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PME SESSIONS (NON-CME) The Rest of the Hormone Story - How Estrogen Metabolism and the Microbiome Characterize Patient Health Presented by: Laura Neville, ND 11:30 am Location: Grand A 6:00 pm Location: Grand A 12:00 pm Location: Georgian Treating Adult Growth Hormone Deficiency Presented by: Thierry Hertoghe, MD (Remote) The Effect of Zonulin and Food Sensitivities on Gut Health Presented by: Robert G. Silverman, DC, DACBN, DCBCN, MS, CCN, CNS, CSCS, CIISN, CKTP, CES, HKC, FAKTR Sponsored by: Sponsored by: Sponsored by: FRIDAY | SEPTEMBER 16TH 8 ANTI-AGING MEDICAL NEWS | FALL 2022
Aligning HRT Monitoring Practices with Peer-Reviewed Clinical Data Presented by: Mark Newman, MS 12:00 pm Location: Grand A 6:15 pm Location: Grand A 12:00 pm Location: Avenue 34 Stress And Hormones: The Role Of Cortisol On Hormone Dysfunction Presented by: Michael Chapman, ND System Synergy: Using Technology to Track Clinical Outcomes, Optimize Adherence, and Deliver Personalized Precision Medicine Presented by: James LaValle, RPh, CCN, MT Sponsored by: Sponsored by: Sponsored by: SATURDAY | SEPTEMBER 17TH ® 9ANTI-AGING MEDICAL NEWS | FALL 2022
Colorado; compounding pharmacist, men’s health specialist, and director of marketing and business development at Stanley Specialty Pharmacy and Stanley Pharma Group, Charlotte, North Carolina; and member
Greg McKettrick, Greenwood Village, of the
scientific advisory board of Berkeley Life Professional, Chicago, Illinois. The DysfunctionErectileinSupplementationNitricRoleEssentialofDietaryOxideReversing 10 ANTI-AGING MEDICAL NEWS | FALL 2022
GregBy: McKettrick RPh The following article is not endorsed and/or supported by The American Academy of Anti-Aging Medicine. The purposes of this publication do not imply endorsement and/or support of any author, company or theme related to this article. Corresponding Author Greg McKettrick, RPh, Stanley Specialty Pharmacy, 3120 Latrobe Drive, Charlotte, North Carolina 28211; telephone number, 704-370-6612; Greg@stanleyrx.com; website: https://www.stanleyrx.com/.
RPh, is the director of men’s health for Revelation Pharma Corporation,
Introduction
Many men who experience refractory ED from any cause are unprepared for its severity and persistence (the effects of which, in PC survivors, are compounded by the trauma of having undergone invasive procedures for a lifethreatening disease), and most such patients are unaware that effective, noninvasive treatment is available. To address the needs of those men, the author and his pharmacy-practice partner designed a novel protocol that has consistently proven effective in restoring erectile function. Oral dietary NO supplementation is an essential component of that program, in which each participating patient works closely with an assigned compounding pharmacist. As the patient’s dedicated contact during treatment, that compounder coordinates clinical care with prescribers; provides
from prostatectomy, radiotherapy, or both as therapy for prostate cancer (PC); and the effects of chronic systemic disease and its treatment. An adequate systemic level of NO (the endogenous form of which is produced from arginine by a family of 3 calmodulin-dependent NO synthase enzymes) [1] is necessary to achieve and sustain penile erections, but that level decreases as aging progresses due to numerous factors, including the breakdown of the NO synthase pathway. In men who are deficient in NO and experience some degree of ED, supplementation with a dietary form of that vasodilator/neurotransmitter can increase blood flow to an adequate level and thus assist the restoration of sexual function.
Abstract
The author of this report is an experienced compounding pharmacist and specialist in men’s health. Over decades, his treatment of men afflicted with erectile dysfunction (ED) has revealed that many such patients and their physicians are unaware of the essential role of supplemental dietary nitric oxide (NO) in recovery from that disorder and that effective, noninvasive therapy for the loss of erectile function exists. Among the causes of ED that afflict the patient population so affected are aging; complications
ED in Survivors of PC
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This article describes the role of oral dietary nitric oxide supplementation as part of a noninvasive protocol for recovery from erectile dysfunction caused by aging; prostatectomy, radiotherapy, or both as therapy for prostate cancer; and chronic systemic disease and its treatment. Many men who experience refractory erectile dysfunction are unprepared for its severity and persistence (the effects of which in prostate-cancer survivors are compounded by the trauma of having undergone invasive procedures for a life-threatening disease), and most are unaware that effective treatment is available. The endogenous production of nitric oxide, which is necessary to achieve and sustain penile erections, decreases as aging progresses. In men who are deficient in that vasodilator/ neurotransmitter and are experiencing some degree of impotence, supporting nitric oxide levels with a dietary nitrate facilitates the return of erectile function and sexual response. Supplemental nitric oxide is an essential component of the protocol described in this report, which also examines the mechanisms of impotence and its most common causes and reviews the role of that supplement in penile erections.
Supplemental dietary NO is an essential component of the protocol described in this report, which also examines the mechanisms of impotence and its most common causes and reviews the role of NO in penile erections.
The Role of NO in Penile Erection
information about the uses and effects of drugs and dietary supplements; ensures that prescribed medications, nutraceuticals, and equipment are readily available and instructs the patient in their use; modifies protocol components as prescribed when medical needs change; and provides compassionate support. Offering those services unquestionably encourages compliance and results in better outcomes. Most protocol patients achieve a degree of erectile function that they themselves deem satisfactory, regardless of whether participation in that program is initiated soon after the onset of ED or years thereafter.
