April 2025 | Volume 20 | Issue 4 : simplebooklet.com

Chronic Fatigue Syndrome (CFS), also known as Myalgic Encephalomyelitis (ME), is a complex and debilitating condition characterized by persistent, unexplained fatigue that is not alleviated by rest. The exact cause remains elusive, but research suggests a combination of immune dysfunction, hormonal imbalances, and post-viral complications contribute to its onset[1].The Energy Crisis: Mitochondrial DysfunctionOne of the hallmarks of CFS is an energy production failure at the cellular level. Mitochondrial dysfunction has been observed in CFS patients, with muscle biopsies revealing abnormal mitochondrial degeneration[2] and severe deletions in mitochondrial DNA linked to bioenergy production[3]. This dysfunction leads to increased oxidative damage, reduced essential metabolic compounds like L-carnitine[4], and impaired oxidative metabolism, contributing to fatigue and muscle weakness. Additionally, studies have shown decreased intracellular pH and lower ATP synthesis rates after exercise, indicating impaired energy recycling in mitochondria[5]. The mitochondrial dysfunction would lead to muscle fatigue and an inability to relax properly[6]. This results in painful muscle contractions, making even simple movements exhausting.The Hypothalamus “ Circuit Breaker” Beyond the mitochondria, the hypothalamus—a master regulator of hormones, sleep, and autonomic functions—appears to flip off like a circuit breaker in CFS patients, perhaps to shield against further strain. This dysfunction acts like a circuit breaker shutting down to prevent further damage, disrupting sleep, energy regulation, and immune response[7]. Cortisol, the most important effector hormone of the hypothalamic-pituitary-adrenal (HPA) axis, often shows up dysregulated—either stubbornly low or blunted in response to stress. A meta-analysis[8] found that 75% of studies report mild hypocortisolism, flattened diurnal cortisol rhythms, or weakened feedback sensitivity, hinting at chronic stress or neuroimmune shifts as culprits.Signs & SymptomsCFS presents with a range of symptoms, including:• Flu-like symptoms – Muscle aches, feverish sensations, and joint pain.• Fatigue and exhaustion – A profound lack of energy that is not relieved by rest.• Chronic pain – Widespread pain resembling fibromyalgia.• Sleep disturbances – Inability to sleep despite extreme exhaustion.• Cognitive difficulties – Often referred to as “brain fog,” affecting memory and concentration.• Digestive issues - gut inflammation, irritable bowel syndrome [9]Triggers and Related ConditionsCommon triggers may include:• Physical Trauma: Surgery, accidents • Psychological Stress: Life events, trauma • Hormonal Changes: Pregnancy, menopause • Immunological Stressors: Vaccines, allergies, autoimmune disorders, cancers• Environmental Exposures: Toxins, mold • Overexertion: Extreme physical or mental strain CFS can also be triggered by infections. Post-viral fatigue syndromes, including Long-COVID, share many overlapping symptoms with CFS[10]. Other conditions such as Lyme disease[11] and Epstein-Barr virus (EBV)[12] have been implicated as potential triggers.Restoring Function: Flipping the “Circuit Breaker” Back OnSince there is no single test to diagnose CFS, physicians rely on symptom-based questionnaires, such as the Chalder Fatigue Scale and SF-36 Health Survey help quantify symptoms.[13] Treatment is similarly complex and requires a multifaceted approach. The SHINE protocol, developed by Dr. Jacob Teitelbaum, offers a structured method to manage CFS, Fibromyalgia (FM), and Long-COVID: 1. Sleep - Addressing sleep disorders through natural aids, such as melatonin[14], magnesium (bisglycinate), ashwagandha, and phosphatidylserine; and sleep hygiene improvements.2. Hormones & Hypotension – Prioritize adrenal support to steady the HPA Dr. Joseph Cheng, NDAdvertisementaxis with adaptogenic herbs, such as cordyceps (Cs-4), rhodiola, Panax ginseng, and astragalus; then address thyroid or sex hormone imbalances as needed.3. Infections – Treating viral and bacterial infections commonly associated with CFS. SIBO/IBS, a common co-morbid, should be addressed if indicated. Modulate immune/inflammatory responses by balancing the microbiota.[15]4. Nutritional Support – Promoting mitochondrial biogenesis is the most critical process to help break the vicious cycle in CFS as it enhances cellular responses to signals from neurotransmitters and hormones. Key natural ingredients known to support mitochondrial regeneration include PQQ (pyrroloquinoline quinone)[16],[17], Coenzyme Q10[18],[19], L-carnitine (or acetyl-L-carnitine)[20], R-alpha-lipoic acid[21], and NMN (nicotinamide mononucleotide)[22]. In addition, implementing a diet rich in essential nutrients or supplements, such as magnesium, selenium, D-ribose, B vitamins, and proteins would help facilitate tissue repair and recovery.5. Exercise – Engaging in gentle, structured movement to prevent deconditioning while avoiding post-exertional malaise.Final ThoughtsChronic Fatigue Syndrome remains a misunderstood and challenging condition to treat. However, emerging research, post-viral studies, and integrative treatment approaches like SHINE provide hope for those suffering. Addressing sleep, hormones, infections, nutrition, and gentle exercise can help restore function and gradually “turn the circuit breaker” back on. Ongoing research into Long-COVID and CFS will continue to shed light on effective treatments and potential cures.Chronic Fatigue Syndrome: Understanding the Energy Crisis & RecoveryVita Aid SHINE ProtocolSleep:•Melatonin-3 – 1 cap HS, or if feeling wide awake at bedtime, take 1 cap of Melatonin-5, 3-5 hours before bedtime.•Cortilief (lowers nighttime cortisol) – 2 caps 3-5 hours before bedtime.Hormones & Hypotension:•Adrenergyn (support daytime adrenal function) – 2 caps in the AM, 1 cap in the PM. May choose AdrenoForte DP if patients showing signs of depleted adrenal function. •Thyroaide (support healthy thyroid function, if indicated) – 2 caps in the AM QD.•Estrolief (for women showing estrogen-dominance, if indicated) – 2 caps QD.Infections/Immune Support:•Defenxin (boost immune system against acute viral infection) – 2 c aps AC BID, 2 weeks.•Immutonin (long-term immune tonic support) – 2 caps QD.•Ultra-PB100 DF+ (featuring well-researched probiotics like LrGG, BL-04, and HN001) – 1 scoop QD.•SIBO Treatment Protocol (if indicated)Nutritional & Mitochondrial Support:•C-Nergy (vitamin C energy drink with 2.5g D-Ribose) – 1 scoop BID. •Neuromin (Mitochondrial Biogenesis Support) – 2 caps QD.•NMN 300 (NAD+ Precursor) - 1 cap QD.Full Ref.:© 2025 Vita Aid Professional Therapeutics Inc. All Right Reserved.P: 1.800.490.1738www.vitaaid.comModulate the ‘High Cortisol State’ in HPA Axis Dysregulation**The statements made herein have not been evaluated by the Food and Drug Administraon. Products are not intended to diagnose, treat, cure, or prevent disease. If you have any concerns about your own health, you should always consult with a physician or healthcare professional.Proudly in Collaboraon with:• High-Dose Phosphadylserine (150 mg/cap) from sunower seeds - helps reduce acvaon of the HPAA under stress*• Synergized with Unique, Mul-Mechanisc Herbal Combinaon - exerts powerful anxiolyc & corsol-modulang acons and opmize stress-coping response*Learn More:Cortilief

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Clinical pearlsCase management/case studiesNaturopathic philosophyPractice building and business managementCurrent trends and issues that affect naturopathic physicians in your areaNews, announcements, and event noticesDevelopment of new techniques or protocolsAbstracts and reviewsDiscussions pertaining to diagnosticsPublic/media relations and networkingUsing technology to make practices more efficient and profitableEducational and grassroots programs that further the naturopathic causeAny other trend, event, or development you believe is pertinent to theprofessionFor more information regarding article submission, or to receive a copy ofsubmission guidelines, please contact editor@ndnr.com or scan the QR code formore information. Opinions expressed in Naturopathic Doctor News & Review do not necessarilyreflect those of this publication and its publishers.Copyright © 2024 Naturopathic Doctor News & Review. All rights reserved. No portionof this publication may be copied, reproduced, or redistributed without express writtenpermission from the publisher. Reprint information is available by contactingpublisher@ndnr.com.Naturopathic Doctor News & Review reserves the right to edit or reject any submittededitorial or advertising. Opinions expressed by contributors and advertisers are notnecessarily the opinions of Naturopathic Doctor News & Review or its principals.Naturopathic Doctor News & Review is published and circulated as an annualsubscription (12 issues) to licensed naturopathic doctors (NDs) and students andgraduates of CNME recognized naturopathic colleges in North America, and certainsuppliers to the profession. Annual subscriptions (12 issues) are available to other healthcare providers and NDs outside of North America: $199 USDINSIDEOptimizing Healthy Aging for Older Adults: Insightsfrom a Case Series Using a Novel Supplement Regimen Optimizing Healthy Aging for Older Adults: Insightsfrom a Case Series Using a Novel Supplement Regimen 07Jen Palmer, ND; Joseph M. Keenan, MDThis case series explores the impact of a novelsupplement regimen on healthy aging. It demonstratesthat the regimen can improve cardiovascular health,metabolic function, and cognitive well-being whilereducing reliance on statins in older adults.The Integrative Management of Psoriasis: A Case Study inHomeopathy, Nutrition, and Lifestyle MedicineMarisa Kassimir, NDThis article examines an integrative, patient-centered approach totreating severe psoriasis by targeting root causes such as systemicinflammation, gut health, metabolic balance, and emotional well-being through homeopathy, nutrition, and lifestyle modifications.Occupationally Exacerbated PalmoplantarDermatitis with Systemic TriggersCarrie Phillips, NDAn integrative approach to treating occupationally exacerbatedpalmoplantar dermatitis, focusing on gut dysbiosis, mycotoxinexposure, and systemic triggers for lasting skin healthimprovement.Topical Treatments for Rosacea: A Clinical Comparison of Efficacyand Patient OutcomesJordan Robertson, NDThis article explores the efficacy, mechanisms, and patientconsiderations for ivermectin, azelaic acid, and metronidazole,empowering clinicians and patients to make informed decisions.Geriatric Syndrome—Bone Up, Muscle Up, and More withMyostatin InhibitionChris D. Meletis, NDThis article explores how inhibiting myostatin, using interventionslike Fortetropin and lifestyle changes, can improve bone density,prevent sarcopenia, and enhance overall musculoskeletal healthin aging individuals.From Pain to Relief: A Shingles Victory with HomeopathyMichael Knapp, ND, DHANPA case study detailing the successful treatment of shingles in a 51-year-old female using individualized homeopathy, resulting infaster recovery, reduced pain, and no postherpetic complications.Breaking the Cycle: Understanding PCOS-Related SkinManifestationsGalina Mironova, NDThis article explores the complex connection between polycysticovarian syndrome (PCOS) and skin conditions such as acne,hirsutism, androgenic alopecia, and acanthosis nigricans. It delvesinto the underlying pathophysiology and offers evidence-basednaturopathic strategies, including dietary modifications, targetedsupplementation, and functional medicine interventions toaddress the root causes and improve skin health.Mechanisms of Aging and Neurodegeneration: Exploring Thiamine Deficiency, Catecholamine Toxicity, andAngiotensin IIQuinn Rivet, NDThis article investigates key mechanisms in neurodegenerationand aging, focusing on thiamine deficiency, catecholamine-induced toxicity, and Angiotensin II-related inflammation, withinsights into potential therapeutic strategies.Targeting Menopausal Acne: Hormone Balancing and Skin Barrier Support in PracticeAarti Patel, NDThis case study explores the successful treatment of menopausalacne in a 55-year-old female using a combination of hormonebalancing, adrenal support, and gentle skincare to restore skinhealth and improve overall well-being.Resolving Acne Vulgaris Through Gut and Hormone Support: A Case StudyChelsea Smithback, NDThis case study highlights a 90% improvement in acne for a 24-year-old female following a naturopathic treatment plan thataddressed gut health, hormone balance, and liver function.Article Submissions: Articles should be original,previously unpublished, and should cover aspecific topic, protocol, modality, diagnostic,philosophy, commentary, or case study pertainingto naturopathic medicine rather than a generaloverview. Illustrations, photographs, charts, andprotocols are encouraged. Naturopathic DoctorNews & Review does not reprint articles fromother publications except under unusualcircumstances. Typical word requirements are 700 to 2000 words per article. Topics of interestinclude:TOLLE TOTUM312172335JOIN THE CONVERSATIONAPRIL 2025 - VOLUME 20 | ISSUE NO. 043039502645

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20YEAREST. 2005ANNIVERSARYLetter from the PublisherDear Colleague,We are pleased to share with you the latest issue ofNDNR, focused on Dermatology and Aging—twoareas where naturopathic medicine continues to offerdistinct value through personalized, root-causeapproaches to care. As our patients increasingly seeksupport for both skin health and healthy aging, thisissue brings together timely clinical insights and case-based research to inform and inspire your practice.One of the lead articles, authored by Jen Palmer, ND,and Joseph M. Keenan, MD, explores the impact of anovel supplement regimen on the aging process.Through a compelling case series, they highlight howthis approach can support cardiovascular function,metabolic health, and cognitive well-being in olderadults—all while potentially reducing reliance on statinmedications.Also featured is an integrative case study from MarisaKassimir, ND, which examines the management ofsevere psoriasis through a multifaceted protocolcombining homeopathy, targeted nutrition, and lifestylemedicine. By addressing systemic inflammation, guthealth, metabolic balance, and emotional well-being,this patient-centered approach offers a practicalroadmap for clinicians treating complex dermatologicconditions.Skin health remains a central concern for many patients,and Jordan Robertson, ND, offers a comparativeanalysis of topical treatments for rosacea. Her articleevaluates the clinical efficacy, mechanisms of action,and patient considerations for commonly usedtherapies, including ivermectin, azelaic acid, andmetronidazole—providing valuable context forinformed decision-making in practice.Applied Naturopathic Medicine 20th Annual Dermatology and Aging Issue 4NATUROPATHIC DOCTOR NEWS & REVIEWIn the realm of aging and musculoskeletal health, ChrisD. Meletis, ND, explores the emerging role of myostatininhibition in the prevention of sarcopenia and bone loss.His discussion of Fortetropin, alongside lifestyle-basedinterventions, sheds light on strategies to enhancestrength, resilience, and overall quality of life in olderadults.Rounding out this issue, Carrie Phillips, ND, presents anintegrative approach to treating occupationallyexacerbated palmoplantar dermatitis, with an emphasison uncovering systemic triggers such as gut dysbiosis andmycotoxin exposure. Her focus on underlyingcontributors offers a fresh perspective on restoring lastingskin health in patients with complex environmental andoccupational exposures.We hope you find this issue to be a rich resource forclinical application, as well as a testament to the evolvingscope of naturopathic dermatology and anti-aging care.Thank you for your ongoing commitment to theadvancement of integrative medicine, and for being partof the NDNR community.In Health,Razi BerryPublisher, NDNRwww.ndnr.comDERMATOLOGY AND AGING ISSUERazi Berry

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Dietary supplements can provide older adults a therapeutic option for maintaining optimal health without relying onprescription drugs. This article summarizes key findings from a recent case series1 demonstrating the ability of onenovel supplement regimen to promote healthy aging in older adults. The regimen can treat dyslipidemia, promotephysical and mental well-being, and eliminate the burden of statin drugs and their associated adverse effects. Study ProtocolThis case series, conducted from September 2022 to August 2024, included a convenience sample of 10 adults (7 menand 3 women) living in the United States. The average age of the participants was 80, ranging from 62 to 91. Notably,the majority of the participants (7 out of 10) were taking a statin drug at the start of the study.Each participant was required to share the study protocol with their personal doctor and request blood tests atbaseline, 6 weeks, 12 weeks, and quarterly thereafter to monitor benefits and potential side effects, with closermonitoring as needed. The routine blood test protocol included a blood lipid profile, including lipoprotein (a) (Lp[a]),a comprehensive metabolic profile, and uric acid, homocysteine, and glycated hemoglobin (HbA1c) levels. Insights from a Case Series Using a Novel Supplement RegimenInsights from a Case Series Using a Novel Supplement RegimenJEN PALMER, ND; JOSEPH M. KEENAN, MD7NATUROPATHIC DOCTOR NEWS & REVIEWPRIMUM NON NOCEREAPRIL 2025 - VOLUME 20 | ISSUE NO. 04Optimizing Healthy Agingfor Older AdultsOptimizing Healthy Agingfor Older Adults

