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Gaylord Palms Orlando, FL

Belmond Charleston Place Charleston, SC

Spring Congress May 14-16 ABAARM & ABAAHP Written Exams May 13

FEBRUARY/MARCH Terranea Resort Rancho Palos Verdes, CA BHRT Symposium February 27-29

ABAARM Oral Exams May 14-16 Module I - Endocrinology May 14-16 Module V: Clinical Intensives May 14-16

Module IV: Gastroenterology October 15-17 Module VII: Autoimmune October 15-17 IV Therapy Symposium October 16-17 Pellet Therapy October 16-17

Module XVI C: Advanced Cardio May 14-16

Module II - Cardiology February 27-29 Module VI - Mitochondrial Restoration February 27-29 Peptide I February 27-28


Peptide II February 29-March 1


Venetian/Palazzo Las Vegas, NV

Boston Park Plaza Boston, MA

World Congress December 11-13

BHRT Symposium September 9-12 ABAARM & ABAAHP Exams September 9-12 Module III: Neurology September 10-12 Module VIII: Weight Management September 10-12


Peptides III September 10-11 Peptides III and IV September 12-13

ABAARM & ABAAHP Written Exams December 10 ABAARM Oral Exams December 11-13 Module I - Endocrinology December 11-13 Module V: Clinical Intensives December 11-13 Module XVI D: Advanced Cardio December 11-13

A4M | MMI Planning Committee

Pamela W. Smith

Andrew Heyman



Mark C. Houston MD, MS, MSc, FAARM, ABAARM

James LaValle RPh. CCN, MT, ND(trad)

Mark Rosenberg MD, FAARM, ABAARM

A4M Founders Ronald Klatz MD, DO Co-Founder

Robert Goldman MD, PhD, DO, FAASP






FALL 2019

Methylation Status as an Indicator of Cellular Aging


By: Michael J. Chapman, ND


Fasting: Role in Wellness, Metabolic Health and Inflammation


By: Kurt Hong, M.D. Ph.D. F.A.C.N.

Ways to Weed, Seed, and Feed the Endocannabinoid System Targeted strategies to support your body’s own homeostatic modulator By Kari Hamrick, PhD, RD, and Elnaz Karimian Azari, PhD


Leadership vs. Management in Your Anti-Aging Practice By: Tim Sawyer President & Co-Founder, Crystal Clear


Oral Liposomal Vitamin C as an Adjunct to Intravenous Ascorbic Acid

By: Lucie Kotlarova, PharmD





Rooted in comprehensive and holistic health, the Fellowship in Anti-Aging, Metabolic and Functional Medicine (FAAMFM) develops forward-thinking practitioners to effectively practice a new form of medicine that is both personalized and preventive. Our fellows are equipped to lead at the forefront of the chronic health crisis with a firm focus on root causes and an extensive array of personalized approaches and strategies. Adaptively designed with you in mind, this fellowship allows practitioners to continue treating patients while gaining the most clinically current education needed to prevent, diagnose, and treat chronic diseases.

The World’s Only Fasting Mimicking Diet®

Clinically Studied to Support WEIGHT MANAGEMENT & HEALTHY AGING


Role in Wellness, Metabolic Health and Inflammation By: Kurt Hong, M.D. Ph.D. F.A.C.N. Professor of Clinical Medicine. Executive Director, Center for Clinical Nutrition. Keck School of Medicine, USC. Davis School of Gerontology, USC. Member, L-Nutra Scientific Board. The article has been sponsored by L-Nutra 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.

Introduction Fasting is an ancient practice that has its roots in religious and healing practices, tracing back to ancient Greece and days of Hippocrates and Plutarch, who famously said “Instead of using medicine, rather, fast a day.” During 14th century Renaissance, fasting was frequently employed to bring about physical and spiritual renewal, as well as a form of cleanse before warriors were sent to wars. In different religions, the practice of fasting is associated with penitence, including with Muslims during Ramadan and with Roman Catholics during Lent1. Fasting is also practiced by Buddhists during times of intensive meditation as a method of practicing self-control. The definition of fasting is “to abstain from food.” In the 18th century, fasting was used by European physicians to prevent and treat various illness, ranging from bowel ailments to respiratory diseases to joint symptoms. More recently, there is ample evidence based on recent clinical studies that fasting or intermittent caloric restriction - when carefully employed by healthcare providers - can improve patients’ wellness and health outcomes. The obesity epidemic is now recognized as a global chronic disease with significant metabolic consequences, including coronary heart disease, hyperlipidemia, hypertension, and diabetes2. While weight loss leads to beneficial changes in these metabolic conditions, the degree of improvement seen in the reduction of blood glucose level, fasting lipids, and inflammation profiles occurs independent of the weight loss3,4. In recent years, various caloric restriction regimens have also been shown to reduce fasting insulin levels and improve hepatic


insulin sensitivity, leading to a reduction in visceral adiposity and fatty liver disease3,4. One of the main benefits of fasting rests in our body’s natural ability to downregulate important nutrient-sensing pathways, which in turn stimulate a protective response that results in stress resistance5,. Perhaps the most well-categorized nutrient sensing pathways are the target of rapamycin (mTOR), insulinlike growth factor 1 (IGF-1), and protein kinase A (PKA). It has been established that the key regulators of these nutrient sensing pathways include glucose, amino acids, and the energy status within the cell5-7. There are several distinct methods of fasting, including time-restricted eating, modified fasting (including alternate-day fasting and 5:2 regimens), and fasting mimicking diets (See Table 1)3,7,8. These categories are separated by differences in duration of fasting, as well as the different physiological impact induced by distinct dietary restriction. It has been hypothesized that there is an optimal amount of time during which the body needs to be in the fasting mode in order to induce prolonged and physiologically pronounced changes. This brief review of the various regimens of fasting aims to define the rationale to support each type of fast as it pertains to optimal metabolic health. Time Restricted Eating Time restricted eating (TRE) gains its roots from original studies on circadian rhythms9-10. Disruptions in these daily cycles of ~24 h that control a multitude of physiological and behavioral processes lead to physiologic effects on energy metabolism11, gastrointestinal motility and microbiota12, and


FASTING: Role in Wellness, Metabolic Health and Inflammation

Table 1: Types of Fasting Types of Fasting



Time-Restricted Eating (TRE)

A daily pattern of eating usually conducted between 4-8 hours. The rest of the day would be non-eating hours or fasting.

16:8 Diet or 20:4 (Warrior) Diet

Modified Fasting

A pattern of eating little to no calorie intake conducted 2 to 3 times per week.

