Agenda October, 2026

• Evidence vs. Practice Gap
• Regulatory Risk Overview
• Case Based Learning Emphasis

Advanced Peptide Pharmacology
Luis Martínez, M.D., MPH
President, XanoGene Clinic, San Juan, Puerto Rico
Member, AMMG Planning Committee

• Receptor Targeting & Signaling
• Pharmacokinetics & Dosing
• Stacking Strategies
• Failure Patterns

• 3–5 Advanced Cases
• Protocol Design
• Complication Handling
• Audience Discussion

• Metabolic & Longevity Cases
• Protocol Integration
• ACRI Framework
• Audience Decision Points

• FDA Trends
• 503A vs 503B
• Risk Zones
• Future Outlook

Presented by TBA

Open to all attendees and includes a complimentary lunch

Non-CME Symposium Sponsored by TBA

• Off-label Use
• Documentation
• Consent
• Liability Scenarios

• Pipeline peptides
• Mechanistic promise
• Clinical positioning
• Risk stratification

• Live case submissions
• Protocol building
• Faculty moderation

• Controversial peptides
• Future outlook
• Open discussion

Open to all conference attendees, spouses and guests

Held in Conference Networking and Exhibits Center

The extensive data from the Japanese microbiome studies evaluating centenarians as they have the longest longevity among any nations for the last 40 consecutive years suggests a particular microbiome profile that allows for enhanced resistance to sepsis, less sarcopenia, less intestinal permeability and less chronic inflammatory burden. The lecture will go into the details of that and how to achieve that along with clinical applications such as the specific uses of probiotics, prebiotics, synbiotics, postbiotics, fecal transplants, nutritional strategies, anti-microbials, and multi-tiered methods to manipulate colon bacterial profile.

The metabolomics status suggests that the microbial metabolites which are products of the 265 million microbial genes in the human microbiome is responsible for creation of metabolites that directly interact with the central clock in our human genomic transcription-translation complexes that offer precise moment by moment regulation of our genetic expression; this allows for more precise regulation of our circadian rhythm, which at a macro level is regulated by our diurnal-HPA axis. By offering microbiome-based treatments, we can thereby resolve constitutional symptoms such as fatigue, insomnia, brain fog, digestive complaints, exercise intolerance and autonomic dysfunction by improving this metabolomic physiology.

Hepatic Applications of enteroimmunology is predicated on the data that suggests the degree of severity of child’s based grouping of cirrhosis is based on degree dysbiotic inflammation, thereby we can improve the health of our chronic cirrhotic patients along with reversing to some degree of tendency toward cirrhosis along with fatty liver and metabolic liver dysfunction by growing commensal keystone species, eliminating LPS burden at the level of the colon, lessening toxic biological amines and this is also substantiated by the data of benefit from Rifaximin and preobiotic foods such as higher fiber diverse diets in the health of liver patients.

Cardiac Applications of enteroimmunology treatments involve suppression of trimethylamine oxide and LPS along with addressing the 45 steps in atherogenesis that begin with dysbiotic inflammatory signalling; endothelial repair and health start with enterocyte site repair and health at the level of the gut microbiome. This lecture will offer strategies to improve both cardiac and hepatic health in one treatment plan.

The science on microbes intrinsic to the brain is developing, however, plentiful data is available for gut microbiome related to the brain. There are plentiful brain and gut connections, and there is evidence to show the neurologic disease can occur as a consequence of partial gastrectomy. Autism spectrum disorder, anxiety, depression, Alzheimer’s and Parkinson’s are all associated with gut dysbiosis; consider the phrase that a “leaky gut” is associated with a “leaky brain.” In Parkinson’s disease, LPS is associated with aggregated alpha-synuclein which leads to motor dysfunction characteristic of Parkinson’s. We will review the multiple clinical studies have shown the benefits of probiotics for cognitive dysfunction, dementia, anxiety, and depression; it is important to remember that the microbes actually make neurotransmitters including GABA and norepinephrine. Meanwhile, Firmicutes species in the colon make AADC which catalyzes conversion of 5-HTP into serotonin which is essential for optimal mood and gut health.

Open to all attendees and includes a complimentary lunch

Non-CME Symposium Sponsored by TBA

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We live in the GLP-1 era. Know that GLP-1 is an enteric peptide that is made by L cells in the distal small intestine and the colon. The gut microbiome’s production of butyrate is the major molecule responsible for endogenous GLP-1 production. This lecture will cover optimizing GLP-1 use by minimizing side effects, improving efficacy, and helping you ultimately wean patients off GLP-1 treatments.