Erectile Dysfunction
Synthesized in and released by endothelial cells, endogenous NO has been shown to affect the physiologic process of penile erection [7] when it
12 ANTI-AGING MEDICAL NEWS | FALL 2022
Parkinson’s disease, [5] or depression. Evidence suggests that ED may also serve as a general marker for occult CVD and as an indicator of overall physical and emotional health. [5] According to Gurtner and colleagues, persistent failure to sustain a penile erection affects all races and social classes and is documented in ancient medical treatises, such as those found in Egyptian tombs, on Greek cups, and in the Old Testament. [6] Those authors state that treatments for ED were recorded early as the eighth century, when, in Rome and Greece, talismans of rooster and goat genitalia were thought to promote sexual function, and that in the thirteenth century, cures for ED included ingesting roasted wolf penis. [6] Fortunately, patients today who experience ED intermittently or chronically can access more palatable and effective therapies for reversing that condition.
ED, which is defined as “the inability to achieve or maintain a [penile] erection sufficient for satisfactory sexual performance,” [4] can be caused by aging; complications from prostatectomy, radiotherapy, or both to treat PC; obesity; lifestyle choices such as smoking; psychologic, neurologic, vasculogenic, hormonal, or pharmaceutical factors; and/or a range of recurring or chronic diseases such as hypertension, hypercholesterolemia, lower–urinary-tract disease, diabetes mellitus, cardiovascular disease (CVD), metabolic syndrome,
Evidence suggests that NO is the primary vasoactive, nonadrenergic, noncholinergic neurotransmitter and chemical mediator of penile erection. [5] Burnett reports that after its release by nerve and endothelial cells in the penile corpora cavernosa, NO activates soluble guanylyl cyclase to cause an increase in the levels of 3’,5’-cyclic guanosine monophosphate (cGMP), which acts as a second messenger molecule and regulates calcium-channel activity and the levels of intracellular contractile proteins that affect the relaxation of penile corpus cavernosum smooth muscle. [5] He further notes that impaired NO bioactivity is a major mechanism in ED. [5]
In this article, the mechanisms of ED are briefly described and its most common causes are summarized, the role of NO in penile erections is examined, an effective protocol that includes dietary NO supplementation in a regimen for reversing ED is presented, and the results of that program are demonstrated in a brief case report. Detailed information about restoring erectile dysfunction caused by the effects of prostatectomy, radiotherapy, or both in PC survivors is provided in a series published in the International Journal of Pharmaceutical Compounding (IJPC). [2,3]
NO Supplementation in Recovery from ED
The Essential Role of Dietary Nitric Oxide Supplementation in Reversing Erectile Dysfunction
Identifying Low Levels of NO
Dietary NO Supplementation in the Treatment of ED: A Case Report
In the case summarized below, the use of dietary NO supplementation as part of an effective program for recovery from ED is described. The patient profiled and his recovery from that disorder and concomitant urinary incontinence
Case report
(UI) are typical of most PC survivors who complete the rehabilitation protocol, which relies on the purity, potency, safety, and efficacy of prescribed supplements and drugs; is customized for each participant; can easily be incorporated into the spectrum of most pharmacy services; and (because patient care is coordinated by an assigned pharmacist) saves time for busy practitioners.
13ANTI-AGING MEDICAL NEWS | FALL 2022
causes the relaxation of corporal cavernosal smooth muscle tissue and the subsequent increase in blood flow into the penis. [8] It could thus be concluded that impaired NO activity greatly impacts the pathogenesis of ED in a manner similar to that occurring in other forms of vascular disease or in patients with cardiovascular risk factors such as smoking, dyslipidemia, diabetes, or hypertension. [7]
Conclusion
This report describes the use of supplementary dietary NO in an effective ED-treatment protocol
Drugs such as sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra), and avanafil (Stendra) support the maintenance of healthful levels of endogenous NO by blocking its breakdown, but if the patient’s NO level is already low, those medications will be ineffective. There are now available saliva test “strips” that can be used in the home setting or a pharmacy to reveal, in 15 seconds and via an easy-to-read color code, the NO level at baseline and, if a dietary NO supplement is required, before and after dosing. Those test results can be provided to the patient’s prescriber, who will determine whether a change in the treatment protocol is required. If exogenous NO is needed, then selecting a quality-controlled concentrated dietary NO supplement is advised. Choosing a supplement that has demonstrated verifiable potency, purity, and safety; is provided in a precise dose; requires minimal dosing; and is both easy to swallow and convenient to use ensures compliance and results in a better treatment outcome.
DF, a 60-year-old African-American man, was referred to the author’s compounding pharmacy practice to undergo treatment for refractory ED and UI, both of which developed after prostatectomy for localized PC. His prior failed treatments for ED consisted of sildenafil and the use of a vacuum-erection device (VED) before attempted sexual activity, and his UI was untreated (he wore disposable padded undergarments). The following regimen ultimately proved effective in resolving this patient’s ED and UI to his satisfaction: oral treatment with a dietary NO supplement, tadalafil, and sildenafil; intracavernosal injections of Trimix (a compounded combination of prostaglandin E1, 10 mcg/mL; phentolamine mesylate, 1 mg/mL; and papaverine hydrochloride, 30 mg/mL); adherence to a program of prescribed Kegel exercises; use of a VED as instructed; and voluntary stop-andstart interruption of urine flow during urination. This patient experienced resolution of his ED to a degree that he deemed acceptable and became completely continent of urine approximately 6 months and 3 months, respectively, after protocol participation was initiated. Both of those successful outcomes persist at the time of this writing.
