812 in Subjects with Mild to Moderate Dementia with Lewy Bodies. https://www.clinicaltrials.gov/ study/NCT05225415?term=CT1812&rank=9
4. Cognition Therapeutics, Inc. (2024, December 18). Cognition Therapeutics Announces Positive Results in Phase 2 Study of CT1812 in Dementia with Lewy Bodies. https://ir.cogrx.com/ press_releases/cognition-therapeutics-announces-positive-resultsin-phase-2-study-of-ct1812-in-dementia-with-lewy-bodies/
5. Elder, G.J., Lazar, A.S., Alfonso‐Miller, P., & Taylor, J. (2022). Sleep disturbances in Lewy body dementia: A systematic review. International Journal of Geriatric Psychiatry, 37(10). https://doi. org/10.1002/gps.5814
6. Jiang, Y., Alam, J.J., Gomperts, S.N., Maruff, P., Lemstra, A.W., Germann, U.A., Stavrides, P.H., Darji, S., Malampati, S., Peddy, J., Bleiwas, C., Pawlik, M., Pensalfini, A., Yang, D., Subbanna, S., Basavarajappa, B.S., Smiley, J.F., Gardner, A., Blackburn, K., Chu, H-M., Prins, N.D., Teunissen, C.E., Harrison, J.E., Scheltens, P., Nixon, R.A. (2022). Preclinical and randomized clinical evaluation of the p38α kinase inhibitor neflamapimod for basal forebrain cholinergic degeneration. Nature Communications, 13(1). https://doi.org/10.1038/s41467-022-32944-3
7. Lemstra, A.W., & Van De Berg, W.D.J. (2025). Temporal and biological heterogeneity in Lewy body disease. The Lancet Neurology, 24(5), 378–379. https://doi.org/10.1016/s14744422(25)00113-9
8. National Institute of Neurological Disorders and Stroke. (n.d.). Lewy body dementia. https://www.ninds.nih.gov/health-information/disorders/lewy-body-dementia
9. Lizama, B.N., Kahle, J., Catalano, S.M., Caggiano, A.O., Grundman, M., & Hamby, M.E. (2023). Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases. International Journal of Molecular Sciences, 24(7), 6251. https://doi.org/10.3390/ijms24076251
10. Matar, E., & Halliday, G.M. (2025). Biological effects of pathologies in Lewy body diseases: why timing matters. The Lancet Neurology, 24(5), 441–455. https://doi.org/10.1016/s14744422(25)00085-7
11. Stallard, P.J.E., Ukraintseva, S.V., & Doraiswamy, P.M. (2025). Changing story of the dementia epidemic. JAMA. https://doi. org/10.1001/jama.2025.1897
12. United States Cost of Dementia Research Team. (2025, April 23). The Cost of Dementia in 2025. USC Leonard D.Schaeffer Institute for Public Policy & Government Service. https://schaeffer.usc.edu/research/the-cost-of-dementia-in-2025/
Gregory Michael Tomlinson, OMS-II, is a medical student at the University of the Incarnate Word School of Osteopathic Medicine, Class of 2027. He is passionate about preventative and lifestyle medicine and interested in pursuing psychiatry or neurology.
Ramaswamy Sharma, MS, PhD, is a Professor of Histology and Pathology at the University of the Incarnate Word School of Osteopathic Medicine. He is interested in delineating the multiple molecular and cellular roles of melatonin in maintaining our quality of life. Dr. Sharma is a member of the BCMS Publications Committee.
By Alison Bartak, OMS-II; Crista Thyvelikakath, OMS-1; and Ramaswamy Sharma, MS, PhD
Despite its remarkable resilience in a multitude of situations, the human brain faces unprecedented vulnerability due to chronic stress — a silent and progressive epidemic that elevates cortisol levels, triggers inflammation, which damages neuronal connections over time, erodes neuronal architecture, particularly in the prefrontal cortex and the hippocampus, and negatively impacts cognitive function. Preventative approaches to lower stress, as listed below, can help protect brain health and improve our quality of life.
Neurological resilience against stress stems from three interconnected physical pillars: exercise, sleep and nutrition, each of which works through distinct but complementary biological mechanisms to protect the brain. Physical exercise, such as 30-45 minutes of moderate activity, three to five times per week, promotes neuroplasticity by increasing BDNF (Brain-Derived Neurotrophic Factor), a trophic factor directly associated with cognitive improvement. Different types of exercises offer their own unique advantages. Aerobic exercise boosts cardiovascular health and BDNF levels, while coordination exercises strengthen neural pathways governing balance and spatial awareness. Ensuring a good night’s sleep, perhaps by having a consistent sleep schedule, and practicing sleep hygiene to reduce cortisol levels, also significantly improves cognitive resilience. During deep sleep, the efficiency of clearance of accumulated waste products in the brain via the glymphatic system increases by approximately 60% as compared to the awake state, and memory, including perceptual memory related to emotions, is consolidated. Adequate nutrition incorporating omega-3 fatty acids, antioxidants and B vitamins, directly affects brain function by activating anti-inflammatory pathways. Additionally, consuming diverse plant foods and fermented products helps in maintaining healthy gut bacteria and optimal function of the gut-brain axis, which, in turn, prevents inflammation and promotes mental health.
A variety of cognitive strategies have been identified to alleviate stress, including meditation practices, attention management and Cognitive Behavioral Therapy (CBT) techniques. Meditation enhances activity in brain regions associated with control of cognition and emotion. Applications (apps) such as Calm and Headspace are used by college students to decrease their stress levels — virtual mindfulness
apps such as these increase accessibility. To experience the benefits of meditation, consistent daily practice is key, even if only meditating for a few minutes, as it may take eight weeks or longer to improve attention and mood. Similarly, the practice of mindfulness is effective for various psychiatric disorders such as depression. The Mindfulness-Based Stress Reduction protocol (MBSR), an 8-week program developed by Dr. Jon Kabat-Zinn in 1979 that combines mindfulness, meditation and yoga practices, is widely used in clinical practice to reduce chronic pain, stress, depression and anxiety. MBSR may also benefit healthcare workers in managing their own stress.
Attention management is important for decreasing the stress involved with day-to-day responsibilities. While multitasking can be appealing, fMRI studies show that it places additional demand on the brain, ultimately decreasing efficiency rather than enhancing productivity. Therefore, avoiding multitasking and other distractions is critical for preventing excess demand on the brain during a work session. While working through a task, such as a study session, taking preset, timed breaks may improve mood and productivity compared to self-determined break patterns. One such method is the Pomodoro technique, which involves taking 5-minute scheduled breaks between every 25-minutes of work, with longer breaks after four such rounds.
Cognitive Behavioral Therapy involves working with psychologists or licensed therapists to identify and change thinking patterns associated with poor mental health such as anxiety, depression, eating disorders, and other cognitive distortions such as self-blame, mind reading and minimization of positive attributes. For example, individuals experiencing high levels of stress and perceived pain due to “catastrophizing” or irrationally blowing the effect of an event out of proportion, are helped by the introduction of balanced, rational thoughts.
The Social Baseline Theory states that people rely on the presence of others to regulate emotion. Social support can function as a strong buffer against stress, promoting longevity and decreasing mortality. The quality of relationships is important, as secure attachments are highly associated with positive emotional regulation, whereas negative relationships raise physiological signs of stress such as blood pressure. Physicians should encourage patients to consider social support as part of their overall health, perhaps by implementing a “connection prescription” in their practice.
A sense of belonging as well as a sense of purpose can protect against severe depression and anxiety. Helping others in the community decreases activity in regions of the brain associated with stress. Volunteering is associated with benefits to mental and physical health, specifically in those with low neuroticism and higher extraversion.
As remote work has become common, the boundary between work and home has become unclear, which can cause stress that may be further aggravated by interpersonal conflict within families. Active listening techniques, such as eye contact, asking questions, and affirming the speaker, can strengthen relationships. Being assertive also improves communication and interpersonal skills, thereby reducing stress in the social environment.
When implementing effective habit formation strategies for tackling long-term brain health, it is important to understand the underlying neuroscience of behavior change. For example, starting with small steps not only increases the probability of long-term success, but also continuously reinforces new neuronal pathways. Environmental cues as well as meaningful rewards also support consistency, while the utilization of tracking methods provides feedback that can strengthen and help with continued commitment. Personalized approaches are especially helpful due to individual differences in stress-related triggers as well as vulnerabilities. Tailoring habit-changing strategies based on personality, preference and lifestyle greatly increases adherence. Furthermore, maintaining flexibility and adjusting approaches during high stress periods as well as developing a personalized “emergency protocol” enhances resilience. Importantly, when stress overwhelms personal coping strategies, utilization of professional support becomes a valuable resource. Evidence-based models such as CBT provide structured approaches to stress regulation that can be easily integrated with self-directed practice.
Ultimately, stress is multifactorial and may require patients to practice techniques relevant to various aspects of their life to see benefits. By introducing small changes to each facet of health, one can synergize protection from stress. With time, these small interventions can improve long-term brain health. As stress quickens age-related cognitive decline, managing stress with consistent practices may greatly improve the quality of life in old age. While stress can never be eliminated, reducing stress should be a priority for enhancing overall life satisfaction.
References:
1. Afonso, R.F., Kraft, I., Aratanha, M.A., Kozasa, E.H. Neural correlates of meditation: a review of structural and functional MRI studies. Front Biosci (Schol Ed). 2020;12(1):92-115. https://doi. org/10.2741/S542
2. Basso, J.C., McHale, A., Ende, V., Oberlin, D.J., Suzuki, W.A. Brief, daily meditation enhances attention, memory, mood, and emotional regulation in non-experienced meditators. Behav Brain Res. 2019;356:208-20. https://doi.org/10.1016/j. bbr.2018.08.023
3. Berding, K., Vlckova, K., Marx, W., Schellekens, H., Stanton, C., Clarke, G., et al. Diet and the Microbiota-Gut-Brain Axis: Sowing the Seeds of Good Mental Health. Adv Nutr. 2021;12(4):1239-85. https://doi.org/10.1093/advances/nmaa181
4. Eilert, D.W., Buchheim, A. Attachment-Related Differences in Emotion Regulation in Adults: A Systematic Review on
Attachment Representations. Brain Sci. 2023;13(6). https://doi. org/10.3390/brainsci13060884
5. Giunchi, M., Pena-Jimenez, M., Petrilli, S. Work-Family Boundaries in the Digital Age: A Study in France on Technological Intrusion, Work-Family Conflict, and Stress. Med Lav. 2023;114(4):e2023039. https://doi.org/10.23749/mdl.v114i4.14510
6. Huberty, J., Green, J., Glissmann, C., Larkey, L., Puzia, M., Lee, C. Efficacy of the Mindfulness Meditation Mobile App “Calm” to Reduce Stress Among College Students: Randomized Controlled Trial. JMIR Mhealth Uhealth. 2019;7(6):e14273. https://doi. org/10.2196/14273
7. King, H.R., Jackson, J.J., Morrow-Howell, N., Oltmanns, T.F. Personality Accounts for the Connection Between Volunteering and Health. J Gerontol B Psychol Sci Soc Sci. 2015;70(5):691-7. https://doi.org/10.1093/geronb/gbu012
8. Lewis, N.A., Hill, P.L. Sense of Purpose Promotes Resilience to Cognitive Deficits Attributable to Depressive Symptoms. Front Psychol. 2021;12:698109. https://doi.org/10.3389/ fpsyg.2021.698109
9. Madore, K.P., Wagner, A.D. Multicosts of Multitasking. Cerebrum. 2019;2019
10. Martino, J., Pegg, J., Frates, E.P. The Connection Prescription: Using the Power of Social Interactions and the Deep Desire for Connectedness to Empower Health and Wellness. Am J Lifestyle Med. 2017;11(6):466-75. https://doi. org/10.1177/1559827615608788
11. Romero Garavito, A., Diaz Martinez, V., Juarez Cortes, E., Negrete Diaz, J.V., Montilla Rodriguez, L.M. Impact of physical exercise on the regulation of brain-derived neurotrophic factor in people with neurodegenerative diseases. Front Neurol. 2024;15:1505879. https://doi.org/10.3389/fneur.2024.1505879
12. Vandekerckhove, M., Wang, Y.L. Emotion, emotion regulation and sleep: An intimate relationship. AIMS Neurosci. 2018;5(1):117. https://doi.org/10.3934/Neuroscience.2018.1.1
13. Xie, L., Kang, H., Xu, Q., Chen, M.J., Liao, Y., Thiyagarajan, M., et al. Sleep drives metabolite clearance from the adult brain. Science. 2013;342(6156):373-7. https://doi.org/10.1126/science.1241224
14. Zhan, L., Lin, L., Wang, X., Sun, X., Huang, Z., Zhang, L. The moderating role of catastrophizing in day-to-day dynamic stress and depressive symptoms. Stress Health. 2024;40(4):e3404. https://doi.org/10.1002/smi.3404
Alison Bartak, OMS-II, is a medical student at the University of the Incarnate Word School of Osteopathic Medicine, Class of 2027. Her current interests include Preventative Medicine and Surgery.