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Dihydroberberine was included primarily to supportmetabolic health. Dihydroberberine is a highly bioavailableform of berberine¹¹, requiring a lower therapeutic dosage thateliminates the digestive upset commonly associated withberberine use. Clinical research supports the therapeutic useof berberine for common age-related diseases such as type 2diabetes, dyslipidemia, hypertension, stroke, metabolicsyndrome, polycystic ovarian syndrome, and nonalcoholicliver disease.¹²′¹³Taxifolin (dihydroquercetin) was included primarily tosupport immune health, an action primarily attributed to itsability to reduce oxidative stress.¹⁴ Interestingly, taxifolin hasbeen shown to improve pneumonia recovery in otherwisehealthy men when used as an adjuvant to standard therapy.¹⁵Mixed tocotrienols were included primarily for theirneuroprotective properties. Mixed tocotrienols are reportedto help reduce neurotoxicity and protect againstmitochondrial dysfunction¹⁶, delay progression of whitematter lesions and reduce the incidence and severity ofstroke¹⁷, reduce elevated total and LDL cholesterol¹⁸, andprotect LDL cholesterol from oxidation.¹⁹Supplement Delivery Forms and Dosing ScheduleWax-matrix controlled-release tablets manufactured byEndurance Products Company, Inc. (Sherwood, Oregon)were chosen for the supplements providing water-solubleingredients (niacin, dihydroberberine, and taxifolin). Aproprietary tableting process is used to overcome the “dosedumping” challenge of typical modified-release tablets andprovide a steady nutrient release over 4 to 8 hours, dependingon the supplement. This delivery form serves two importantfunctions. First, it helps maintain effective therapeutic bloodlevels without requiring higher or more frequent doses.Second, it reduces the risk of side effects from rapid nutrientabsorption. For the mixed tocotrienols supplement, animmediate-release softgel with a fat-soluble suspension (“bio-enhanced”) was chosen to help ensure optimal absorptioneven if not taken with fat in a meal.The participants' medical background and currentmedication use dictated the supplement choice and dosingschedule (see Table 1). Participants were informed thatsupplementing with niacin in the form of NA may initiallycause mild skin flushing that typically improves within a fewweeks. To help prevent flushing, participants were advised touse aspirin or a non-steroidal anti-inflammatory drug(NSAID), if needed, and to increase their intake of methyldonor foods to support liver metabolism of NA.Quarterly in-person home visits were also conducted. Thefirst meeting aimed to provide a detailed study protocol,obtain informed consent, and assess each participant's healthhistory, lifestyle and dietary habits, and support system.Subsequent visits focused on delivering the supplementsupply for the next quarter, reviewing diet and lifestyle goalsand lab results, and adjusting supplement dosages as neededto minimize side effects or enhance benefits.Participants also completed the Self-AdministeredGerocognitive Exam 2 (SAGE 2) cognitive assessment tool,an early diagnostic tool for cognitive impairment, and a self-reported assessment of physical/mental well-being at baselineand at the final home visit.Supplement SelectionThe supplement regimen included four research-backeddietary ingredients (niacin, dihydro berberine, taxifolin, andmixed tocotrienols) that have the potential to support keyhealth concerns of older adults, including cardiovascularhealth, metabolic function, immune defense, and cognitivehealth. Niacin was included primarily as nicotinic acid (NA) orniacinamide to support cardiovascular health and cellularmetabolism. Extensive clinical research² supports using NA,including wax-matrix NA, for treating dyslipidemia andcardiovascular disease despite skepticism from a recent meta-analysis³ based on two high-profile, flawed clinical trials.⁴′⁵NA has also been reported to help reverse chronic kidneydisease⁶ and offer therapeutic potential for certainneurological disorders and early stroke recovery.⁷ Both typesof niacin (NA and niacinamide) serve as precursors for thebody’s production of nicotinamide adenine dinucleotide(NAD+), essential for cellular metabolism and stem cellproduction.⁸ Finally, niacinamide may help prevent or delaythe progression of glaucoma, the leading cause of age-relatedblindness.⁹′¹⁰8DERMATOLOGY AND AGING ISSUE

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Table 1. Supplement Regimen for Healthy Aging: Dosing ScheduleKey NutrientSupplementDeliveryDosageNiacin*Nicotinic Acid (250mg to 750mg per tablet)WM ER tablet (6-8hours)Week 1, 250mg bid; week2,500mg bid; week3,750mgbid maintained for 3 more weeksNicotinicAcid/Pantethine(500mg/200mg per tablet)WM ER tablet (5-7 hours)For participants taking a statin at baseline: 1 tablet bidincreased to 2tablets bid after week6; tapered down/offstatin use if blood lipids as good as or betterthanbaselineNicotinamide(750mg per tablet)WM SR tablet (5-7 hours)2tablets bidDihydroberberineDihydroberberine (150mg/tablet)WM SR tablet (5-7 hours)2tablets bid for participants with metabolic syndromeor type 2 diabetes, otherwise 1tablet bidTaxifolinTaxifolin Complex(150mgtaxifolin, 500mgvitamin C,15mgzinc per tablet)WM SR tablet (5-7 hours)1tablet bidMixed TocotrienolsMixed Tocotrienols (Bio-enhanced)(50mg per softgel)IR softgel4 softgels bidWM indicates wax-matrix; ER, extended-release, SR, sustained-release; IR, immediate-release; bid, twice daily (taken with meals).*Form of niacin dictated by a participant’s medical background and current medication use.APRIL 2025 - VOLUME 20 | ISSUE NO. 049Key FindingsThe supplement intervention lasted 16 months, onaverage, resulting in significant improvements in bloodlipid profiles, enhanced physical and mental well-being,and a reduced reliance on statin drugs. Key findingsinclude the following:Reduction in Lp(a) levels. Three participants hadelevated Lp(a) levels at baseline (85, 125, 256 mg/dl)and were able to achieve normal levels (<30 mg/dl)after 6 weeks of supplementation with wax-matrixNA/pantetheine and wax-matrix dihydroberberine.This is an important outcome given Lp(a) issignificantly more atherogenic than LDLcholesterol.20 The participant with the highestbaseline Lp(a) level initially improved to 148 mg/dl,but then appeared to develop liver hypersensitivity toNA. NA therapy was temporarily stopped to allow theside effect to resolve, then resumed at a lower dose.NATUROPATHIC DOCTOR NEWS & REVIEWStatin withdrawal with comparable blood lipid benefits.Of the participants (7 out of 10) taking a statin atbaseline, all achieved comparable lipid benefits post-statin withdrawal with a 25% decrease in totalcholesterol, 35% decrease in LDL cholesterol, 52%increase in HDL cholesterol, and 46% decrease intriglycerides, on average, compared to baseline. Oneparticipant discontinued his supplement regimen andresumed statin therapy due to digestive upset that hisdoctor attributed to the supplement regimen.Improved mental and physical well-being. All 10participants completed the cognitive and well-beingassessments, reporting generally stable or positivephysical and mental functions compared to baseline,including improved balance, energy level, andalertness.

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10Occurrence and Management of Side EffectsSide effects were successfully managed by adjustingsupplement regimens. Four participants experienced skinflushing, which was managed by instructing them to avoidchewing tablets; take tablets with meals without hot foods orbeverages (which can accelerate tablet dissolution); or takeaspirin or an NSAID if needed. Three participantsexperienced elevated blood homocysteine and were instructedto add a vitamin B12/folate supplement until thehomocysteine level returned to normal. Four participantsexperienced an upset stomach, which was managed by rulingout abnormal liver enzymes and recommending antacids oracid-blocking agents for relief. Finally, two participants experienced liver hypersensitivity.NA was temporarily withdrawn until liver enzymes (AST,ALT) returned to normal, then gradually resumed at a lowermaintenance dose (usually 500 mg twice daily). Theseparticipants were also reminded to consume more methyl-donor foods to support NA metabolism. Discussion and ConclusionThis case series demonstrates the therapeutic potential of anovel dietary supplement regimen to promote healthy agingby addressing dyslipidemia, enhancing physical and mentalwell-being, and reducing the reliance on prescription drugssuch as statins. Importantly, it offers valuable insight fordesigning a larger controlled clinical trial to address thegrowing healthcare needs of the aging population.Notably, all participants taking a statin drug at the start ofthe study could discontinue use while maintaining bloodlipid levels that were equal to or often better than theirinitial levels. The clinical value of discontinuing statins isprofound as it also eliminates their associated adverse sideeffects, which can be especially troubling for older adults.For example, statins are known to deplete intracellularlevels of coenzyme Q10 (CoQ10)²¹, which is crucial formuscle health and function. Up to 20% of cases of statinintolerance are attributed to statin-induced CoQ10depletion.²² Additionally, statins are reported to increaseatherogenic Lp(a) by up to 20%²³, and statins with highCellular Aging ContentUPCOMING EVENTSAAMPCARDIOLOGY CONFERENCEScottsdale, AZ May 30 - June 1, 2025BIMCBELIZE INTEGRATIVEMEDICINE CONFERENCE:San Ignacio, Belize July 27 - Aug 2Dr. Anderson’sConferences:ACCME & AANP-APPROVED | 30+ YRS OF EXPLive or Virtual AAMP Conference:AAMP: 18 AMA Cat-1 CMELive or Virtual Oncology:AAMP 18 Cat-1 AMA CME Integrative OncologymTOR-Rapamycin1.5 CE Total | 1.5 PharmGlutathione-ReDox 4 CME Total | 3 PharmMethylene Blue2.0 CE Total | 2.0 PharmMitochondrial UpdatesCLICK ON THE VIDEO PREVIEW LINKS BELOW(Bundle)Other Speaking Venues: BELIZE INTEGRATIVE MEDICINE CONFERENCE

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REFERENCESlipophilicity (atorvastatin, simvastatin) are associated withan increased risk of dementia in older people.²⁴ Finally,results from one systematic review²⁵ provide compellingevidence statins are significantly associated with a decreasein insulin sensitivity, regardless of the type of statin used.The supplement regimen also enhanced physical and mentalfunctions such as balance, energy, and alertness, which areimportant considerations for older individuals who want tostay active and independent. The fact that all participantsmaintained or improved their SAGE 2 cognitive assessmentscores is encouraging and suggests that supplementationmay directly support the preservation of cognitive function. It is promising to effectively manage the transient sideeffects through supplement dose adjustment, dietarymodifications, or other relatively simple solutions.However, this underscores the need for routine care so thatdoctors can monitor progress and tailor the protocol toeach patient's specific needs.1. Keenan J. A novel supplement regimen for healthy aging: a case series. Med ResArch. 2024;12(10):2375-1924. doi:10.18103/mra.v12i10.58302. Keenan J. The niacin rebirth: revisiting the potential of nicotinic acid therapy forcardiovascular disease and niacin supplementation for healthy aging. Med Res Arch.2024;12(7):1-9. doi:10.18103/mra.v12i7.55213. D'Andrea E, Hey SP, Ramirez CL, Kesselheim AS. Assessment of the role ofniacin in managing cardiovascular disease outcomes: a systematic review and meta-analysis. JAMA Netw Open. 2019;2(4):e192224.doi:10.1001/jamanetworkopen.2019.22244. AIM-HIGH Investigators. The role of niacin in raising high-density lipoproteincholesterol to reduce cardiovascular events in patients with atheroscleroticcardiovascular disease and optimally treated low-density lipoprotein cholesterolRationale and study design. The Atherothrombosis Intervention in Metabolicsyndrome with low HDL/high triglycerides: Impact on Global Health outcomes(AIM-HIGH). Am Heart J. 2011;161(3):471-477.e2. doi:10.1016/j.ahj.2010.11.0175. HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design,pre-specified muscle and liver outcomes, and reasons for stopping study treatment.Eur Heart J. 2013;34(17):1279-1291. doi:10.1093/eurheartj/eht0556. Park CW. Niacin in patients with chronic kidney disease: is it effective and safe?.Kidney Res Clin Pract. 2013;32(1):1-2. doi:10.1016/j.krcp.2013.02.0017. Wuerch E, Urgoiti GR, Yong VW. The promise of niacin in neurology.Neurotherapeutics. 2023;20(4):1037-1054. doi:10.1007/s13311-023-01376-28. McReynolds MR, Chellappa K, Baur JA. Age-related NAD+ decline. ExpGerontol. doi:10.1016/j.exger.2020.1108889. Tribble JR, Otmani A, Sun S, et al. Nicotinamide provides neuroprotection inglaucoma by protecting against mitochondrial and metabolic dysfunction. RedoxBiol. 2021;43:101988. doi:10.1016/j.redox.2021.10198810. Hui F, Tang J, Williams PA, et al. Improvement in inner retinal function inglaucoma with nicotinamide (vitamin B3) supplementation: a crossover randomizedclinical trial. Clin Exp Ophthalmol. 2020;48(7):903-914. doi:10.1111/ceo.1381811. Feng R, Shou JW, Zhao ZX, et al. Transforming berberine into its intestine-absorbable form by the gut microbiota. Sci Rep. 2015;5:12155. doi:10.1038/srep1215512. Song D, Hao J, Fan D. Biological properties and clinical applications ofberberine. Front Med. 2020;14(5):564-582. doi:10.1007/s11684-019-0724-613. Imenshahidi M, Hosseinzadeh H. Berberine and barberry (Berberis vulgaris): aclinical review. Phytother Res. 2019;33(3):504-523. doi:10.1002/ptr.625211DERMATOLOGY AND AGING ISSUE14. Das A, Baidya R, Chakraborty T, Samanta AK, Roy S. Pharmacological basis andnew insights of taxifolin: a comprehensive review. Biomed Pharmacother.2021;142:112004. doi:10.1016/j.biopha.2021.11200415. Kolhir VK, Bykov VA, Teselkin YO, et al. Use of a new antioxidant diquertin as anadjuvant in the therapy of patients with acute pneumonia. Phytother Res. 1998;12:606-608, 10.1002/(SICI)1099-1573(199812)12:8<606::AID-PTR367>3.0.CO;2-U16. Naomi R, Shafie NH, Kaniappan P, Bahari H. An interactive review on the role oftocotrienols in the neurodegenerative disorders. Front Nutr. 2021;8:754086.doi:10.3389/fnut.2021.75408617. Gopalan Y, Shuaib IL, Magosso E, et al. Clinical investigation of the protectiveeffects of palm vitamin E tocotrienols on brain white matter. Stroke. 2014;45(5):1422-1428. doi:10.1161/STROKEAHA.113.00444918. Zuo S, Wang G, Han Q, et al. The effects of tocotrienol supplementation on lipidprofile: a meta-analysis of randomized controlled trials. Complement Ther Med.2020;52:102450. doi:10.1016/j.ctim.2020.10245019. O'Byrne D, Grundy S, Packer L, et al. Studies of LDL oxidation following alpha-,gamma-, or delta-tocotrienyl acetate supplementation of hypercholesterolemic humans.Free Radic Biol Med. 2000;29(9):834-845. doi:10.1016/s0891-5849(00)00371-320. Björnson E, Adiels M, Taskinen MR, et al. Lipoprotein(a) is markedly moreatherogenic than LDL: an apolipoprotein B-based genetic analysis. J Am Coll Cardiol.2024;83(3):385-395. doi:10.1016/j.jacc.2023.10.03921. Qu H, Guo M, Chai H, Wang WT, Gao ZY, Shi DZ. Effects of coenzyme Q10 onstatin-induced myopathy: an updated meta-analysis of randomized controlled trials. JAm Heart Assoc. 2018;7(19):e009835. doi:10.1161/JAHA.118.00983522. Saxon DR, Eckel RH. Statin intolerance: a literature review and managementstrategies. Prog Cardiovasc Dis. 2016;59(2):153-164. doi:10.1016/j.pcad.2016.07.00923. Zhu L, Fang Y, Gao B, et al. Effect of an increase in Lp(a) following statin therapyon cardiovascular prognosis in secondary prevention population of coronary arterydisease [published correction appears in BMC Cardiovasc Disord. 2022 Dec 30;22(1):577.doi: 10.1186/s12872-022-03027-4]. BMC Cardiovasc Disord. 2022;22(1):474.doi:10.1186/s12872-022-02932-y24. Prasanna P, Liu S, Silverman D. Lipophilic statins in subjects with early mildcognitive impairment: associations with conversion to dementia and decline in posteriorcingulate brain metabolism in a long-term prospective longitudinal multi-center study. JNucl Med. 2021;62(supp 1):Abstract 102. doi.org/10.1002/alz.06939425. Dabhi KN, Gohil NV, Tanveer N, et al. Assessing the link between stans and insulinintolerance: a systematic review. Cureus. 2023;15(7):e42029. doi:10.7759/cureus.42029Jen Palmer, ND, is a recognized leader in thedietary supplement industry, with expertise indriving growth for professional supplement brandsthrough strategic educational marketing. Her pastroles have included serving as a subject matterexpert, educator, and managing continuingmedical educational conferences for healthcareprofessionals.Joseph Keenan, MD, is a physician, researcher, andProfessor Emeritus, University of Minnesota,Department of Family Medicine & CommunityHealth. Dr. Keenan is a leading expert on the useof niacin therapy in the treatment ofcardiovascular disease and dyslipidemia andauthor of The Niacin Breakthrough, The KeenanProtocol for Heart Health and Healthy Aging.Finally, it’s interesting to note that, although the case seriesincluded two severe winter seasons, no deaths, strokes, heartattacks, cancer, or serious infections occurred in this group ofolder adults.