Alternate Day Fasting or 5:2 Diet (2 days per week of severe caloric restriction of 500-600 kcal/d)

Fasting Mimicking Diet (FMD)

Dietary plan utilizing specific food ingredients x 5 consecutive days each month, which seeks to replicate the benefits of fasting while still providing calories and nutrients

sleep-wake cycles. TRE has been defined as a daily eating pattern that involves consumption of all daily nutrients within a < 4-8-hour time frame; there is no distinction as to the composition of the nutrition; rather, the focus is restriction of timing as to when food is consumed. The mechanism by which the circadian rhythm is regulated is complex and can be impacted by nutrient consumption. The transcription activators, which are involved in circadian regulation are closely influenced by the nutrient sensing pathways, including mTOR and AKT, as well as other pathways that are downregulated during fasting. As such, perturbations in timing of food/nutrient intake result in metabolic changes through disruptions of the circadian control and downstream transcription activation. There is new evidence to support that TRE may help to reinforce circadian rhythmicity leading to weight loss efficacy and improvement in insulin sensitivity. While clinical data are still sparse in this emerging field, in a recent 16-week feasibility trial, eight overweight individuals were instructed to consume their entire daily caloric intake over the span of a self-selected 8 h period to determine if this would lead to a reduction in body weight. The study found all subjects not only were able to reduce their eating duration, but this was associated with lost weight (average of 3.27 kg)13. Although the reduction in eating time also induced a decrease in estimated caloric intake - which may have contributed to the weight loss observed - there is new evidence to show that the benefits of TRE may be independent of weight loss. Additional metabolic benefits seen include reduction in total cholesterol, TGs, glucose, insulin, inflammatory biomarkers interleukin 6 and CRP, as well as improvements in insulin sensitivity13,14. The long-term metabolic benefits associated with eating or not eating breakfast are of great research and public interest since previous studies showed greater weight loss and better metabolic profile in those with

3 consecutive cycles of Fasting Mimicking Diet.

regular breakfast intake. In one recent study, participants skipping breakfast were hungrier at lunchtime and had higher plasma levels of ghrelin (important in triggering hunger)15. Fully understanding the potential importance of aligning food intake with daytime hours for metabolic health in humans requires additional large-scale studies. Modified Fasting (MF) Regimens Modified fasting (MF) regimens go by many definitions in the literature, but will be defined as very little (~25% energy restriction) to no calorie intake conducted 2-3 times per week; the majority of studies discussed here will represent the 2-day non-contiguous food restriction each week (5:2 diet) or alternate days of 24-hour water only fast (ADF). Animal studies with MF regimens have shown upregulation of autophagy, stress resistance, and antioxidant activity, as well as extension of lifespan while decreasing cellular proliferation16,17. However, in clinical studies, the results have been conflicting. In a 1-year trial, 112 subjects who had a BMI between 30-45 kg/m2 followed the 5:2 diet meal plan18. After 1 year, the treatment group with intermittent caloric restriction had similar weight loss as compared to those on continuous energy restriction (8.0 kg in the MF group versus 9.0 kg, p = 0.6) and improvements in their metabolic profile were also similar. Both groups reduced energy intake by average of 27%. In a separate study, 107 premenopausal women with a BMI between 24-40 kg/m2 followed a 5:2 regimen or continuous calorie restriction over 6 months19. In this study, the women in the MF group had comparable weight loss with the group on continuous calorie restriction (6.4 kg compared to 5.6 kg, respectively; P= 0.4). Comparable body fat reduction and cardiovascular risk marker reduction were also observed between the groups; however, in this one trial, there was



FASTING: Role in Wellness, Metabolic Health and Inflammation

slightly greater reduction in fasting serum insulin levels in the MF group19. Given the totality of current evidence, the overall metabolic benefits of MF regimens are not superior to those of continuous energy restriction. As such, additional large-scale prospective studies would be needed to determine true long-term metabolic benefits. Fasting Mimicking Diet (FMD) Prolonged fasting (PF) can be described as an extension in duration of the fast, in that it is longer than 2-3 days; PF typically is defined by water only fasting of 4 or more consecutive days. In animal and clinical studies, PF effects a metabolic switch triggering ketosis as well as induction of autophagy and reversal of immunosenescence20,21. With an extended period of fasting (>72hrs), studies have demonstrated a greater upregulation of aging resistance transcription factors such as FOXO as well as antioxidant enzymes SOD2, Gpx1, and GSR22,23. Moreover, there is evidence that with an extended >72h fast, there is an augmented down-regulation of key regulators of the nutrient sensing pathways, which accelerate aging, such as IGF-1 and mTOR24. While metabolic benefits of prolonged fasting (PF) are well defined, barriers of this regimen include poor compliance, increased risk of dehydration and electrolyte imbalance, particularly in the elderly. Due to these difficulties the Fasting Mimicking Diet (FMD) was developed, a novel modality that mimics fasting with a diet while still allowing consumption of limited calories and selected nutrients25. The diet is a five-day regimen of low protein, moderately low carbohydrate, and moderately high fat that is moderately restricted in calories (800-1100 calories). In recent animal studies, the Fasting Mimicking Diet was found to decrease IGF-1, reduce visceral fat mass, extend median lifespan, promote neurogenesis, enable hepatic regeneration, and increase hematopoietic and mesenchymal stem and progenitor cells25. In a published clinical study, just following three consecutive cycles of FMD, participants lost an average of 3% of body weight while maintaining lean muscle mass. Improvements in metabolic parameters such as C-reactive protein, triglycerides, fasting blood sugar, and blood pressure, were observed26. Currently, multiple clinical studies are ongoing to evaluate the effects of the FMD in patients with metabolic syndrome, inflammatory bowel disease, and breast cancer (FMD was previously found to differentially sensitize tumors to chemotherapy in murine models27). Beyond Metabolic Benefits Autoimmune and allergic diseases such as lupus, asthma, multiple sclerosis, Hashimotoâ&#x20AC;&#x2122;s thyroiditis, and rheumatoid arthritis are characterized by dysfunctional T cell