Crista Thyvelikakath, OMS-1, is a medical student at the University of the Incarnate Word School of Osteopathic Medicine, Class of 2028. Her current interests include Behavioral Neurology and exploring public health measures to improve mental health.
Ramaswamy Sharma, MS, PhD, is a Professor of Histology and Pathology at the University of the Incarnate Word School of Osteopathic Medicine. He is interested in delineating the multiple molecular and cellular roles of melatonin in maintaining our quality of life. Dr. Sharma is a member of the BCMS Publications Committee.
By Brandon Goff, DO; Cooper Allenbrand, OMS-IV; and Austin Smith, OMS-IV
As physicians, one of our fears is the acute or gradual decline in our cognitive abilities. When we buy disability insurance, this is one of the issues we are paying for coverage but we hope to never have to use. Whether physicians or not, one of our greatest assets is our brain health, and there are simple ways to ensure it is safeguarded. How many times do we see children and adults engaged in high-risk activities without helmets? Frequently. Reinforcing helmet wear among our family, friends and patients is crucial, whether it is for recreational activities or in industrial settings. In our experience, people are often not aware that even mild brain injuries can lead to an increased risk of cognitive decline and dementia.1 That fact can be an effective starting point in a conversation to capture attention. Protecting our brains is essential for leading a fulfilling life and preventing the long-term effects of traumatic brain injuries (TBIs). As awareness of TBIs grows, understanding the importance of helmet use in preventing these injuries is even more evident.
Traumatic brain injuries can result from a variety of common recreational activities, including cycling, skateboarding, skiing, snowboarding and contact sports as well as in industrial settings. In fact, contact sports such as football, basketball and soccer accounted for 45% of all sport-related TBI and concussion-related emergency room visits for children 17 years and under.18 TBIs can range in severity from mild to moderate to severe. We all understand the potential of significant repercussions in a catastrophic TBI (a continuum leading up to unresponsive wakefulness syndrome or death) but the repercussions of a mild or moderate TBI can be life-altering as well, impacting cognitive function, emotional well-being and overall quality of life. Research shows that the brain’s functioning before an injury influences recovery, so taking good care of our brains before an accident is also important. Even mild TBIs can lead to many unfortunate sequelae, including dementia, psychiatric disorders and sleep disturbance.1,3,4 If patients understand that even the mild end of the continuum can radically change their life, helmets seem much more reasonable.
Neurocognitive decline and dementia are a significant concern following traumatic brain injuries (TBIs). A Swedish study found that individuals with TBI had a markedly increased risk of dementia, even 30 years later, with higher risks associated with multiple TBIs.1 A separate study estimat-
ed TBIs account for as high as 15% of the attributable risk for dementia.20 One acute manifestation of TBI is diffuse axonal injury (DAI), caused by rotational trauma, which can lead to the accumulation of pathological proteins like tau and amyloid, commonly seen in Alzheimer’s disease and chronic traumatic encephalopathy (CTE).2 Additional studies support that TBI victims are also at greater risk for neurodegenerative disorders such as Alzheimer’s, amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Parkinson’s disease.3,5,19 Wear that helmet!
Neuropsychiatric symptoms such as depression, anxiety and apathy are more likely to arise within 12 months post-TBI, with sleep disturbances in the acute phase predicting these issues.4 A meta-analysis indicated that individuals with TBI double their risk for psychiatric disorders, and another study with a large cohort found that 75.2% of participants received a psychiatric diagnosis.5,6 Although anxiety rates decreased over time, mood disorders and substance use remained stable, influenced by pre-injury diagnoses and accompanying limb injuries.
Sleep is the time when our brain performs its clean-up duties. When the brain is injured, its self-regulatory processes are diminished. Research by Werner et al. on 138 warfighters with chronic mild TBI showed that poorer sleep quality correlated with higher plasma neurofilament levels, a TBI biomarker and impaired executive function.7 This highlights the long-term impact of TBIs on sleep and mental health. Wear that helmet!
Helmets are crucial for reducing the risk of TBI during high-risk activities. They absorb impact and protect the skull, significantly lowering the chance of injuries like subdural hematomas and skull fractures, especially for cyclists.8-10 The evolution and acceptance of bicycle helmets is an interesting story. From pith helmets in the 1880s to the helmets of today, helmet wear has become ubiquitous in cycling. The same goes for skiing. In the 2000s, it was unusual to see helmets on the ski mountains. Now the un-helmeted skier stands out to the observer and, at many ski mountains, helmets are now mandatory. When advising on proper helmet selection, the Consumer Product Safety Commission (CPSC) has an easy-to-understand e-brochure that is helpful and user-friendly.11
Promoting helmet use among patients, family and friends is essential. Encourage others to wear helmets, support initiatives that empha -
size helmet safety, and continue the process of creating a culture where wearing helmets is the norm. Education on helmet safety can shift perceptions and behaviors toward prevention. Some of us remember when cyclists and skiers wearing helmets were scorned. Wear that helmet!
Conclusion
Taking proactive steps to prevent TBIs through helmet use is crucial to prioritizing brain health. As physicians, we can also promote long-term cognitive resilience by encouraging healthy lifestyle choices like good nutrition, regular exercise, proper sleep, cognitive stimulation and effective stress management.12-17 By embracing these strategies, you are protecting your mind and enhancing its strength and functionality. Safeguard your brain and wear that helmet!
References:
1. Nordström, A., Nordström, P. Traumatic Brain Injury and the Risk of Dementia Diagnosis: A Nationwide Cohort Study. PLoS Medicine. 2018;15(1):e1002496. doi:10.1371/journal. pmed.1002496
2. Graham, N.S., Sharp, D.J. Understanding Neurodegeneration After Traumatic Brain Injury: From Mechanisms to Clinical Trials in Dementia. Journal of Neurology, Neurosurgery, and Psychiatry. 2019;90(11):1221-1233. doi:10.1136/jnnp-2017-317557
3. Brett, B.L., Gardner, R.C., Godbout, J., Dams-O’Connor, K., Keene, C.D. Traumatic Brain Injury and Risk of Neurodegenerative Disorder. Biological Psychiatry. 2022;91(5):498-507. doi:10.1016/j.biopsych.2021.05.025
4. Rao, V., McCann, U., Han, D., Bergey, A., Smith, M.T. Does Acute TBI-related Sleep Disturbance Predict Subsequent Neuropsychiatric Disturbances? Brain Injury. 2014;28(1):20-6. doi:10. 3109/02699052.2013.847210
5. Perry, D.C., Sturm, V.E., Peterson, M.J., et al. Association of Traumatic Brain Injury With Subsequent Neurological and Psychiatric Disease: A Meta-Analysis. Journal of Neurosurgery. 2016;124(2):511-26. doi:10.3171/2015.2.JNS14503
6. Always, Y., Gould, K.R., Johnston, L., McKenzie, D., Ponsford, J. A Prospective Examination of Axis I Psychiatric Disorders in the First 5 Years Following Moderate to Severe Traumatic Brain Injury. Psychological Medicine. 2016;46(6):1331-41. doi:10.1017/ S0033291715002986
7. Werner, J.K., Shahim, P., Pucci, J.U., et al. Poor Sleep Correlates With Biomarkers of Neurodegeneration in Mild Traumatic Brain Injury Patients: A CENC Study. Sleep. 2021;44(6):zsaa272. doi:10.1093/sleep/zsaa272
8. Forbes, A.E., Schutzer-Weissmann, J., Menassa, D.A., Wilson, M.H. Head Injury Patterns in Helmeted and Non-Helmeted Cyclists Admitted to a London Major Trauma Centre With Serious Head Injury. PloS One. 2017;12(9):e0185367. doi:10.1371/ journal.pone.0185367
9. Sethi, M., Heidenberg, J., Wall, S.P., et al. Bicycle Helmets Are Highly Protective Against Traumatic Brain Injury Within a Dense Urban Setting. Injury. 2015;46(12):2483-90. doi:10.1016/j.injury.2015.07.030
10. Lee, L.K., Flaherty, M.R., Blanchard, A.M., Agarwal, M. Helmet Use in Preventing Head Injuries in Bicycling, Snow Sports, and Other Recreational Activities and Sports. Pediatrics. 2022;150(3):e2022058877. doi:10.1542/peds.2022-058877
11. U.S. Consumer Product Safety Commission. Which helmet for which activity? Bethesda (MD): CPSC; 2022 May 13 [cited 2025 May 7]. Available from: https://www.cpsc.gov/safety-ed-
ucation/safety-guides/sports-fitness-and-recreation-bicycles/ which-helmet-which-activity
12. Siervo, M., Shannon, O.M., Llewellyn, D.J., Stephan, B.C., Fontana, L. Mediterranean Diet and Cognitive Function: From Methodology to Mechanisms of Action. Free Radical Biology & Medicine. 2021;176:105-117. doi:10.1016/j.freeradbiomed.2021.09.018
13. Ahlskog, J.E., Geda, Y.E., Graff-Radford, N.R., Petersen, R.C. Physical Exercise as a Preventive or Disease-Modifying Treatment of Dementia and Brain Aging. Mayo Clinic Proceedings. 2011;86(9):876-84. doi:10.4065/mcp.2011.0252
14. Beyer, J.L., Dix, E., Husain-Krautter, S., Kyomen, H.H. Enhancing Brain Health and Well-Being in Older Adults: Innovations in Lifestyle Interventions. Current Psychiatry Reports. 2024;26(8):405-412. doi:10.1007/s11920-024-01513-4
15. Kimura, N., Sasaki, Y., Masuda, T., et al. Lifestyle Factors That Affect Cognitive Function—a Longitudinal Objective Analysis. Frontiers in Public Health. 2023;11:1215419. doi:10.3389/ fpubh.2023.1215419
16. García-García, I., Donica, O., Cohen, A.A., et al. Maintaining Brain Health Across the Lifespan. Neuroscience and Biobehavioral Reviews. 2023;153:105365. doi:10.1016/j.neubiorev.2023.105365
17. Lazar, R.M., Howard, V.J., Kernan, W.N., et al. A Primary Care Agenda for Brain Health: A Scientific Statement From the American Heart Association. Stroke. 2021;52(6):e295-e308. doi:10.1161/STR.0000000000000367
18. Waltzman, D.W., Thomas, K.E., Sarmiento, K. Trends in Emergency Department Visits for Contact Sports-Related Traumatic Brain Injuries Among Children — United States, 2001–2018. Morbidity and Mortality Weekly Report. 2020
19. Barker, S., Paul, B.D., Pieper, A.A. Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury. Biomedicines. 2023;11(4):1154. Published 2023 Apr 11. doi:10.3390/biomedicines11041154
20. Shively, S., Scher, A.I., Perl, D.P., Diaz-Arrastia, R. Dementia Resulting from Traumatic Brain Injury: What Is the Pathology? Arch. Neurol. 2012;69:1245–1251. doi: 10.1001/archneurol.2011.3747
Brandon Goff, DO, FAAPMR, is an Adjunct Associate Clinical Professor at the University of the Incarnate Word School of Osteopathic Medicine and Associate Professor at F. Edward Hebert School of Medicine Uniformed Services University of Health Sciences. He completed residency at Walter Reed Army Medical Center and fellowship at Johns Hopkins. He served as his specialty Consultant to the Army Surgeon General, as Program Director for the local military Multidisciplinary Pain Medicine fellowship, as the Director of the Center for the Intrepid, and as Chief of the Department of Rehabilitation before retiring from the Army. He has worked as a civilian PM&R physician and pain specialist in various capacities in San Antonio. Dr. Goff volunteers at the Corazon Medical Clinic and is a member of the Bexar County Medical Society.