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Medical HistoryBRCA2 positiveDouble mastectomy and reconstructive surgery(2015)G1P1A0, history of postpartum depressionPrevious use of oral contraceptivesCurrent Medications & SupplementsNo prescription medicationsMedical cannabis for anxiety and insomniaMelatonin 10 mg QHS for insomniaSymptoms & Systemic ReviewChronic diarrhea when consuming restaurant-prepared foodDysmenorrhea and menorrhagia with a regular cycleDifficulty losing weightInsomnia with racing thoughts (5–7 hours of sleepper night)Seasonal allergies, vertigo, photophobiaDry skin, nail changesSocial History & LifestyleOwner of a fitness studio; exercised regularlyReported energy level: 7/10Hydration: 32 oz of water per dayPsoriasis PresentationDL exhibited widespread psoriatic plaques, with themost severe involvement on her anterior lower legs andscalp (notably the occiput). Additional lesions werepresent on her knees, thighs, arms, glutes, and vulva. Thescalp lesions were thick and covered with silver scales,causing noticeable hair thinning. The lower leg lesionswere erythematous with scales and scabbing,continuously spreading. All plaques were severelypruritic, and excessive scratching led to bleeding.Psychosocially, DL experienced significant emotionaldistress. She avoided mirrors, wept multiple times perday, and expressed despair over finding relief. She fearedmedical treatments, supplements, and food, stating, “Ican’t trust anything anymore.” She was anxious abouther daughter developing psoriasis, particularly given herhusband’s history of the condition. Although resistant tomedical intervention, she was desperate for a solution.13DERMATOLOGY AND AGING ISSUE

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14NATUROPATHIC DOCTOR NEWS & REVIEWPsychosocially, DL experienced significant emotionaldistress. She avoided mirrors, wept multiple times per day,and expressed despair over finding relief. She fearedmedical treatments, supplements, and food, stating, “I can’ttrust anything anymore.” She was anxious about herdaughter developing psoriasis, particularly given herhusband’s history of the condition. Although resistant tomedical intervention, she was desperate for a solution.Previous treatments tried: Topical steroids (provided temporary relief)Acupuncture and Chinese herbal formulas (causeddiarrhea) Tanning beds (discontinued during and afterpregnancy) Self-guided food elimination challenge (providedtemporary relief) Laboratory FindingsComprehensive laboratory analysis revealed multiplesystemic imbalances:Iron metabolism: Low iron saturation (13%) with low-normal serum iron and adequate ferritinHormonal findings: Suboptimal day 21 progesterone(5.3 ng/mL), LH:FSH ratio of 3:1Nutrient status: Suboptimal vitamin D (35 ng/mL)Adrenal function: Elevated AM cortisol (20.8 µg/dL)Glucose metabolism: Elevated fasting glucose (106mg/dL), HOMA-IR of 3.0 (indicative of insulinresistance)Thyroid function: TSH 3.310 µIU/mL, Free T4 0.99ng/dL, Free T3 3.2 pg/mL (suggestive of suboptimalthyroid function)These findings pointed to dysregulation of thehypothalamic-pituitary-adrenal (HPA), hypothalamic-pituitary-ovarian (HPO), and hypothalamic-pituitary-thyroid (HPT) axes, alongside insulin resistance andprobable gut hyperpermeability.Therapeutic Strategy and RationalePsoriasis is now understood as a condition that affectsseveral different systems in the body, which is why a whole-body approach is key. Therefore, the treatment approach centered on reducingsystemic inflammation, improving gut health and optimizingnutrient status, restoring hormonal balance, optimizingmetabolic function, supporting detoxification pathways, andmanaging stress. For example, problems with the gut barrier can contributeto inflammation and worsen psoriasis, making gut-healingstrategies an important area to focus on.⁵ Additionally,metabolic health was a priority due to the link betweeninsulin resistance and psoriasis.³ A systematic review from2022 even found that mindfulness and meditation can helpimprove both the severity of the skin and the quality of lifefor people with psoriasis.⁴ There’s no strong evidence thatvitamin D supplementation alone is a cure for psoriasis, butdeficiency has been linked to autoimmunity. It plays animportant role in immune function, making it a valuableaddition to treatment.¹Given the complex, multi-system nature of psoriasis, it wasclear that an integrative approach was necessary. Along withaddressing factors above, I felt confident from the outsetthat homeopathy would complement these strategieseffectively for this patient. In fact, research backs the use ofhomeopathy in treating psoriasis. A 2023 double-blind,randomized, placebo-controlled trial demonstrated thatindividualized homeopathic remedies significantly alleviatedsymptoms of psoriasis vulgaris, reinforcing homeopathy as apromising treatment for chronic skin conditions. In thisstudy, the most commonly prescribed remedies includedCalcarea carbonica, Mercurius solubilis, Arsenicum album,and Petroleum.²Initial Recommendations (first visit)Increased water intake for hydrationCompletion of a 7-day food, bowel movement, andsymptom diary for a more complete look at nutritionand any correlation with symptomsCastor oil packs to support liver health and itsassociation with metabolic disease, hormonemetabolism, and detoxificationInitiation of homeopathic treatment Homeopathic Evaluation & PrescriptionThe lesions were pathognomonic for psoriasis and notunique from a homeopathic perspective. APRIL 2025 - VOLUME 20 | ISSUE NO. 04

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October2024November2024December2024February2025Symptom TrackingTwo-week aggravation of itching, followed by reduction in pain and itching; lesions still spreading;mood is better from pain reduction; feels anxious about food qualityNo itching most days of the week; some lesions resolving, others still spreading; flare of redness andscales after eating processed foods; noticeable decrease in hyperkeratosis in officeA downward spread of lower leg lesions, commonly seen in healing processes; itchy on the border wherethey spread; scalp itching is starting to improveScalp lesions resolved and hair regrowth; lower leg lesion without any scabs or scales significantly lessred, and still spreading downward; lesions on other body parts have resolved (glutes, thighs, knees,vulva, and elbows); noticeable reduction in anxiety, increased optimism about healing, and limitedstress around foodFollow upsAt this visit, additional interventions were introduced:Dietary modifications:Increased protein intake (20-30g per meal) for hormone andimmune optimizationAdjusted macronutrient timing for adrenal supportEmphasis on low-sugar fruits (e.g., berries over tropical fruits)for metabolic healthBotanicals: Nettle and/or dandelion leaf long-infusion once daily for theiralterative and nutritive propertiesSupplementation:Multivitamin with iron to replenish nutrients and antioxidantsVitamin D for suboptimal levelsGut support powder (L-glutamine, mucilaginous and anti-inflammatory herbs) to improve the intestinal barrier15After considering polycrest remedies fordermatologic conditions (Sulphur, Phosphorus,Arsenicum album, and Calcarea carbonica),Arsenicum album emerged as the most appropriatechoice. Key confirmatory symptoms included:health-related anxiety, racing thoughts at night,emotional despair over healing.Key Rubrics Used (Schroyens F. Synthesis TreasureEdition 2009V)Skin – Eruptions – psoriasis Skin – Eruptions – painfulHead – Eruptions – Occiput Head – Eruptions - scalpMind – Despair – recovery, ofMind – Anxiety – Health; about – about one’sown healthMind – Anxiety – children – about his Prescription: Arsenicum album 30C, 2 pellets perday Clinical Course & ProgressionAt the first follow-up two months later, DL reportedshe had started the homeopathic remedy. Shereported an initial two-week aggravation ofsymptoms, after which her itching and painmarkedly improved. Although the plaques persisted,the emotional burden had lightened, and dailyweeping had ceased.DERMATOLOGY AND AGING ISSUENETTLE & DANDELION LEAF

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Aranow C. Vitamin D and the Immune System. J Investig Med.2011;59(6):881-886. doi:10.231/JIM.0b013e31821b87551.Balamurugan D, Nayak C, Chattopadhyay A, et al. Individualizedhomeopathic medicines in the treatment of psoriasis vulgaris:double-blind, randomized, placebo-controlled trial. ComplementMed Res. 2023;30(4):317-331. doi:10.1159/000530180.2.Chan AA, Li H, Li W, et al. Association between baseline insulinresistance and psoriasis incidence: the Women's Health Initiative.Arch Dermatol Res. 2022;314(9):869-880. doi:10.1007/s00403-021-02298-93.Javadian Y, Sadeghi N, Sadeghi M, et al. The effect of mindfulnessand meditation on psoriasis: a systematic review. J Dermatol Treat.2022;33(1):1-7. doi:10.1080/09546634.2021.19090724.Sikora M, Stec A, Chrabaszcz M, et al. Clinical Implications ofIntestinal Barrier Damage in Psoriasis. J Inflamm Res. 2021;14:237-243. Published 2021 Jan 27. doi:10.2147/JIR.S2925445.REFERENCESDr. Marisa Kassimir received her Doctor ofNaturopathic Medicine (ND) from theSonoran University of Health Sciences inTempe, Arizona. Her clinical trainingprimarily focused on the care and treatmentof mental, pelvic, digestive, and hormonalhealth. She treats mainly with the modalitiesof homeopathic medicine, botanical medicine,mind-body medicine, nutrition, lifestyle, andnatural supplementation. Dr. Kassimir hasadditional training in craniosacral therapythrough the Upledger Institute. Prior tomedical school, she received her Bachelor ofScience in Biology and Genetics from theUniversity of Georgia and received acertificate in permaculture design from Havav’ Adam ecological farm in Israel. 16DERMATOLOGY AND AGING ISSUEAt subsequent visits, further refinements included:Omega-3 supplementation (fish oil) for its anti-inflammatory propertiesElectrolytes for improved hydrationInositol for insulin resistance, sleep support, andhormone balanceMind-body interventions, including vagus nerveexercises, grounding techniques, and guided meditation(which she later incorporated daily)Outcome & DiscussionOver the next several months, DL's psoriasis improvedgradually, as shown in Table 1 and Figures 1 and 2. Herprimary relief came from reduced pain and itching, greatlyenhancing her quality of life. She reported progressivelesion regression, with patches becoming smaller, lesshyperkeratotic, and less erythematous. A downward spreadof lower leg lesions, commonly seen in healing processes,was noted.At the five-month mark, her scalp lesions had fullyresolved, with noticeable hair regrowth, confirmed by bothher hairdresser and physical examination. Her mentalhealth showed profound improvement—in office, she wasnotably less anxious and more optimistic. Her outlook onfood shifted from avoidance to empowerment, focusing onresilience rather than restriction. This case is ongoing andwe are carefully monitoring for any plateau or regression insymptoms that would indicate the need for an increase inhomeopathic potency. ConclusionThis case underscores the importance of a multi-factorial,individualized approach to psoriasis. While homeopathyappeared to be the catalyst for healing, addressing guthealth, metabolic health, systemic inflammation, and stressmanagement played equally critical roles. The resolution ofDL’s most distressing symptoms illustrates the potential forintegrative therapies in complex chronic conditions.Her case signifies the importance of further research on theinterplay between stress, metabolic health, and gut integrityon skin disorders, as well as the role of homeopathy as amodulator of systemic inflammation and immune balance. Left Leg Before Treatment ProtocolLeft Leg After Treatment Protocol

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A skin condition is never just a skin condition—it is often areflection of deeper imbalances within the body. Gut health,in particular, plays a crucial role in dermatologic conditions,as disruptions in the microbiome, intestinal permeability,and systemic inflammation can manifest on the skin.³ Byaddressing digestive function, reducing inflammatorytriggers, and supporting detoxification pathways, we canachieve meaningful and lasting improvements in skin health. This case study exemplifies the power of this approach,demonstrating significant clinical improvement in a patientwith an undiagnosed skin condition. It highlights the efficacyof individualized, holistic treatment strategies—an essentialcomponent of naturopathic medical practice, even without adefinitive diagnosis. As naturopathic physicians, we have aprofound opportunity to help our patients heal from chronicskin concerns by looking beyond the surface and treating thewhole person. Case Presentation 35-year-old female FarrierIt all started with her hands—the very tools of her trade. As a farrier, she spent her days gripping metal, hammeringhorseshoes, and working in the elements, exposed to dust,sweat, and friction. The calluses were expected, but thepainful fissures and thickened, scaling skin that developedover time were not. At first, she brushed it off as anoccupational hazard, something a bit of balm andperseverance would fix. But as the seasons passed, her handsworsened. Soon, her feet followed, cracking painfully at theheels, making even walking uncomfortable. She had always prided herself on her resilience. A tough jobrequired a tough person, and she wasn’t one to complain.But when winter came, her symptoms eased—only to flareback up with a vengeance as soon as the warmer monthsreturned. The cycle was relentless. She tried everything: bagbalm, silver sulfadiazine, salves, homemade detergents.Nothing seemed to help. The more she worked, the worse itbecame. As a new mother determined to get healthy and tobe able to model this for her child, she realized it was time towork on herself more deeply. Unraveling the Underlying CausesHer medical history painted a telling picture. Though therewas no family history of chronic skin conditions like eczemaor psoriasis, and having struggled with recurrent bladderinfections from a young age, often enduring at least three tofour infections per year.Diagnosed with short ureters as a child, she surmised wasprescribed more than 100 rounds of antibiotics over theyears! The relentless cycle of UTIs had driven her to learnhow to be healthy, and in 2023, she attempted to manage herinfections with Uqora supplements. But by the end of thatyear, as she prepared for motherhood, she knew she needed amore comprehensive approach to her health. Resolute to findanswers, she sought naturopathic care, hoping for a solutionthat went beyond just symptom management.Digging Deeper: Testing & CluesDuring pregnancy, we focused on foundational health – diet,lifestyle, and nutraceuticals, improving her overall vitality.Five months postpartum, as she returned to work, her palmsand soles began thickening, cracking, peeling, and itching. Iknew it was time to dig deeper based on her skin symptomsalone as she did not report any GI symptoms and reportedregular well-formed daily bowel movements. Functional labtesting revealed critical insights. And treatment was targetedat the results of the GI-MAP. She remained committed to herdiet and nutraceuticals, experiencing steady progress—untilthe holidays triggered a setback. Indulging in comfort foods,she soon experienced a significant flare—the holidays.Letting her guard down, she indulged in comfort foods: a biteof mac and cheese, a cookie, a celebratory beer. Within days,her skin erupted, red and inflamed, her body seeminglyrevolting against her choices. When nausea set in, followedby vomiting, she knew something deeper was at play. It wasno longer just her hands and feet; her entire system seemedoff-balance.Functional testing provided striking insights. GI-MAP Results. - H. pylori: 1.02e3 (Elevated)- Inflammatory dysbiosis: Low Escherichia spp., Bacteroidesfragilis, Faecalibacterium prausnitzii; High Proteus mirabilis,Staphylococcus spp., Streptococcus spp.- Pancreatic Insufficiency: Elastase = 383 (Low, ideally >750)- Gut Inflammation: Calprotectin = 1227 (Normal <173) &Steatocrit = 8 (High)- Low Secretory IgA: <210 (Low)18DERMATOLOGY AND AGING ISSUE

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OAT & Mycotoxin Testing:Ochratoxin A positive =27.56 (Normal <7.5)Yeast & fungal overgrowth markers: 3-Oxoglutaric,Tartaric, Arabinose elevated, but not significantlyClostridia markers detectedNeurotransmitters & mitochondrial markers low, likelydue to gut dysbiosis and environmental exposuresHer GI-MAP results confirmed what her history suggested—her gut microbiome was imbalanced. H. pylori waselevated, and beneficial bacteria such as Faecalibacteriumprausnitzii and Bacteroides fragilis were alarmingly low. Atthe same time, opportunistic bacteria like Proteus mirabilis,Staphylococcus spp., and Streptococcus spp. thriving withovergrowth. Worse, her pancreatic enzyme production wasdeficient, suggesting she wasn’t digesting and absorbingnutrients effectively. Chronic inflammation was evident,with calprotectin levels soaring at 1227 (normal <173) andsecretory IgA dangerously low, leaving her gut barriercompromised. Further testing revealed the presence of yeast and fungalovergrowth markers on her Organic Acids Test (OAT),which suggested a systemic fungal burden. At the sametime, imbalances in neurotransmitters and mitochondrialfunction hinted at underlying stress and energy productiondeficits. This led us to Mycotoxin testing which provedpositive with elevated Ochratoxin A, a mycotoxin linked tomold exposure. This patient reports regular exposure tovisible mold, having a small farm and working withanimals and feed. I suspected it would have been muchhigher and it’s likely she was not detoxifying and excretingwell. Her symptoms were no longer a mystery. The combinationof gut dysbiosis, mycotoxin exposure, and foodintolerances had created a perfect storm that manifestedthrough her skin.It all started with her hands—the very tools of her trade. As a farrier, she spenther days gripping metal, hammering horseshoes, and working in the elements,exposed to dust, sweat, and friction. The calluses were expected, but thepainful fissures and thickened, scaling skin that developed over time were not. 19Connecting the Dots: A Root-Cause DiagnosisRather than viewing her condition as merely dermatologic, itbecame clear that her skin was reflecting internal dysfunction.Still unsure of the exact diagnosis, I focused on fungalovergrowth and trusting this intuitive instinct. Althoughtesting was positive for fungal overgrowth, it was not assignificant as I had predicted. My differential diagnosisincluded; Psoriasis (Palmoplantar type)Tinea pedis (chronic moccasin type)Hyperkeratotic palmar dermatitis/hand eczemaSevere xerosis or ichthyosis. Final Diagnosis:1. Palmoplantar Hyperkeratotic Dermatitis— chronic irritantcontact dermatitis exacerbated by repeated metal exposureand mechanical trauma. Partially responsive to barrierrestoration and emollients.Underlying Systemic Triggers:2. Gut Dysbiosis & Pancreatic Insufficiency →Compromising nutrient absorption, immune function, andskin repair3. Mycotoxin Exposure (Ochratoxin A) → Contributing tooxidative stress and immune dysregulation4. Food Intolerance-Induced Inflammation→ Drivingintestinal permeability and systemic immune activationAddressing only the skin would have been a temporary fix. Adeeper, whole-body approach was and always is necessary.A Comprehensive Treatment ApproachHealing had to happen from the inside out. Her treatmentplan targeted multiple systems, restoring gut health,eliminating mycotoxins, and reinforcing her skin’s naturalbarrier.APRIL 2025 - VOLUME 20 | ISSUE NO. 04NATUROPATHIC DOCTOR NEWS & REVIEW

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Phase 1: 1 Gut & Mycotoxin DetoxificationBroad-spectrum antimicrobial and biofilm disruptor, 2 capsBIDA dairy free immunoglobulin concentrate for mucosalimmune support and binder, 4 caps dailyOrganic Chlorella tablets to support metal binding anddetox, 5 tablets qdPhase 2: Skin Barrier Repair & Symptom ManagementNeem Oil topical applied post-shower to calm irritation, 1-2x/dayPatient preferred to mix this with Bag BalmPhase 3: Hydration & Lifestyle AdjustmentsStrict elimination of dairy, and potato-grain combinationsDaily water and electrolyte intake to support detoxificationand hydrationWearing gloves: To reduce metal exposure (initial resistance,later compliance)With patience and adherence, she slowly saw improvements—first in digestion, then in her energy levels, and finally, inher skin.Follow up Visit:One month later, patient-initiated plan, and then the holidayindulgences induced vomiting followed by chronic diarrhealasting 6 weeks. It is unclear to me what caused this flare. Itcould have resulted from die-off, and an additional bindershould have been included, possibly due to acute gastritis. Treatment Plan AdjustmentsPhase 1: Gut & Mycotoxin DetoxificationA broad-spectrum antifungal and antimicrobial, → 2 capsBID which includes; Neem (Azadirachta indica) leaf extract300 mg, and a blend of AmlaOxy (Phyllanthus emblica)fruit, Belleric myrobalan (Terminalia bellerica) fruit,Chebulic myrobalan (Terminalia chebula) fruit, Indianmadder (Rubia cordifolia) stem, Indian tinospora(Tinospora cordifolia) stemA dairy free immunoglobulin concentrate for mucosalimmune support and binder - mucosal immune support,binder, → 2 caps BIDACS spray for Ochratoxin A (aflatoxin). To help treat themold →12 sprays po BID, hold and swallow. No food ordrink for 2 minutes. (prescribed but the patient did not use). 20Phase 2: Skin Barrier Repair & Symptom ManagementNeem Oil topical applied post-shower to calm irritation,1-2x/dayPatient preferred to mix this with Bag BalmPhase 3: Hydration & Lifestyle AdjustmentsStrict elimination of dairy, and potato-graincombinationsDaily water and electrolyte intake to supportdetoxification and hydrationWearing gloves: To reduce metal exposure (initialresistance, later compliance)With patience and adherence, she slowly saw improvements—first in digestion, then in her energy levels, and finally, in herskin.Follow up Visit:One month later, patient-initiated plan, and then the holidayindulgences induced vomiting followed by chronic diarrhealasting 6 weeks. It is unclear to me what caused this flare. Itcould have resulted from die-off, and an additional bindershould have been included, possibly due to acute gastritis. Treatment Plan AdjustmentsPhase 1: Gut & Mycotoxin DetoxificationA broad-spectrum antifungal and antimicrobial, → 2caps BID which includes; Neem (Azadirachta indica) leafextract 300 mg, and a blend of AmlaOxy (Phyllanthusemblica) fruit, Belleric myrobalan (Terminalia bellerica)fruit, Chebulic myrobalan (Terminalia chebula) fruit,Indian madder (Rubia cordifolia) stem, Indian tinospora(Tinospora cordifolia) stemA dairy free immunoglobulin concentrate for mucosalimmune support and binder - mucosal immune support,binder, → 2 caps BIDACS spray for Ochratoxin A (aflatoxin). To help treat themold →12 sprays po BID, hold and swallow. No food ordrink for 2 minutes. (prescribed but the patient did notuse). Phase 2: Skin Barrier RepairNeem Oil topical, applied 2x/dayAgain, I urge the patient to wear gloves when working tominimize potential reaction to metal.APRIL 2025 - VOLUME 20 | ISSUE NO. 04NATUROPATHIC DOCTOR NEWS & REVIEW