The most dominatingly beneficial data on the vagus nerve is coming from the academic publications on the applications of yoga for medical problems. Yoga offers alignment of breath intention, body postures, mindfulness all applied in one syncretic activity which offers the most amount of vagus nerve stimulation. Exercise and other forms of other practices and technologies while they may offer some temporary benefits, they do not have the overwhelming effects on the vagus nerve that yoga does. This lecture will go into how to help you apply the basics of yoga therapy in your practice to help learn how to not use their stress response in daily life.

Sarcopenia and frailty are the most malignant aspects of chronic disease whether it be CHF or dementia or osteoporosis. This lecture will go into the microbiome basis of sarcopenia and efforts to use both endocrine and enteroimmunologic microbiome-based treatments, peptides, anabolic hormones, and nutritional strategies customized to each patient’s gut bacterial profile, to increase healthy body mass including optimization of fat and muscle stores.

Open to all conference attendees, spouses and guests

Held in Conference Networking and Exhibits Center

Introduction to functional laboratory interpretation using optimal physiologic ranges and systems-based pattern recognition. Topics include metabolic and inflammatory markers, insulin resistance, cardiovascular risk, thyroid physiology, autoimmune thyroid disease, nutrient deficiencies, and foundational serum hormone evaluation.

This session begins with the latest information about FSH as a longevity marker. Then, we explore how different laboratory matrices reveal various aspects of hormone physiology, including circulating levels, bioavailable fractions, circadian rhythms, and metabolic pathways. Exploration of hormone assessment using serum, salivary, and urinary testing methodologies. Includes FSH as a longevity biomarker, adrenal stress patterns, circadian cortisol rhythms, estrogen and androgen metabolism, neurosteroid pathways, and clinical applications for hormone optimization.

The microbiome and intestinal barrier represent a major driver of systemic inflammation and endocrine dysfunction. This session will review of microbiome analysis, intestinal permeability, SIBO testing, inflammatory markers, and gut-immune interactions. Emphasis on the relationship between gastrointestinal dysfunction, systemic inflammation, metabolic disease, and endocrine imbalance.

This lecture explores laboratory evaluation of mitochondrial metabolism, nutrient status, and toxic exposures. Discussion of organic acids testing, micronutrient evaluation, mitochondrial function, and environmental toxicology. Participants will learn how nutrient deficiencies and toxic exposures contribute to immune activation, neurotoxicity, metabolic dysfunction, and chronic disease.

Advanced cardiovascular risk assessment using ApoB, Lp(a), MPO, GlycA, oxidized LDL, lipoprotein particle analysis, and inflammatory biomarkers to identify early atherosclerotic and vascular disease risk.

Presented by TBA

Open to all attendees and includes a complimentary lunch

Non-CME Symposium Sponsored by TBA

This lecture examines laboratory evaluation of bone turnover and endocrine influences on skeletal health. Evaluation of bone turnover, endocrine influences on skeletal health, vitamin D physiology, inflammatory bone loss, and laboratory markers used in osteoporosis risk assessment and prevention.

How laboratory markers identify early immune dysregulation and autoimmune activation. Overview of laboratory markers used to identify immune dysregulation, autoimmunity, mast cell activation, cytokine activity, and chronic inflammatory states associated with complex chronic illness.

Interactive systems-based case presentation of a 25-year-old female with PCOS and Hashimoto’s thyroiditis. Participants will review stepwise laboratory evaluation, interpretation strategies, and integrated treatment approaches including metabolic therapy, gut restoration, hormone balancing, and anti-inflammatory interventions.

Chronic disease arises from interactions among physiologic systems, not from isolated organ dysfunction. Final discussion emphasizing the interconnected nature of physiologic systems and the role of comprehensive laboratory analysis in identifying root causes of chronic disease.