Cooper Allenbrand, OMS-IV, is a medical student at the University of the Incarnate Word School of Osteopathic Medicine.
Austin Smith, OMS-IV, is a medical student at the University of the Incarnate Word School of Osteopathic Medicine.
By Claire Kowalick, UT Health San Antonio
For Jeremy Tanner, MD, behavioral neurologist and assistant professor of neurology at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) and Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, and Shayanne Martin, MPH, senior project manager at the Charles E. Cheever, Jr. Center for Medical Humanities and Ethics at UT Health San Antonio, what began as a personal journey transformed into a global mission of advocacy to understand and research an ultra-rare neurogenetic disease. When their daughter, Cora, was diagnosed with a rare neurogenetic disease, it shifted their career paths and priorities in unexpected ways. They realized the path toward real progress involved a coordinated effort to understand and find treatments for these conditions that, until recently, have remained largely unexplored.
Jeremy and Shayanne’s journey together began at Johns Hopkins University, where both were studying public health. Jeremy, a Houston native, had been drawn to medicine after witnessing the devastating effects of Alzheimer’s disease on his grandmother. His career trajectory led him to specialize in neurology, with a focus on Alzheimer’s and dementia, recognizing early on the growing impact of these diseases. Shayanne spent her early career working in global health, particularly in infectious diseases. Her work involved securing grants and collaborating with governments and universities to improve healthcare delivery in low- and middle-socioeconomic status countries. When the couple moved to Texas, Shayanne’s focus shifted to community-based public health, where she leads initiatives such as training community health workers.
In 2022, the couple was living in San Francisco where Jeremy was finishing his neurology residency and behavioral neurology fellowship. The couple planned to move to Africa for a year for a global neurology fellowship before accepting a faculty position in the United States.
Those plans changed dramatically when the couple learned they were expecting their first child. Initially, the only concern was a clubfoot seen on ultrasound — which the physician said was treatable. Recommended prenatal genetic testing came back normal. After Cora’s birth in March 2022, however, additional features prompted the couple to push for whole exome sequencing, a cutting-edge genetic test that can evaluate a range of genes at the same time and see all protein-coding portions of those genes. Whole genome sequencing has only become widely available in the past five to 10 years and was often only used if a genetic condition was suspected.
At six weeks old, Cora was diagnosed with an ultra-rare and severe neurodevelopmental disease called CLIFAHDD — Congenital
Contracture of the Limbs and Face, Hypotonia and Developmental Delay. At the time, with fewer than 30 documented cases worldwide, there was little information available. Many children with this condition did not survive early childhood, and those who did required lifelong care. “As first-time parents, we were devastated. We didn’t know what to expect going forward, or what to expect at all,” Jeremy said.
Faced with uncertainty, Jeremy and Shayanne immersed themselves in research, reaching out to scientists and medical experts around the world. They discovered that CLIFAHDD is a result of a random genetic mutation affecting the sodium leakage channel protein (NALCN), which plays a crucial role in neural function. While NALCN research was advancing in Europe, there was no active work being conducted in the United States. “Where Alzheimer’s disease was 20 years ago is where the neurogenetic disease space is now. But this also means there is a huge opportunity for growth and development,” Jeremy said.
The family moved to San Antonio, where UT Health San Antonio staff and faculty supported them both professionally and personally. Jeremy said prior to moving, they were able to meet with physicians at the UT Health San Antonio complex care clinic, including Cora’s current specialist Glen Mendellin, MD, to review her care. They also met with neurogenetics care staff at the Texas Children’s Hospital. Jeremy said along with his regular duties, Sudha Seshadri, MD, director of the Biggs Institute, encourages his research into NALCN-related conditions. Shayanne said the Cheever Center for Medical Humanities and Ethics provides flexibility in her schedule to take Cora to medical appointments. “It was a great fit for our family; they really went above and beyond anywhere else,” Jeremy said.
Jeremy and Shayanne realized that the best way to advocate for more research and treatment development for CLIFAHDD and other ultra-rare conditions would be to create a focused nonprofit organization. “The only way to develop a treatment is to have a strong patient advocacy organization and nonprofit bring together the resources, raise funds, bring communities together and bring the scientists together,” Jeremy said.
In 2023, they co-founded the Channeling Hope Foundation along with other parents of children with ultra-rare diseases. The organization’s mission is to unite families, scientists and clinicians to advance research and treatments for CLIFAHDD and other NALCN-related conditions. With no prior experience in nonprofit management, the couple quickly learned how to navigate the new challenges of fundraising and a new direction for their prior experiences in advocacy, scientific collaboration and capacity building.
At the first international NALCN conference in Spain, the couple connected with researchers who had already developed disease models. These collaborations created the groundwork for potential treatments, including drug repurposing to identify existing Food and Drug Administration-approved medications that may help patients with CLIFAHDD.
The Channeling Hope Foundation has rapidly expanded its network, engaging families and scientists worldwide. With support from the Chan Zuckerberg Initiative Rare As One Network, the foundation recently secured $800,000 in funding over the next five years. While this funding is not for research, it provides critical support for organizational growth and capacity building.
On the research front, Jeremy is working with UT Health San Antonio scientists at the Center for Innovative Drug Discovery and international collaborators to develop the first high-throughput screening and drug discovery program for NALCN-related conditions. He is also working with Baylor College of Medicine scientists to develop the first induced pluripotent stem cell line as an open resource for the scientific community to study these conditions and to begin to develop genetic therapies.
The next major milestone will be the second international NALCN conference, set to take place in October 2025 in San Antonio. This gathering will bring together families, researchers and clinicians to share the latest findings and launch a natural history study — an essential step for future clinical trials. “In order to test a treatment, you have to see the natural course of the disease and how treatment changes that course,” Jeremy said.
Despite the demands of leading a nonprofit while raising a child with special needs, Jeremy and Shayanne remain deeply committed to their professions. Shayanne balances her role as executive director of the Channeling Hope Foundation with her professional responsibilities while also pursuing a doctorate in public health. She credits the support of her colleagues at the Charles E. Cheever, Jr. Center for Medical Humanities and Ethics for enabling her to continue her work. “For me, it’s the support system,” she said. “Being given that flexibility and freedom to pursue this work has enabled me to stay in the workforce.”
As advancements in genetic testing and treatments develop, the landscape for rare disease research is evolving rapidly. More widespread availability of whole exome sequencing has made it possible for rare genetic conditions to be discovered sooner and correctly diagnosed. “This space is growing fast,” Jeremy said. “More diseases are being diagnosed, and with better genetic testing, we’re identifying conditions that were previously misclassified. The capabilities of UT Health San Antonio provide a great opportunity for us to become leaders in the space of ultra-rare diseases.”
The couple welcomed their second child in January. At the UT Health San Antonio obstetrics and gynecology center, the genetic counseling team conducted whole exome sequencing prenatally and confirmed that the child did not carry the CLIFAHDD mutation. “Here, the genetic counselor listened to us. She said, ‘I’ll advocate for you.’ At the lab she explained that there was a reason [for the sequencing test]. This is a new space in science and medicine. The sooner you know, the sooner you can prepare and consider treatment options,” Shayanne said. With unwavering determination, Jeremy and Shayanne are proof that when families and scientists work together, there is hope for even the rarest diseases. Their journey shows what is possible when science, collaboration and determination come together.
Learn more about the Channeling Hope Foundation at https://www.channelinghope.org/
Claire Kowalick is a science writer and senior public relations specialist with The University of Texas Health Science Center at San Antonio. She is a graduate of the University of North Texas. As a science writer, she combines her passion for writing with a deep appreciation of biomedical science to tell people about the groundbreaking research and novel discoveries happening at South Texas’ largest academic research institution.
By Russel J. Reiter, PhD
Melatonin was isolated from the bovine pineal gland sevenand-a-half decades ago by the dermatologist, Aaron Lerner and colleagues, hoping it would be useful to treat abnormal skin pigmentations. This assumption was based on a study published 50 years earlier, which reported that the consumption of minced animal pineal tissue profoundly changed pigment distribution in the skin of tadpoles. The observations reported for amphibian skin, however, proved not to directly apply to the pigment distribution in the human epidermis.
Shortly after the seminal discovery by Lerner, a physiologist, Wilbur Quay, observed that the synthesis of melatonin in the pineal gland of mammals exhibited a circadian rhythm, which was driven by the light:dark cycle to which the animals were exposed with high levels of this molecule being produced and released at night and virtually none during the day. This observation set the stage to what is usually known about melatonin by most individuals today.
In humans, the blood melatonin rhythm, which is initiated in the newborn at 4 to 6 months of age and is like that in all other mammals such that during the day circulatory levels are barely measurable, while at night they increase 10 to 20-fold. Noteworthy is that the cerebrospinal fluid exhibits a melatonin cycle like that in the blood except the nighttime increase is an order of magnitude greater than the levels in the circulation; the cycle of melatonin in the cerebrospinal fluid may be the one that drives the circadian rhythms of the body by interacting with neurons situated in the master circadian clock, the suprachiasmatic nucleus, located in the hypothalamus just above the optic chiasm.1 This action depends on specific melatonin receptors on the neurons of this nuclear group. Exposure to sufficiently bright and appropriate wavelength light at night interrupts pineal melatonin synthesis and accordingly disrupts circadian rhythms such as occurs during jet lag and in night shift workers. Likewise, in advanced age the melatonin rhythms wane, a change that contributes to the circadian destabilization that occurs in the elderly. Well-controlled circadian rhythms are an important factor in maintaining optimal health.
Since melatonin is a circadian regulator and given its levels are elevated during darkness, it was initially presumed to be associated with sleep.2 This idea is strongly ingrained in the mind of the public with dozens of supplemental melatonin products being sold for sleep promotion. Melatonin, however, is not a direct soporific and its efficacy as a sleep aid is variable with its effectiveness in terms of sleep dependent on it being given during a restricted time interval during the 24-hour period, an interval that is sometimes difficult to identify and seems to vary among individuals. The lack of its direct association with sleep is also obvious in nocturnal species that sleep during the day and are active during darkness when their melatonin levels are at their peak.