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Dr. Carrie Phillips, ND, RH (AHG), is alicensed naturopathic physician specializingin dermatology, pediatrics, and shamanicmedicine. She operates a hybrid clinic inLakebay, WA, combining traditionalhealing practices with modern naturopathiccare. With a deep respect for the body'sinnate wisdom, she focuses on uncoveringroot causes and restoring balance. When notin practice, she enjoys life with her husband,four children, and a small menagerie ofanimals. Her approach is both practical andintuitive, bridging science and traditionsupporting whole-body health in an effort tohelp patients glow from the inside out—because skin rarely keeps secrets. In ConclusionThis case highlights the importance of addressing systemicinflammation, gut dysbiosis, and mycotoxin burden inchronic occupational dermatitis while emphasizing the valueof trusting our clinical intuition as healers. The patient’ssignificant reduction in fissuring and scaling confirmsintegrative efficacy, while persistent erythema suggeststransient inflammatory reactivity from diet and detoxprocesses. Ongoing monitoring of gut health and mycotoxinclearance remains essential. If symptoms persist or continueto flare, I could consider a referral for colonoscopy. Additionally, even after the skin clears up, it is crucial tocontinue treating systemically to ensure complete resolutionof underlying dysfunction. If treatment stops prematurely,the root causes—whether gut dysbiosis, toxic burden, orimmune dysregulation—may re-emerge, leading to symptomrelapse. Long-term management should include maintenanceprobiotic support, periodic detoxification, and avoidance ofdietary triggers to sustain remission and prevent future flare-ups. This case also underscores the growing need for naturopathicdermatology in patients with chronic, treatment-resistantskin conditions. Many individuals find little relief inconventional dermatology and seek our help to treat theircomplex chronic skin conditions, as suppressive therapies failto address underlying systemic imbalances. Naturopathicmedicine is critical in providing patients with sustainable,root-cause solutions to persistent skin concerns.1. Lim HW, Collins SAB, Resneck JS, et al. *The burden of skindisease in the United States. American Academy of Dermatology.Published 2017. Accessed February 28, 2025.[https://www.aad.org/about/burden-of-skin-disease] 2. Lio P. The naturopathic approach to skin disorders. Get WellHere. Published 2022. Accessed February 28, 2025.[https://getwellhere.com/the-naturopathic-approach-to-skin-disorders]3. Naturopathic and integrative dermatology series. LearnSkin.Published 2023. Accessed February 28, 2025.[https://www.learnskin.com/series/naturopathic-and-integrative-dermatology-series] 4. Hengge UR, Ruzicka T, Schwartz RA, Cork MJ. Adverse effectsof topical glucocorticosteroids. J Am Acad Dermatol. 2006;54(1):1-15.5. Bowe WP, Logan AC. Acne vulgaris, probiotics, and the gut-brain-skin axis—back to the future? Gut Pathog. 2011;3(1):1-11.REFERENCES22DERMATOLOGY AND AGING ISSUERight Heel Before Treatment ProtocolRight Palm Before Treatment Protocol

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Topical Treatments for RosaceaA Clinical Comparison of Efficacy & PatientOutcomesJORDAN ROBERTSON, NDA detailed evaluation of the most commonlyprescribed topical treatments for rosacea,comparing efficacy, patient suitability, and clinicaloutcomes.Rosacea significantly affects patients' quality of life, andevidence indicates that any treatment enhances quality of lifecompared to pre-treatment status. However, recent researchshows that treatment patterns have not aligned with evolvingguidelines. This article reviews the evidence for major topicaltreatments, emphasizing their comparative efficacy,mechanisms of action, and practical considerations. Patientsshould understand the range of options available to treattheir rosacea, especially since the evidence for each choice isrelatively similar. The Standard of Care DiscrepancyThe guidelines for rosacea have moved away from strictclassifications of rosacea to phenotypic descriptions,accounting for the fact that many patients with rosacea fallin multiple sub-categories¹, and prescriptions should bechosen based on shared decision making and patient-centricgoals. Current guidelines recommend three primary topicalmedications for rosacea: ivermectin, azelaic acid, andmetronidazole.² However, a recent survey of 6,000 USdermatologists revealed that 98% primarily prescribemetronidazole, with only 9.1% using azelaic acid and 4.1%ivermectin.³TOLLE TOTUM23NATUROPATHIC DOCTOR NEWS & REVIEWDERMATOLOGY AND AGING ISSUEMany practitioners, especially those in group practices,demonstrate little flexibility in treatment selection regardlessof patient presentation. Despite the evidence for equivocalresults, and possible subtypes of rosacea patients who benefitfrom one treatment over another, patients are being deniedthe opportunity to understand all available options beforebeing handed a prescription. Comparing Treatment Options for Rosacea Ivermectin (1%)Ivermectin therapy targets the dermatological mite,Demodex, and reduces the Demodex lesion count by directlydecreasing mite density through anti-inflammatorymechanisms.⁴ Despite its high cost, ivermectin offers lastingimprovements beyond the acute phase of treatment. It mayaddress the root cause of rosacea in many patients, which forsome may include a high density of Demodex mites.⁵ Pros:Superior mite-killing efficacy against Demodex, a keyfactor in rosacea pathophysiologyAnti-inflammatory properties independent of mitereduction⁶Faster improvement (visible by week 4) than othertopicalsLow relapse rate—many patients maintain improvementfor 32+ weeks after a 16-week treatment course⁵Fewer side effects than other optionsTreats both papules/pustules and shows some efficacy forerythema⁷

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24NATUROPATHIC DOCTOR NEWS & REVIEWCons:Cost ($150-250 for a 16-week supply)Prescription requiredLimited accessibility in some regionsAzelaic Acid (15-20%)Originally formulated to treat hyperpigmentation, azelaic acidhas emerged as a viable solution for rosacea, with bothantimicrobial and anti-inflammatory effects.⁸ Available inhigher concentrations as a prescription, azelaic acid has neverbeen formally studied in a dose lower than 15%. In head-to-head trials, it outperforms metronidazole and performs equallywell to ivermectin.² Pros:61-74% reduction in inflammatory lesions by 12 weeks⁹′¹⁰Fewer side effects than metronidazole¹¹Some effect on erythema⁸ Lower-concentration versions (10-14%) available over-the-counter** **this has not been formally studied in clinical trialsCons:Higher concentrations (15-20%) require a prescriptionPotential for skin irritation, especially at 20% concentrationTwice-daily application required for optimal resultsNo studies on concentrations below 15%, leavinguncertainty about OTC product efficacyMetronidazole (0.75-1%)Metronidazole is the most commonly prescribed treatmentfor rosacea and operates through two mechanisms of action:antimicrobial and anti-inflammatory.² As a topical agent, itcan cause fewer side effects than long-term antibiotic use forrosacea. It has remained the most affordable treatmentoption for patients.¹² Newer research suggests thatmetronidazole may be the third most effective choice(following ivermectin and azelaic acid).¹³ Pros:More affordable than alternativesLong history of useWidely prescribed and availableAnti-inflammatory propertiesCons:Performs equal to or worse than alternatives in head-to-head studies²′¹³Less effective at treating erythemaUncertain mechanism against specific rosacea pathogensMay require longer-term use with higher relapse ratesDERMATOLOGY AND AGING ISSUEThese collagen peptides are specifically formulated to enhance the quality ofskin, hair, and nails. With small peptides consisting of only 4-5 amino acids,they are designed for superior absorption, minimizing the need for digestionand ensuring optimal bioavailability.• Clinically proven to speed nail growth, reduce nail chipping and reduce cellulite appearance after 2 to 3 months• Clinically proven to reduce eye wrinkles in 4 weeks• Speeds wound healing and helps reduce scarringRebuild, repair, and restorewith bioactive peptides.ONLY AVAILABLE IN CANADA

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25NATUROPATHIC DOCTOR NEWS & REVIEWOverall, these three treatment options provide substantialsupport for patients with various phenotypes of rosacea andcan enhance quality of life and skin health in as little as 12weeks. In a recent systematic review of rosacea solutions, eachoption discussed here emerged as viable, presenting positive andnegative considerations unique to every patient. Clinicians havethe opportunity to educate patients about these options andassist in selecting a solution that aligns with both the patient’sgoals and their clinical picture. Key Takeaways: The decision to select a topical treatment should consider:1. Primary symptoms – predominance of papules/pustulesversus erythema2. Skin type and tolerance** – consider potential for irritation3. Cost and accessibility – including insurance coverage andprescription access4. Patient preferences – compliance with application frequencyand vehicle formulation5. Skin of color considerations – certain treatments such asazelaic acid may affect melanocytes. APRIL 2025 - VOLUME 20 | ISSUE NO. 04Concluding ThoughtsEvidence indicates that ivermectin may provide the highesteffectiveness and lasting results, especially for patients withpronounced papulopustular components. Azelaic acid serves asa robust alternative with fewer side effects than metronidazole. Timely, targeted treatment for rosacea is essential to preventirreversible changes like telangiectasia. The tendency to rely onmetronidazole despite evidence supporting alternativesunderscores the need for practitioner flexibility in treatmentselection and ongoing evaluation of treatment effectiveness. Thechronicity of rosacea may lead us to deprioritize completeresolution, which can compromise patient quality of life andresult in irreversible skin changes. Dr. Jordan Robertson ND is on a mission to createa standard of care of evidence based naturopathicmedicine while reducing the unpaid-research-labour of naturopathic clinicians. She is thefounder of The Confident Clinician, a clinicaldecision making tool and database builtspecifically for Naturopathic Doctors. She is agraduate of CCNM (2008) and has a 15 yearcareer teaching critical appraisal, research inintegrative medicine and clinical nutrition atMcMaster University Canada. Jordan can bereached at hello@theconfidentclinicianclub.com 1. Schaller M, Almeida LMC, Bewley A, et al. Recommendations for rosaceadiagnosis, classification and management: update from the global ROSaceaCOnsensus 2019 panel. Br J Dermatol. 2020;182(5):1269-1276.doi:10.1111/bjd.184202. Frazier W, Zemtsov RK, Ge Y. Rosacea: Common Questions and Answers.Am Fam physician. 2024;109(6):533-542.3. Nicholas A, Spraul A, Fleischer AB. Prescriber Phenotypes: Variability inTopical Rosacea Treatment Patterns Among United States Dermatologists. JClin Med. 2024;13(20):6275. doi:10.3390/jcm132062754. Li J, Wei E, Reisinger A, French LE, Clanner-Engelshofen BM, Reinholz M.Comparison of Different Anti-Demodex Strategies: A Systematic Review andMeta-Analysis. Dermatology. 2023;239(1):12-31. doi:10.1159/0005262965. Trave I, Micalizzi C, Cozzani E, Gasparini G, Parodi A. PapulopustularRosacea Treated With Ivermectin 1% Cream: Remission of the Demodex MiteInfestation Over Time and Evaluation of Clinical Relapses. Dermatol PrConcept. 2022;12(4):e2022201. doi:10.5826/dpc.1204a2016. YEH MCH, TSAI J, HUANG YC, WANG HH. Topical MetronidazoleVersus Ivermectin for Low-density Demodex Rosacea: A Rater-blinded,Randomized, Split-face Trial. Acta Derm-Venereol. 2022;102:4391.doi:10.2340/actadv.v102.43917. Singh R, Perche PO, Kelly KA, et al. Topical Ivermectin Is Associated WithImproved Erythematotelangiectatic, Papulopustular, and Phymatous Rosaceain a Secondary Analysis. J drugs Dermatol : JDD. 2023;22(10):1063-1064.REFERENCES8. Feng X, Shang J, Gu Z, Gong J, Chen Y, Liu Y. Azelaic Acid:Mechanisms of Action and Clinical Applications. Clin, Cosmet InvestigDermatol. 2024;17:2359-2371. doi:10.2147/ccid.s4852379. Hua NJ, Chen J, Geng RSQ, Sibbald RG, Sibbald C. Efficacy ofTreatments in Reducing Facial Erythema in Rosacea: A Systematic Review.J Cutan Med Surg. Published online 2024:12034754241287546.doi:10.1177/1203475424128754610. King S, Campbell J, Rowe R, Daly M, Moncrieff G, Maybury C. Asystematic review to evaluate the efficacy of azelaic acid in the managementof acne, rosacea, melasma and skin aging. J Cosmet Dermatol.2023;22(10):2650-2662. doi:10.1111/jocd.1592311. Williamson T, LaRose A, Cameron J, et al. Rosacea TreatmentSatisfaction: Matching Adjusted Indirect Treatment Comparison Analysis ofMetronidazole Gel or Cream vs Azelaic Acid Foam. J drugs Dermatol : JDD.2020;19(3):295-304.12. Xiao W, Chen M, Wang B, et al. Efficacy and safety of antibiotic agentsin the treatment of rosacea: a systemic network meta-analysis. FrontPharmacol. 2023;14:1169916. doi:10.3389/fphar.2023.116991613. Geng RSQ, Sood S, Hua N, Chen J, Sibbald RG, Sibbald C. Efficacy ofTreatments in Reducing Inflammatory Lesion Count in Rosacea: ASystematic Review. J Cutan Med Surg. 2024;28(4):352-359.doi:10.1177/12034754241253195

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A Novel Way To Support Muscles and BonesFortetropin is a bioactive myostatin inhibitor derived fromfertilized egg yolk extract. Fortetropin increases muscleprotein synthesis and inhibits muscle atrophy by reducingcirculating myostatin. Fortetropin increases lean body mass,reduces markers of protein breakdown consistent withinhibition of myostatin, and increases mTOR signaling,which is associated with muscle growth. All of these actionsare beneficial to both muscle and bone strength.⁷⁻⁹Research demonstrates Fortetropin's effects on proteinsynthesis and muscle health. For example, 21 days ofFortetropin supplementation in 10 healthy older men and 10women resulted in 18% higher muscle protein synthesiscompared with a placebo.⁸ According to the lead researcher,"Stimulating muscle protein synthesis in elderly patientscould potentially result in increased muscle mass and betteroutcomes for those with sarcopenia."In another human study of 37 resistance-trained college-agemales, lean body mass dramatically increased in patientsgiven Fortetropin compared with placebo.⁷ The men taking19.8 grams had greater lean body mass improvements thanthose given 6.6 grams. In both groups, there werepronounced increases in muscle thickness, and Fortetropindecreased markers of protein breakdown. Clearly, a better alternative is needed, which may very wellbe the inhibition of myostatin. Myostatin inhibition is avital clinical consideration for functional medicine providerswho want to get at one of the root causes of low bonedensity. What Is Myostatin?Myostatin is a growth differentiation factor (GDF-8) in thetransforming growth factor-beta (TGF-β) superfamily. Itblocks skeletal muscle growth and is involved in sarcopenia(muscle wasting).² However, emerging research suggests thatmyostatin also involves bone breakdown and osteoporosis.From Building Muscle to Protecting BoneA lot of the initial research on the inhibition of myostatinindicates that blocking myostatin can lead to increasedprotein synthesis, improved lean body mass, and musclegrowth. It is becoming apparent that inhibiting myostatinalso can play a role in bone health.Muscle and bone health are connected. By increasing musclemass, more mechanical load is generated on bones. Whenthis happens, it stimulates the activity of bone-building cellsknown as osteoblasts, which enhances bone mineral density(BMD). Myostatin is highly expressed in sites of fractures.³Increasing muscle mass by inhibiting myostatin improvesbone mineral density and reduces fracture risk.³ In addition, inhibiting myostatin improves bone resorption,the process by which damaged bone is broken down andabsorbed by the body.³ Bone remodeling regulates both thequantity and quality of bone.⁴ During bone remodeling,osteoclasts first resorb bone, and then bone-buildingosteoblasts fill in the spaces created by this process.⁴ Bone formation is a balancing act between the activity ofbone-building osteoblasts and bone-destroying osteoclasts.Blocking myostatin can lead to bone formation byincreasing the activity of osteoblasts and suppressingosteoclasts.³ The relationship between the muscles and bones is morethan just mechanical; muscle increases the load, and boneacts as an attachment site. Emerging evidence suggests thatbone and muscle act as secretory endocrine organs thataffect each other's function.⁵ The crosstalk that occursbetween muscle and bone occurs due to a number of factors,including bone-destroying signals conveyed by myostatin.⁵ 27DERMATOLOGY AND AGING ISSUESarcopenia's Connection to Bone LossSarcopenia is a progressive decline of skeletal muscle massand function. Up to 29% of older persons have this muscledisease.² The presence of low muscle mass plus low musclestrength or low physical performance indicates a sarcopeniadiagnosis.²Inhibiting myostatin leads to the prevention of sarcopenia,which indirectly supports bone health.⁶ The connectionbetween muscle and bone health is evident in the newlycreated term osteosarcopenia, which refers to the existence ofboth osteoporosis and sarcopenia in a patient.⁶ Muscle-boneinteractions at the biomechanical, cellular, paracrine,endocrine, neuronal, or nutritional levels may play a role inthe development of osteosarcopenia.⁶