1. Bredt DS. Endogenous nitric oxide synthesis: biological functions and pathophysiology. Free Radic Res. 1999;31(6):577-596.
2. McKettrick G, Yoch D. Reversing erectile dysfunction and urinary incontinence after prostatectomy or radiotherapy: the Stanley Prostate-Cancer Treatment Protocol. Int J Pharm Compd. 2021;25(1):18-23.
time for busy practitioners and their staff. Readers who are interested in additional information about the benefits of dietary NO supplementation in patients with ED or the described protocol used to treat that condition are invited to contact the author at the address provided in this article or visit the website also listed.
3. McKettrick G, Yoch D. The Stanley Prostate-cancer Treatment Protocol for Erectile Dysfunction After Prostatectomy and/or Radiotherapy: a case report. Int J Pharm Compd. 2021;25(2):94-98.
DisclaimerReferences
Mr. McKettrick serves as an independent consultant for Berkeley Life Professional, Chicago, Illinois, and its clients and a member of the scientific advisory board of Berkeley Life Professional but is not reimbursed directly for those services. A Berkeley Life Professional product is recommended for patients treated in the protocol described in this report.
5. Burnett AL. The role of nitric oxide in erectile dysfunction: implications for medical therapy. J Clin Hypertens (Greenwich). 2006;8(12 suppl 4):53-62.
4. U. S. Department of Health and Human Services. National Institutes of Health. Impotence. NIH Consens Statement. 1992, Dec 7-9;10(4):1-31.
7. Sullivan ME, Thompson CS, Dashwood MR, et al. Nitric oxide and penile erection: is erectile dysfunction another manifestation of vascular disease? Cardiovasc Res. 1999;43(3):658-665.
The views expressed herein are those of the author.
that provides an alternative to surgical options for restoring the loss of erectile function. Feedback from program participants and their prescribing clinicians has consistently shown the effectiveness of that regimen in restoring male sexual function. In addition, the protocol can be easily integrated into the spectrum of pharmacy services, and the patient-physician communication it facilitates saves
14 ANTI-AGING MEDICAL NEWS | FALL 2022
8. Davies KP. Development and therapeutic applications of nitric oxide releasing materials to treat erectile dysfunction. Future Sci OA. 2015(1):FSO53.
6. Gurtner K, Saltzman A, Hebert K, Laborde E. Erectile dysfunction: a review of historical treatments with a focus on the development of the inflatable penile prosthesis. Am J Mens Health. 2017;11(3):479-486.
Financial Disclosure
The Essential Role of Dietary Nitric Oxide Supplementation in Reversing Erectile Dysfunction
As we age, we lose 85% of our ability to make Nitric Oxide. • Available exclusively through practitioners • All ingredients and batches tested for safety • Full marketing support and non-stocking options available Become a distributing practitioner at berkeleylife.comBecome a distributing practitioner at berkeleylife.com Test and support your patients’ Nitric Oxide levels with Berkeley Life’s Complete Nitric Oxide System.
JoelBy: Kahn, Chen Chen, Jon Ward, Caroline Dombrowski The following article is not endorsed and/or supported by The American Academy of Anti-Aging Medicine. The purposes of this publication do not imply endorsement and/or support of any author, company or theme related to this article. Blood Pressure and AArterialtheWall:Root-CauseApproach to Healthy Life Extension 16 ANTI-AGING MEDICAL NEWS | FALL 2022
Longevity: Reframing the Story
Hypertension is one of the most significant threats to both the quality and length of human life. Elevated blood pressure is correlated with organ damage,1 worsened brain health,2 and shorter lifespan.3
Conversely, effective control of blood pressure has been associated with a 5-7 year longer lifespan.4 Healthy blood pressure is also associated with improved, more youthful brain function.5
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Figureseriously.1. 6 , 7 , 8 , 9 The numbers don’t lie. Current approaches to hypertension leave a huge opportunity for improvement.
Many patients today are motivated to protect brain health and pursue a longer life. Framing blood pressure in these terms can motivate increased compliance. However, this requires patients to understand the bigger picture: to see their blood pressure in the context of their overall vascular health. Hypertension is both an indication of, and contributor to, a deteriorating vascular system. It is exacerbated by failures in the endothelium to sustain adequate vasodilation. At the same time, high blood pressure inflicts damage on the but the therapy is not without challenges, both in compliance and side effects.
withisLDLofprimarilycommonpressuremostishowFirst,endothelialarterialtoatInleadingofincreasingendothelium,thelikelihoodinflammatoryprocessestoatherosclerosis.thisarticle,wewilllookbloodpressureinrelationtwosignificantfactors:elasticityandtheglycocalyx.wemustrecognizecardiovascularhealthcurrentlyaddressedinclinicalpractices.Bloodapart,itisstillpracticetofocusonthelipidcontenttheblood,particularlyandtriglycerides.Thisconventionallytackledtheuseofstatins,
A range of medications to control blood pressure is available to clinicians, but patient compliance (as with most medications) is low.