Within the last two decades it has become apparent that melatonin production is not unique to the pineal gland as originally thought. In fact, it is now estimated that of the total amount of melatonin synthesized in the human, that of pineal origin is miniscule (<5%). The
alternate source of melatonin is the mitochondria of perhaps every cell.
Phylogenetically, melatonin is an extremely ancient molecule having evolved in prokaryotic organisms such as bacteria 3-2.5 billion years ago. 3 Subsequently, with the advent of single cell eukaryotes, which came into being about 2 billion years ago, they fed on the prokaryotes by engulfing/phagocytizing them for their nutrient value. Over additional eons, the engulfed bacteria established a permanent residence and evolved into mitochondria, and they carried with them the ability to produce melatonin. The transformation of engulfed bacteria into mitochondria in eukaryotes is known as the widely accepted endosymbiotic theory. Even today, mitochondria in every human cell have many molecular characteristics of bacteria, attesting to their origin from these prokaryotes.
The early melatonin synthesizing single cell eukaryotes eventually became multicellular with the earliest vertebrates only appearing about 525 million years ago during the Cambrian Explosion. Vertebrates are the only species that have a pineal gland, so melatonin was present for an estimated 2 billion years before vertebrates and the pineal gland existed.
Additional data supporting the synthesis of melatonin in human mitochondria comes from experiments that examined the melatonin synthetic activity of recently ovulated oocytes from two mammalian species. When provided the necessary precursor, serotonin, melatonin production was quickly activated. This is relevant given that during embryo development, oocyte mitochondria are the exclusive antecedents of all mitochondria of every cell in the body.
The current evidence is that melatonin evolved as an especially-potent antioxidant, a function that has been documented in thousands of scientific publications during the last two decades.4 The function of an antioxidant is to neutralize unstable toxic derivatives of oxygen referred to as free radicals or reactive oxygen species; the damage these brigands inflict on lipid, proteins, DNA, etc., is referred to as oxidative stress. Excessive oxidative stress is a feature on most chronic diseases and unequivocally contributes to age-associated organ deterioration, for example, neurodegenerative diseases, visual deterioration, cardiovascular dysfunction, bone loss, hepatorenal failure, auditory loss and others.5-8
There is a plethora of antioxidants available to cells, some of which humans ingest in the diet (vitamins A, C, E, flavonoids and polyphenols) and some of which cells produce (glutathione, melatonin, lipoic acid, coenzyme Q10, antioxidative enzymes). Melatonin is both endogenously produced and exogenously acquired in the diet since all plants also produce melatonin. Since free radicals damage any molecule in the vicinity of where they are generated within an infinitesimally short period of time, a scavenging molecule must be within the immediate neighborhood of where the free radical originated.
In addition to being an uncommonly multifunctional radical scavenger, melatonin acts synergistically with other antioxidants and stimulates antioxidant enzymes. Like real estate, an essential feature of a potent and reliable antioxidant also is its location because the damage a radical inflicts is essentially instantaneous. During oxidative phosphorylation
(OXPHOS), which results in energy (ATP) production, free radicals are often produced in abundance especially in the mitochondria of diseased cells with melatonin being at the ready to neutralize them.
Since OXPHOS is unique to the inner mitochondrial membrane, this organellar fragment is a major source of destructive free radicals. Thus, the high levels of melatonin in the mitochondrial matrix puts this antioxidant in a strategic position to scavenge the radicals before they mutilate a neighboring molecule. Despite the high efficacy of melatonin and other antioxidants in doing their jobs, some free radicals invariably escape being neutralized and indiscriminately create molecular havoc. Over the course of a lifetime, the accumulated oxidative stress erodes cells and renders them less capable of carrying out their respective functions, thereby contributing to signs of aging.9
Many serious ailments have a free radical component, including cardiovascular diseases, arthritis, cancer, chronic obstructive pulmonary disease, skin deterioration, neurodegenerative diseases, viral and bacterial infections, autoimmune disorders, bone loss, inflammation and others.5-9 Also, ultraviolet and ionizing radiation, toxin ingestion, legal and illegal drug ingestion, nicotine use and air pollutants promote OXPHOS inefficiency and generate massive numbers of free radicals. The ubiquity of actions of melatonin stems from it being a highly efficient radical scavenger which targets mitochondria, the home base for the production of many toxic derivatives of oxygen. The molecular mutilation resulting from oxidative stress is a common denominator for many diseases.
Melatonin’s protection against these conditions has been repeatedly confirmed in experimental animals and some in human clinical trials. The major bottlenecks for the more frequent examination of melatonin in clinical trials are two-fold; melatonin is inexpensive, and the molecule is not patentable. Thus, in the absence of pharmaceutical industry endorsement, funding of clinical trials, especially those of long duration which are important to adequately evaluate the consequences of melatonin use, has been a monumental obstacle for scientists/clinicians in the performance of these much-needed trials. Because of the shortage of funding, most of the clinical trials that have been performed are underpowered, too short a duration, inappropriate melatonin dose, or have provided incomplete endpoints. I have had a front row seat for 60 years in observing the progress of research on this highly beneficial molecule, and to not further test it in appropriate clinical trials almost seems unethical.
The list of diseases where melatonin has been shown to be of experimental and clinical value is extensive. There are hundreds of scientific publications in medical journals supporting its use to combat atherosclerotic plaque formation and the rupture of such plaques in the heart microvascular, with the latter being a frequent cause of heart attack. Also, the consequence of cardiac arrest relative to tissue damage is attenuated when melatonin is administered.10,11 There are an equal number of reports documenting its ability to lessen the symptoms of and to defer the progression of neurodegenerative disorders, with the bulk of these studies being focused, but not exclusively, on Alzheimer’s and Parkinson’s diseases.5 Due to its anti-viral actions, more than 250 publications have encouraged the use of melatonin to treat viral infections including COVID-19, as well as symptoms of post-COVID, with a few small inadequate trials in humans that yielded some success.12 Given that bone loss during aging involves osteoclastic-mediated free radical destruction of bone matrix, its use in both experimental and clinical trials have proven melatonin’s utility
in delaying osteopenia/osteoporosis.13 Other pathological disorders where melatonin has shown significant ameliorative effects include protection from ionizing and ultraviolet radiation, colitis, hearing loss and others. A check of PubMed with the appropriate search terms will uncover many other disorders where melatonin has proven beneficial. There may be no subdiscipline of medicine where melatonin does not have some potential applications.
With an excess of 3,000 publications on this subject, perhaps no disease has been more thoroughly tested relative to the favorable effects of melatonin than has been cancer, including from the perspectives of prevention, therapy and quality of life of individuals with this disease. This research has involved multiple cancer types with a notable emphasis on breast cancer.14 Likewise, multiple molecular mechanisms have been examined in relation to the ability of melatonin to counteract cancer initiation, proliferation and metastasis with the presumption that its oncostatic actions are multifactorial. A well-documented Hallmark of Cancer is excessive free radical generation in mitochondria. Due to its highly efficient protection against free radicals, this may be one of many mechanisms by which melatonin modulates tumor metabolism and growth.
Chemotherapeutic agents are major elements of the anti-cancer arsenal. A limitation to their use is their collateral toxicity, especially when it involves critical organs such as the heart. Melatonin has been examined in animals relative to its ability to reduce cardiotoxicity of chemotherapies such as doxorubicin and the side effects of 5-fluorouracil on neurobehavioral performance with significance success. Warburg metabolism, which many tumors and other pathological cells use to enhance proliferation and cellular survival, is a factor in the development of cancer cell chemo- and radio-resistance. Current evidence indicates that this metabolic phenotype is reversed with the use of melatonin;15 this being the case, melatonin may also re-establish chemosensitivity. The proposed rationale for utilizing melatonin as a potential treatment of cancer include its intrinsic tumor inhibiting properties, its ability to limit chemotherapeutic toxicity, and due to its apparent reversal of chemoresistance.
High levels of melatonin are not sustained throughout life. By late middle age, the circadian melatonin rhythm begins to attenuate with its deterioration continuing during late life such that in most elderly a melatonin rhythm is barely discernible.9 Mitochondrial production of melatonin also is believed to wane. Thus, mitochondria and cells lose an important safeguard against functional degradation leaving them increasingly vulnerable to dysfunction and disease. The frequency and severity of disorders that melatonin normally opposes are unequivocally exaggerated in late life; thus, its diminished levels may be a contributing factor in determining the degree of infirmity. As an example, a recent retrospective epidemiological study provided evidence for this when it was shown that age-related macular degeneration, a condition with a highly oxidizing environment in retinal mitochondria, was significantly delayed in individuals who had regularly used melatonin in previous years.7 While the loss of melatonin may be consequential to the enhanced rate of physical and mental regression in the elderly due to both its reduced circadian regulatory actions and its disease resistance functions, loss of melatonin is not the only feature that determines the impairment of health span.
A discussion about the loss of melatonin with age and its use to blunt the frequency or the progression of age-associated debilitating
conditions is apropos currently. Humans, for several reasons, are living longer such that the common aging diseases are becoming increasingly manifested. For example, the number of individuals suffering with Alzheimer’s or Parkinson’s diseases are predicted to increase substantially over the next 25 years. Unless treatments are found to hinder the initiation, or the progression of these degenerative conditions, the social and medical welfare systems will become grossly overtaxed.
Comments regarding the safety of melatonin have been a feature of every clinical trial that has been performed. There is general agreement that melatonin is an uncommonly safe molecule with a wide safety profile. Doses between 1 mg and 1 gram have been given to humans for prolonged periods without serious side effects being noted. Complaints associated with melatonin ingestion have been mostly subjective and include sleepiness, dizziness and fatigue, like those of placebo-treated individuals. While not reported in clinical trials, some individuals who initially take melatonin report having vivid dreams. In animals, a LD50 (lethal dose for 50% of the animals) for melatonin has not been defined despite attempts to do so.
Most individuals who use melatonin, especially for sleep, take daily doses in the range of 1-10 mg at night. While these doses may be sufficient for its chronobiologic synchronizing actions, they may not be adequate for other purposes. A recent detailed statistical analysis of currently available data suggested that the optimal anticipated human equivalent doses of melatonin relative to those used in animals are in the range of 1.0 to 1.5 mg per kg body weight daily.12 While melatonin is usually recommended to be taken in the early evening, circumstances may justify its use at other times during a 24-hour period, e.g., to reduce molecular damage from conventional diagnostic radiation exposure. Pathological processes are often highly complex and involve more than oxidatively mutilated critical molecules which thereafter contribute to pathophysiology. While the radial scavenging actions of melatonin are emphasized in the current article, the actions of melatonin are extraordinary and uncommonly diverse as noted. These varied actions are currently under intensive investigation, including in some ongoing clinical trials, to further define melatonin’s worthiness in disease prevention and treatment. The extensive positive accumulated data engenders confidence that the experimental findings from animal and human studies will support the expanded use of melatonin in a variety of clinical disorders as a sole treatment or in combination with other medications. Trials using melatonin as a treatment should have high priority.
References:
The majority of the references cited are to recent review articles, so the reader is given a broad perspective and ready access to the field as a whole.