regulation, which in part is propagated by age associated inflammation. In the example of multiple sclerosis, which is characterized by T cell mediated demyelination and neurodegeneration of the central nervous system, Fasting, with an FMD regimen, lead to improvement in patient symptoms and positive changes in self-reported HealthRelated Quality of Life (HRQoL) in a clinical trial28. In the animal model, fasting results in improvements in neuronal regeneration along with remyelination at the demyelinated lesions through simulation of myelin production and suppression of inflammation28. Similarly, in murine models of rheumatoid arthritis and inflammatory bowel disease, caloric restriction through prolonged fasting resulted in reversal of autoimmunity generated by aberrant pathways of similar T cell activation 29,30. In a study with 53 RA patients, randomly assigned to either a control diet or prolonged fasting, patients in the fasting group reported significant improvement in clinical parameters as well as laboratory parameters such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) that are correlated with RA disease severity31. Similarly, a recently published study in patients with inflammatory bowel disease with active flares associated with elevated CRP, intervention with a fasting simulating regimen lead to improvement in multiple inflammatory markers29. The beneficial immunomodulatory effect seen with disease improvement after fasting is also, in part, related to changes in gut microflora which reduce T cell numbers and intestinal infiltration while promoting gut regeneration32. Whatâ&#x20AC;&#x2122;s Next? In murine models as well as other preclinical and preliminary clinical studies involving human subjects, caloric restriction through various fasting regimens has shown early promise in providing health benefits such as weight loss (particularly of visceral adipose tissue), reduction in markers of systemic inflammation, improvement in metabolic parameters (including blood pressure and fasting glucose), as well as reversal of hepatic steatosis18,20,25,26. However, important clinical questions remain: Is employment of a routine, fasting regimen sustainable for most patients long term? Which patient will most benefit from a specific fasting regimen in promoting his/her metabolic health? In animal studies, it has been shown that various forms of fasting reduce progression of cancers (including colorectal, liver, breast, and kidney), likely through an impact on inflammatory as well as epigenetic modulation through nutrient sensing pathways33,45. While additional studies are needed, it is exciting to note that the one major metabolic change associated with caloric restriction is a dramatic improvement in insulin sensitivity and reversal of age-related oxidative stress â&#x20AC;&#x201C; both of which are important


FASTING: Role in Wellness, Metabolic Health and Inflammation

drivers of progression of diabetes and cardiovascular diseases. While this represents a tremendous opportunity to improve cardiometabolic health, it is important to appreciate that not all caloric restriction regimens confer similar or equal benefits. As such, future studies evaluating efficacy of fasting interventions for specific diseases or health conditions should carefully be defined based on the type of fasting regimen employed. Given the wealth of new published studies, fasting regimens may present a safe, promising, nonpharmacological approach for weight loss as well as to facilitate metabolic improvements for healthy individuals and certain patient populations.

Modified Alternate Day Fasting: A Novel Dietary Strategy for Weight Loss and Cardioprotection in Obese Adults. Am. J Clin Nutr. 2009; 90(5):1138-43

17. Patterson RE, Laughlin GA, Sears DD, LaCroix AZ, Marinac C, Gallo LC, Hartman SJ, Natarajan L, Villasenor A. Intermittent Fasting and Human Metabolic Health. J Acad Nutr Diet. 2015; 115(8) 1203-1212 18. Sundfør TM, Svendsen M, Tonstad S. Effect of intermittent versus continuous energy restriction on weight loss, maintenance and cardiometabolic risk: A randomized 1-year trial. Nutr Metab Cardiovasc Dis. 2018 Jul;28(7):698-706.

19. Harvie MN, Pegington M, Mattson MP, et al. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomised trial in young overweight women. International journal of obesity (2005). 2011;35(5):714-727.

20. Balasse EO, Fery F. Ketone Body Production and Disposal: Effects of Fasting, Diabetes, and Exercise. Diabetes Metab Rev. 1989; 5(3) 247-70 21. Anton SD, Moehl M, Donahoo WT, Marosi K, Lee S, Mainous AG, Mattson MP. Flipping the Metabolic Switch: Understanding and Applying Health Benefits of Fasting. Obesity. 2018; 26(2) 254-268

Reference: 1. Trepanowski J, Bloomer RJ. The impact of Religious Fasting on Human Health. Nutrition J. 2010; Nutr J. 2010; 9:57 2. Singla P, Bardolio A, Parkash AA. Metabolic Effects of Obesity: A review. World J Diabetes. 2010; 1(3): 76-88

3. Longo VD, Mattson MP. Fasting: Molecular Mechanisms and Clinical Applications. Cell metabolism. 2014;19(2):181-192. 4. Gustafson C. Alan Goldhamer, dc: Water Fasting—The Clinical Effectiveness of Rebooting Your Body. Integrative Medicine: A Clinician’s Journal. 2014;13(3):52-57.

5. Efeyan A, Comb WC, Sabatini DM. Nutrient Sensing Mechanisms and Pathways. Nature. 2015; 517 (7534): 302-310.

6. Bettedi L, Foukas LC. Growth Factor, Energy, and Nutrient Sensing Signaling Pathways in Metabolic Aging. Biogerontology. 2017; 18(6): 913-929. 7. Cheng C-W, Adams GB, Perin L, et al. Prolonged Fasting reduces IGF-1/PKA to Promote Hematopoietic Stem Cell-Based Regeneration and Reverse Immuno- Suppression. Cell Stem Cell. 2014;14(6):810-823.

8. Mattson MP, Longo VD, Harvie M. Impact of Intermittent Fasting on health and Disease Processes. Ageing Res Rev. 2017; 39: 46-58 9. Zheng X, Sehgal A. AKT and TOR Signaling Set the Pace of the Circadian Pacemaker. Current biology : CB. 2010;20(13):1203-1208. 10. Lamia KA, Sachdeva UM, DiTacchio L, et al. AMPK Regulates the Circadian Clock by Cryptochrome Phosphorylation and Degradation. Science (New York, NY). 2009;326(5951):437-440.

11. Froy O. Metabolism and Circadian Rhythms, Implications for Obesity. Endocrine Review. 2010; 31(1): 1-24. 12. Deaver. JA, Eum SY, Tobroek M. Circadian Disruption Changes Gut Microbiome Taxa and Functional Gene Composition. Front Microbiol. 2018; 9:737

13. Sutton EF, Beyl R, Early KS, et al. Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes. Cell Metab. 2018 Jun 5;27(6):1212-1221. 14. Gabel K, Hoddy KK, Haggerty N, et al. Effects of 8-hour time restricted feeding on body weight and metabolic disease risk factors in obese adults: A pilot study. Nutrition and Healthy Aging. 2018;4(4):345353.

15. Kral TV, Whiteford LM, Heo M, Faith MS. Effects of Eating Breakfast Compared with Skipping Breakfast on Ratings of Appetite and Intake at Subsequent Meals in 8-10 Year Old Children. Amer J Clini Nutr. 2011; 93(2) 284-291.

22. Lee C, Safdie FM, Raffaghello L, et al. Reduced IGF-I differentially protects normal and cancer cells and improves chemotherapeutic index in mice. Cancer research. 2010;70(4):1564-1572.

23. Verweij M, van Ginhoven TM, Mitchell JR, Sluiter W, van den Engel S, Roest HP, Torabi E, Ijzermans JN, Hoeijmakers JH, de Bruin RW. Preoperative fasting protects mice against hepatic ischemia/reperfusion injury: mechanisms and effects on liver regeneration. Liver Transpl. 2011 Jun;17(6):695-704. 24. Parrella E, Longo VD. Insulin/IGF-I and Related Signaling Pathways Regulate Aging in Nondividing Cells: from Yeast to the Mammalian Brain. The Scientific World Journal. 2010;10:161-177.