A study by Gascon et al.5 revealed two of the most prevalent reasons. First, patients have an aversion to hypertension drugs, which they associate with negative side effects and damage to long-term health. Secondly, and more worryingly, they tend not to take high blood pressure
to Healthy Life Extension Figure 2.10 , 11 , 12
Blood Root-Cause Approach
The main problem with a focus of lowering blood lipids is that it’s an extraordinarily simplistic approach to a complex problem. LDL is just one step in a chain of events leading to cardiovascular disease, and many other factors must be in place for it to become a threat. Specifically, lipids become a problem only when they penetrate the blood vessel wall and are retained in the presence of other plaque-forming elements in the subendothelial space. This requires a failure in reverse transport by HDL and — more importantly — a vulnerability in the arterial wall itself.
Here we get to the nub. The most direct assessment of vascular health focuses not on the contents of the lumen, but on the condition of the blood vessel wall. Placing blood pressure in this context makes it more understandable to both practitioners and patients.
Pressure and the Arterial Wall: A
The primary threat to the vascular wall is atherosclerosis: the buildup of plaque which may break off to form fatal clots in the coronary arteries or the brain.16 It has been shown that hypertension contributes to the development of atherosclerosis, which is increasingly viewed as an inflammatory disorder.17 High blood pressure is directly associated with oxidative stress, which can lead to inflammation of the blood vessel wall. Oxidative stress (and the resulting reactive oxygen species, ROS) likely plays a causative role in the development of hypertension. 18
In brief, once we begin to explore the larger
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Arterial stiffness is directly correlated with high blood pressure,15 and it seems there is a causative connection — very likely, a two-way connection or vicious circle, meaning hypertension increases arterial stiffness by damaging the blood vessel wall, and arterial stiffness exacerbates hypertension by reducing vasodilation.
The Blood Vessel Wall
One of the most fundamental changes that can occur in the vascular wall is the development of arterial stiffness. A healthy vascular system maintains an adequate degree of elasticity. With age and a decline in vascular function, arterial elasticity declines. Arterial stiffness is a reliable and independent predictor of cardiovascular events.13 One inexpensive and non-invasive measurement uses pulse wave velocity (PWV). High PWV reliably indicates arterial stiffness.14
Currently, 90% of hypertension cases presenting in the clinical setting do not have a known cause.29 Nevertheless, we can be confident that blood pressure dysregulation develops in relation to the overall condition of the vascular system.
As a semi-permeable barrier, the EGX provides essential protection to the endothelium,
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However, the EGX is far more than a passive barrier. It plays active regulatory roles in several key respects. Most relevant to hypertension, the EGX responds to the shear stress of flowing blood, triggering the production of nitric oxide (NO), through the eNOS enzyme.22 NO is an essential signaling molecule. Among its many physiological roles, it functions as a vasodilator and is therefore essential to maintaining blood pressure in the healthy range.26 When the EGX is compromised, natural production of NO declines and arterial elasticity is impaired, an inflammatory response is triggered.23 This initiates the vicious cycle, whereby blood pressure continues to rise.
prohibiting the inflammatory intrusion or adhesion of harmful substances while allowing the passage of fluids, proteins, and solutes.25
The EGX is an extracellular matrix on the luminal side of the endothelium comprising a negatively charged mesh of membranous glycoproteins, proteoglycans, glycosaminoglycans and associated plasma proteins.19 The gel-like EGX covers the entire endothelium in both the larger blood vessels and in the microvasculature, serving several functions essential to the health of the vascular system.
In fact, a healthy, robust endothelial glycocalyx protects against arterial stiffness.28
Nature provides its own answer to this question; the endothelial glycocalyx (EGX). The EGX plays a unique role in both protecting and regulating the entire vascular system, with direct implications for blood pressure, arterial stiffness, and atherogenesis.
Important Intersections
Specific to hypertension, the EGX buffers sodium homeostasis.27 In the absence of a robust EGX, sodium in the blood gets uncontrolled access to the endothelium. In the presence of aldosterone, excess sodium stiffens the endothelium and reduces NO release, with a resulting risk of increased blood pressure.
context of hypertension, all roads eventually lead to the blood vessel wall. For clinicians, this raises the question: How do we best protect and support the health of the blood vessel wall?
In the first place, the EGX provides a semipermeable barrier between the flowing blood and the endothelium.20 This barrier controls the access of circulating LDL to the endothelium.21 In other words, the EGX provides the first line of defense against the subendothelial space lipid accumulation, the hallmark of atherosclerotic plaque.22
At the center of the story lies the vascular wall, in particular its protective and regulatory lining, the EGX. We know there are correlations between
In its protective barrier function, the EGX also prevents adhesion to the endothelium of inflammatory circulating molecules.22 Studies have shown that when the EGX is degraded, endothelial adhesion significantly increases. This means that the EGX plays a key role in regulating vascular inflammation,23 which is now seen at the root of atherosclerosis.24
The Glycocalyx
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A root-cause analysis of cardiovascular dysfunction will inevitably lead to focus on the begins, and atherosclerosis develops. Understanding hypertension as a disorder of the vascular wall invites more far-reaching clinical interventions. In particular, regeneration of the endothelial glycocalyx can bring lifelong benefits beyond the control of blood pressure, important as that is. The latest research in this field points to exciting clinical opportunities.
Figure 3.
Blood Pressure and the Arterial Wall: A Root-Cause Approach to Healthy Life Extension
The upside of a vicious circle is that intervention at any point may arrest the process. This means that in addition to addressing blood pressure with the currently available medications, the clinician can open a new front and focus on repairing the EGX.