1. Lian, X., Liu, Z., Gan, Z., Yan, Q., Tong, L., Qiu, L., Liu, Y., Chen, J.F., Li, Z. Targeting the glymphatic system to promote alpha-synuclein clearance: a novel therapeutic strategy for Parkinson’s disease. Neural Regen Res. 2025. doi: 10.4103/NRR. NRR-D-24-00764
2. Bjørklund, G., Oleshchuk, O., Ivankiv, Y., Venger, O., Liuta, O., Mocherniuk, K., Lukanyuk, M., Shanaida, M. Melatonin Interventions in Autism Spectrum Disorder: Sleep Regulation, Behavioral Outcomes, and Challenges Across the Lifespan. Mol Neurobiol. 2025. doi: 10.1007/s12035-025-04809-5
3. Zhao, D., Yu, Y., Shen, Y., Liu, Q., Zhao, Z., Sharma, R., Reiter, R.J. Melatonin Synthesis and Function: Evolutionary History in Animals and Plants. .Front Endocrinol (Lausanne). 2019 7;10:249. doi: 10.3389/fendo.2019.00249
4. Reiter, R.J., Mayo, J.C., Tan, D.X., Sainz, R.M., Alatorre-Jimenez, M., Qin, L. Melatonin as an antioxidant: under promises but over delivers. .J Pineal Res. 2016;61(3):25378. doi: 10.1111/jpi.12360
5. Steinbach, M.J., Denburg, N.L. Melatonin in Alzheimer’s Disease: Literature Review and Therapeutic Trials. .J Alzheimers Dis. 2024;101(s1):S193-S204. doi: 10.3233/JAD-230760
6. Lu, X., Yu, S., Chen, G., Zheng, W., Peng, J., Huang, X., Chen, L. Insight into the roles of melatonin in bone tissue and bone-related diseases (Review). Int J Mol Med. 2021;47(5):82. doi: 10.3892/ijmm.2021.4915
7. Jeong, H., Shaia, J.K., Markle, J.C., Talcott, K.E., Singh, R.P. Melatonin and Risk of Age-Related Macular Degeneration. .JAMA Ophthalmol. 2024;142(7):648-654. doi: 10.1001/jamaophthalmol.2024.1822
8. Alshahrani, S., Sultan, M.H., Rashid, H., Alam, F., Khan, A., Akhter, M.S., Qamri, D., Beigh, S., Riyaz, F. Melatonin Rescues Renal Mitochondria From Multiple Stressors-Induced Oxidative Stress. Basic Clin Pharmacol Toxicol. 2025;136(5):e70031. doi: 10.1111/bcpt.70031
9. García-Domínguez, M. Pathological and Inflammatory Consequences of Aging. Biomolecules, 2025,15:404, doi: 10.3390/ biom15030404’
10. Reiter, R.J., Sharma, R., Romero, A., Simko, F., Dominguez-Rodriguez, A., Cardinali, D.P. Melatonin stabilizes atherosclerotic plaques: an association that should be clinically exploited. Front Med (Lausanne). 2024;11:1487971. doi: 10.3389/ fmed.2024.1487971
11. Gu, P., Wu, Y., Lu, W. New Perspectives on the Role and Therapeutic Potential of Melatonin in Cardiovascular Diseases. .Am J Cardiovasc Drugs. 2024;24(2):171-195. doi: 10.1007/s40256024-00631-x. Epub 2024
12. Qin, J., Wang, G., Han, D. Benefits of melatonin on mortality in severe-to-critical COVID-19 patients: A systematic review and meta-analysis of randomized controlled trials. Clinics (Sao Paulo). 2025;80:100638. doi: 10.1016/j.clinsp.2025.100638
13. Cardinali, D.P. Melatonin as a chronobiotic/cytoprotective agent in bone. Doses involved. J Pineal Res. 2024;76(1):e12931. doi: 10.1111/jpi.12931
14. Zhang, B., Tang, M., Li, X.A. narrative review of sleep and breast cancer: from epidemiology to mechanisms. Cancer Causes Control. 2024. doi: 10.1007/s10552-024-01951-8
15. Reiter, R.J., Sharma, R., Bai, Y., Chuffa, L.G.A., Loh, D., Fan, L. Cardinali DP Function of intramitochondrial melatonin and its association with Warburg metabolism.Cell Signal. 2025 21;131:111754. doi: 10.1016/j.cellsig.2025.111754
Russel J. Reiter, PhD, is Professor of Cell Biology in the Department of Cell Systems and Anatomy at the UT Health San Antonio. In addition to his PhD, Dr. Reiter has received four honorary MD degrees and one honorary DSc degree from international universities. He has received many awards for his research including the A. Ross McIntyre Gold Metal (USA), US Senior Scientist Award (Germany), Lizoni Lincee Award (Italy), Inaugural Aaron B. Lerner Pioneer Award (USA), Chulabhorn Royal Academy Medal (Thailand), etc. He has published numerous research papers, reviews and chapters and he has written or edited 25 books. Based on Google Scholar, his papers have been cited in scientific literature more than 222,000 times and his h-index is 227. Thomson Reuters/Clarivate Analytics has identified Dr. Reiter as a Highly Cited Scientist (top 1%) and listed him as one of the World’s Most Influential Scientific Minds in 2014. He is ranked in the top 200 list of Best Scientists in the World-2024 by Research.com.
By Pendleton Wickersham, MD
Systemic Lupus Erythematosus (SLE) is a complex multisystem autoimmune disease frequently encountered in clinical medicine, both in initial diagnosis and long-term management. Its heterogeneity presents ongoing diagnostic and therapeutic challenges. This update highlights both key areas of progress and important clinical reminders.
While the 2019 EULAR/ACR classification criteria are intended primarily for research, the use of a positive ANA as an entry criterion followed by weighted clinical and immunologic domains does reflect current clinical thinking. The clinician must consider many diverse presentations with myriad symptoms including fatigue, fever, mouth and nasal sores, rash (especially photosensitive), arthritis, serositis, cytopenia, nephritis and neuropsychiatric manifestations. A high index of suspicion is crucial, especially in young women presenting with vague multisystem complaints. Key autoantibodies beyond ANA testing include anti-dsDNA (suggesting nephritis risk), anti-Sm (highly specific), antiphospholipid antibodies (associated with thrombosis and pregnancy morbidity) and anti-Ro/SSA and anti-La/SSB (often associated with photosensitive rash).
Research continues to underscore the central role of the Type I interferon (IFN) pathway in SLE pathogenesis. Overproduction of Type I IFNs drives immune dysregulation, autoantibody production and subsequent tissue damage. This understanding has directly led to targeted therapies.
1. Hydroxychloroquine (HCQ): HCQ remains a foundational therapy, which is crucial for nearly all SLE patients, regardless of severity. It can improve skin and joint manifestations, reduce flare rates, lower organ damage accrual, decrease thrombotic risk, and improve survival. Dose optimization (ideally ≤5 mg/kg actual body weight/day) and regular ophthalmologic screening to exclude retinal toxicity are essential.
2. Standard Immunosuppression: Glucocorticoids are used for flares at the lowest effective dose for the shortest duration possible due to long-term toxicities. The EULAR guidelines recommend 5mg of prednisone daily as the maximum safe dose. New data suggests that corticosteroids increase cardiovascular risk in lupus patients independently of other factors. Mycophenolate mofetil (MMF), methotrexate (MTX), leflunomide (LFN) and azathioprine (AZA) remain key steroid-sparing agents, particularly in visceral disease such as lupus nephritis. Cyclophosphamide is reserved for severe, life-threatening organ involvement.
3. Biologics & Targeted Therapies: Much as has occurred in other rheumatologic diseases, biologics are becoming the standard of care for the treatment of patients with moderate to severe SLE. The landscape of biologic treatment options is expected to expand dramatically over the next five to 10 years. Current treatment options include:
• Belimumab (Anti-BLyS/BAFF): Approved for non-renal SLE and, more recently, for lupus nephritis in combination with standard therapy. Belimumab targets B-cell activation and survival. Potential risks of therapy include serious infection, malignancy, infusion reactions and depression.
• Anifrolumab (Anti-Type I IFN Receptor): A significant advance directly targeting the IFN pathway. Approved for moderate-to-severe SLE (non-renal) in patients inadequately controlled on standard therapy, anifrolumab offers another option for patients with persistent disease activity, particularly those with prominent skin and joint involvement. Potential risks of therapy include serious infection (especially viral) and infusion reactions. Malignancy risk is not completely known but trials suggest minimal risk.
• Voclosporin (Calcineurin Inhibitor): Approved specifically for active lupus nephritis in combination with MMF and lowdose steroids. Voclosporin provides rapid reduction in proteinuria by stabilizing podocytes and inhibiting T-cell activation. Potential risks include elevated blood pressure and decreased renal function as well as serious infections.
A major cause of morbidity and mortality; regular screening with urinalysis (hematuria, pyuria, casts) and urine protein-to-creatinine ratio (UPCR) is vital in all SLE patients. Induction regimens for proliferative LN (Class III/IV) have typically included MMF or cyclophosphamide, often combined with glucocorticoids. Voclosporin (with MMF) and belimumab (with standard therapy) are newer approved induction options that have rapidly eclipsed cyclophosphamide in utilization because of both lower toxicity and better results. Maintenance therapy usually involves MMF or AZA (and now belimumab). Achieving rapid and complete renal response is the goal to preserve long-term kidney function.
Non-rheumatologists are central here.
• Cardiovascular Disease: SLE confers a significantly elevated risk of accelerated atherosclerosis, which is independent of traditional risk factors. Aggressive management of hypertension, dyslipidemia, diabetes and smoking cessation is paramount as are inflammatory disease control and steroid dosing limitation.
• Infections: Increased risk due to both underlying immune dysregulation and immunosuppressive therapies. Ensure appropriate vaccinations (pneumococcal, influenza, COVID-19, HPV, Zoster; avoid live vaccines in significantly immunosuppressed patients).
• Osteoporosis: Screen and manage risk, especially with cumulative glucocorticoid exposure.
• Mental Health: Depression and anxiety are common; screen and facilitate appropriate care. The most common neuropsychiatric manifestation of SLE is mood disorder (generally depression and/ or anxiety). This level of central nervous system involvement is present in more than half of all SLE patients in some studies.
SLE management is increasingly nuanced, moving towards targeted therapies based on pathogenic pathways and more personalized approaches. While HCQ remains central, biologics like belimumab and anifrolumab, along with voclosporin for LN, offer valuable additions. More targeted therapies including biologics are expected to be approved in the next few years. Vigilant screening for organ involvement (especially renal) and aggressive management of comorbidities, particularly cardiovascular risk, are essential components of care.
Pendleton Wickersham, MD, graduated from Rice University in 1996, attended Baylor College of Medicine in Houston and earned his medical degree with honors in 2000. He completed his internship, residency and fellowship at University of Colorado Health Sciences Center in Denver where he worked in a basic sciences lab as part of his research training. Dr. Wickersham moved to San Antonio in early 2006 to join a large rheumatology practice. He is a partner in the San Antonio-based Arthritis Associates, PA, where he has created a Lupus Center of Excellence to care for over 500 active lupus patients. A frequent national and international speaker and consultant, he has invented several medical devices, a molecule for pain, and a nutraceutical for arthritis. He is a principal investigator for clinical trials with Flourish Research. Dr. Wickersham is a member of the Bexar County Medical Society.
By John Suder, MD, and Meilinh Thi, DO
The landscape of cystic fibrosis (CF) continues to evolve and is important to recognize. Cystic fibrosis is an autosomal recessive genetic mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) and was historically known as a pediatric illness. Due to advancements for early diagnosis and treatment, CF is currently considered an adult disease and requires lifelong and adult-specific care. In 1970, only 10% of the CF population survived into adulthood with a median predicted survival of 16 years old.1 According to the 2023 CF Foundation Patient Registry, the median survival for those born between 2019-2023 is 68 years old and currently 60.4% of patients are > 18 years old. The demographic evolution highlights the need for adult-specific specialized CF centers.