25. Brandhorst S, Choi IY, Wei M, et al. A periodic diet that mimics fasting promotes multi-system regeneration, enhanced cognitive performance and healthspan. Cell metabolism. 2015;22(1):86-99. doi:10.1016/j. cmet.2015.05.012. 26. Wei M, Brandhorst S, Shelehchi M, et al. Fasting-mimicking diet and markers/risk factors for aging, diabetes, cancer, and cardiovascular disease. Sci Transl Med. 2017 Feb 15;9(377). 27. DiBiase S, Lee C, Brandhorst S, Manes B, Buono R, Cheng CW, Cacciottolo M, Cabo R, Wei M, Morgan TE, Longo VD. Fasting Mimicking Diet Reduces HO-1 to Promote T Cell Mediated Tumor Cytotoxity. Cancer Cell. 2016; 30(1) 136-146. 28. Choi, IY, Piccio L, Childress P, Bollman B, Ghosh A, Brandhosrt S, Suarez J, Morgan TE, Wei M, Bock M, Longo VD. Diet Mimicking Fasting Promotes Regeneration and Reduces Autoimmunity and Multiple Sclerosis Symptoms. Cell Report. 2016; 15(10): 2136-46.

29. Rangan P, Choi IY, Wei M, Navarrete G, Guen E, Brandhosrt S, Pasia G, Maesincee D, Abdulridha M, Longo VD. Fasting-Mimicking Diet Modulates Microbiota and Promotes Intestinal Regeneration to Reduce Inflammatory Bowel Disease Pathology. Cell Report. 2019; 26(10) 2704-19 30. Khanna S, Jaswal KS, Gupta B. Managing Rheumatoid Arthritis with Dietary Intervention. Front Nutrition. 2017; 4:52.

31. Kjeldsen-Kragh J, Haugen M, Laerum E, Hovi K, Forre O. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet. 1991;338:899–902

32. Cignarella F, Cantoni C, Salter A, Dorsett Y, Weinstock GM, Fontana L, Piccio L. Intermittent Fasting Confers Protection in CNS Autoimmunity by Altering the Gut Microbiota. Cell Metab. 2018; 27(6) 1222-1235. 33. Lee C, Longo VD. Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients. Oncogene. 2011; 30:3305–3316.

34. Lee C, Raffaghello L, Longo VD. Starvation, detoxification, and multidrug resistance in cancer therapy. Drug Resist Updat Rev Comment Anti-microb Anticancer Chemother. 2012. 5:114–122.

16. Varady KA, Bhutani S, Church EC, Klempel MC. Short-Term




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Leadership vs. Management in Your Anti-Aging Practice By: Tim Sawyer President & Co-Founder, Crystal Clear 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.

Over the past several years, I have had the pleasure of participating with A4M in many meaningful lectures, forums, and panel discussions on all facets of practice management. As I have often stated, successful practice management education should always speak to the underlying question of, “How is this going to help me and my practice find, serve/treat, and keep more patients profitably?” The assumption going into these lectures is that attendees are not only interested in refining their treatment protocols, improving operational efficiencies, etc., but they are ALL also interested in increasing profits and effectively growing their practice. I think we can all agree on that. Where I depart somewhat is the traditional approach taken regarding how and what is discussed to achieve true profitability and growth.


First, I would like to challenge the mere fact that this type of education is universally referred to as practice management. The word “management” implies tactics, and these tactical discussions are focused on the usual topics such as the deployment of new technology and treatment protocols, the hot topics around marketing, social media, search engine optimization, email, website development, in-office technologies like EMR and online scheduling, incorporating cash-pay services, compliance, financial management, and the list goes on. If you have attended a practice management event anywhere in the world, you will recognize these topics as classic menu items. While these are important topics worthy of research and exploration, they largely ignore what I feel are essential elements needed when creating and implementing sustainable growth strategies. These tactical discussions focus on the how and not the WHY. I refer to this paradigm as Management vs. Leadership. As a serial entrepreneur, three times listed in the Inc. 500/5000 List of America’s FastestGrowing Private Companies, in two different startups, I have significant experience (good

and bad) on what I call tuition with the practice of both leadership and management. Hopefully, you can tell by this point that I value both, almost equally, but not quite. As it relates to your elective anti-aging practice, let’s take a minute to discuss the important role of leadership, which is simply defined in Webster’s dictionary as “the quality of character and personality giving a person the ability to gain the confidence of and lead others.” Volumes about leadership have been written by people a lot smarter than me, so I will keep the conversation closely and practically related to the impact on your practice. So, let’s start here. Some important questions to determine where you are with this include: 1.

Do you value leadership as an integral part of growing your practice?


How much time do you spend and have you spent contemplating your role as THE leader?


Do you consider yourself an effective leader?


When would be a good time to start asserting yourself as a true leader?

There are close to no leadership skills taught in medical school. Hence, it’s not a priority in the education and matriculation of the modern elective physician. This makes no sense because many of you are ultimately responsible for leading your teams in growing your private practice. Very few people are natural born leaders. Like any other skill, this requires education and lots of practice. Over the past 15 years, we have developed a simple guide to practical leadership in elective medicine that includes what we have seen as the common elements shared by effective leaders in high-growth practices.


Leadership vs. Management in Your Anti-Aging Practice

First, leaders have a strong sense of purpose. This is their big why. It’s their reason for getting up every day and doing what they do. This purpose often leads to passion. Passion, as we all know, is infectious for everyone around them including team members and the patients they treat. Leaders will often use words like “belief ” and statements that begin with, “The reason for doing this…” They have conviction, and that conviction breeds trust. Second, these leaders operate under a set of core principles they refuse to sacrifice, from patient care standards to employee conduct and beyond. They know that the further they move away from their core principles, the harder it becomes to sustain rapid growth. There are certain things they just will not do for short-term gain. Period. Third, leaders operate with a plan. The plan often originates from their vision for the practice. They see their vision clearly and consistently develop and modify their plan based on current circumstances. They never modify or veer from their VISION. Equally as important, they are consistent in the way they share this vision with everyone in the practice. They believe everyone must buy into the “drink the Kool-Aid” moment in culture and those who do not pose a threat to long-term success. Fourth, because effective leaders operate with principle, and because they believe they are doing what’s right for the organization, you will never hear a strong leader say, “I wish I could implement this in my practice, but you know how it goes, I have to pick my battles.” Strong leaders are not concerned with picking battles or negative pushback from employees. They believe in their vision and operate in such a fashion that team members prefer NOT to pick battles with them. Lastly, they stay consistent over the long run. They avoid the temptation to hop from one model to the next or chase the latest and greatest. Instead, they consistently ask themselves how new ideas, treatments, and investments fit into their longterm vision. They stay the course and do not get distracted with quick fixes or short-term gains, even in the face of adversity. In business, the important role of leadership is undeniable. It has been researched and refined for thousands of years. As a former business student at Bryant University, we were bombarded with leadership concepts from the first day we walked on campus. Even in this environment, not all students placed the same value on its importance. That said, in the times I have attended the Inc. 500 conferences, there was not a person or organization in that room who had not dedicated countless hours to developing their own leadership style.