This is where good news begins. It is likely that a compromised EGX can be restored quickly and effectively with purely natural interventions. As always, part of this strategy must include lifestyle factors, because the same behaviors that exacerbate hypertension and cardiovascular disease directly undermine the EGX: excess glucose, excess sodium, stress, sleep deprivation, and lack of exercise. In addition to rectifying these lifestyle components, the clinician can directly restore and protect the EGX by the use of one particular natural compound: rhamnan sulfate (RS) from the green seaweed Monostroma nitidum. The cardiovascular benefits of RS have been studied for many years, and today clinicians are specifically using it to support the health of the EGX.
hypertension and loss of NO production. We also know that hypertension can be triggered or exacerbated by excess sodium in the plasma. In both cases, the EGX plays a critical role. In addition, hypertension is correlated with arterial stiffness, which in turn is correlated with a compromised EGX because the loss of NO reduces vascular tone.30
While hypertension can independently lead to serious cardiovascular events, it is best viewed systemically within the broader context of the many inter-connected features of the human vascular system. The advantage of this approach is that it opens the door to more effective interventions, including non-pharmaceutical therapies. Since blood pressure rises with age, many can benefit.
Conclusion
16. Sakakura K, Nakano M, Otsuka F, Ladich E, Kolodgie FD, Virmani R. Pathophysiology of Atherosclerosis Plaque Progression. Heart, Lung and Circulation. 2013;22(6):399-411. doi:10.1016/j. hlc.2013.03.001
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9. Rethy L, Shah NS, Paparello JJ, Lloyd-Jones DM, Khan SS. Trends in Hypertension-Related Cardiovascular Mortality in the United States, 2000 to 2018. Hypertension. doi:10.1161/HYPERTENSIONAHA.120.151532020;76(3):e23-e25.
5. Cherbuin N, Walsh EI, Shaw M, et al. Optimal Blood Pressure Keeps Our Brains Younger. Frontiers in Aging Neuroscience. 2021;13. Accessed June 29, article/10.3389/fnagi.2021.6949822022.https://www.frontiersin.org/
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10. Vrijens B, Antoniou S, Burnier M, de la Sierra A, Volpe M. Current Situation of Medication Adherence in Hypertension. Frontiers in Pharmacology. 2017;8. Accessed July 1, 2022. frontiersin.org/article/10.3389/fphar.2017.00100https://www.
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19. Nieuwdorp M, Meuwese MC, Vink H, Hoekstra JB, Kastelein JJ, Stroes ES. The endothelial glycocalyx: a potential barrier between health and vascular disease. Current Opinion in Lipidology. 2005;16(5):507-511. doi:10.1097/01.mol.0000181325.08926.9c
20. Kolářová H, Ambrůzová B, Švihálková Šindlerová L, Klinke A, Kubala L. Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions. Mediators Inflamm. 2014;2014. doi:10.1155/2014/694312
24. Zhu Y, Xian X, Wang Z, et al. Research Progress on the Relationship between Atherosclerosis and Inflammation. Biomolecules. 2018;8(3):E80. doi:10.3390/biom8030080
7. Santos D, Dhamoon MS. Trends in Antihypertensive Medication Use Among Individuals With a History of Stroke and Hypertension, 2005 to 2016. JAMA Neurology. 2020;77(11):13821389. doi:10.1001/jamaneurol.2020.2499
12. Casula M, Mozzanica F, Scotti L, et al. Statin use and risk of new-
11. May HT, Knowlton KU, Anderson JL, Lappé DL, Bair TL, Muhlestein JB. High-statin adherence over 5 years of follow-up is associated with improved cardiovascular outcomes in patients with atherosclerotic cardiovascular disease: results from the IMPRES study. Eur Heart J Qual Care Clin Outcomes. 2022;8(3):352-360. doi:10.1093/ehjqcco/qcab024
1. Triantafyllidi H, Benas D, Schoinas A, et al. Hypertension‐mediated organ damage regression associates with blood pressure variability improvement three years after successful treatment initiation in essential hypertension. J Clin Hypertens (Greenwich). 2021;23(6):1150-1158. doi:10.1111/jch.14209
23. Schierke F, Wyrwoll MJ, Wisdorf M, et al. Nanomechanics of the endothelial glycocalyx contribute to Na+-induced vascular inflammation. Sci Rep. 2017;7(1):46476. doi:10.1038/srep46476
6. CDC. Facts About Hypertension | cdc.gov. Centers for Disease Control and Prevention. Published July 12, 2022. Accessed August 8, 2022. https://www.cdc.gov/bloodpressure/facts.htm
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15. Safar ME, Asmar R, Benetos A, et al. Interaction Between Hypertension and Arterial Stiffness. Hypertension. 2018;72(4):796805. doi:10.1161/HYPERTENSIONAHA.118.11212
21. Liu X, Fan Y, Deng X. Effect of the endothelial glycocalyx layer on arterial LDL transport under normal and high pressure. Journal of Theoretical Biology. 2011;283(1):71-81. doi:10.1016/j. jtbi.2011.05.030
22. Mitra R, O’Neil GL, Harding IC, Cheng MJ, Mensah SA, Ebong EE. Glycocalyx in Atherosclerosis-Relevant Endothelium Function and as a Therapeutic Target. Curr Atheroscler Rep. 2017;19(12). doi:10.1007/s11883-017-0691-9
2. Hajjar I, Goldstein FC, Martin GS, Quyyumi AA. Roles of Arterial Stiffness and Blood Pressure in Hypertension-Associated Cognitive Decline in Healthy Adults. Hypertension. doi:10.1161/HYPERTENSIONAHA.115.062772016;67(1):171-175.