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0428In 24 healthy young men whounderwent single-leg immobilization fortwo weeks, Fortetropin also blocked therise in circulating myostatin that wouldhave normally occurred.¹⁰Animal research supports Fortetropin'suse, such as a study in dogs sufferingfrom disuse muscle atrophy afterundergoing tibial plateau levelingosteotomy (TPLO) surgery.⁹ The dogsgiven Fortetropin experienced nochange in myostatin levels. Bycomparison, myostatin levels increasedover eight weeks in the placebo-treateddogs. Thigh circumference did notchange in the animals givenFortetropin, while the placebo-treateddogs had a reduction in thighcircumference over eight weeks. Fortetropin's Effects on BonesBy inhibiting protein breakdown andpromoting protein synthesis,Fortetropin may also benefit bonehealth.⁸ A low-protein diet or a reducedability to synthesize protein cansuppress bone formation, resulting inlower bone density and fragility.¹¹Additionally, Fortetropin's ability toinhibit muscle loss is connected toprotein metabolism⁷ and can potentiallyimprove bone weakness and reducefracture risk.Inhibiting Myostatin Through LifestyleIn addition to supplementing withFortetropin, I encourage patients tofocus on lifestyle-related approachesthat can support myostatin inhibition.These include:• Engaging in resistance exercise• Eating a high-protein diet• Consuming a nutritious diet with avariety of phytonutrients• Getting enough sleep to help the bodyhealNATUROPATHIC DOCTOR NEWS & REVIEW

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REFERENCESLeBoff MS, Greenspan SL, Insogna KL, et al. The clinician's guide toprevention and treatment of osteoporosis. Osteoporos Int.2022;33(10):2049-2102.1.Cho MR, Lee S, Song SK. A Review of Sarcopenia Pathophysiology,Diagnosis, Treatment and Future Direction. J Korean Med Sci.2022;37(18):e146.2.Cui Y, Yi Q, Sun W, et al. Molecular basis and therapeutic potentialof myostatin on bone formation and metabolism in orthopedic disease.Biofactors. 2023;49(1):21-31.3.Ikeda K, Takeshita S. The role of osteoclast differentiation andfunction in skeletal homeostasis. J Biochem. 2016;159(1):1-8.4.Li G, Zhang L, Wang D, et al. Muscle-bone crosstalk and potentialtherapies for sarco-osteoporosis. J Cell Biochem. 2019;120(9):14262-14273.5.Gielen E, Dupont J, Dejaeger M, Laurent MR. Sarcopenia,osteoporosis and frailty. Metabolism. 2023;145:155638.6.Sharp MH, Lowery RP, Mobley CB, et al. The Effects of FortetropinSupplementation on Body Composition, Strength, and Power inHumans and Mechanism of Action in a Rodent Model. J Am CollNutr. 2016;35(8):679-691.7.Evans W, Shankaran M, Nyangau E, et al. Effects of Fortetropin onthe Rate of Muscle Protein Synthesis in Older Men and Women: ARandomized, Double-Blinded, Placebo-Controlled Study. J GerontolA Biol Sci Med Sci. 2021;76(1):108-114.8.White DA, Harkin KR, Roush JK, Renberg WC, Biller D.Fortetropin inhibits disuse muscle atrophy in dogs after tibial plateauleveling osteotomy. PLoS One. 2020;15(4):e0231306.9.Lim C, McKendry J, Giacomin T, et al. Fortetropin supplementationprevents the rise in circulating myostatin but not disuse-inducedmuscle atrophy in young men with limb immobilization: A randomizedcontrolled trial. PLoS One. 2023;18(5):e0286222.10.Genaro Pde S, Martini LA. Effect of protein intake on bone andmuscle mass in the elderly. Nutr Rev. 2010;68(10):616-623.11.ConclusionEmerging evidence indicates that inhibition of myostatin is aneffective way to promote muscle and bone health.Osteoporosis and fractures can severely limit the independenceof older patients, and taking a proactive approach tosupporting bone health can lead to greater mobility as patientsage. Fortetropin, a bioactive myostatin inhibitor derived fromfertilized egg yolk extract, effectively inhibits myostatin andpromotes lean body mass, protein synthesis, and musclehealth. Combining Fortetropin with lifestyle approaches suchas resistance exercise and eating enough protein can yieldexcellent results.29DERMATOLOGY AND AGING ISSUEDr. Chris D. Meletis is an educator, internationalauthor, and lecturer. His mission is “Changing theWorld’s Health One Person at a Time.” He believesthat when people become educated about theirbodies, actual change and wellness begin.He has written over 200 nationally published articlesand over a dozen books to share his passion andamazement of the human body and what is requiredto maintain health. Dr. Meletis served as Dean ofNaturopathic Medicine and Chief Medical Officerfor seven years at NCNM, the oldest naturopathicuniversity in North America. The AmericanAssociation of Naturopathic Physicians awardedhim the 2003 Physician of the Year.

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Case Analysis Despite the current therapies she has undergone, whichinclude more invasive procedures and medications withstrong pharmacologic effects (CBD), the vital force stillmanages to express a clear symptom profile on which tobase the homœpathic diagnosis. This indicates a verygood prognosis. Often, these interventions cancomplicate a case because key symptoms necessary toselect the best remedy are altered or obscured. The factthat the pain continues to increase suggests that thedisease is still in its ascendancy and that properhomœpathic treatment should significantly and rapidlyshorten the course of illness without postherpeticsequelae. Homeopathic case-taking in acute diseases emphasizeschanges from a previously healthy state. The primarycomplaints and sensations described as "as if” areexamined thoroughly. Specific anatomical locations andaffected tissues are documented. Natural factors causingslight increases or decreases in symptoms, even minorrelief, are known as modalities and receive specialattention because they often represent the mostindividualized symptoms. The same approach is appliedto all secondary or accessory complaints, referred to asconcomitants. While the information necessary fordiagnosis is important, identifying specific details aboutthis individual case that distinguish it from genericmedical diagnoses is vital for finding the besthomeopathic remedy. This also includes the patient'soverall condition and sensitivity, such as theirperceptions of temperature, thirst, and mood, to name afew. If symptoms diverge from the normal baselinestate, they should be considered significant forindividualizing the acute disease. For instance, ifsomeone usually feels chilly but experiences heat duringthe acute illness, or if they typically have low thirst butsuddenly become very thirsty, these changes arenoteworthy. The greater the change in these symptoms,the more likely they need a genuine acute remedy ratherthan the chronic remedy that addresses their long-standing health issues. In this case, the vesicular eruptions are located on theleft lateral thigh and are accompanied by a burning andtingling sensation that worsens with cold air and initialmovement. Additionally, the case is marked by aconcurrent feeling of heaviness in the lumbar spine thatincreases during stepping. She is shivering, experiencingchills, and has a strong craving for cold drinks.Initial Case History A 51-year-old female presents with acute shingles. She takes amethylated B-complex, internal CBD that “takes the edge off,”and an antiviral herbal tincture containing Lomatium, SaintJohn's Wort, Cayenne, and Echinacea. She has also received IVinfusions of Vitamin C and lysine without benefit and isscheduled for IV ozone the following day. Symptoms began 10 days ago with tingling in the left thigh. Shehas been experiencing stress from work, traveling to visitfamily, and especially the recent illness of her son, who was outof school with the flu. She feels significant stress when he is illdue to his history of seizures and the fear that they may return. The tingling sensation has intensified into pain shooting upand down the leg, accompanied by numbness. After five days,blisters appeared on the outer thigh. The friction from clothingand dressing aggravates the blisters. Getting up in the morningor from bed at night is extremely painful. The blisters burn andtingle, and sharp pain is experienced upon first movement,which eases as she continues to walk. The cool air is painful,and she begins to shiver; however, she starts to feel better onceshe warms up. She wishes to have the heating pad in bed. Her entire spine aches when she walks. "It feels like a heavysensation moving downward with each step, almost like thepounding of each step vibrating through it.” Today, the itchingfrom the blisters has intensified, and she has a new achyheadache at the back of her head and cervical pain thatworsens with noise. Sleep is fitful, with tossing and turning and bizarre dreams. “IfI can lie in one place, then I feel good, but I have to move. It’slike I need to move and stretch and roll over.” She gets deepchills to the bone, shivers, and needs blankets. She frequentlythirsts for cold water, even after drinking. She also experiencesmild nausea in the epigastric region after eating. She experiences symptoms of menopause, such as hot flashes,but has no other medical diagnoses. Additionally, there are norelevant psychosocial factors, review of systems findings, pastmedical history, or family history related to this acutecondition. Objectively, I note the presence of many red singular vesiclesalong the entire surface of the left lateral thigh from hip toknee, with larger coalescing grayish vesicles. There is nodischarge and no surrounding discoloration of the skin.Regrettably, an initial photo was not taken, but the lesions andarea affected were impressively extensive.31DERMATOLOGY AND AGING ISSUE

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0432TBR2¹ - The full rubric breadcrumbs have been left intact for complete reference.1. General [non regional]{776 1686}; Generals; Eruptions; Vesicles [and bullæ [blisters]] {1511}; zoster [zona, shingles] {1521}(11)2. General [non regional]{776 1686}; Generals; Eruptions; Vesicles [and bullæ [blisters]] {1511} (77) 3. Modalities {1687 1694}; Temperature, Seasons, Weather; Warm [& warmth] in general, from [+ amel. Cold in general]{1725}; Covering [warm covers], from {1731} [+ amel. Uncovering]; amel. {1732} [+ aggr. Uncovering] (56) 4. Systemic {301 775}; Thermoregulatory; Chill; Shivering [shuddering, trembling], with {681} (30)5. General [non regional]{776 1686}; Generals; Generals; Sensibility altered [paræsthesiæ, pseudoæsthesiæ] {1071}; prickling[tingling, ‘pins & needles’], outer parts {1078}; single parts, as if asleep [‘pins & needles’] {1080} (106)6. Modalities {1687 1694}; From Situation & Circumstance; Rising, on [on straightening-up, becoming erect] {2120}; bed, onrising from [on getting out of bed] {2122} (76) 7. Regional {001 300}; Extremities; Lower Limbs; Hip, region of [loins] {275} (111) 8. Modalities {1687 1694}; From Situation & Circumstance; Stepping [treading] hard, from {2170} (68) 9. Regional {001 300}; Trunk [torso]; Back; lumbosacral region [small of back] {252} (111)10. General [non regional]{776 1686}; Generals; Generals; Pressing [& aching], outer parts {1050}; weight, as if from a heavy{1057} (94) NATUROPATHIC DOCTOR NEWS & REVIEWDifferentiating remedies by briefly utilizing both acomprehensive materia medica like Hahnemann, T.F. Allen,or Hering and a summary materia medica such as Phatak orMorrison is an effective strategy to capture both the detailsand the overall context of how the remedy relates to the caseat hand. Rhus ToxicodendronAllen’s Encyclopedia of Pure Materia Medica1200 - Vesicles, most of which contain a milky but some alsocontain a clear liquid, become confluent; this condition laststhree days, after which the skin desquamates [4]. 1201 - A burning eruption of small blisters, filled with water,with redness of the skin of the whole body except on the scalp,palms of the hands, and soles of the feet [23]. Repertorization was completed using The Bönninghausen Repertory (TBR2). Some commonly indicated remedies for shingles,like Ranunculus bulbosus and Mezereum, are underrepresented in this repertory. If the best options identified throughrepertorization don't seem suitable, one can refer directly to the materia medica of these remedies for a quick review.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0433Phatak’s Materia Medica of HomœopathicMedicinesAffections of Nerves.Pains are Tearing, Shooting, Stitching, worse at Night,Cannot Rest in any position.Numbness.Worse: Cold air, Uncovering parts, Beginning of Motion.Better: Continued motion. Heat. Change of position.Stomach: Craves cold drinks. Great thirst.Neck and Back: Lumbago.Extremities: Pains down the back of thighs.Skin: Skin sensitive to cold air. Eruptions: Vesicular.Fever: Easily chilled, worse least uncovering.Morrison’s Desktop Guide to Keynotes andConfirmatory Symptoms General aggravation from coldGeneral aggravation from uncoveringGeneral amelioration from motionDesires cold drinksLow back painBack pain, better heatShinglesHe experiences restless sleep, constantly shifts, and can notfind a comfortable position.NATUROPATHIC DOCTOR NEWS & REVIEWCocculus indicus causes numbness but does not prominentlyexhibit relief from motion as a significant symptom, nor is ithighly associated with vesicular or herpetic eruptions.Pulsatilla is well represented in analysis, but many of itssymptoms contradict the patient’s condition, such asimprovement from uncovering and a lack of thirst. Bryoniaalba is considered because of its aggravation from stepping,and while symptoms of vesicles are noted for this remedy, itdoes not improve with continued motion. Rhus Toxicodendron is one of the most commonly indicatedremedies for acute uncomplicated shingles, but there is nospecific homeopathic remedy for any diagnosis.Administering this remedy blindly based on pathology willmostly lead to failure, with occasional success. Thisparticular case involves Rhus-t shingles because theindividual symptoms of Rhus-t are clearly present in thepatient, unlike the symptoms associated with Arsenicum,Lachesis, or any other common shingles remedy.Plan: Rhus Toxicodendron 200c in 1oz dropper with 80%water, 20% brandy, one dropperful immediately, succussing5 times before a dose. Follow-up check in 5 hours to evaluateresponse to the initial dose.5 Hours After Initial Prescription: The itching from thelesions has turned into more of a stinging sensation. There isno longer any shooting pain down the legs. Plan: There is a clear positive response to the remedy. Repeatif shooting pains return and at bedtime.Follow-up after 24 Hours: The shooting pains, back pain, andchills have improved. Each remedy dose increases thetingling and burning in the blisters, which lasts for a longtime. Plan: She continues to respond positively but experienceslocalized tingling and burning sensations in the lesions aftereach dose. The remedy is adjusted to 1 dropperful in 4 oz ofwater, stirred gently, and one teaspoon is taken from theglass. Repeat if symptoms worsen and at bedtime.Follow-up Day 2: The blisters are scabbing. There is noheadache or back pain, and the burning pain does notaggravate after a dose.Plan: Adjusting the dosage alleviated therapeuticaggravation, and she still responded positively to thetreatment. If symptoms recur, repeat the treatment asneeded. Call if there is no further improvement. 1410 - While walking in the cold air, he cannot be warmed byany covering; he has a shaking chill in the open air, withviolent thirst and mucus between the lips that makes themstick together [1]. 932 - One hand's index and middle fingers feel numb and asleepin the morning [1].1042 - Pain, like a tingling, in the tibiæ at night while the feetare crossed; she is constantly obliged to move the legs back andforth, and on this account, she cannot sleep [1]. 970 - A pressive pain in both hip joints on every step and aparalyzed sensation in the anterior muscles of the thighs [1].979 - A left thigh tension extending downward from the hipjoint [3].836 - Heaviness and pressure in the small of the back, as if onehad received a blow while sitting (after six days), [3].