I get it. That’s different; those are businesspeople. But let’s go back to the beginning of this article. The entire premise of practice management is creating strategies to help you find, serve/treat, and keep more patients profitably. Aren’t these ALL business functions? This leads to my central theme: Modern anti-aging practices offering elective treatments such as HRT, medical weight loss, diets, nutrition plans, precision medicine, HCG, etc. are 100% retail businesses by virtue of the fact that these are ELECTIVE in nature, meaning patients have choices. They can choose to be treated by you, by your competitors, or NOT at all. That puts us all in the retail category, which means that every law of retail that applies to Nordstrom, Nike, and Gucci applies to YOU. And one of those laws is the irrefutable need for strong leadership to create long-term sustainable growth for your practice. Ignoring it is simply not an option. As we get ready for the exciting practice management discussions at the upcoming A4M World Congress in Las Vegas, my encouragement is that we all take some time to think about WHY we are going. There will be plenty of opportunity to discuss the who, what, when, and where. And I will be right there leading and participating in these discussions. If we go with a strong sense of purpose, otherwise referred to as the why, the rest will be much more meaningful when it comes to the real-life implementation of these best practices when we return to reality. And as I always like to say, “That’s what I believe. But it doesn’t matter what I believe; it only matters what YOU believe.” Best of luck, safe travels, and I hope to see you in Las Vegas.

AUTHOR BIO Tim Sawyer President & Co-Founder, Crystal Clear 407-793-9254 Tim Sawyer is a luminary speaker and published author within the aesthetic and anti-aging industries. He currently is the President & Co-Founder of two-time Inc. 500/5000 company Crystal Clear – also named Best Practice Marketing Company by THE Aesthetic Guide and Top Aesthetic Service Provider by Aesthetic Everything®.





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Methylation Status as an Indicator of Cellular Aging By: Michael J. Chapman, ND 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.

In the last two decades, there have been a variety of ways that researchers and clinicians try to gain insight into the factors that lead to, or accelerate, the aging process. A few examples include telomere analysis, genotyping, oxidative stress evaluation, or even just a thorough cardiovascular assessment. However, recent advancements in technology have increased our capacity to evaluate cellular methylation status through both genotyping and novel biomarker analysis. The importance of methylation status is not new to the anti-aging and functional medicine communities. Proper methylation is crucial in an enormous number of biochemical processes, including creatine production for skeletal muscle contraction, DNA and RNA synthesis, gene regulation (epigenetics), hormone regulation and detoxification, energy production, cell membrane repair, fat metabolism, myelination, and immune function.1-5 Methylation also plays a critical role in vascular endothelial function and maintaining cardiovascular health.

DNA methylation occurs when methyl groups are attached to specific “non-coding” regions of certain genes. These regions are commonly referred to as CpG islands. Generally speaking, methylation of CpG islands lead a decrease in that particular


While it is certainly clinically useful to have a firm grasp on all the processes in the body that are affected by methylation perturbation, it is also important to widen the lens so we can put methylation in perspective regarding cellular health overall. Furthermore, evidence has suggested that methylation dysfunction is associated with the aging process overall, including higher incidence of most age-related pathologies.6 But, how is it that methylation status can be referred to as an indication of cellular health?

METHYLATION AND DNA HEALTH It is well-understood that genome instability is one of the most crucial determinants of cellular senescence, and it is also a large risk-factor for tumerogenesis.7 One factor that contributes to genomic instability is alterations in gene expression within the cell, which is also called epigenetic regulation. Epigenetic regulation is accomplished through DNA methylation.8

gene’s expression. The greater number of methyl groups that are attached to these islands, the more gene expression is suppressed. Conversely, removal of these methyl groups increase a gene’s expression.


Methylation Status as an Indicator of Cellular AgingT

The relationship between DNA methylation and carcinogenesis is nuanced. For example, hypomethylation of many genes has been implicated in several forms of cancer, whereas other types of cancers have been associated with CpG hypermethylation.9 This does make sense given some genes may code for proteins that are more or less associated with neoplasm (such as the various types of estrogen receptors). Regardless, attempts have been made to interpret specific patterns of DNA methylation to assess cancer-risk as well as predict overall age.6 While DNA assessment for age-associated methylation dysfunction remains relegated to the realm of research-useonly, there are metabolic markers that have been shown to correlate well with DNA methylation changes.10 Plasma levels of S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), and the ratio between the two (SAM/SAH) have been used as biomarkers for cellular methylation status.11-13 To note, the SAM/SAH ratio is resistant to fluctuations owing to multiple backup pathways and feedback mechanisms. It is more likely that SAH variability will lead to alterations in the methylation index.14 This is because methylation reactions become compromised with a decreased SAM:SAH ratio and as SAH levels become elevated.15 Therefore, assessing these novel biomarkers in context of the entire methylation pathway is ideal.

METHYLATION AND OXIDATIVE STRESS Another significant contributor to cellular aging is oxidative stress.16 A host of cellular reactions generate large amounts of reactive oxygen species (ROS) every second. The electrontransport chain, in particular, is a source of a tremendous amount of free radical production, which must be neutralized in order to prevent mitochondrial dysfunction.17 One of the main intracellular antioxidants to combat this insult is glutathione. Oxidative stress has been clinically correlated to innumerable chronic diseases and age-related pathologies.16 Cellular accumulation of ROS causes damage to multiple structures inside the cell, which can culminate in many downstream dysfunctions.16 Common sequelae include protein & lipid damage, altered enzyme activity, and DNA damage. One important mediator of oxidative stress is the enzyme catechol-o-methyltransferase (COMT). The COMT enzyme is responsible for phase 2 detoxification of many intrinsic chemical, such as catecholamines. It accomplishes this by methylating these substrates using SAM as a cofactor. Also,

proper COMT activity is crucial for adequate elimination of endogenous estrogens which, at high-levels, could be metabolized into DNA adducts (capable of DNA damage).18 Another way that methylation impacts oxidative stress is through its influence on glutathione production. As mentioned, glutathione is one of the bodyâ&#x20AC;&#x2122;s most potent antioxidants. Glutathione is produced in a step-wise fashion from homocysteine (a methylation byproduct and independent cardiovascular risk marker) through a process call transsulfuration. The the first step in transsulfuration is accomplished by the enzyme cystathionine beta-synthase (CBS). To note, CBS activity is dependent on adequate availability of the main methyl donor, SAM.19 Ultimately, when SAM is low, glutathione production will be slowed down. Therefore, poor methylation status can indirectly lead to lower glutathione levels which makes the cell more susceptible to oxidative damage. METHYLATION AND CELLULAR ENERGY Within each cell, there is a vast and dynamic interplay between many biochemical pathways to ensure cellular energy demands are met. Methylation imbalances can influence the ebb and flow of products used by the mitochondria. For example, SAM availability increases the transsulfuration pathway (discussed above). Interestingly, the transsulfuration pathway also contributes to the production of pyruvate used in cellular ATP synthesis. Therefore, adequate SAM can influence pyruvate production for cellular energy metabolism. Another important methylation product is creatine. Creatine is as crucial energy source for muscle contraction. Creatine production in the body is accomplished by subsequent methylation reactions using SAM as a cofactor. Therefore, an inadequate supply of SAM may impair the systemâ&#x20AC;&#x2122;s ability to adequate generate creatine for optimal muscle contraction which could potentially manifest as muscle weakness.