3. Franco OH, Peeters A, Bonneux L, de Laet C. Blood Pressure in Adulthood and Life Expectancy With Cardiovascular Disease in Men and Women. Hypertension. doi:10.1161/01.HYP.0000173433.67426.9b2005;46(2):280-286.
8. WHO Fact Sheet. Hypertension. World Health Organization. Published August 25, 2021. Accessed August 8, 2022. https://www. who.int/news-room/fact-sheets/detail/hypertension
onset diabetes: A meta-analysis of observational studies. Nutrition, Metabolism and Cardiovascular Diseases. 2017;27(5):396-406. doi:10.1016/j.numecd.2017.03.001
25. Hellenthal KEM, Brabenec L, Wagner NM. Regulation and Dysregulation of Endothelial Permeability during Systemic Inflammation. Cells. 2022;11(12):1935. doi:10.3390/cells11121935
27. Korte S, Wiesinger A, Straeter AS, Peters W, Oberleithner H, Kusche-Vihrog K. Firewall function of the endothelial glycocalyx in the regulation of sodium homeostasis. Pflugers Arch - Eur J Physiol. 2012;463(2):269-278. doi:10.1007/s00424-011-1038-y
30. konomidis I, Voumvourakis A, Makavos G, et al. Association of impaired endothelial glycocalyx with arterial stiffness, coronary microcirculatory dysfunction, and abnormal myocardial deformation in untreated hypertensives. J Clin Hypertens (Greenwich). 2018;20(4):672-679. doi:10.1111/jch.13236
29. Oparil S, Zaman MA, Calhoun DA. Pathogenesis of hypertension. Ann Intern Med. 2003;139(9):761-776. doi:10.7326/0003-4819139-9-200311040-00011
22 ANTI-AGING MEDICAL NEWS | FALL 2022
Jon Ward earned an MA in English literature from Cambridge University and an MSW from Sussex University. He is a strategic consultant to Calroy Health Sciences and CEO of Braincat, an education and software company.
26. Klahr S. The role of nitric oxide in hypertension and renal disease progression. Nephrology Dialysis Transplantation. 2001;16(suppl_1):60-62. doi:10.1093/ndt/16.suppl_1.60
Caroline Dombrowski is an AMWA-certified medical writer and holds a Master of Library and Information Science from the University of Washington. She is a content strategist with Calroy Health Sciences.
Author Bios
28. Mahmoud M, Mayer M, Cancel LM, Bartosch AM, Mathews R, Tarbell JM. The glycocalyx core protein Glypican 1 protects vessel wall endothelial cells from stiffness-mediated dysfunction and disease. Cardiovasc Res. 2021;117(6):1592-1605. doi:10.1093/cvr/ cvaa201
Blood Pressure and the Arterial Wall: A Root-Cause Approach to Healthy Life Extension
Joel Kahn, MD, FACC is an integrative cardiologist. He serves as Clinical Professor of Cardiology at Wayne State University School of Medicine and is founder of the Kahn Center for Cardiac Longevity in Michigan.
Dr. Chen Chen, PhD in Nutritional Science, has researched cardiometabolic diseases and led a natural product and botanical drug program at a pharmaceutical company. He currently directs the glycotherapeutics research program at Calroy Health Sciences.
is for
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glycocalyx.*Thesestatementshavenotbeenevaluated by
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Who It’s For
This product is not intended to diagnose, treat, cure or prevent any disease. Healthy CompromisedArteryArtery Endothelial Glycocalyx
The special polysaccharides in Arterosil® help rebuild the endothelial glycocalyx—the slippery inner lining of every artery, vein, and capillary in the body. This supports endothelial health, protects and stabilizes plaque, may regress plaque, and enhances NO production.
BURKE, MD
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Arterosil® delivers powerful support to patients with: • Arterial or Carotid Plaque • Coronary Artery Disease • Cardiovascular Disease • Erectile Dysfunction • Diabetic Neuropathy • Hyperglycemia • Raynaud’s • Angina • Diabetes • Hypertension • Hypercholesterolemia • Peripheral Artery Disease
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Arterosil® is a proprietary dietary supplement formulated with a rare seaweed that contains specialized polysaccharides clinically proven to support arterial and endothelial health. material licensed healthcare providers only.
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SaharBy: PHARM.D.,SwidanABAAHP, FAARFM, FACA The following article is not endorsed and/or supported by The American Academy of Anti-Aging Medicine. The purposes of this publication do not imply endorsement and/or support of any author, company or theme related to this article. Use PainLow-DoseInforNaltrexoneLow-DoseofPainandammationNaltrexoneforandInflammation 26 ANTI-AGING MEDICAL NEWS | FALL 2022
Experiments with LDN have been done in a narrow spectrum of chronic pain syndromes. One such condition is fibromyalgia (FM). Musculoskeletal discomfort and sensitivity to mechanical stimulation are characteristics of FM, which also causes extreme weariness, cognitive impairment, and sleep issues. Although FM does not appear to be an inflammatory condition in the conventional sense, it does not seem to react to widely used antiinflammatory medicines.1 There is a possibility that inflammatory processes are still active.2
Is LDN an effective treatment for FM?