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SulfurAllen’s Encyclopedia of Pure Materia Medica3414 - Rash over the whole body, with itching sticking [1]. 3416 - *Nettlerash, with fever (twenty-sixth day), [1].1289 - Great thirst, always more thirst than hunger [3].1399 - At night, qualmish nausea and working at the pit ofthe stomach, as in waterbrash [1].Arsenicum album and Nux vomica rank higher than Sulphurin the repertory chart, yet intense coldness accompaniesnearly all the complaints associated with these remedies.Additionally, Sulphur causes skin eruptions with itching andmay present with increased thirst and reduced appetite. It isalso frequently indicated to address lingering symptomsfollowing acute illness.Plan: Sulfur 200c in 1oz dropper with 80% water and 20%brandy, one dropper immediately, succussing 5 times beforea dose, and to be repeated if symptoms relapse.The patient reported a complete resolution of the remainingsymptoms with Sulphur 200c.APRIL 2025 - VOLUME 20 | ISSUE NO. 0434NATUROPATHIC DOCTOR NEWS & REVIEWFollow-up Day 7: Nausea woke her in the middle of thenight, so she took charcoal. A new symptom, a "heat rash,"has also appeared on her arms, legs, and stomach. RhusToxicodendron does not relieve either of these issues. Mildtingling is present in the shingles lesions, which areimproving slightly each day.Plan: She is no longer responding to Rhus toxicodendron;her symptoms have changed, and a new remedy is needed tocomplete the cure. She is advised to monitor any modifyingfactors in her symptoms until the next day to provideadditional clarity for the second prescription. Clearmodalities often serve as significant indicators that helpdetermine the best remedy choice (§133).Follow-up Day 8: She reports her energy is back to normal,but her appetite is low. She is very thirsty. The pain in theshingles is gone, and there is very slight itching. The heatrash is a bit better but very itchy. She is no longer cold. Case AnalysisThe case was re-repertorized based on the new symptoms andremedies complementary to Rhus Toxicodendron. Dr. Michael Knapp attended National University ofNatural Medicine in Portland, OR and completed aone year teaching and clinical residency at theuniversity. His practice has an emphasis in theinterconnection of digestive problems, (dis-)stress,hormonal and immune system complaints.Dr. Knapp is a certified mindfulness meditationteacher and has taught meditation in jail for inmatesin substance misuse treatment. He has providedoutreach to the homeless and at domestic violenceshelters in Northern Arizona. He is currentlypresident of the Homœopathic Academy ofNaturopathic Physicians.REFERENCESDimitriadis, G. (2010). The Bönninghausen Repertory: TherapeuticPocketbook Method (2nd ed.). Hahnemann Institute.1.Centers for Disease Control and Prevention. (n.d.). Shingles (HerpesZoster). U.S. Department of Health & Human Services.https://www.cdc.gov/shingles/about/index.html2.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0436NATUROPATHIC DOCTOR NEWS & REVIEWIntroduction: The Link Between PCOS &DermatologyPolycystic Ovarian Syndrome is the most common endocrinedisorder in reproductive-aged women, affectingapproximately 10-15% of the population.1 It is diagnosedbased on the Rotterdam criteria, requiring at least two of thefollowing three features: oligo- or anovulation,hyperandrogenism (clinical or biochemical), and polycysticovarian morphology on ultrasound.² While PCOS is oftenassociated with reproductive dysfunction, its dermatologicimpact is significant and frequently serves as a visibleindicator of underlying metabolic and hormonalimbalances.³ For many women seeking treatment for PCOS,the visible impact on their skin is the most distressing aspectof the condition. While internal imbalances causediscomfort, outward symptoms—such as facial hair, cysticacne, and hair thinning—often prompt them to seek medicalhelp. These symptoms affect physical appearance and take asignificant emotional and psychological toll, makingdermatologic concerns a primary driver for consultation.⁴Hyperandrogenism, insulin resistance, and systemicinflammation are the primary drivers of skin manifestationsin PCOS. The excessive androgen production characteristicof PCOS stimulates sebaceous gland activity, leading toacne, and promotes hair follicle changes that cause hirsutismand androgenic alopecia.⁵ Simultaneously, insulin resistanceexacerbates hyperandrogenism by reducing sex hormone-binding globulin (SHBG) and increasing ovarian androgensynthesis.⁶ Furthermore, chronic low-grade inflammationcontributes to oxidative stress, compromising skin barrierfunction and accelerating dermatologic aging.⁷Understanding the pathophysiology of PCOS-related skinconditions is crucial for implementing a holistic, integrativetreatment strategy that addresses the root causes ofdysfunction rather than merely managing symptoms.Common Dermatologic Manifestations of PCOSAcnePCOS-related acne is typically inflammatory, cystic, andconcentrated along the lower face, jawline, and upper back.Androgens, particularly dihydrotestosterone (DHT), bind tosebaceous gland receptors, stimulating excessive sebumproduction and promoting the proliferation of Cutibacteriumacnes bacteria.⁵ Elevated androgens also increasekeratinocyte proliferation, leading to follicular plugging andcomedone formation. Acne can be both physically and emotionally distressing forwomen with PCOS, and its severity often reflects the level ofhormonal imbalance.⁸A study published in the Journal of the American Academy ofDermatology found that women with PCOS havesignificantly higher sebum excretion rates and increasedsensitivity to circulating androgens compared to non-PCOSindividuals. This heightened sensitivity explains why evennormal androgen levels can trigger persistent acne in somewomen.HirsutismHirsutism is characterized by excessive terminal hair growthin androgen-sensitive areas, including the face, chest,abdomen, and back. Androgens stimulate hair follicletransition from vellus (fine) to terminal (coarse) hair, leadingto coarse, pigmented hair growth in affected regions.⁹Hirsutism is a common source of distress and social anxietyfor many women with PCOS, and conventional treatments,such as anti-androgenic medications, may not always addressthe root causes of hair growth.Androgenic AlopeciaIn contrast to hirsutism, androgenic alopecia presents asscalp hair thinning, typically manifesting as a widening partline and diffuse shedding over the crown. The underlyingmechanism involves androgen-induced follicularminiaturization, where DHT shortens the anagen (growth)phase and prolongs the telogen (resting) phase.⁴ Reducedscalp blood flow and inflammation further contribute tofollicular atrophy. Androgenic alopecia in PCOS oftenresults in a gradual, diffuse thinning of hair, which may bemore challenging to address through traditional hair losstreatments alone.Acanthosis NigricansAcanthosis nigricans present as hyperpigmented, velvetyplaques in flexural regions such as the neck, axillae, andgroin. It is a clinical marker of insulin resistance, ashyperinsulinemia stimulates epidermal proliferation andmelanocyte activity.¹⁰ The severity of acanthosis nigricanscorrelates with fasting insulin levels, making it an importantdermatologic sign of metabolic dysfunction in PCOS. Thisskin condition can be a physical manifestation of themetabolic disturbances common in PCOS and may indicatethe need for more aggressive management of insulinresistance.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0437NATUROPATHIC DOCTOR NEWS & REVIEWRoot Causes and Pathophysiology of SkinManifestationsAndrogen DysregulationExcess androgens originate from both the ovaries and adrenalglands in PCOS. Hyperinsulinemia exacerbates this by reducingSHBG, thereby increasing free testosterone levels. Additionally,upregulated 5-alpha reductase activity converts testosterone toDHT, a more potent androgen that drives sebaceous glandhypertrophy and hair follicle changes. Elevated DHT levels area key factor in both acne and hirsutism in women with PCOS.Insulin Resistance & HyperinsulinemiaInsulin resistance, present in up to 70% of women with PCOS,contributes significantly to hyperandrogenism by stimulatingovarian theca cells to produce excess androgens. Insulin alsoimpairs hepatic SHBG synthesis, further increasing freeandrogen availability. Addressing insulin resistance is central tomanaging the dermatologic manifestations of PCOS, as itdirectly influences androgen levels and sebaceous gland activity.Chronic Inflammation & Gut DysbiosisElevated markers such as C-reactive protein (CRP) and pro-inflammatory cytokines evidence systemic inflammation inPCOS. Dysbiosis, characterized by reduced microbial diversityand increased intestinal permeability, exacerbates systemicinflammation and influences androgen metabolism. Studiesindicate that gut microbiota alterations can modulatetestosterone levels, further linking gut health to dermatologicmanifestations. Addressing gut health and systemicinflammation is essential for managing the skin symptoms ofPCOS.Naturopathic and Functional Medicine ApproachDietary InterventionsA low-glycemic, anti-inflammatory diet is foundational inmanaging PCOS-related skin conditions. The Mediterraneandiet, rich in omega-3 fatty acids, polyphenols, and fiber, hasimproved insulin sensitivity and androgen balance.¹¹ Reducingdairy intake may be beneficial for acne-prone individuals, asdairy proteins stimulate insulin-like growth factor-1 (IGF-1),which enhances androgenic activity and sebaceous glandproliferation..¹² A nutrient-dense, whole-food approach helps toreduce systemic inflammation, which in turn can improve bothskin health and overall well-being.The ketogenic diet has also gained attention for itspotential benefits in PCOS. By significantly reducingcarbohydrate intake, the diet can improve insulinsensitivity, lower circulating insulin levels, and reduceandrogen production.¹⁰ Studies suggest that ketogenicinterventions may help regulate menstrual cycles andimprove dermatologic symptoms by targeting theunderlying metabolic dysregulation seen in PCOS. Thisdietary strategy focuses on reducing blood sugar spikeslinked to higher insulin and androgen levels.Nutritional & Herbal SupportZinc: Zinc plays a critical role in regulating sebumproduction and inhibiting the conversion oftestosterone to DHT.¹³ It also promotes woundhealing, making it a beneficial supplement forwomen with acne and other inflammatory skinconditions.Omega-3 Fatty Acids: Omega-3 fatty acids are anti-inflammatory and help reduce testosterone levels,improving acne and hirsutism.¹¹ These essentialfatty acids in fatty fish, flaxseeds, and walnuts arekey to supporting skin health in women with PCOS.Inositol (Myo & D-chiro): Inositol is a naturallyoccurring substance that helps to enhance insulinsensitivity and reduce hyperandrogenism.¹² Studiesshow that inositol supplementation can reducesymptoms such as acne and irregular menstrualcycles in women with PCOS.Spearmint Tea: Spearmint tea has been shown toreduce free testosterone levels, helping to alleviatesymptoms of acne and hirsutism.¹⁴ Drinkingspearmint tea regularly may provide a simple,effective natural remedy for managing PCOS-related skin issues.Saw Palmetto & Licorice: Both herbs have anti-androgenic effects. Saw palmetto blocks 5-alphareductase, reducing the conversion of testosteroneto DHT, while licorice helps reduce cortisol levels,indirectly reducing androgen excess.¹³Hormone & Metabolic RegulationAdaptogens: Herbs such as ashwagandha andrhodiola are used in naturopathic medicine tosupport adrenal function and reduce cortisol-drivenandrogen excess. Chronic stress and elevatedcortisol levels exacerbate the hormonal imbalance inPCOS, so adaptogens can help modulate the stressresponse and balance hormone levels.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0438NATUROPATHIC DOCTOR NEWS & REVIEWLiver Detoxification: The liver plays a crucial role in estrogenmetabolism. Supplements such as DIM (diindolylmethane)and N-acetylcysteine (NAC) enhance liver detoxificationprocesses, aiding in the clearance of excess hormones andsupporting hormonal balance.Topical & Lifestyle StrategiesNon-Toxic Skincare: Choosing non-toxic skincareproducts is essential for women with PCOS. Avoidingendocrine-disrupting chemicals (EDCs) in personal careproducts can help prevent further hormonal disruption,which may exacerbate acne and other skin issues.Exercise: Regular physical activity, particularly strengthtraining, improves insulin sensitivity and metabolichealth. Exercise helps reduce insulin levels andinflammation, which can reduce the severity of PCOS-related skin issues.Stress Management: Practices like yoga, meditation, andmindfulness can lower cortisol levels, which in turn mayreduce the androgenic effects of elevated stresshormones. Stress management is an importantcomponent of a holistic approach to managing PCOS.Conclusion: A Holistic Path to Clear SkinThe dermatologic manifestations of PCOS are indicative ofdeeper systemic imbalances that require comprehensive root-cause interventions. By addressing insulin resistance,androgen excess, inflammation, and gut health, naturopathicmedicine provides a holistic, patient-centered approach toimproving skin health. Integrating dietary, lifestyle, andbotanical therapies empowers patients to improve theirdermatologic and overall well-being.¹⁵ Taking apersonalized, holistic approach is key to managing PCOSsymptoms and restoring balance for the skin and overallhealth and vitality.Dr. Galina Mironova is a Naturopathic Doctorspecializing in women’s health and the founder ofPCOSDr.com. As a PCOS warrior, her personaljourney fuels her passion for helping women addressthe root causes of polycystic ovarian syndrome. Shecreated a holistic PCOS program focused onevidence-based, integrative care for hormonalbalance and metabolic health. Galina earned herPsychology degree from Miami University and aDoctorate in Naturopathic Medicine from theUniversity of Bridgeport. Her mission is toempower women with the tools and knowledge totake control of their health and well-being.Website: www.DrGalinaND.comPCOS Program: www.PCOSdr.comThiboutot D. Acne in women: The role of hormones. J InvestDermatol. 2004;123(1):1-12.1.Carmina E, Lobo RA. Polycystic ovary syndrome (PCOS): Symptoms,diagnosis, and management. J Clin Endocrinol Metab. 2006;91(1):2-7.2.Yildiz BO, Ozturk S, Kirazli S, et al. The role of androgens in thepathophysiology of polycystic ovary syndrome. J Clin EndocrinolMetab. 2004;89(6):2746-2751.3.Strowig SM, Coste SL. Dermatologic manifestations of polycysticovary syndrome: Clinical presentation and management. Cutis.2008;81(1):31-36.4.Diamanti-Kandarakis E, Koukkou E, Papavassiliou AG, et al. Therole of inflammation in the pathogenesis of polycystic ovary syndrome.Endocr Rev. 2006;27(3):264-283.5.Lindheim SR, Zeng Y, Pirelli G, et al. Insulin resistance and obesity inpolycystic ovary syndrome: Implications for treatment. J ClinEndocrinol Metab. 2017;102(2):678-687.6.Barrea L, Muscogiuri G, Nappi C, et al. Nutritional aspects inpolycystic ovary syndrome: From obesity to vitamin D. Nutrients.2019;11(6):1413.7.Kaymak Y, Atmaca S, Avci I, et al. Clinical characteristics of patientswith polycystic ovary syndrome and dermatologic findings. JDermatol. 2009;36(3):146-153.8.Oner G, Oner C, Erem C, et al. Dermatological manifestations ofpolycystic ovary syndrome and their impact on the quality of life. JEndocrinol Invest. 2017;40(4):367-375.9.Unfer V, Carlomagno G, Yildiz BO. Use of inositols in the treatmentof polycystic ovary syndrome. Eur Rev Med Pharmacol Sci.2017;21(1):27-36.10.Grant P. The use of botanical medicine in managing acne andhirsutism in polycystic ovary syndrome. Phytother Res. 2010;24(2):186-188.11.Russo M, Spagnuolo C, Tedesco I, et al. The effects of spearmint onfree testosterone and acne in polycystic ovary syndrome. J AlternComplement Med. 2014;20(9):732-738.12.Nestler JE, Jakubowicz DJ, de Vargas F, et al. Insulin resistance inpolycystic ovary syndrome: Pathogenesis and therapeutic implications.Fertil Steril. 2005;83(2):441-444.13.Hutchison SK, Depenbusch M, Fader AN, et al. Management ofpolycystic ovary syndrome: A focus on dermatologic manifestations. JClin Endocrinol Metab. 2011;96(7):E1160-E1168.14.Morrow-Baez K. Thriving with PCOS. [Publisher]; 2024.15.REFERENCES

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0440NATUROPATHIC DOCTOR NEWS & REVIEWThe paper also examines catecholamine-induced neurotoxicity,which results from the spontaneous oxidation and/ormetabolism of catecholamines through the monoamine oxidasesystem, producing neurotoxic aldehydes. This process isregarded as a key pathogenic mechanism in stress-relatedneurological damage linked to conditions such as Alzheimer’sand Parkinson’s, as well as in general brain aging. Finally, the role of Angiotensin II—typically associated with thecardiovascular and renal systems–is examined in the context ofneurodegeneration. Emerging evidence indicates thatAngiotensin II is synthesized locally in the brain, where itcontributes to neurodegeneration by upregulating microglia andpromoting neuroinflammation, linking it to both disease-relatedand age-related cognitive decline.While other mechanisms, such as the gut-brain axis,neurotrauma, and infection, have been explored in separateresearch articles, this paper focuses on understanding theaforementioned mechanisms. It aims to enhance clinicians'understanding of the pathophysiological processes contributingto both age-related and disease-related neurological deficits.Thiamine Associated NeurodegenerationDr. Rudolph Peters, an English medical doctor and biochemist,could arguably be considered the father of functional medicine.He became the chair of chemistry at Oxford at age 34 and wasassociated with over 200 published papers throughout hiscareer.¹ His first paper, published in 1912, elucidated oxygenand its relationship to hemoglobin.²He later researched the toxicity of certain gases using protozoal,which led him to investigate the nutritional requirements of themedia used to sustain these organisms. This explorationeventually motivated him to study B-complex vital amines (i.e.,vitamins). He worked with the factor that helped cure pigeonsand other fowl suffering from beriberi. He observed thatpigeons with this factor deficiency exhibited certain symptoms,such as ataxia and opisthotonos.By 1932, he and his colleagues had isolated a factor from yeastthat demonstrated high vitamin B1 activity. He observed thatwhen this factor (thiamine) was administered to birds with adeficiency induced by a polished rice diet, there was animprovement in symptoms, particularly head retraction. Hebelieved this deficiency indicated "underlying damage to thenervous system." While thiamine deficiency caused peripheralpolyneuropathy, he thought it also had a significant centralimpact, specifically in the brain. Fundamentally, Peters was the first to demonstrate themode of action of a vitamin; in this case, he concludedthat it influenced a pyruvate enzyme.³ Notably, he alsocoined the term “biochemical lesions” to refer to a lowfunctional enzyme state caused by “cofactor”insufficiency or a toxicant that negatively impacts thefunction of certain biochemical pathways (hence, he isregarded as the father of functional medicine).⁴ Science has also noted over time that thiaminedeficiency (beriberi/Wernicke-Korsakoff syndrome) hassimilar neurological symptoms to those of otherneurological conditions such as dementias andAlzheimer’s.⁵⁻⁹ Over time, papers were publishedexploring thiamine and its role in brain metabolism,including the cholinergic system.¹⁰⁻²² It has beendetermined that thiamine insufficiency profoundlyinfluences three main enzymes involved in energymetabolism²³: Transketolase influences the pentose phosphateshunt, which is important for myelin and NADPHproduction involved in glutathione activity.Pyruvate dehydrogenase fundamentally linksglycolysis to the Krebs cycle and alpha-ketoglutarate complex, serving as the rate-limitingstep in the citric acid cycle. Alpha-ketoglutarate complex is a rate-limiting stepin the Krebs cycle.The downregulated activity of these enzymes may bedue to several factors: low intake of thiamine (e.g.,alcoholism), interrupted absorption, poor transport intothe cell, or issues with enzyme activation. With theseenzymes downregulated, primarily essential cellularfunctions, including beta-amyloid production andincreased oxidative stress, have been noted.²⁴′²⁵ The endresult is poor functioning of neurons and upregulationof microglial activation, which is related toneuroinflammation, damage, and expression of clinicalentities. It is now understood how apparent insulin resistancecan occur in neurodegenerative diseases, particularlyAlzheimer’s²⁶′²⁷, when glucose metabolism issignificantly altered downstream. Additionally, a highoxidative environment can influence receptor andsecondary messenger systems, exacerbatingmitochondrial dysfunction due to sustained andunabated oxidative stress within the neuro-microenvironment.²⁸′²⁹

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0441NATUROPATHIC DOCTOR NEWS & REVIEWFigure 1 depicts the three main enzymes that use thiamine as acofactor. Insufficient cofactors can lead to reduced enzymeactivity, which may result in a cellular degenerative state anddecreased functionality. This can instigate clinical symptomssuch as poorer cognition and psychic, motor, andsomatosensory disturbances. The clinical application of thiamine pyrophosphate (ThPP)during periods of overt deficiency has been noted to becurative (R). However, in chronic cases of mild cognitivedeficit or early Alzheimer’s, water-soluble thiamine does notappear to cross the blood-brain barrier or remaininterneuronally in sufficient quantities (R). Therefore,synthetic thiamine has been developed with greater fatsolubility, allowing for better absorption and a moreenhanced effect on the enzymes: transketolase, pyruvatedehydrogenase, and the alpha-ketoglutarate complexintraneuronally. Small human clinical trials have yieldedpromising results.³⁰⁻⁴¹“Among these, the thioester benfotiamine (BFT) has beenextensively studied and has beneficial effects both in rodentmodels of neurodegeneration and in human clinical studies.BFT has antioxidant and anti-inflammatory properties thatseem to be mediated by a mechanism independent of thecoenzyme function of ThDP. BFT has no adverse effects andimproves cognitive outcome in patients with mild Alzheimer’sdisease (AD). Recent in vitro studies show that anotherthiamine thioester, dibenzoylthiamine (DBT), is even moreefficient than BFT, especially with respect to its anti-inflammatory potency.”³⁰Angiotensin II-Related NeurodegenerationAngiotensin II (Ang II) is usually considered in the contextof renal and cardiac disease; however, in recent decades, ithas been found localized in the brains of rats⁴¹, which has ledto human studies revealing its role as a pro-inflammatorymolecule.⁴²′⁴³ It is suggested that part of its inflammatoryeffects result from an upregulation of NADPH oxidase,causing increased oxidation related to brain injury andneurodegenerative diseases.⁴⁴′⁴⁵