Methylation Status as an Indicator of Cellular Aging

SUMMARY The previous examples discussed just a few (among many) ways that the methylation cycle relates to optimal cellular health. The methylation cycle assists in maintaining DNA integrity and appropriate expression, mitigating oxidative stress, and cellular energy production. Given this insight, we can make the case that adequate methylation is a hallmark for optimal cellular aging. Therefore, it is critical to consider



Moore LD, Le T, Fan G. DNA methylation and its basic function. Neuropsychopharmacology. 2013;38(1):23.


Brosnan JT, Jacobs RL, Stead LM, Brosnan ME. Methylation demand: a key determinant of homocysteine metabolism. ACTA BIOCHIMICA POLONICAENGLISH EDITION-. 2004;51:405-414.


Smazal AL. Oral S-adenosyl methionine (SAM) mediates disruptions in methyl group metabolism due to retinoic acid therapy and alters neurotransmitter metabolism: Implications for major depressive disorder, Iowa State University; 2013.


Lawson BR, Eleftheriadis T, Tardif V, et al. Transmethylation in immunity and autoimmunity. Clinical Immunology. 2012;143(1):8-21.


Abu-Lebdeh HS, Barazzoni R, Meek SE, Bigelow ML, Persson X-MT, Nair KS. Effects of insulin deprivation and treatment on homocysteine metabolism in people with type 1 diabetes. The Journal of Clinical Endocrinology & Metabolism. 2006;91(9):3344-3348.


Jung M, Pfeifer GP. Aging and DNA methylation. BMC Biol. 2015;13:7-7.


Finkel T, Serrano M, Blasco MA. The common biology of cancer and ageing. Nature. 2007;448(7155):767-774.


Deroo LA, Bolick SC, Xu Z, et al. Global DNA methylation and one-carbon metabolism gene polymorphisms and the risk of breast cancer in the Sister Study. Carcinogenesis. 2014;35(2):333-338.


Issa JP, Ottaviano YL, Celano P, Hamilton SR, Davidson NE, Baylin SB. Methylation of the oestrogen receptor CpG island links ageing and neoplasia in human colon. Nature genetics. 1994;7(4):536-540.

10. Yi P, Melnyk S, Pogribna M, Pogribny IP, Hine RJ, James SJ. Increase in plasma homocysteine associated with parallel increases in plasma S-adenosylhomocysteine and lymphocyte DNA hypomethylation. The Journal of biological chemistry. 2000;275(38):29318-29323.

when addressing all age-related pathologies, as well as the symptoms that accompany the aging process as a whole.

BIBLIOGRAPHY Michael Chapman, N.D. works as Product Development Manager at Genova Diagnostics. Dr. Chapman has no prior publications.

11. Hao X, Huang Y, Qiu M, et al. Immunoassay of S-adenosylmethionine and S-adenosylhomocysteine: the methylation index as a biomarker for disease and health status. BMC research notes. 2016;9(1):498. 12. Mason JB. Biomarkers of nutrient exposure and status in one-carbon (methyl) metabolism. The Journal of nutrition. 2003;133 Suppl 3:941s-947s. 13. James SJ, Cutler P, Melnyk S, et al. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. The American journal of clinical nutrition. 2004;80(6):1611-1617. 14. Guerra-Shinohara EM, Morita OE, Pagliusi RA, Blaia-dâ&#x20AC;&#x2122;Avila VL, Allen RH, Stabler SP. Elevated serum S-adenosylhomocysteine in cobalamin-deficient megaloblastic anemia. Metabolism-Clinical and Experimental. 2007;56(3):339347. 15. Williams KT, Schalinske KL. New insights into the regulation of methyl group and homocysteine metabolism. The Journal of nutrition. 2007;137(2):311-314. 16. Finkel T, Holbrook NJ. Oxidants, oxidative stress and the biology of ageing. Nature. 2000;408(6809):239-247. 17. Kudryavtseva AV, Krasnov GS, Dmitriev AA, et al. Mitochondrial dysfunction and oxidative stress in aging and cancer. Oncotarget. 2016;7(29):44879-44905. 18. Zahid M, Kohli E, Saeed M, Rogan E, Cavalieri E. The greater reactivity of estradiol-3,4-quinone vs estradiol-2,3-quinone with DNA in the formation of depurinating adducts: implications for tumor-initiating activity. Chemical research in toxicology. 2006;19(1):164-172. 19. Pey AL, Majtan T, Sanchez-Ruiz JM, Kraus JP. Human cystathionine betasynthase (CBS) contains two classes of binding sites for S-adenosylmethionine (SAM): complex regulation of CBS activity and stability by SAM. The Biochemical journal. 2013;449(1):109-121.



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Genova’s Methylation Panel is an innovative genotypic and phenotypic assessment designed to offer insight into the biochemical methylation pathway. This profile directly measures levels of key amino acids and intermediate metabolites involved in methylation, homocysteine transsulfuration, and folate metabolism to help clinicians design more targeted and specific treatment strategies to optimize patient outcomes. Single nucleotide polymorphisms (SNPs) are also assessed to offer insight into genetic predispositions that affect enzymes within these pathways.

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Ways to Weed, Seed, and Feed the Endocannabinoid System Targeted strategies to support your body’s own homeostatic modulator By: Kari Hamrick, PhD, RD, and Elnaz Karimian Azari, PhD 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.

In school, we are taught that the human body is most commonly divided into 11 major organ systems that function together to carry out specifics tasks. However, a new system has emerged in research over the last 30 years called the endocannabinoid system (ECS), which is described as “one of the most important physiologic systems involved in establishing and maintaining human health.”1 This article aims to shed light on the size and scope of the ECS, its role in the body, and strategies support your body’s internal homeostasis.