Participants with fibromyalgia who received daily LDN therapy reported an improvement in their symptoms.5
In two small clinical investigations, LDN was demonstrated to be an effective treatment for FM. In all investigations, LDN was administered orally once daily at a dosage of 4.5 mg before bedtime. Published in 2009 was the first crossover experiment3, LDN reduced fibromyalgia pain significantly in six of the 10 women compared to placebo. There were several limitations to the pilot study, including a single-blind design. Another 30 women with fibromyalgia were surveyed in a follow-up study to ensure that the findings were accurate. A significant reduction in pain was seen in 57% of those taking LDN in the double-blind, crossover, counterbalanced experiment described above. At the end of the
Involvement with inflammatory markers in general
27ANTI-AGING MEDICAL NEWS | FALL 2022
treatment, half of the respondents reported feeling “far better” or “very much improved.” There is strong evidence from these two studies that LDN is superior than placebo in the treatment of fibromyalgia’s pain symptoms.
In this review, we will look at how low-dose naltrexone (LDN) may be used as a new antiinflammatory drug for chronic pain problems that are known to be caused by inflammatory processes. Opioid antagonists, such as naltrexone, may have a “paradoxical” analgesic effect within a narrow dosage window.
In the early phases of clinical research on LDN, there are no human studies that replicate the results seen in animal models. Indirect data, however, suggests that LDN may be a novel anti-inflammatory. Fibromyalgia patients were given LDN in a pilot study.3 One of the most reliable predictors of LDN’s clinical response is the baseline erythrocyte sedimentation rate (ESR). ESR is frequently used as a clinical test which may identify both long-term and shortterm inflammation.6 A greater reduction in pain was seen in patients with higher baseline ESRs even though FM is not traditionally classified as an inflammatory disorder, and ESR levels were in the normal to high-normal range.
Published research show that 4.5 mg of LDN is the most often used dosage. Most individuals take this medication an hour or so before going to bed, however some people with insomnia are prescribed it in the morning. Those experiencing adverse effects should cut their dose to 3mg. Because a commercial formulation of LDN does not exist, you can only obtain LDN currently from compounding pharmacies across the country. The most common fillers are standard gelatin capsules and microcrystalline cellulose.
It’s important to remember that there are no clinical guidelines for the usage of LDN right now. For the treatment of chronic pain or inflammatory diseases, naltrexone has not been authorized by the FDA for use at any dosage. In addition, the FDA has not approved LDN for use in treating any medical condition. In order to perform LDN research, an FDA IND application must be submitted. A multitude of ways have been suggested by doctors to administer LDN, but none have been empirically proven. Rather than offering therapeutic advice, we’ll have a look at how LDN has been used in previous studies. This section is not meant to be taken as such.
Adverse drug reactions
On one hand, the low reported incidence of negative side effects is an intriguing
28 ANTI-AGING MEDICAL NEWS | FALL 2022
Use of Low-Dose Naltrexone for Pain and In ammation - Low-Dose Naltrexone for Pain and In ammation
Why it has different MOA in inflammation and pain?
Additionally, Naltrexone has shown some promise in lowering multiple sclerosis’s severity,8 It’s not as clear that LDN is successful as it was in the previous cases. Even while some clinical endpoints and one study fail to show a difference from the placebo, there is some evidence of reduced stiffness and improved mental wellbeing,9 improvements in any of the clinical outcomes were not found.
Although LDN’s distinct anti-inflammatory pathways are supported by a large body of data, there are other compelling explanations for the LDN mechanism. According to Dr. Ian Zagon and colleagues, the body will compensate by upregulating both endogenous opioids and opioid receptors if an opioid blockade is moderate and temporary. In the past, naltrexone or naloxone blocking has been shown to have an
The nature of the chronic illnesses that react to LDN therapy is a third piece of evidence suggesting LDN may have anti-inflammatory capabilities in humans. LDN has been found in studies to be effective in the treatment of Crohn’s disease.7 CD is a systemic inflammatory bowel disease that affects the whole body. Evidence shows that LDN may assist with self-reported pain as well as objective markers of inflammation and disease severity in this illness (including the severity scores from endoscopic evaluation). If you have Crohn’s disease, LDN may be more beneficial than fibromyalgia in helping you get well.
opioid upregulation effect. It is possible that the “opioid rebound” effect might have a variety of deleterious impacts on health and quality of life, including increased endogenous analgesia and the suppression of critical immunological components.4
Use of LDN in research
Efficacy in the treatment of wellcharacterized inflammatory diseases
The adverse effects of LDN treatment are minimal. LDN was shown to be somewhat more acceptable than placebo by participants in our research (91.0 versus 89.5 percent, not significant). In around 37 percent of instances, participants report experiencing more vivid dreams as a side effect. There are just a few occasions in which patients report having nightmares. Dreams become vivid as soon as the initial dosage is taken, and then fade away over time.
There have been no reports of LDN interfering with the effects of any other medications. However, since the research populations were so tiny, many possible interactions were unnoticed. Despite the absence of pharmacological interactions, synergistic effects with anti-inflammatory and diseasemodifying antirheumatic medications should be investigated. The use of LDN in combination with an opioid analgesic is an evident exception.
LDN has been shown to be a potential treatment option for chronic pain issues that are thought to be caused by inflammatory processes, according to a large body of research. Before it may be widely supported, additional research is needed to confirm its efficacy in clinical trials. Important aspects like dose need to be fine-tuned. For now, LDN may be the first in a series of glial cell modulators that might be utilized to address a variety of long-term health conditions.