Open to all conference attendees, spouses and guests

Held in Conference Networking and Exhibits Center

After more than three decades as a pharmacist and physician, I have witnessed remarkable advances in medicine. Yet some of the greatest insights into disease prevention, treatment response, and patient outcomes have come not from new drugs, but from understanding the genetic blueprint each patient carries. In this thought-provoking and clinically practical presentation, Dr. Laura Lile shares the lessons learned from implementing applied genomics in real-world patient care. Through compelling case studies spanning cardiovascular disease, neurodegeneration, cancer risk, metabolic dysfunction, hormone optimization, and longevity medicine, attendees will explore how genomics has transformed clinical decision-making and challenged many long-held assumptions in healthcare. What if the patient with “normal” cholesterol is actually at high cardiovascular risk? Why do some patients fail standard therapies while others thrive? How can genomics help identify hidden drivers of inflammation, cognitive decline, hormone imbalance, detoxification challenges, and treatment response years before disease develops? Drawing from thousands of patient encounters and years of genomic interpretation, Dr. Lile will discuss what she knows now that she wishes she had known earlier in her career. Attendees will leave with practical strategies for incorporating genomic insights into everyday clinical practice, improving patient engagement, personalizing treatment plans, and ultimately moving from reactive disease management to truly predictive and preventative medicine.

There has been a recent explosion of products that claim to reverse aging. Many are using telomere lengths to demonstrate the products efficacy. But other biomarkers such as DNA methylation, IgG Glycosylation, Total RNA Sequencing, among others, are also being used. The products claiming to reverse aging include supplements, lifestyle changes, therapies, etc.

Though the biomarkers are good at measuring aging, none of them can truly be used to measure the reversal of aging. They can only show reversal of the biomarkers themselves. It’s not even possible to show the slowing of aging.

I will show alternate explanations, besides reversal of aging, for the results that vendors are presenting to their clients. And these explanations actually represent an acceleration of aging, not the reversal of aging. That is, these products can preferentially kill the older cells in the blood, or elsewhere, causing the average age of the remaining cells to appear younger. Likewise, these products can also induce immunologic responses that will drive naive immune cells and/or memory immune cells, all of which are biologically younger, to divide and expand into the blood. Again, this will cause the average age of the cells in the blood to appear younger. Unfortunately, replicative aging throughout the body will be increased, not decreased, as a result.

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Presented by TBA

Open to all attendees and includes a complimentary lunch

Non-CME Symposium Sponsored by TBA

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This lecture explores inflammaging as a central, modifiable driver of age-related decline in physiological capacity and resilience. Drawing on five years of clinical experience using IgG glycosylation (GlycanAge) testing, it will present a biomarker-guided framework for measuring and targeting chronic immune activation in longevity medicine. Through case-based examples, the talk will illustrate how metabolic health, cumulative estrogen exposure, and hormone optimization significantly influence inflammatory aging trajectories, and how these interventions can be monitored in real time using glycan biomarkers. The session will conclude by positioning hormone optimization, in both women and men, as a first-line strategy in the clinical management of inflammaging and the preservation of “Healthspan.”

Hair loss is one of the most common complaints and complications for age management practices, especially with the rising use of GLP-1s. Evaluating and treating it well is an important opportunity to serve your patients and burnish your reputation. But hair is complicated, with multiple factors such as hormones, micronutrients and lifestyle habits coming together to affect the growth and loss of hair. Through a combination of didactic instruction and case studies, learn the causes and remedies for hair loss that are most relevant for age management practices.

From head to toe: vascular dementia, cerebral atrophic changes, inflammatory fat in the chest, abdomen, liver, muscles, pancreas, GI tract. Plaques in the arteries: carotid images with stable and unstable soft tissue plaques, as well as calcified ones.  Aorta dilation and the imaging pathology steps: how it starts, where it starts, progression, imaging biomarkers. Reversal strategies and imaging results. Radiology as a gate keeper: diagnosing before major abnormal laboratory tests and symptoms