ECS at a glance Endocannabinoids, our body’s own cannabinoids, and cannabinoid receptors are found throughout the body, including the brain, connective tissues, and immune cells.2 The ECS performs different tasks in each tissue, but the goal is always homeostasis. For example, when a stressful event occurs, the brain responds to coordinate and regulate a response. Preclinical evidence demonstrates that 1) the ECS helps modulate stress signals,3 and 2) the ECS helps regulate immune responses to prevent them from going haywire, thus relieving pain and inflammation.4

What is clinical endocannabinoid deficiency? Everyone has an underlying endocannabinoid tone. Endocannabinoid tone describes the overall functioning of the ECS- the function or density of cannabinoid receptors, endocannabinoid levels and their metabolic enzymes.5 Dysregulation of the endocannabinoid tone,


which is known as clinical endocannabinoid deficiency (CED), is implicated in various pathological conditions,6 and declining homeostasis as part of the aging process.7 One example of CED is the impact of posttraumatic stress on the ECS among survivors of the World Trade Center attacks. Endocannabinoid levels were lower in victims with PTSD, suggesting an inability of the body to reset a healthy ECS tone and resume homeostasis after a traumatic event for some individuals.8 CED has been linked with health conditions such as pain and psychiatric disturbances, with the greatest evidence present for migraine, fibromyalgia and irritable bowel syndrome.5,6

Strategies to correct clinical endocannabinoid deficiency Several strategies have been suggested to restore balance of CED and enhance the endocannabinoid functioning. Genetics, nutrition and lifestyle, and overall health status can impact endocannabinoid tone and functionality. Considering the wide range of systems that the ECS helps regulate, supporting it and ensuring optimal function is an important part of overall health. The following outlines the “weeding, seeding and feeding” of the ECS to provide targeted support to your body’s own homeostatic modulator.

WEEDING: Cleansing our lifestyle of ECS disruption


Ways to Weed, Seed, and Feed the Endocannabinoid System

Targeted strategies to support your body’s own homeostatic modulator


Stress is a stimulus that challenges our body’s homeostasis. Stress is inevitable in our lives and in some cases can be beneficial, such as for solving problems. However, both acute and chronic stress are common cause of disruption to our ECS tone, and animal models indicate that ECS impairment may be involved in stress-related mental health perturbations.3 Numerous effective stress-reduction methods exist, including: meditation, yoga, acupuncture, massage, exercise, and social support. For example, a human trial of osteopathic manipulative treatment showed increased endocannabinoid levels 168% over pretreatment.9 Even dancing and emotional support, such as talking to friends and family, can benefit stress levels and significantly enhance ECS function.10


Some evidence suggests that chronic/long-term use of alcohol (moderate to high quantities) can impair ECS by increasing levels of endocannabinoids, which leads to the reduction of cannabinoid receptors expression and function.11 The downregulation of cannabinoid receptors in the brain is linked with tolerance to alcohol, and therefore, it is recommended to use moderation when drinking.12

SEEDING: Promoting healthy lifestyle factors Dietary changes

There is increasing research indicating a dietary component in the modulation of the ECS. Endocannabinoids are products of dietary polyunsaturated fatty acids (PUFA), and cannabinoid receptor function can be modulated via modification of dietary fatty acid intake.13 A diet rich in n-3 fatty acids has shown the potential to properly modulate the endocannabinoid signaling in dysregulated tissues such as liver and adipose tissue.14 In contrast, a diet that is high in n-6 PUFA, such as Western diet, causes overstimulation of ECS that ultimately decreases insulin sensitivity in muscle and promotes fat accumulation in the adipose tissue.15 Excellent dietary sources with a healthy n-6:n-3 fatty acid ratio include cold water fatty fish like salmon and tuna, krill oil, chia seeds, ground flax seeds or flax oil, walnuts and hemp seeds. Supplementation with fish oil is also a practical way to address the widespread omega-3 gap.


Aerobic exercise training results in weight loss and improved mood; it is also linked to higher endocannabinoid levels in

healthy people.16 It is even thought that the so called “runner’s high,” a neurobiological phenomenon associated with exercise may be connected to the activation of the ECS.17 It is interesting to note that moderate intensity exercise (but not low or high intensity exercise) has significant impact on circulating endocannabinoids.17 Additionally, animal and human studies indicate that exercise that is forced or prescribed can be interpreted by the body as stress and result in a negative impact on ECS tone , whereas exercise that is self-selected is preferred and contributes to positive mood outcomes.18

FEEDING: Endocannabinoid system enhancers Although lifestyle modification is considered a first line therapy for most chronic disease management, for some individuals, targeted nutritional approaches can be utilized to support the ECS.

Probiotics and prebiotics

Many researchers believe that the ECS is the communication link between the gut and the brain that enables them to speak to each other.19 Researchers have demonstrated that probiotics, such as lactobacillus acidophilus, modulate the ECS in the colon.20 Probiotic-rich foods include fermented items like yogurt, kefir, kombucha and kimchi, and probiotic supplementation can provide one or more strains for targeted support. Additionally, preliminary studies demonstrate that prebiotics play a role in maintaining healthy intestinal ECS tone.21,22


Another potential approach is utilization of phytocannabinoids found in plants such as hemp. Cannabis sativa is an herb containing hundreds of bioactive compounds including phytocannabinoids and terpenes.23 The most well- known phytocannabinoids in cannabis are ∆9-tetrahydrocannabinol (∆9-THC) from the marijuana variety and cannabidiol (CBD) from the hemp variety. Both phytocannabinoids can confer health benefits; however, ∆9-THC induces psychoactive effects while CBD does not. The mechanisms of ∆9-THC extend beyond the scope of this article. Cannabis extracts have metabolically active phytocannabinoids with biologic and therapeutic relevance as ECS enhancers.24 A review of evidence on the health effects of Cannabis extracts and cannabinoids determined that CBD has substantial evidence of effectiveness for



Ways to Weed, Seed, and Feed the Endocannabinoid System

Targeted strategies to support your body’s own homeostatic modulator

some conditions such as chronic pain, chemotherapy-induced nausea and spasticity in multiple sclerosis.25 Ongoing phytocannabinoid therapeutic research is promising. While CBD has received the most attention, evidence suggests that whole-plant Cannabis extract that contains other phytocannabinoids, terpenes and flavonoids is superior to isolated compounds from the plant.26 Terpenes are organic hydrocarbons found in the essential oils of plants that may also act on cannabinoid receptors and neurotransmitters.27 Terpenes are found in citrus fruit rinds, mango, thyme, black pepper, and peppermint, to name just a few. In fact, over 100 terpenoid compounds are responsible for the unique aroma of Cannabis.28 Further, flavonoids, antioxidants found in many fruits and vegetables, may exert an additional synergistic effect by inhibiting the enzymes that breaks down endocannabinoids, thereby allowing them to continue to exert their therapeutic effect.29


compounds in tea that are thought to function as antioxidants, and accumulating research describes numerous potential benefits from reducing heart disease and cancer risk to facilitating weight loss.30,31 We now understand that catechins also mimic endocannabinoids so some of their health impact may be related to an effect on ECS tone. Catechins are found in high concentrations in green tea, but are also found in wine and dark chocolate.32


Since its discovery in the 1990’s, and ECS has captivated the scientific community, and we are continually describing its extensive involvement in health. The growing body of knowledge paved the way for legalization of the medical Cannabis, and is now helping us uncover lifestyle approaches to balance the ECS. A deficient ECS has significant health consequences, therefore the proposed “weed, seed, and feed” concept outlined in this article embraces the multifactorial nature of cultivating a healthy ECS.