Cystic fibrosis mutations have been included in newborn screening in the U.S. since 2004 but was not adopted by every state until 2010, and Texas did not initiate newborn screening for CF until 2009. Despite improved screening methods, patients are still being diagnosed in adulthood. While newborn screening should allow us to detect the disease earlier, there have been concerns raised that the
tests only include the common 23 variants largely favoring the identification of CF in non-Hispanic white infants.2 While CF is typically diagnosed early in life, 831 individuals received this diagnosis after the age of 18 in 2000.1 The delayed diagnoses of CF raises important questions about adult evaluations for CF and what clinical indicators should prompt physicians to consider this diagnosis in older patients.
Many factors contribute to a delayed diagnosis of CF with > 4000 genetic variants in the CFTR gene, which causes variable phenotypic presentations. Depending on the combination of genetic mutations, phenotypic expression can range from severe disease with resulting respiratory failure to mild disease with an asthma-like syndrome. The most common mutation is the F508del variation, which is most prevalent among most individuals, but the frequency is lower in the Black and Hispanic population. The most common genetic test available may only detect common genetic variants, which has a lower mutation detection rate in non-Caucasian patients. Patients that are diag -
nosed as adults typically complain of chronic respiratory problems and frequently have milder lung disease, less frequent Pseudomonas colonization, and increased frequency of pancreatic insufficiency. Unfamiliarity of the full spectrum of phenotypic presentations may delay recognition and ultimately a proper diagnosis.1
Multiple organ systems beyond the lung and gastrointestinal tract are also frequently affected. Patients presenting with symptoms in other organ symptoms can easily go unrecognized. Some examples of atypical presentations include chronic sinusitis, chronic or recurrent pancreatitis, or infertility due to congenital bilateral absence of the vas deferens (CBAVD). While the diagnosis of CF may be more obvious in symptomatic patients with multiple organ system involvement, the diagnosis of CF may not be as clear in patients with isolated organ involvement. Patients with CBAVD can be particularly challenging as many patients do not exhibit other features of CF, but 50 to 60% of them will have at least one CF mutation.1
The standard initial test for CF is sweat chloride testing but results can vary depending on the severity of the mutations. The spectrum of results of sweat testing includes normal (≤ 29 mmol/L), borderline (30 -59 mmol/L) and positive (≥ 60 mmol/L). A borderline sweat test requires genetic analysis for confirmation. There is no gold standard for routine molecular genetic testing and patients should be evaluated at an accredited CF center to receive appropriate and comprehensive testing.3
Despite milder or atypical presentations, several signs and symptoms should prompt physicians to consider a CF diagnosis.1
• Chronic sinopulmonary disease
» Persistent colonization or infections with organisms typical for CF: Including S. aureus, H. influenzae, P. aeruginosa and B. cepacian.
» Chronic cough with sputum production: Persistent respiratory symptoms even if not severe should be considered.
» Chest radiograph abnormalities: Bronchiectasis, infiltrates and hyperinflation.
» Airway obstruction: Symptoms such as wheezing or pulmonary function tests showing air trapping. Lung function in patients may be variable but may present as mild to severe.
» Nasal polyps: By physical examination or on imaging.
» Digital clubbing: A widening and rounding of the fingertips.
• Gastrointestinal and nutritional abnormalities
» Distal intestinal obstruction syndrome: This may manifest as severe recurrent constipation and abdominal pain.
» Pancreatitis: Acute and recurrent episodes may be noted especially in the absence of other causes.
» Malabsorption: Evidence of fat malabsorption or deficiencies in fat-soluble vitamins. Clinically this may manifest as diarrhea, foul-smelling greasy stools, flatus, abdominal pain or unexplained weight loss/poor weight gain.
» Chronic liver disease: Histologically as focal biliary cirrhosis or multilobular cirrhosis.
• Reproductive issues
» Congenital bilateral absence of vas deferens: This leads to obstructive azoospermia and infertility, therefore patients with infertility with absent vas deferens should be evaluated.
• Bone disease
» Osteoporosis/Osteopenia: Common in CF due to multiple factors including malabsorption and chronic inflammation.
Cystic fibrosis care centers specialize in the evaluation and management of CF to include minimizing disease progression, preventing and treating exacerbations, and reducing complications to support those living with CF to live longer, healthier lives. Multidisciplinary clinic teams provide a clinical environment that is difficult to obtain outside of a care center. The teams include many disciplines including nurses, dieticians, respiratory therapists, social workers and pharmacists, palliative care, gastroenterologists, endocrinologists and pulmonologists. This team-based approach is unique and designed to meet the healthcare needs of those living with CF. If a diagnosis of CF is suspected, patients should be referred to an accredited CF center for evaluation.
References:
1. Cystic Fibrosis Adult Care: Consensus Conference Report. Yankaskas, James, et al. 125, 2004, CHEST, pp. 1S-39S
2. Cystic Fibrosis Newborn Screening: A Systematic Review-Driven Consesus Guideline from the United States Cystic Fibrosis Foundation. McGarry, Meghan, et al. 24, 2025, Internation Journal of Neonatal Screening, Vol. 11
3. Diagnosis of Cystic Fibrosis: Consensus Guidelines from the. Farrell, Philip, et al. Elsevier, 2017, Journal of Pediatrics, Vol. 181S, pp. S4-S15
John Suder, MD, was born in North Carolina but has called Texas home for the last seven years. He completed his undergrad at East Carolina University after serving four years in the military as a combat medic; medical school at University of North CarolinaChapel Hill; internal medicine residency at UT Austin Dell Medical School; and pulmonary and critical care fellowship at UT Health San Antonio. He is currently finishing his last year of fellowship and will be staying on with UT Health San Antonio with clinical and research interests in cystic fibrosis and bronchiectasis. Dr. Suder is a member of the Bexar County Medical Society.
Meilinh Thi, DO, was born in Los Angeles but calls Houston home as she has spent most of her life in the great state of Texas. She completed undergrad at Baylor University; medical school at the University of North Texas Health Science Center; internal medicine residency, pulmonary and critical care fellowship, and cystic fibrosis fellowship at the UT Health San Antonio. She currently serves as an assistant professor and director of the adult cystic fibrosis program at the UT Health San Antonio. Her clinical and research interests include cystic fibrosis and bronchiectasis.
By
I would like to talk with you, my physician colleagues, about Child Advocates San Antonio (CASA).
CASA is a San Antonio nonprofit that recruits and leads VOLUNTEERS who advocate for children in Bexar County who are in foster care. CASA is the organization that, through devoted adult volunteers, champions children in the legal system. CASA is the only agency trusted to speak for these children in court.
How did I get involved in CASA and why are physicians ideal professionals to be involved with CASA?
I will definitely answer the first question and do my best to address the second query. I had a long career as an emergency physician in a trauma center and then a second iteration as a Chief Medical Officer in a large healthcare system. After I retired from my CMO position, I became a full-time medical-legal consultant. It was at this point in my career that I began looking for some volunteer organization to fulfill my need to “give back” to the community. I was fortunate enough to have a colleague/friend to be among the many people I spoke with regarding volunteer efforts.
This dear colleague/friend, Kathryn Goertz, had recently completed a long-time commitment to CASA. When I reached out to Kathryn, she immediately sang the praises of CASA and what they did for children in our community. My biggest challenge was getting Kathryn to stop advocating for CASA, as she articulately laid out for me what great things CASA does for children experiencing foster care here in Bexar County. I decided CASA sounded good for me. I also realized that the only way to silence Kathryn for the moment was to commit to joining up with CASA. I joined the Board of Directors of CASA a few years ago and currently serve as its Secretary. As the saying goes, I have truly gotten more from CASA than I have put into it.
Having put forth my personal story about CASA, I will attempt to sell you on why physicians are ideal professionals to become involved, in some way, with CASA. I know first-hand how busy we are as physicians. I know how precious your time is, in particular when you are not directly involved in patient care. I also know that you, as an experienced medical professional, can make a real difference in a child’s future, outside of a physician-patient relationship.
Traits of physician practice ideally lend themselves to physicians being uniquely qualified candidates to work with CASA. Many of the children CASA serves have significant medical problems that have not been adequately addressed. As a CASA volunteer advocate, you would
not in any way have a physician-patient relationship with a child. However, your expertise and knowledge in the medical field will enable you to be a strong advocate in promoting appropriate medical care for the child.
In addition, we as physicians are skilled communicators. This expertise is ideal to enable you to advocate for a child in the legal and community areas. Most importantly, we physicians have a sense of a true “calling.” We know what it is to advocate for patients. This skill would make you an ideal CASA volunteer.
Being a CASA advocate does involve a time commitment. There is an initial training period, and then ongoing involvement once you are assigned a child as a case to manage. I admit this time commitment may be something that is burdensome on top of your extremely busy schedule as a clinician. I also realize this CASA involvement may be a better fit for physicians with set schedules, in certain less time-demanding specialties, or physicians in semi-retirement or full retirement.
These facts do not eliminate any physician who has the desire to become involved with CASA. You just need to make it a priority for you. One obvious way that any physician who feels his/her schedule does not now permit a time allocation to CASA is through a monetary contribution to CASA. Any donation to CASA has the benefits of nonprofit support. We are fortunate as physicians to be in a position to donate to worthy organizations such as CASA.
I will summarize my argument for physician involvement in CASA in the well-known SOAP format utilized by physicians:
S - Many children in the foster care system in Bexar County need an advocate to make their best interest a top priority for their benefit in the system.
O - CASA is an organization that supports the best interest for children in foster care in the community and legal system and ensures their voice is heard.
A - It makes sense that a physician is an ideal candidate, through his/ her knowledge and experience, to volunteer for CASA and financially support CASA.
P - Get involved as a volunteer for CASA; Donate to support CASA.
Thank you, gracias, toda raba, for your support of CASA.
You can get information about CASA, learn how to join the efforts at CASA, and also how to financially support CASA at www.casa-satx.org, 210-225-7070.
With heavy hearts, we share the news that Dr. Phillip William Voltz Jr, MD, 1975 BCMS President, passed away peacefully at home on May 1, 2025, at the age of 95. We are grateful for his dedicated service with the Bexar County Medical Society and for the San Antonio community.
In 1959, Dr. Voltz moved to San Antonio, where he became a founding force in diagnostic radiology and nuclear medicine at Christus Santa Rosa Hospital. He later served as Clinical Associate Professor at the University of Texas Health Science Center at San Antonio, mentoring generations of physicians. Dr. Voltz was one of the founding partners of Radiology Associates, which later transitioned to South Texas Radiology Imaging Center (STRIC), and now has 22 facilities serving the San Antonio area. He served as President of the Texas Radiological Society and was awarded its highest honor, the Gold Medal, in 1997.
In 1975, Dr. Voltz was elected the 77th President of the Bexar County Medical Society, guiding the organization through the Texas malpractice insurance crisis. Throughout his BCMS membership, he served on various committees and boards, including the Executive Board, Delegation to TMA, and Patient Relations Committee. He remains the only physician recognized as both the youngest and, in later years, the oldest serving BCMS president.
Bexar County Medical Society extends its deepest condolences to the Voltz family and friends. Dr. Phillip Voltz leaves behind a lasting impact on his community and is fondly remembered by his fellow physicians.
The Texas Medical Association installed Jayesh “Jay” Shah, MD, as its 160th President during TexMed, the association’s annual conference, held in San Antonio on May 8-10 this year.
“I am deeply honored to serve as the president of TMA,” said Dr. Shah. “This role is both a privilege and a responsibility, and I see it as an opportunity to amplify the voices of physicians across Texas.”