Open to all conference attendees, spouses and guests

Held in Conference Networking and Exhibits Center

The lecture, The Two “Eyes” of Hypogonadism: The Influence of Ibuprofen and Inflammation on Testosterone Production, presents a paradigm-shifting perspective on the etiology of hypogonadism by emphasizing dual, often overlooked drivers: chronic inflammation and the widespread use of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly ibuprofen. Rather than viewing testosterone deficiency solely as a primary endocrine disorder requiring replacement therapy, this work reframes hypogonadism as a consequence of upstream disruptions within the neuroimmune–endocrine axis. The first “eye” of hypogonadism described in this paper is inflammation—particularly neuroinflammation—which impairs hypothalamic signaling and disrupts the hypothalamic-pituitary-gonadal (HPG) axis. Inflammatory cytokines such as IL-1β, TNF-α, and IL-6 interfere with gonadotropin-releasing hormone (GnRH) pulsatility, ultimately reducing luteinizing hormone (LH) output and downstream testosterone production. This mechanism is especially relevant in populations exposed to repetitive trauma, including military personnel and athletes, where chronic inflammatory states are common and persistent. The second “eye” focuses on ibuprofen and other NSAIDs as endocrine-disrupting chemicals (EDCs). The paper details how ibuprofen interferes with steroidogenesis at multiple levels: directly impairing Leydig cell function, suppressing key transcription factors such as steroidogenic factor-1 (SF-1), and downregulating critical enzymes including StAR, CYP17A1, and 17β-HSD. In addition, ibuprofen alters neuroglial function—specifically astrocyte-mediated prostaglandin E2 (PGE2) production—which is essential for proper GnRH signaling. The inhibition of PGE2 disrupts GnRH pulsatility, further compounding reductions in LH and testosterone levels. Importantly, the lecture extends beyond immediate endocrine effects to explore transgenerational implications. NSAID exposure during pregnancy is shown to alter fetal steroidogenesis and induce epigenetic modifications that may impair reproductive function in subsequent generations. These findings elevate NSAIDs from benign over-the-counter medications to agents with potentially profound long-term biological consequences. Finally, the presentation proposes a therapeutic framework centered on restoring physiological function rather than replacing hormones. Strategies include reducing neuroinflammation, restoring redox balance (e.g., selenium supplementation), and reactivating endogenous HPG axis signaling through selective estrogen receptor modulators (SERMs). This integrative approach aims to address root causes of hypogonadism and reestablish endogenous testosterone production. Overall, this work provides a comprehensive, mechanistic, and clinically actionable model linking inflammation, NSAID use, and endocrine dysfunction, advocating for a shift toward causation-based diagnosis and treatment of hypogonadism.

Despite widespread use of aggressive anti hormone strategies, many early stage breast cancer survivors are left with persistent symptoms, metabolic deterioration, and substantial quality of life impairment, including damage to intimacy and relationships. In many cases, these interventions deliver limited lived benefit while imposing long term physiologic cost. At the same time, a growing body of clinical and observational data suggests that, in carefully selected women, menopausal hormone therapy does not uniformly increase the risk of breast cancer recurrence or mortality. In this lecture, Estradiol: Friend or Foe in the Breast Cancer Survivor?, we will review the key studies evaluating hormone therapy after completely treated stage I–II breast cancer, with specific attention to recurrence, breast cancer–specific mortality, and overall survival. The goal is not reassurance, but clarity—what the data actually show, where the risks appear concentrated, and where long held assumptions deserve re examination. Particular emphasis will be placed on the distinction between older estrogen–progestin regimens and contemporary protocols utilizing bioidentical 17β estradiol with micronized progesterone. Available evidence suggests that breast outcomes differ meaningfully depending on the progestogen used, with more favorable outcomes observed when micronized progesterone is employed rather than synthetic progestins. We will also examine mechanistic and clinical data indicating that bioidentical progesterone may exert antiproliferative and de differentiating effects in breast tissue. The lecture will further review evidence that testosterone, including in some studies at supraphysiologic levels, can counter estrogen driven breast proliferation, may be associated with reduced breast cancer risk, and frequently improves quality of life parameters in women. These findings challenge the simplistic framing of hormones as uniformly harmful in breast cancer survivors and instead demand a more nuanced, physiology based discussion. This presentation does not argue that hormone therapy is universally safe, nor does it minimize the seriousness of breast cancer risk. Rather, it highlights the often under appreciated morbidity and mortality associated with prolonged hormone deprivation. We will compare outcomes associated with anti hormone therapy to those observed in carefully selected women treated with hormone therapy in the post cancer setting. The objective is to provide a structured, evidence based framework for considering bioidentical hormone replacement, including estradiol, micronized progesterone, and testosterone, in select women with fully treated stage I–II disease. The approach is grounded in rigorous literature review, physiologic reasoning, and explicit shared decision making, recognizing that quality of life, long term health, and individual risk tolerance matter, perhaps more to some patients.

Intimacy can be a challenge as we age. ED affects 77% of men worldwide and increases with age. Female sexual dysfunction Incidence is reported as 40% worldwide but that is greatly underreported due to definition. What causes sexual dysfunction in men and women? What tools exist to address the issues? What role does hormone therapy play? Who should provide the care? What is the best way to incorporate sexual health into your practice?