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0442NATUROPATHIC DOCTOR NEWS & REVIEWInterestingly, Angiotensin-II associated brain inflammation hasbeen linked to hypertension⁴⁶, heart disease⁴⁷, heart failure andremodeling⁴⁸′⁴⁹, activated microglia in heart failure⁵⁰′⁵¹ rats, agingin heart failure, and depression in heart failure.⁵²⁻⁵⁴ Moreover,Angiotensin-II mediated neuroinflammation contributes tocognitive impairment⁵⁵′⁵⁶ including a potential association withAlzheimer’s disease.⁵⁷ One proposed mechanism behind Ang II-mediated neuroinflammation is that the angiotensin II type 2receptor (with Ang II as its ligand) can modulate a pro-inflammatory response in microglia and other cells, such asmacrophages.⁵⁸⁻⁶³ Neurological damage arises from an increase inNADPH oxidase, which generates free radicals and pro-inflammatory transcription factors, leading to the elaboration ofpro-inflammatory cytokines and ensuing neuronal damage,including damage to the blood-brain barrier.Another mechanism at play is that Ang II has a detrimental effecton the blood-brain barrier⁶⁴⁻⁷⁰, increasing its permeability. Thisincreased permeability allows Ang II to drift into brain areas, suchas the hypothalamus and brainstem, which subsequently causesbrain disruption.⁶⁷ Ang II can also modulate sympathetic outflowby stimulating sympathoexcitatory centers.⁶⁹ The latter results inincreased catecholamine release, which enhances the aminochromeredox cycling pattern that, in itself, is neurodegenerative. However, the brain appears to have a counteracting system tobalance this Ang II neuroinflammation, which is Ang 1-7.⁷¹⁻⁷⁵Literature reveals that when Ang 1-7 (with ACE 2 required forconversion from Ang II) binds to the Mas receptor, a coolingeffect occurs, signaling a more anti-inflammatory and antioxidantstate. With this anti-inflammatory state, neurodegeneration and,consequently, cognition may be mitigated. Fig 2. Ang II triggers microglial activation, leading to cytokinerelease that contributes to neurodegeneration and increases blood-brain barrier permeability.Fig 3. Basic outline of the angiotensinogen pathway,showing receptor-dependent outcomes based on eitherAng II or Ang 1-7, as well as therapeutic targeting, suchas ACE inhibition. Studies have shown that ACE andACER blockers may have neuroprotective qualities. With this association in mind–that is, the link betweenAng II-mediated inflammation and its role inneuroinflammation and brain degeneration–severaltherapeutic strategies have been explored. Theseinclude:Decrease Ang II synthesis (via Renin or ACEinhibitor)locking its receptor (using ACE receptor blockers)Increasing Ang 1-7 levels or enhancing Masreceptor ligandMitigating the intracellular effects of toxic radicalsNatural ACE inhibitors have been investigated; manyare polyphenolic in origin.⁸⁴⁻⁸⁶ However, these naturalcompounds often have relatively high IC50 values, sotheir effectiveness may be less pronounced in loweringcritically elevated Ang II (e.g., renal-associatedhypertension). Nonetheless, they may prove successfulas a long-term addition to treatment. Theirantioxidant qualities are undoubtedly advantageous.

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Catecholamine-Related NeurodegenerationChronic stress in midlife has been observed to correlate withlater life neurodegeneration, particularly Parkinson’sdisease, Alzheimer’s, and age-related dementia⁸⁷⁻⁸⁹, as well asstress-induced cardiomyopathy.⁹⁰ Literature shows thatchronic stress, and consequently high neuro-catecholamineexposure, has a multifaceted cytotoxic effect on centralneural tissue.⁹¹⁻¹⁰⁰The metabolism of catecholamines (e.g., dopamine,norepinephrine) through the monoamine oxidase (MAO)enzyme system, along with spontaneous oxidation, results inthe accumulation of toxic molecules such as aminochromeand its o-semiquinone radical. These molecules undergoREDOX cycling (see Fig. 4), producing hydrogenperoxide⁹⁷, which can trigger a Fenton reaction whenexposed to iron, generating hydroxyl radicals. This cascadeleads to progressive damage to cellular mechanisms andarchitecture, particularly impacting mitochondrialfunction.⁹⁵⁻⁹⁸This pathway has been linked to the neurodegenerationprocesses involved in Parkinson’s disease, Alzheimer’s, andaging.¹⁰¹⁻¹⁰⁶A simplified version of catecholamine metabolism via MAOand spontaneous oxidation produces aminochrome, andthrough a one-electron reduction, forms the o-semiquinoneradical. This radical subsequently generates hydrogenperoxide, which can create damaging hydroxyl radicals. Thehydrogen peroxide is converted to water and oxygen byglutathione, which is then re-reduced to its active form byglutathione reductase, which requires NADPH from thepentose phosphate pathway. If aminochrome redox cyclingoutpaces the in situ activity of glutathione—either due to alack of substrates, insufficient selenium for glutathioneperoxidase, or an issue with NADPH—a high concentrationof oxidative molecules will form, leading to eventualneurodegeneration. 43NATUROPATHIC DOCTOR NEWS & REVIEWAPRIL 2025 - VOLUME 20 | ISSUE NO. 04Fig. 4This heightened redox cycling can also deplete NADH as it isdiverted to the redox cycling, reducing its availability formitochondrial electron transport and subsequently loweringATP synthesis. This reduced ATP synthesis, combined withthe increased redox cycling of aminochrome and itssemiquinone producing neurotoxic hydrogen peroxide,disrupts neuronal allosteric balance, contributing toneurodegeneration and all the associated cascades, ultimatelyleading to cognitive and psychiatric pathologies.Chronic stress has been shown to trigger inflammatoryactivity not only in peripheral immune cells and cytokinesbut also by enhancing the activation of glial cells within aninflammatory context.¹⁰⁷ This leads to increased productionof inflammatory cytokines in the brain, which contributes tosubsequent clinical manifestations such as anxiety,depression, psychosis, and central degeneration, includingcognitive deficits. Activated MAO also contributes to amyloid (Aβ)aggregation by producing two successive cleavages ofamyloid precursor protein (APP) via beta-secretase andgamma-secretase.¹⁰⁷′¹⁰⁸ This process and the destruction ofcholinergic neurons lead to cognitive impairment. Given this association, it seems prudent to inhibit MAO as apotential treatment for neurodegeneration–an approach thathas been utilized for some time. Depression in dementia hasbeen treated with MAO inhibitors since at least 1985.¹⁰⁹Furthermore, MAO inhibitors have remained a key focus oftreatment over the years for Alzheimer’s¹¹⁰⁻¹¹⁷, and perhapsthis model could be adapted for prevention strategies tomitigate neurodegeneration.

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A combination of MAO oxidase inhibitors andacetylcholinesterase inhibitors has also been explored forAlzheimer’s disease.¹¹⁸ This combined approach may offeranti-Alzheimer's and neuroprotective effects by reducingoxidative stress caused by MAO enzyme activity.Certain plants may have therapeutic effects with this modelin mind. Ege et al. report⁶⁹ that quercetin, epigallocatechingallate, resveratrol, curcumin, as well as Angelica gigas andScutellaria baicalensis exhibit MAO inhibition effects andpossess antioxidant properties. Hypericum perforatum hasbeen noted as an MAO inhibitor.⁷⁰ Dat, T., et al. report that51 plants were evaluated for their MAO inhibitor properties,though human trials are still lacking.⁷¹ Finally, Polygonatumsibiricum has been investigated for its neuroprotectiveproperties.⁷² It appears clinically prudent to support glutathione (e.g.,NAC, selenium), enhance intraneuronal antioxidant capacityincluding mitochondrial protection (e.g., ALA, CoQ10,carnitine), and replenish cofactors involved in protectingagainst highly cytotoxic hydrogen peroxide. Lastly, andmost obviously, it is essential to minimize catecholamineinflux to avoid overburdening neural cells, which couldperpetuate and/or accelerate existing neurodegeneration; inother words, one must manage sympathetic output. Quinn Rivet, ND graduated from CCNM in 1994.From 1997-2000 he instructed at CCNM and was aclinical supervisor. From 2001 to 2012 he was aninstructor of pathology, laboratory diagnosis,nutrition, clinical medicine, and the chair ofNutrition (2004-2010) at Boucher Institute ofNaturopathic Medicine. After returning from 3years in China (2017-2020) where he taught Englishand explored TCM for IgA nephropathy, Dr Rivetnow pursues further work in clinical research,education, and consultation services at TheMiramichi Naturopathiuc Health Clinic(MiramichiNaturopathic.com). Inquiries:drquinn@shaw.ca.REFERENCESThomson, R. H., & Ogston, A. G. (1983). Rudolph Albert Peters.Biographical Memoirs of the Fellows of the Royal Society, 29, 421–449. https://doi.org/10.1098/rsbm.1983.00161.Peters, R. (1912). Chemical nature of specific oxygen capacity inhaemoglobin. Journal of Physiology, 44(3), 131–149.https://doi.org/10.1113/jphysiol.1912.sp0015062.Banga, I., et al. (1939). Pyruvate oxidation in the brain. The activeform of vitamin B1 and the role of C4 decarboxylic acids. BiochemicalJournal, 33(7), 1109–1121. https://doi.org/10.1042/bj03311093.Peters, R. (1963). Biochemical lesions and lethal synthesis. Elsevier.https://doi.org/10.1016/C2013-0-07764-14.Gibson, G., et al. (2011). Modeling neurodegenerative diseasepathophysiology in thiamine deficiency: Consequences of impairedoxidative metabolism. Neurochemistry International, 58(3), 248–260.https://doi.org/10.1016/j.neuint.2010.12.0075.Matsushita, S., et al. (2008). Elevated cerebrospinal fluid tau proteinlevels in Wernicke’s encephalopathy. Alcoholism: Clinical andExperimental Research, 32(6), 1091–1095.https://doi.org/10.1111/j.1530-0277.2008.00671.x 6.Butterworth, R. F. (2003). Thiamine deficiency and brain disorders.Nutrition Research Reviews, 16(2), 277–284.https://doi.org/10.1079/NRR2003677.Ramamoorthy, K., et al. (2022). Alzheimer's disease is associated withdisruption in thiamin transport physiology: A potential role forneuroinflammation. Neurobiology of Disease, 171, 105799.https://doi.org/10.1016/j.nbd.2022.1057998.Gibson, G. E., et al. (2016). Vitamin B1 (thiamine) and dementia.Annals of the New York Academy of Sciences, 1367(1), 21–30.https://doi.org/10.1111/nyas.129909.Kennedy, A. (2001). The potential role of thiamine in the pathogenesisand treatment of Alzheimer’s disease [Master’s thesis, University ofManitoba]. University of Manitoba Repository.10.Unknown author. (1982). The role of the cholinergic system in thiamindeficiency. Annals of the New York Academy of Sciences, 378, 382–403. https://doi.org/10.1111/j.1749-6632.1982.tb50291.x11.Zhang, Q., et al. (2011). Thiamine deficiency increases β-secretaseactivity and accumulation of β-amyloid peptides. Neurobiology ofAging, 32(1), 42–53.https://doi.org/10.1016/j.neurobiolaging.2009.01.00212.Reggiani, C., et al. (1984). Nervous tissue thiamine metabolism in vivo.I. Transport of thiamine and thiamine monophosphate from plasma todifferent brain regions of the rat. Brain Research, 293(2), 319–327.https://doi.org/10.1016/0006-8993(84)91215-513.Gibson, G. E., et al. (1988). Reduced activities of thiamine-dependentenzymes in the brains and peripheral tissues of patients withAlzheimer's disease. Archives of Neurology, 45(8), 836–840.https://doi.org/10.1001/archneur.1988.0052032006202114.Gold, M., et al. (1998). Plasma thiamine deficiency associated withAlzheimer’s disease but not Parkinson’s disease. Metabolic BrainDisease, 13(1), 43–53. https://doi.org/10.1023/A:102065810346115.Ke, Z. J., & Gibson, G. E. (2004). Selective response of various braincell types during neurodegeneration induced by mild impairment ofoxidative metabolism. Neurochemistry International, 45(2–3), 361–369. https://doi.org/10.1016/j.neuint.2003.11.00316.Bubber, P., et al. (2005). Mitochondrial abnormalities in Alzheimerbrain: Mechanistic implications. Annals of Neurology, 57(5), 695–703.https://doi.org/10.1002/ana.2045217.Gibson, G. E., et al. (2013). Abnormal thiamine-dependent processesin Alzheimer’s disease: Lessons from diabetes. Molecular and CellularNeuroscience, 55, 17–25. https://doi.org/10.1016/j.mcn.2012.12.00518.Osiezagha, K., et al. (2013). Thiamine deficiency and delirium.Innovations in Clinical Neuroscience, 10(4), 26–3219.Reference 20-120 on NDNR.comAPRIL 2025 - VOLUME 20 | ISSUE NO. 0444NATUROPATHIC DOCTOR NEWS & REVIEW

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0446NATUROPATHIC DOCTOR NEWS & REVIEWWhat is Menopausal Acne?While the term ‘menopausal acne’ is not always classifiedseparately, the American Academy of Dermatology¹ defines arelated term, ‘adult acne,’ as breakouts that occur at agesthirty and older. The term ‘menopausal acne’- commonly usedin academic articles, healthcare culture, and on social mediaand blogs- would be considered a subset of that age group.The Academy further explains that among these ages,menopausal acne is the most prevalent form of acne. Menopause has historically been regarded as a reproductivephase during which acne is expected to resolve for womenwho experience it, and it was assumed to be a non-relevantclinical topic for those with no prior experience. However, a2006 survey² revealed that the prevalence of acne in womenaged 50 and over was 15.3%, indicating that more than 10% ofwomen in this age group continue to experience acne,challenging the assumption that menopausal women are freeof this condition. Khunger and Mehrotra² report that hormone imbalances,such as the relative increase of androgens during menopausecompared to the more rapidly declining female hormones likeestrogen and progesterone, significantly contribute tomenopausal acne. The rise in androgens, such as testosterone,can overstimulate hair follicles and the sebaceous glandswithin them, producing skin oils (sebum). This can result inclogged pores and acne. We must also consider a few underlying factors that affectmenopausal acne, which are harder to detect and operate on amind-body level. These factors include the mental pursuit ofanti-aging; skin dysmorphia linked to social media or otherprevalent physical ideals; and increased self-consciousnessregarding appearance and aging skin among menopausalwomen. These elements can significantly impact the skin’slong-term ability to heal and maintain an intact barrier toprevent future acne. How does this work?Menopausal women may turn to quick-fix methods toimprove their complexions rapidly, but these approaches candisrupt the skin’s natural ability to renew, heal, detoxify, andbalance oils. Quick-fix methods may include potent, moisture-stripping acne skincare routines, extraction techniques usingesthetic tools, skin picking while looking in the mirror,excessive or prolonged use of pharmaceuticals and harsh acnemedications, and heavy application of makeup that can clogpores and exacerbate acne. These methods, whether usedalone or in combination, can create vulnerability in the skinbarrier for menopausal women, which tends to worsen overtime. This damage to the skin barrier occurs at a time when women’smaturing menopausal skin is already challenged by hormonedeficiencies, unbalanced hormones and oils, a reduction incollagen and elastin within skin cells, and increasedtransepidermal water loss (TEWL) compared to what womentypically experience in their 20s, 30s, and 40s. It appears that, on the surface, there are many similaritiesbetween teenage acne and menopausal acne; however, there arealso significant differences beneath the skin worth noting. Both occurring during a phase of natural hormonefluctuations, menopausal and teen acne can manifest asinflammatory and non-inflammatory lesions, includingwhiteheads, blackheads, large pustules, and even cysts, whichhave often been regarded as a symptom exclusive to teenagers.²The facial regions affected overlap with those in teenagers aswell, comprising what is known as the “beard” distributionalong the lower cheeks, jawline, the submental space betweenthe chin and neck, and the distal part of the throat.² When menopausal women seek treatment for their acne, theyare often prescribed the same prescription-grade topicalsoffered to teenagers, as well as potent over-the-counter acneskincare products, or both. However, the skin characteristics ofa teenage girl are vastly different from those of a menopausalwoman. These contrasting characteristics include abundant collagenand elastin in the skin of teenagers, significantly lowertransepidermal water loss (TEWL) and increased naturalmoisture retention within skin cells, rising hormone levels thatsupport skin tone and strength, and a more resilient skinbarrier typical of young age. Using potent topical treatments,young skin can recover more quickly if the skin barrier isdamaged. When a medication, such as prescription retinoids that can bedrying or customized skincare formulas that combine topicalhydroxy acids, topical antibiotics, and benzoyl peroxide atvarious dosages, impairs the skin barrier of a menopausalwoman, new therapies with a similarly suppressive or harshlyeradicative approach to treatment are often prescribed. Patients are often advised to apply multiple potentially harshor damaging products or ingredients simultaneously on theirskin. This approach causes the skin barrier to lose its integrity,healthy oils, and moisture levels, leading to increasedsusceptibility to acne, slower healing, and more significantscarring over time.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0447NATUROPATHIC DOCTOR NEWS & REVIEWMenopausal women can benefit from a naturopathicapproach to acne treatment that employs internal measuresto support the health of the organs, nourishing the skin andproviding gentle, nourishing, yet effective topical skin care.Providers specializing in hormone balancing for womenshould exercise caution when prescribing bio-identicalandrogens, as they can increase the incidence of acne.Additionally, providers can collaborate with their patients onstress management and adrenal health, treatment for hotflashes and sleep disruption, immune and gut health,androgen excess, and estrogen dominance to offer a well-rounded approach to treating menopausal acne. CASE PRESENTATIONS // A 55-year-old female CW with a decades-long history ofpreviously diagnosed hormonal and cystic acne presents withsevere skin barrier damage and a worsening of her acnesymptoms. CW went through menopause three years ago, after whichher acne worsened instead of improving as she had expected.An eight-step topical skincare routine, prescribed by aclinical provider fourteen years ago, had improved hercomplexion for several years. However, it may havecontributed to excess skin dryness over the past six months,particularly on the bilateral cheeks, chin, and nose. The dryskin exacerbated her acne symptoms, leading to redness,sensitivities, and increased wrinkles. Her skincare routineincluded multiple active ingredients used simultaneously,such as a high-dose topical antibiotic, mandelic acid, salicylicacid, glycolic acid, and antiseptic components.The patient was also receiving a 1.5 mg estradiol injectiononce a week from a different provider, a 0.75 mg testosteroneinjection weekly, and a 200 mg progesterone capsule eachnight. Other medications included a prescription stimulantfor ADHD symptoms and an over-the-counter allergymedication. No family history of acne or any other chronicskin conditions was reported. Supplements she was already taking included omega-3 fattyacids and magnesium. CW engaged in low-to-moderateintensity workouts four days a week for 30-40 minutes persession, combining cardiovascular exercise with lightresistance training. She shared her history of high stresslevels related to a previous divorce years ago and changes inher position at work. She felt that stress played a significantrole in acne flare-ups, which tended to vary in frequency.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0448NATUROPATHIC DOCTOR NEWS & REVIEWTreatment OverviewDiscontinue testosterone injections by gradually reducingthe frequency to every other week initially, and thenstopping altogether. High testosterone levels in salivatesting, along with persistent acne breakouts, served asthe primary rationale. The patient was started on a skin-specific probiotic thatcontains 50 billion CFU‡ from a diverse blend ofbacterial strains, including S. boulardii, B. coagulans,various Lactobacillus (e.g., L. plantarum, L. rhamnosus,L. acidophilus) and Bifidobacterium species (e.g., B. lactis,B. breve, B. bifidum, B. longum), along with B. subtilisand B. clausii. These strains were selected to support theskin microbiome and gut-skin axis. The formula alsoincludes phytoceramides and a proprietary blend ofAyurvedic herbs to support sebum balance andinflammation modulation, including fermented Indianfrankincense, triphala, holy basil, fenugreek, elecampane,camu camu, mangosteen, açaí, ginger, white peony, rosehip, asparagus, and Huang Qi. Vitamin C from acerolacherry extract was included for antioxidant support. Inaddition to targeting acne-related factors internally, theformula helps modulate immune response through theenteric immune system. An adrenal support formula containing 60 mg ofRhodiola per capsule, 16 mg of Holy Basil, and aproprietary blend of Ashwagandha, Oats, andSchisandra was prescribed as one capsule to be taken inthe morning and one capsule before lunchtime on anempty stomach. The focus on chronic stress during CW’shealth history and intake process, coupled with Phase 2moderate adrenal fatigue and low cortisol levels,highlighted the need for adrenal support. Her facial skinwas severely red and inflamed, and the slow healing ofscars also indicated that low cortisol levels were noteffectively supporting her immune system for overall skinhealth. CW also received customized mind-body techniques tohelp her manage stress daily, including breathingexercises during the day and a positive skin affirmationto reduce excessive anxiety about her skin. As sheimplemented the recommended changes, the patient wasencouraged to address stressful and discouragingthoughts related to her skincare routine. Hormonal changes leading to occasional hot flashesdisrupted CW’s sleep, further increasing her stress levels forthe following day. At times, her energy could be notably lowthroughout the day. The patient sometimes experiencedmigraines due to chronic stress and also reported having coldhands and feet. O// The facial skin appeared red and crepey in all areasexcept beneath the eyes, with two cystic bumps on the chinand multiple regions of post-inflammatory erythema (PIE)and post-inflammatory hyperpigmentation (PIH). The PIEand PIH scarring seemed slow to heal, and the skinsurrounding these areas did not regain its tone, moisture, orluminosity.Hormones were assessed using a comprehensive salivarypanel that included eight analytes: estradiol, progesterone,testosterone, DHEA, and four cortisol readings (morning,noon, evening, and night). Results indicated moderate (orphase 2) adrenal fatigue, characterized by low cortisol levelsin the morning, noon, and night. DHEA was low,testosterone was on the upper end of normal, and estrogenwas within range. CW’s progesterone was moderately low,and the progesterone-to-estrogen ratio was severely low,which indicates estrogen dominance. A// The patient was diagnosed with menopausal acne, aconclusion drawn from the presenting symptoms and CW’shistory of acne dating back to high school. Rosacea wasconsidered for differential diagnosis because of the rednessvisible on the skin. However, the cystic bumps and slow-healing distinct spots of post-inflammatory erythema (PIE)and post-inflammatory hyperpigmentation (PIH) scars alignmore closely with the typical presentation of acne and itshealing process.CW was also diagnosed with phase 2 or moderate adrenalfatigue, androgen excess, and estrogen dominance based onsalivary hormone results.