29ANTI-AGING MEDICAL NEWS | FALL 2022
Endogenous opioid blocking may produce anxiety in certain individuals since it is a known sign of opioid withdrawal. More research will be needed to discover how prevalent this adverse occurrence is and how to effectively handle it.
feature of LDN. LDN is well tolerated as has bene reported in numerous studies..13
However, more research is needed before conclusive evidence can be drawn about the statistical significance of the difference between LDN and placebo in the occurrence of headaches. Patients with fibromyalgia are more likely to have unpredictable headaches, which have been documented in research studies at every stage.
Drug interactions
Summary
The most often asked question about LDN is whether it may be used with opiate medicines. Even a low dosage of naltrexone might cause enough opioid receptor blockage to reduce the effectiveness of opioid analgesics. All patients who used opioid analgesics were excluded from our research. While there is human data supporting the use of ultralow-dose naltrexone in conjunction with opioid analgesics. 14,15
30 ANTI-AGING MEDICAL NEWS | FALL 2022
14. Burns LH, Wang HY. Ultra-low-dose naloxone or naltrexone to improve opioid analgesia: the history, the mystery and a novel approach. Clin Med Insights Ther. 2010;2:CMT. S4870.
13. Pini LA, Ferretti C, Trenti T, Ferrari A, Sternieri E. Effects of long-term treatment with naltrexone on hepatic enzyme activity. Drug Metabol Drug Interact. 1991;9(2):161-174.
2. Wallace DJ. Is there a role for cytokine based therapies in fibromyalgia. Curr Pharm Des. 2006;12(1):17-22.
10. Weerts EM, Kim YK, Wand GS, et al. Differences in δ-and μ-opioid receptor blockade measured by positron emission tomography in naltrexone-treated recently abstinent alcohol-dependent subjects. Neuropsychopharmacology. 2008;33(3):653-665.
12. Tempel A, Gardner EL, Zukin RS. Neurochemical and functional correlates of naltrexone-induced opiate receptor up-regulation. J Pharmacol Exp Ther. 1985;232(2):439-444.
References
6. Sharma R, Rauchhaus M, Ponikowski PP, et al. The relationship of the erythrocyte sedimentation rate to inflammatory cytokines and survival in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors. J Am Coll Cardiol. 2000;36(2):523-528.
4. Younger J, Noor N, McCue R, Mackey S. Low-dose naltrexone for the treatment of fibromyalgia: findings of a small, randomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels. Arthritis Rheum. 2013;65(2):529-538.
Use of Low-Dose Naltrexone for Pain and In ammation - Low-Dose Naltrexone for Pain and In ammation
1. Clauw L. Arnold et al. Sci Fibromyalgia Mayo Clin Proc 86. Published online 2011:907-911.
5. Younger J, Parkitny L, McLain D. The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic pain. Clin Rheumatol. doi:10.1007/s10067-014-2517-22014;33(4):451-459.
9. Sharafaddinzadeh N, Moghtaderi A, Kashipazha D, Majdinasab N, Shalbafan B. The effect of low-dose naltrexone on quality of life of patients with multiple sclerosis: a randomized placebo-controlled trial. Mult Scler J. 2010;16(8):964-969.
8. Cree BA, Kornyeyeva E, Goodin DS. Pilot trial of low-dose naltrexone and quality of life in multiple sclerosis. Ann Neurol. 2010;68(2):145-150.
15. Davis M, Goforth HW, Gamier P. Oxycodone combined with opioid receptor antagonists: efficacy and safety. Expert Opin Drug Saf. 2013;12(3):389-402.
11. Glazner GW, Morrison AE, Ishii DN. Elevated insulin-like growth factor (IGF) gene expression in sciatic nerves during IGF-supported nerve regeneration. Mol Brain Res. 1994;25(34):265-272.
3. Younger J, Mackey S. Fibromyalgia symptoms are reduced by low-dose naltrexone: a pilot study. Pain Med. 2009;10(4):663672.
7. Smith JP, Bingaman SI, Ruggiero F, et al. Therapy with the opioid antagonist naltrexone promotes mucosal healing in active Crohn’s disease: a randomized placebo-controlled trial. Dig Dis Sci. 2011;56(7):2088-2097.
phytonutrient-treated human immune cells 20
tailinDNA% DNA stability Post-hoc pair-wise comparison (p<0.0001)
PhytoMulti is a patented formula of high-quality essential vitamins and minerals enhanced with a proprietary blend of 13 concentrated extracts and phytonutrients to protect cells and maintain DNA stability. It’s formulated with phytonutrients and essential nutrients that support cellular health and certain cell signaling processes.1* Phytonutrients provide antioxidant protection against potentially damaging free radicals that increase with age, poor lifestyle choices, and pollutants.1,2 Antioxidants can help protect cells from oxidative stress, which can be particularly damaging to the immune system. 3*
1. Lerman RH et al. Glob Adv Health Med. 2014;3(2):34-39.
References:
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PhytoMulti supports healthy aging1* PhytoMulti is designed to promote healthy functioning in multiple systems for healthy aging support.1* A sophisticated Comet assay demonstrated the potential of PhytoMulti’s proprietary phytonutrient blend to promote DNA stability in human immune cells.1 As shown in Figure 1, in this study, cells pretreated with the PhytoMulti phytonutrient blend maintained 52% greater DNA stability when compared to untreated cells.1*
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3. Knight JA. Ann Clin Lab Sci. 2000;30(2):145-158.
2. Kaplan P et al. Int J Mol Sci. 2020;21(20):7698.
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1. Rudrappa GH et al. Medicine (Baltimore). 2020;99(28):e20373.
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