Weight management is among the most prevalent and complex challenges in clinical practice, yet it is frequently addressed through a narrow lens by targeting a single hormone, lab value, or lifestyle factor in isolation. Emerging evidence reframes adipose tissue as a dynamic endocrine organ whose receptors span metabolic, hormonal, inflammatory, and neuroendocrine pathways, placing the fat cell at the center of whole-body health and longevity. Similarly, hormones tend to be treated as one or two at a time, while they too are made and metabolized in organ systems throughout the body. This presentation aims to equip mixed-specialty practitioners with an integrated, evidence-based framework for evaluating and treating weight and hormonal dysregulation through their interconnected systems, including sex hormones, adrenal and stress physiology, metabolic hormones, and thyroid function. Key findings highlight that intervening in any one hormonal system produces measurable effects across multiple organ systems- including the gut, brain, liver, and musculoskeletal system- underscoring why single-target approaches so often fall short of lasting results. This talk synthesizes current evidence on GLP-1 receptor agonist therapies, hormone replacement therapy (HRT), functional and conventional laboratory assessment, and lifestyle interventions including diet, circadian rhythm, stress management, and supplementation. Equally important is the role of mindset and behavior change, grounded in neurohormonal biology, as essential and underutilized clinical tools for counseling patients in incorporating these day to day changes. Rooted in a naturopathic philosophy of treating the whole person, this framework invites practitioners across specialties to recognize that in thoughtfully addressing hormonal health, weight, and the full patient picture, we are practicing preventive care and meaningfully supporting each patient’s longevity.

Presented by TBA

Open to all attendees and includes a complimentary lunch

Non-CME Symposium Sponsored by TBA

There are 3 primary indices of longevity typically recognized in the standard biomedical model: VO2, Muscle Mass (SMI) and Insulin Resistance. Functional Medicine however understands and recognizes additional metrics that complete and provide a broader and more useful clinical picture. This lecture will present a comprehensive in-depth look at the complete “Functional Indices for Longevity”: Cardiorespiratory (VO2, Ventilation Efficiency,Lactic Acid, Tissue exchange/saturation, Baseline HR, HR recovery and HRV); Body Composition (SMI, % Fat, VAT, Bone Density, Strength Index); Metabolomics Profile (Insulin resistance and dynamics, CHO-Fat metabolism and metabolic flexibility, Inflammation and acidity); Endocrine/Hormonal–Anabolic–Performance (HAP) Signaling (HPA axis balance, Sleep, Circadian and cortisol rhythm, Sex and growth hormone/IGF 1, mTOR vs. AMPK signaling, and performance related pathways).

This lecture will discuss that dysbiotic inflammation originating in the microbiome will inevitably lead to the endocrinopathy we see in alarmingly increasing incidence today. We see an epidemic of vitamin D deficiency along with hypogonadism / low testosterone even in young men along estrogen/progesterone imbalances, namely elevated luteal estrogens or depleted luteal progesterone, increasing the risk for estrogen-based diseases in young women. There is an inevitable shift in  the endocrine system when dysbiotic inflammation occurs; loss of bacteria promotes cortisol production (corticosteroids are gut hormones), and as the body shifts towards making more cortisol production, these beneficial health and wellness promoting hormones get depleted. While we work on microbiome, it is important to replace beneficial hormones and optimize thyroid as well. This lecture will give you a protocol on how to reverse Graves’ disease, how to reverse Hashimoto’s thyroiditis, how to resolve menstrual symptom imbalances such as dysmenorrhea, menorrhagia and endometriosis. We will also give you a protocol to help you understand how to begin reversing prostate disease.

Preventive medicine in the longevity model is highly individualized. Risk must be identified early and addressed with targeted, evidence-based intervention. In a 160-patient longevity practice, we implement a systems-based screening protocol accessible through local radiology partnerships, and reference laboratories at clinically feasible cost, replicable in any integrative practice. The key is not a single biomarker; it is an individualized risk framework applied consistently across five clinical domains. Our framework spans five clinical pillars: cardiovascular risk assessment through AI-integrated, coronary imaging; fitness and metabolic health via cardiopulmonary breath analysis measuring, VO2 max and metabolic flexibility; biological age assessment using validated epigenetic clocks; multi-modal cancer risk screening; and neurological and mental performance assessment. Connecting all five is insulin resistance, the single most modifiable upstream driver of, cardiovascular disease, metabolic dysfunction, neurodegeneration, and accelerated biological aging.

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