Dr. Shah is an internist, hyperbaric medicine, and wound care specialist in San Antonio, having previously served as the 2016 BCMS President. He is actively involved in the Bexar County Medical Society, the American Medical Association (AMA) and Texas Medical Association, and is making history as the first Indian American to serve as president of the TMA.
Dr. Shah has served on many TMA councils and committees over the years, and on TEXPAC, TMA’s political action committee. He also chaired the TMA Educational Scholarship and Loan Committee, and the International Medical Graduate Section for both TMA and the AMA. He has served as a delegate to the TMA House of Delegates policymaking body and the AMA House as well.
During his one-year term as president, Dr. Shah seeks to reduce challenges and barriers physicians face so they can focus on caring for patients. Dr. Shah wants to “push for reforms that cut through bureaucratic red tape, fight for physician autonomy, and ensure that the healthcare system supports — not hinders — the doctor-patient relationship.”
Dr. Shah is also a champion of physician well-being. As president, Dr. Shah is launching a podcast called “Let Doctors be Doctors,” where he will visit with fellow physicians about their methods for fighting burnout to provide the best care possible for patients. Addressing this issue is one way he intends to show understanding and value to physicians. He hopes it will help increase TMA’s membership and encourage more medical students, residents and young physicians to get involved in the association.
The Bexar County Medical Society congratulates Dr. Shah on his presidency and looks forward to seeing all he accomplishes in the year to come.
In recognition of his 25 years of exceptional contributions to the medical community, the Texas Medical Association is proud to honor David N. Henkes, MD, with the 2025 TMA Distinguished Service Award.
Dr. Henkes received TMA’s highest honor during the TexMed Opening Session on Friday morning to celebrate his leadership within the Texas Delegation to the American Medical Association (AMA).
When Dr. Henkes joined the Texas Delegation in 2001, he could not have foreseen the profound impact he would have over the next two decades. He was elected as vice chair in 2012 and chair in 2014, a position he held with great distinction until December 31, 2024.
Under his leadership, the Texas Delegation’s influence within the AMA grew significantly. The number of Texas delegates increased and Texans now hold positions in nearly every AMA committee and council. Dr. Henkes’ ability to foster relationships and build coalitions, such as the Big Five — a collaboration between Texas, California, Florida, New York and Pennsylvania — has been instrumental in advocating for key issues like Medicare payment reform.
Dr. Henkes’ leadership style, in which he prioritizes the needs of Texas physicians and the medical community over personal ambition, has earned him widespread admiration and appreciation from his colleagues.
Throughout his tenure, Dr. Henkes championed many key initiatives, including making Medicare payment reform a priority, establishing telemedicine guidelines before COVID19, and advocating for internists facing certification challenges.
Outside of delegation work, Dr. Henkes is a practicing pathologist in Bexar County, where he served as the 2005 BCMS President.
Dr. Henkes’ leadership and dedication will leave a lasting legacy, ensuring that the voice of Texans continue to shape the future of healthcare.
San Antonio and the outstanding leadership of the Bexar County Medical Society (BCMS) were on full display at TexMed 2025, held May 8-10, 2025, in San Antonio at the JW Marriott Resort.
BCMS’ own, Jayesh “Jay” Shah, MD, was installed as the 160th President of the Texas Medical Association (TMA); David N. Henkes, MD, received the TMA Distinguished Service Award for his 25 years of exceptional leadership of the Texas Delegation to the American Medical Association (AMA); Ezequiel “Zeke” Silva, MD, was recognized for his unwavering dedication as the TMA Council on Legislation Chair, testifying multiple times per week to the Texas Legislature on behalf of physicians and patients; current BCMS President John M.
Shepherd, MD, was named the Chair of TEXPAC; and Jenny Shepherd, was celebrated as the outgoing TMA Alliance President.
These are just a few of the BCMS members who were honored, but many more contribute significantly — serving on the BCMS Delegation to the TMA House of Delegates, participating in TMA Councils and Committees, and guiding discussion as part of the reference committees.
A heartfelt THANK YOU to all who dedicate their time and talent to organized medicine. Your service at the local, state and national levels strengthens the profession and improves the health of all Texans.
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“Once a member, always a member. Join today!”
American Health Imaging (HHH Gold Sponsor)
American Health Imaging (AHI) has 5 state-of-the-art imaging centers in San Antonio, TX with industry- boardcertified subspecialized radiologists delivering precise, reliable results. Easy scheduling and prompt report turnaround times, serving both physicians and their patients. Imaging at AHI is priced up to 60% less than hospitals and in-network with 99% of health plans with competitive rates to save patients money. AHI has an additional 37 best-in-class diagnostic imaging facilities in Alabama, Florida, Georgia, Texas and South Carolina. US Radiology Physician Number 210-572-1211
Casey Allen
Regional Sales Director | San Antonio US Radiology Specialists 210-846-0606
Casey.Allen@usradiology.com
Jasmine Mendoza
Jasmine.Mendoza@usradiology.com
Jaime Zamora
Jaime.Zamora@usradiology.com
Sydnie Caradec
Sydnie.Caradec@usradiology.com
Sarah McMindes
Sarah.Mcmindes@usradiology.com
Scott Roberson
Scott.Roberson@usradiology.com
Ryan Denman
Ryan.Denman@usradiology.com
www.americanhealthimaging.com (main site)
www.americanhealthimaging.com/ physician-resources/ (Physician Resources to refer to American Health Imaging)
Bexar Credentials Verification, Inc. (HHHH 10K Platinum Sponsor)
Bexar Credentials Verification Inc. provides primary source verification of credentials data that meets The Joint Commission (TJC) and the National Committee for Quality Assurance (NCQA) standards for healthcare entities.
Betty Fernandez Director of Operations
210-582-6355
Betty.Fernandez@bexarcv.com www.bexarcv.com
“Proudly serving the medical community since 1998”
Avid Wealth Partners (*** Gold Sponsor)
For over 15 years, Avid Wealth Partners has been the trusted financial partner for local physician specialists and practice owners. We specialize in physician-focused financial advising, offering proactive tax planning, customized investment strategies, and comprehensive risk management solutions. Our approach addresses every aspect of your financial life, protecting your hardearned assets and building lasting wealth. With a team of credentialed specialists, we simplify complexity so you can focus on what you do best— caring for patients
MDWealth@avidwp.com www.avidforphysicians.com 210-864-3333
Elizabeth Olney with Edward Jones (HHH Gold Sponsor)
We learn your individual needs so we can develop a strategy to help you achieve your financial goals. Join the nearly 7 million investors who know. Contact me to develop an investment strategy that makes sense for you.
Elizabeth Olney Financial Advisor 210-858-5880
Elizabeth.Olney@edwardjones.com www.edwardjones.com/elizabeth-olney "Making Sense of Investing"
Aspect Wealth Management (HHH Gold Sponsor)
We believe wealth is more than money, which is why we improve and simplify the lives of our clients, granting them greater satisfaction, confidence and freedom to achieve more in life.
Michael Clark President 210-268-1520
MClark@aspectwealth.com www.aspectwealth.com
“Your wealth. . .All aspects”
Hancock Whitney (HH Silver Sponsor)
Since the late 1800s, Hancock Whitney has embodied core values of Honor & Integrity, Strength & Stability, Commitment to Service, Teamwork and Personal Responsibility. Hancock Whitney offices and financial centers in Mississippi, Alabama, Florida, Louisiana and Texas offer comprehensive financial products and services, including traditional and online banking; commercial, treasury management, and small business banking; private banking; trust; healthcare banking; and mortgage services.
John Riquelme San Antonio Market President 210-273-0989
John.Riquelme@hancockwhitney.com
Serina Perez San Antonio Business Banking 210-507-9636
Serina.Perez@hancockwhitney.com
UT Health San Antonio
MD Anderson Cancer Center
(HHH Gold Sponsor)
UT Health provides our region with the most comprehensive care through expert, compassionate
providers treating patients in more than 140 medical specialties at locations throughout San Antonio and the Hill Country.
UT Health San Antonio Physicians
Regina Delgado
Business Development Manager
210-450-3713
DelgadoR4@uthscsa.edu
UT Health San Antonio
MD Anderson Mays Cancer Center
Laura Kouba
Business Development Manager 210-265-7662
NorrisKouba@uthscsa.edu
Appointments: 210-450-1000
UT Health San Antonio 7979 Wurzbach Road San Antonio, TX 78229
Golden Billing & Benefits
(HHH Gold Sponsor)
Golden Billing is owned and operated for over 20 years in Houston, TX. The owner, Marcus Yi, is focused on creating a partnership with clients. We are dedicated to optimizing the small business doctor’s productivity and maximizing practice cash flow by accurate claims coding and timely processing. Call today for a free consultation. If you don’t want to use us at lease maybe we can help you fine tune your decision.
Marcus Yi 713-263-0054
MYi@goldenbilling.com www.goldenbilling.com
Genuine Health Group (HHH Gold Sponsor)
Genuine Health Group partners with primary care providers to help them successfully adopt value-based payment models and demonstrate better health outcomes. Providers choose us for our proven expertise and consistency both for their patients enrolled in Medicare Advantage plans and for their patients with traditional Medicare who can align with one of ACOs. We have a track record of effectively reducing the cost of care while simultaneously improving care quality.
786-878-5500
info@genuinehealthgroup.com www.genuinehealthgroup.com
Health (HH Silver Sponsor)
Equality Health deploys a wholeperson care model that helps independent practices adopt and deliver value-based care for diverse communities. Our model offers technology, care coordination and hands-on support to optimize practice performance for Medicaid patients in Texas.
Cristian Leos
Network Development Manager 210-608-4205 CLeos@equalityhealth.com www.equalityhealth.com “Reimagining the New Frontier of Value-Based Care.”
DialOPS (H Bronze Sponsor)
Dialops is a trusted U.S.-based medical answering service and virtual receptionist solution designed specifically for healthcare practices. We provide 24/7 live call handling, HIPAA-compliant messaging, appointment scheduling, and reliable after-hours and overflow support. Our medically trained agents answer every call with professionalism and care—just like your in-office staff— ensuring your patients always feel heard and supported. From solo providers to busy clinics, Dialops helps reduce missed calls, ease front desk overload, and improve the patient experience—all at a fraction of the cost of hiring in-house.
Rachel Caero Rachel@dialops.net
Call 877-2-DIALOPS/ 210-699-7198 or visit www.dialops.net to get started today.
TMA Insurance Trust
(HHHH 10K Platinum Sponsor)
TMA Insurance Trust is a full-service insurance agency offering a full line of products – some with exclusive member discounts and staffed by professional advisors with years of experience. Call today for a complimentary insurance review. It will be our privilege to serve you.
Wendell England Director of Member Benefits
512-370-1746
Wendell.England@tmait.org 800-880-8181 www.tmait.org
“We offer BCMS members a free insurance portfolio review.”
Texas Medical Liability Trust (HHHH 10K Platinum Sponsor)
With more than 20,000 healthcare professionals in its care, Texas Medical Liability Trust (TMLT) provides malpractice insurance and related products to physicians. Our purpose is to make a positive impact on the quality of healthcare for patients by educating, protecting and defending physicians.
Patty Spann Director of Sales and Business Development 512-425-5932
Patty-Spann@tmlt.org www.tmlt.org
“Recommended partner of the Bexar County Medical Society”
The Bank of San Antonio Insurance Group, Inc. (HHH Gold Sponsor)
We specialize in insurance and banking products for physician groups and individual physicians. Our local insurance professionals are some of the few agents in the state who specialize in medical malpractice and all lines of insurance for the medical community.