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ConclusionSkincare routines that moisturize, soothe, and repair theskin’s lipid barrier externally – combined with internalnatural therapies such as adrenal support, gut and immuneprotocols, androgen balancing, and treatment for estrogendominance – may provide a comprehensive approach totreating menopausal acne without further damaging theskin. REFERENCESAdult Acne. American Academy of Dermatology Association.Accessed March 13, 2025.https://www.aad.org/public/diseases/acne/really-acne/adult-acne1.Khunger N, Mehrotra K. Menopausal Acne - Challenges AndSolutions. Int J Womens Health. 2019 Oct 29;11:555-567. doi:10.2147/IJWH.S174292. PMID: 31754313; PMCID: PMC6825478.2.Dr. Aarti Patel has practiced women’s health,hormone balancing, naturopathic dermatology, andhomeopathy for 15 years. She currently sees patientsat Red Fern Health and Mind Body Acne Doc inVancouver, WA. Using natural therapies and whereappropriate BHRT, Dr. Patel treats common healthissues that can stem from hormone imbalances forwomen of all ages. She also practices holisticdermatology for acne and other chronic skinconditions such as eczema and rosacea. Dr. Patelincorporates the mind-body connection intotreatment plans for enhanced symptomimprovement. She graduated from BastyrUniversity in 2009 from their 4-year ND programand has authored a few natural health books:Picture It: Homeopathy, The Art of Health, andAcne: Just Another Four-Letter Word.APRIL 2025 - VOLUME 20 | ISSUE NO. 0449NATUROPATHIC DOCTOR NEWS & REVIEWCW was started on a new, gentle cleanser andmoisturizer featuring hyaluronic acid and herbalantioxidants for moisture and repair, along with aseparate occlusive oil containing rosehip, sea buckthorn,and serrated wrack. She was to use the oil sparingly,applying 1-2 drops in the last step of her skincare routineto seal in hydration from the cleansing and moisturizingsteps. The patient experienced a gradual allergic reaction overthe first 1-2 months of treatment due to the line ofskincare products recommended to her, most likelybecause of the high antioxidant content in the topicals.She was subsequently switched to a cleansing oil balm,facial serum, and stable vitamin C oil containing olivesqualane, olive oil, olive leaf water, Anchusa Azurea,beet, and chicory for gentler soothing and repair. CW was put on vitamin D3 to support immunity,hormone balance, mood and stress management, and guthealth, all connected to skin health. The patient was put on progesterone cream instead ofcapsules, for better absorption and to help reversepronounced estrogen dominance that had beencoinciding with acne symptoms. She was to apply 10 mgcream 30 minutes before bedtime to thin-skinned areas inrotation.Future Plan: Retest hormones out of range in threemonths, followed by a follow-up appointment. OUTCOME AND FOLLOW-UPCW moved out of state and could not schedule a secondappointment. However, she recently emailed an update (ninemonths after her last appointment) reporting that her skinhad healed significantly due to a gentle skincare routinefeaturing olive oil and olive leaf water. The frequency andduration of her acne symptoms, hot flashes, sleepdisruptions, unmanaged stress, and skin-related anxiety hadalso decreased. She continued using the adrenal supporttherapy, mind-body techniques, probiotics, progesteronecream, and vitamin D3. Improved sleep quality aided skinbarrier renewal overnight. Discontinuing testosteroneinjections also contributed positively. Future considerationsinvolve retesting hormones and adjusting CW’s bio-identicalhormone therapies.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0451NATUROPATHIC DOCTOR NEWS & REVIEWCase PresentationS is a 24-year-old female presenting with acne and mildbloating. She has experienced acne since her teenage years,but it worsened significantly after stopping birth controlfour months ago. She previously tried spironolactone forthree months without improvement and began usingtretinoin (0.25%) eight months ago, which improved herskin texture but did not reduce breakouts. She experiences flare-ups during ovulation and has cysticacne with closed comedones on her jawline and forehead,along with mild closed comedones on her back. Hermenstrual cycle is regular, and she reports mild bloatingafter meals. She rates her acne severity as an 8 out of 10.Her current skincare routine includes:PCA creamy cleanserBenzoyl peroxidePCA collagen hydrator and rebalance serum. Clinical findingsThe patient was experiencing cystic acne with erythemaalong the jawline and forehead, along with closedcomedones. She also had mild comedones on her back.Additionally, she reported symptoms of fatigue, hair loss,anxiety, and depression. Her physical exam was otherwisenormal.She denied abdominal pain, heart palpitations, chest pain,heat/cold intolerance, and shortness of breath.Therapeutic interventionInitial visit: The first visit aimed to identify the root cause of her acne.Top considerations for her acne included androgen-relatedfactors, gastrointestinal issues (such as leaky gut), or acnestemming from blood glucose dysregulation. I orderedcomprehensive labs to assess her general health andpotential causes of her acne, including estrogen,progesterone, testosterone, CBC, CMP, lipid panel, HbA1c,TSH, free T3, free T4, rT3, TPO, TG, SHBG, DHEA-S,IGF-1, androstenedione, iron panel, ferritin, vitamin D,B12, and cortisol. I recommend either saw palmetto orDIM, depending on her results. Treatment PlanAcnutrol supplement for acne-specific nutrientsLiver cleanse herbs to support detoxification and excesshormone excretionInsomnitol supplement for occasional insomniaProbiotics to help with bloating and support acnetreatmentElimination diet: avoid dairy, gluten, and sugarBentonite clay mask for skin carePositive affirmations for promoting a positive mindsetregarding skinBox breathing exercises to manage stressGI map test (consider for the next visit to assess guthealth in depth, if needed)Follow-up and OutcomesFirst Follow-up Visit (3 weeks later):The patient’s acne improved after following the diet andsupplement protocol.Lab Results revealed:Low Progesterone and normal estrogen, indicatingestrogen dominanceLow Testosterone, ruling out the need for saw palmettoTo address estrogen dominance and PMS symptoms, I addedvitex through a supplement and St. John’s wort,passionflower, dandelion, dong quai, and wild yam root topromote progesterone balance. Since DIM can exacerbate acne in testosterone-sensitivepatients, I opted not to introduce it at this moment.Currently, my primary working diagnosis for the cause of heracne is a GI/leaky gut issue, as she has been experiencingconstant bloating and is responding well to the previoustreatment plan. Her elevated ALT suggested mild liver inflammation, soI continued the liver cleanse for three months to reduceALT levels. We continued with previous supplementation, added thevitex supplement, and started reintroducing foods fromthe elimination diet.

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APRIL 2025 - VOLUME 20 | ISSUE NO. 0452NATUROPATHIC DOCTOR NEWS & REVIEW2nd Follow Up Visit: The patient reported that after taking the PMS supporttonic, her acne, mood, and cramping worsened, and hermenses were delayed. Suspecting sensitivity to vitex, Iadvised her to discontinue the PMS support. At her next visit, she reported:90% improvement in her acne, with only occasionaljawline breakouts.Bloating is significantly reduced, occurring onlybefore her period or after consuming certain foods. Given her progress, I:Continued Acnutrol and the probiotic while reducingthe liver cleanse to one cap daily.Instructed her to discontinue the liver cleanse in onemonth if her acne stayed stable.Reduce Acnutrol to 3 capsules daily if her skincontinues to improve.Incorporated fish oil for its benefits on mental health,skin health, and gut health.Due to her significant improvement, no further GItesting or treatments were needed at that time. Discussion Acne can have many causes, so it is essential tounderstand the root cause of acne to treat it properly.Acne results from inflammation of the pilosebaceousgland, which is theorized to involve increased sebumproduction, follicular hyperkeratinization, and C. acnesproliferation.²′³ Potential causes for the inflammation ofthe pilosebaceous gland and increased sebum productionare vast and include medication use, oil-based cosmetics,endocrine disorders, hormonal imbalances, leaky gut,genetic factors, mechanical trauma from scrubbing withsoaps and detergents, high glycemic load diets,psychological stress, and insulin resistance, amongothers.⁴ In this case, eliminating sugar, dairy, and glutensignificantly contributed to the reduction of acne. Dairyconsumption has been linked to a higher risk of acne.Milk-derived amino acids can stimulate the synthesis ofinsulin-like growth factor-1 (IGF-1), which increasessebum production, follicular epithelial growth, andkeratinization, all contributing to acne. Plasma levels ofIGF-1 have also been associated with the severity of acne. A similar mechanism occurs with hyperglycemiccarbohydrates, which promote insulin and IGF-1, leading toacne through increased sebum production. Both dairy andhigh glycemic load foods and meat can activate themTORC1 (mammalian target of rapamycin) pathway,resulting in excess sebum production andhyperkeratinization, ultimately leading to acne.⁵ I oftenprefer to conduct an elimination diet with patients to assesstheir IgG food sensitivities and identify acne triggers. Therefore, gut health is critical to assess in patients withacne. The mTOR pathway has been observed to be moreheavily expressed in individuals with skin diseases. Bacterialmetabolites have been shown to interact with the mTORpathway, which is influenced by gut microbiota. This canlead to alterations in the intestinal barrier and potentiallyexacerbate acne. In some studies, 54% of acne patients werefound to have gut dysbiosis.Probiotics are a viable adjunct treatment option formodulating the intestinal microbiota, which creates an anti-inflammatory response and influences IGF-1 levels.⁶′⁷ Manyprobiotics are helpful, with Lactobacillus, specificallyLactobacillus rhamnosus, and Bifidobacterium rankingamong the top probiotic strains.⁸ I recommended a liver cleanse supplement to her topromote optimal hormonal balance. The liver is the primarysource of IGF-1 and plays a crucial role in mediating growthfactors. IGF-1, insulin, and growth factors are all implicatedin metabolic status, which, as mentioned earlier, is related toacne pathogenesis.⁹ The liver is also responsible formetabolizing hormones. Patients with severe acne exhibitincreased levels of dehydroepiandrosterone sulfate, sexhormone-binding globulin, and androstenedione, all ofwhich can contribute to excess sebum production andacne.¹⁰

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ConclusionAcne has various causes; therefore, it is essential tounderstand its root cause and the many factors that cancontribute to its appearance. Hormones, diet, lifestyle,topical products, gut health, and stress all need to be assessedthoroughly with acne patients. In this case, the patient wasable to resolve her acne by 90% at the last visit bymodulating her gut health, mTOR pathway, hormones, andachieving optimal liver function and nutrient support foracne.Dr. Smithback is a licensed naturopathic medicaldoctor, personal trainer, and nutritionist in SanDiego. She became a doctor because she wants tosee her patients not only be healthy but trulythrive in their lives, becoming their best, strongest,most vibrant, and happiest selves. Her clinicalspecialties include sports medicine, PRPinjections, IV therapy, skin health, mental health,hormones, weight management, and gut health.REFERENCESKurokawa I, Nakase K. Recent advances in understanding andmanaging acne. F1000Res. 2020;9:F1000 Faculty Rev-792. Published2020 Jul 29. doi:10.12688/f1000research.25588.11.Sutaria AH, Masood S, Saleh HM, et al. Acne Vulgaris. [Updated2023 Aug 17]. In: StatPearls [Internet]. Treasure Island (FL):StatPearls Publishing; 2023 Jan-. Available from:https://www.ncbi.nlm.nih.gov/books/NBK459173/2.Juhl CR, Bergholdt HKM, Miller IM, Jemec GBE, Kanters JK,Ellervik C. Dairy Intake and Acne Vulgaris: A Systematic Review andMeta-Analysis of 78,529 Children, Adolescents, and Young Adults.Nutrients. 2018;10(8):1049. Published 2018 Aug 9.doi:10.3390/nu100810493.Rhyu J, Yu R. Newly discovered endocrine functions of the liver.World J Hepatol. 2021;13(11):1611-1628. doi:10.4254/wjh.v13.i11.16114.Sánchez-Pellicer P, Navarro-Moratalla L, Núñez-Delegido E, Ruzafa-Costas B, Agüera-Santos J, Navarro-López V. Acne, Microbiome, andProbiotics: The Gut-Skin Axis. Microorganisms. 2022;10(7):1303.Published 2022 Jun 27. doi:10.3390/microorganisms100713035.Chilicka K, Dzieńdziora-Urbińska I, Szyguła R, Asanova B, NowickaD. Microbiome and Probiotics in Acne Vulgaris-A Narrative Review.Life (Basel). 2022;12(3):422. Published 2022 Mar 15.doi:10.3390/life120304226.Goodarzi A, Mozafarpoor S, Bodaghabadi M, Mohamadi M. Thepotential of probiotics for treating acne vulgaris: A review of literatureon acne and microbiota. Dermatol Ther. 2020;33(3):e13279.doi:10.1111/dth.132797.Fabbrocini G, Bertona M, Picazo Ó, Pareja-Galeano H, MonfrecolaG, Emanuele E. Supplementation with Lactobacillus rhamnosus SP1normalises skin expression of genes implicated in insulin signalling andimproves adult acne. Benef Microbes. 2016;7(5):625-630.doi:10.3920/BM2016.00898.Bowe W.P., and Logan A.C.: Acne vulgaris, probiotics and the gut-brain-skin axis: back to the future? Gut Pathog 2011 Jan 31; 3: pp. 19.Murray, K., Wilkinson-Smith, V., Hatcher, D., Vuksan, V., & Jenkins,D. (2022). The effect of a plant-based low-fat diet on body weight,metabolism, and insulin sensitivity in overweight adults: A randomizedcontrolled trial. Journal of the American College of Nutrition, 41(3),221–229. https://doi.org/10.1080/07315724.2022.204821110.APRIL 2025 - VOLUME 20 | ISSUE NO. 0453NATUROPATHIC DOCTOR NEWS & REVIEW

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April 2025 | Volume 20 | Issue 4

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