Katy Brooks, CIC 210-807-5593
Katy.Brooks@bosainsurance.com www.thebankofsa.com
“Serving the medical community.”
MedPro Group
(HH Silver Sponsor)
Rated A++ by A.M. Best, MedPro Group has been offering customized insurance, claims and risk solutions to the healthcare community since 1899. Visit MedPro to learn more.
Kirsten Baze, RPLU, ARM
AVP Market Manager, SW Division 512-658-0262
Fax: 844-293-6355
Kirsten.Baze@medpro.com www.medpro.com
LASO Health Telemedicine and Rx App (HH Silver Sponsor)
LASO Health is the industry’s only solution that makes healthcare services accessible, cost-transparent and convenient. Its mission is to reinvent “healthcare” in the United States by empowering every individual and employer, insured or uninsured to have easy, timely, predictable, cost-effective care. LASO combines an intuitive, mobile superapp with a marketplace of virtual and in-person health services to give customers a one-touch, onestop-shop, comprehensive health solution.
Ruby Garza, MBA 210-212-2622
RGarza@texaskidneycare.com www.lasohealth.com
Parvus Medical Suites (HHHH 10K Platinum Sponsor)
Parvus Medical Suites offers a new way to start your own private clinical practice, either full-time or part-time, at a much lower cost than a traditional clinic. We take care of providing well-qualified employees, so that you can focus solely on delivering high-quality patient care. Our turn-key practice spaces in San Antonio and New Braunfels are available for short- and long-term lease options, and come complete with all amenities. Micropractice medicine is revolutionizing independent clinical care.
John Rodriguez, MD Chief Medical Officer 210-632-3411
DrJohn@parvussuites.com www.parvussuites.com
Henry Schein Medical (HH Silver Sponsor)
From alcohol pads and bandages to EKGs and ultrasounds, we are the largest worldwide distributor of medical supplies, equipment, vaccines and pharmaceuticals serving office-based practitioners in 20 countries. Recognized as one of the world’s most ethical companies by Ethisphere.
Tom Rosol Field Sales Consultant
210-413-8079
Tom.Rosol@henryschein.com www.henryschein.com
“BCMS members receive GPO discounts of 15 to 50 percent.”
Eleos Virtual Healthcare Solutions (HH Silver Sponsor)
Empowering physicians for a Balanced Future. Our virtual health associates alleviate administrative burdens in the evolving healthcare landscape, combatting burnout. Join us in transforming healthcare delivery, prioritizing your wellbeing and patient care.
Darby Rodriguez Regional Client Executive 281-753-3565
D.Rodriguez@eleosvhs.com www.equalityhealth.com
“Reimagining the New Frontier of Value-Based Care”
Methodist Physician Practices (**Silver Sponsor)
Methodist Physician Practices is committed to providing exceptional care for patients in greater San Antonio and South Texas. As part of Methodist Healthcare, we are dedicated to raising the standards of performance excellence while advancing the health and well-being of the communities we serve. Our extensive network of highly-skilled primary care physicians, specialists and surgical care providers ensures patients receive comprehensive, coordinated and compassionate care.
As part of the Methodist Healthcare System, our physicians are committed to delivering personalized, high-quality services that meet the
diverse needs of our patients. At Methodist Physician Practices, we go beyond healthcare — providing hope, healing and unwavering support for each individual we serve.
Erin Fitzgerald
Methodist Healthcare I Methodist Physician Practices M:281-673-7350
methodistphysicianpractices.com
Healthcare Leaders of San Antonio (HH Silver Sponsor)
We are dedicated to nurturing business connections and professional relationships, exchanging knowledge to enhance leadership, and creating career opportunities for healthcare and other industry leaders in a supportive community.
David Neathery President 210-797-8412
HealthcareLeadersSA@gmail.com
Gary Meyn, LFACHE Vice President 210-912-0120
GMeyn@vestedbb.com https://healthcareleaderssa.com/ “Come, Learn, Connect!”
The Health Cell (HH Silver Sponsor)
“Our Focus is People” Our mission is to support the people who propel the healthcare and bioscience industry in San Antonio. Industry, academia, military, nonprofit, R&D, healthcare delivery, professional services and more! Kevin Barber President 210-308-7907 (Direct) KBarber@bdo.com
Valerie Rogler Program Coordinator 210-904-5404
Valerie@thehealthcell.org www.thehealthcell.org
“Where San Antonio’s Healthcare Leaders Meet”
San Antonio Medical Group Management Association (SAMGMA)
(HH Silver Sponsor)
SAMGMA is a professional nonprofit association with a mission to provide educational programs and networking opportunities to medical practice managers and support charitable fundraising. Jeannine Ruffner President info4@samgma.org www.samgma.org
Favorite Healthcare Staffing
(HHHH 10K Platinum Sponsor)
Serving the Texas healthcare community since 1981, Favorite Healthcare Staffing is proud to be the exclusive provider of staffing services for the BCMS. In addition to traditional staffing solutions, Favorite offers a comprehensive range of staffing services to help members improve cost control, increase efficiency and protect their revenue cycle.
San Antonio Office 210-301-4362
www.favoritestaffing.com
“Favorite Healthcare Staffing offers preferred pricing for BCMS members.”
By Stephen Schutz, MD
The every-new-vehicle-sold-by-2035-must-be-electric fever has broken, and Porsche, along with most other automotive manufacturers, has gotten the memo. Porsche recently announced that they will be investing $1 billion into internal combustion engines (ICE), and they’re no longer pledging that 80% of the vehicles they sell in 2030 will be all-electric (BEV). Thank you, Porsche. I want lower carbon emissions as much as anybody else, but I don’t think BEVs will be the answer until battery technology improves significantly.
With that in mind, I was curious to drive the new 2025 Porsche Cayenne plug-in hybrid luxury SUV with a 26kWh battery that allows around 30 miles of all-electric driving. It’s great for commuting or running errands in town yet provides an internal combustion engine to augment performance and charge the batteries when they run low.
An aside: Porsche, a sports car maker that only about 25 years ago began producing non-sports cars, is a highly successful company. What most observers probably don’t appreciate is that, despite the presence of some very expensive sports cars in their lineup, it’s the SUVs that make the lion’s share of the company’s profits.
The original Porsche non-sports car, the Cayenne SUV, was introduced in 2002 and was derided by most Porsche aficionados, including me, as a sacrilege. Once it became clear that the Cayenne, and later the Panamera and Macan, would earn the profits that enabled the company to continue to manufacture special sports cars like the 2016 911R, 2018 911 GT2 RS, and 2024 911 S/T, all was forgiven.
The Cayenne was comprehensively updated in 2024, and while the newest Cayenne looks a lot like prior models, the interior is better.
Exterior-wise, the Cayenne looks like a Porsche, or at least it looks like what people familiar with the famous 911 would imagine a Porsche SUV would look like. Roughly the size and shape of a Ford Explorer, the Cayenne uses premium-looking lighting and chiseled exterior design elements to stand out from the crowd, but, honestly, it doesn’t stand out that much.
On the other hand, the new Cayenne’s interior has been upgraded noticeably. For starters, a new 12.6-inch curved digital instrument display sits behind the steering wheel alongside the 12.3-inch central touchscreen that controls the updated PCM 6.0 infotainment system.
Porsche has decided to go all-in with Apple CarPlay and Android Auto, which I think is a better choice than forcing a clunky system created by automotive engineers on customers who are quite happy with their phones and don’t want to learn another user interface.
The Cayenne also offers an optional 10.9-inch touchscreen for the front passenger, which allows the front passenger to enjoy their own streaming entertainment, control several vehicle features, and even “help” with navigation. The display’s polarized filter makes it invisible to the driver for safety reasons.
The gear-selector lever, previously located on the central console, has been replaced by a smaller toggle switch that now sits just to the left of the central touchscreen on the dash. And the center console now houses a new haptically controlled climate-control panel (no more knobs or switches — sigh).
As you’d expect, the 5,348 lbs Cayenne is most comfortable driving into town to run errands or cruising on the interstate, maybe especially the latter. It’s fine on curvy back roads, too, of course, but it’s no 911.
My plug-in 463HP V-6 Cayenne E-Hybrid test car starts at $97,200. The base Cayenne, which comes with a 348HP V6 engine that pulls enthusiastically but sounds just OK, goes for $84,700. Just above the plug-in V6 Cayenne E-Hybrid is the 475 HP V8 Cayenne S that will set you back $103,600, and then there’s the Cayenne GTS, which goes for $124,900. Turbo models are more — the performance-oriented Cayenne Coupe GT costs more than $200k, and costly options are plentiful. Cayennes are expensive.
I find it interesting that in 1998 after the first large luxury SUV, the Lincoln Navigator, was introduced, most automotive journalists, including the venerable David E. Davis of Car and Driver and Automobile magazines, predicted that upscale buyers wouldn’t be interested. Those experts were proven wrong as every luxury brand eventually introduced an SUV, and now we’re seeing SUVs from sports car brands, most notably Aston Martin, Lamborghini and Ferrari. It’s a new world.
The Cayenne is a vehicle that I believe many BCMS members will find appealing. It’s expensive, but it combines luxury with performance in a vehicle that provides a lot more space than a sedan. And if you choose one of the plug-in hybrid varieties, it’s even good for the environment.
As always, call Phil Hornbeak to get your best BCMS price for a Cayenne or any other vehicle you’re interested in.
Stephen Schutz, MD, is a board-certified Gastroenterologist who lived in San Antonio in the 1990s when he was stationed here in the U.S. Air Force. He has been writing auto reviews for San Antonio Medicine magazine since 1995.
11911 IH 10 West San Antonio, TX 78230
Coby Allen 210-696-2232
Northside Honda 9100 San Pedro Ave. San Antonio, TX 78216
Jaime Anteola 210-744-6198
Audi Dominion 21105 West IH 10 San Antonio, TX 78257
Anthony Garcia 210-681-3399
14610 IH 10 West San Antonio, TX 78249
Tim Rivers 832-428-9507
Northside Chevrolet 9400 San Pedro Ave. San Antonio, TX 78216
Domingo Saenz 210-341-3311
Auto Group
North Park Lexus 611 Lockhill Selma San Antonio, TX 78216
Jose Contreras 320-308-8900
Mercedes Benz of Boerne 31445 IH 10 West Boerne, TX 78006
James Godkin 830-981-6000
Cavender Toyota 5730 NW Loop 410 San Antonio, TX 78238
Spencer Herrera 210-581-0474
Mercedes Benz of San Antonio 9600 San Pedro San Antonio, TX 78216
Chris Martinez 210-366-9600
North Park Toyota 10703 SW Loop 410 San Antonio, TX 78211
Justin Boone 210-635-5000
9455 IH 10 West San Antonio, TX 78230
Jordan Trevino 210-764-6945
Bluebonnet Chrysler
Dodge Ram 547 S. Seguin Ave. New Braunfels, TX 78130
Matthew C. Fraser 830-606-3463
Auto Group
North Park Lexus at Dominion 25131 IH 10 W Dominion San Antonio, TX 78257
James Cole 210-816-6000
Northside Ford 12300 San Pedro San Antonio, TX 78216
Marty Martinez 210-477-3472
North Park Lincoln 9207 San Pedro San Antonio, TX 78216
Sandy Small 210-341-8841
North Park Subaru 9807 San Pedro San Antonio, TX 78216
Raymond Rangel 210-308-0200
North Park Subaru at Dominion 21415 IH 10 West San Antonio, TX 78257
Phil Larson 877-356-0476