The health advantages of tea have been known for thousands of years in the East. Catechins are bioactive phytonutrient

References 1.

Alger BE. Cerebrum : the Dana forum on brain science 2013;2013:14-.


Kruk-Slomka M, et al. Mol Neurobiol 2017;54:8332-47.


Qin Z, et al. Neuron 2015;85:1319-31.


Barrie N, et al. Eur J Rheumatol 2017;4:210-8.


Russo EB. Cannabis Cannabinoid Res 2016;1:154-65.


McPartland JM, et al. PLOS ONE 2014;9:e89566.


Albayram O, et al. Proceedings of the National Academy of Sciences 2011;108:11256-61.


Hill MN, et al. Psychoneuroendocrinology 2013;38:2952-61.


McPartland JM, et al. J Am Osteopath Assoc 2005;105:283-91.

25. National Academies of Sciences E, and Medicine. The health effects of cannabis and cannabinoids: Current state of evidence and recommendations for research. Washington, DC2017. 26. McPartland JM, et al. Journal of Cannabis Therapeutics 2001;1:103-32. 27. Russo EB, et al. Adv Pharmacol 2017;80:67-134. 28. Turner CE, et al. J Nat Prod 1980;43:169-234. 29. Chen AY, et al. Food Chem 2013;138:2099-107. 30. Peluso I, et al. Br J Pharmacol 2017;174:1195-208.

10. Stone NL, et al. Front Behav Neurosci 2018;12:269. 11. Pava MJ, et al. Alcohol 2012;46:185-204. 12. Basavarajappa BS, et al. Alcohol Alcohol 2005;40:15-24. 13. Naughton SS, et al. International journal of endocrinology 2013;2013:361895-. 14. Banni S, et al. Mol Nutr Food Res 2010;54:82-92.

31. Rains TM, et al. J Nutr Biochem 2011;22:1-7. 32. Gottumukkala RV, et al. Int Sch Res Notices 2014;2014:628196.

Kari Hamrick, PhD, RD is founder of Navigate Nutrition and Wellness, Gig Harbor, WA. She earned her PhD in Nutrition from Texas Woman’s University and is a medical communication fellow at Metagenics.

15. Kim J, et al. Nutrition 2011;27:624-32. 16. Dietrich A, et al. British Journal of Sports Medicine 2004;38:536-41. 17. Raichlen DA, et al. Eur J Appl Physiol 2013;113:869-75. 18. Brellenthin AG, et al. Med Sci Sports Exerc 2017;49:1688-96. 19. Sharkey KA, et al. Gastroenterology 2016;151:252-66. 20. Rousseaux C, et al. Nat Med 2007;13:35-7.; 253-853-7340

Elnaz Karimian Azari, PhD is Therapeutic Platform Lead for

Cardiometabolic and Obesity platforms at Metagenics. She earned her PhD in Nutritional Physiology from ETH Zurich in Switzerland.

21. Russo R, et al. Curr Med Chem 2018;25:3930-52.; 949-369-3306

22. Muccioli GG, et al. Mol Syst Biol 2010;6:392. 23. Turner SE, et al. Prog Chem Org Nat Prod 2017;103:61-101. 24. Di Marzo V, et al. Neurotherapeutics 2015;12:692-8.



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Oral Liposomal Vitamin C as an Adjunct to Intravenous Ascorbic Acid By: Lucie Kotlarova, PharmD 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.

Vitamin C is a micronutrient of interest for its effects on human health and its potential role in immune-related diseases. Yet, unlike other mammals, with the exception of guinea pigs, primates do not synthesize vitamin C in the liver and must therefore rely solely on dietary intake. Specifically, due to a mutation in the gulonolactone oxidase (GULO) gene, humans cannot synthesize ascorbic acid from glucose. This leads to lower plasma levels of vitamin C and oxidative stress, unless counterbalanced with sufficient dietary intake from naturally vitamin C-rich foods, vitamin C-fortified foods, or supplements. Americans consuming a varied diet should have no difficulty obtaining a sufficient daily supply of vitamin C. The availability of citrus fruits and other vitamin C-rich foods is widespread, yet vitamin C deficiency is the fourth most common nutrient deficiency in the United States. In the absence of good health, hypovitaminosis C occurring as manifestation of prescorbutic clinical outcomes presents a significant concern. VITAMIN C AND IMMUNE FUNCTION Vitamin C impacts immune function by influencing multiple pathways including enhancing proliferation and differentiation of T-lymphocytes (T-cells) and B-lymphocytes (B-cells); stimulating natural killer (NK) cell activity; modulating cytokine production; acting as an antioxidant; and increasing collagen production in the fibroblasts. In otherwise healthy individuals, the immune system successfully prevents infections and random cancer cells from gaining a foothold and causing cellular havoc. Conversely, vitamin C deficiency


leads to impaired immunity which increases infection susceptibility, severity of organ failure, and mortality risk. Proponents of vitamin C supplementation encourage its use to prevent and treat respiratory and systemic infections and to strengthen the skin as a barrier against pathogens. Prophylactic use requires dosing in the milligram range, whereas treatment of current infections requires dosing in the gram range. Metabolic demand and elevated inflammatory response necessitate higher dosages to face the different stage of oxidative stress presented. VITAMIN C DEFICIENCY IN CANCER AND SEPTIC SHOCK PATIENTS Research suggests that cancer patients present with a higher incidence of vitamin C deficiency than patients with other diseases. Vitamin C deficiency has been observed in critically ill patients, as great as 75%, despite receiving the standard of care nutritional therapy. According to Carr et al., septic shock patients in the ICU experienced hypovitaminosis C at a rate of nearly 40%, compared to the non-septic, still critically ill patients, at a rate of 25%. The elevated inflammatory response accompanying septic shock is believed to induce the severe vitamin C depletion; inflammation was measured by the pro-inflammatory biomarker C-reactive protein (CRP) and was higher in the septic shock patients. Carrâ&#x20AC;&#x2122;s data also suggests that the ICU septic shock patients have scurvy by its definition (serum vitamin C level < 11.3 u/mol/l). Several clinical trials have begun investigating the use of intravenous vitamin C as an adjuvant in sepsis treatment.,


Oral Liposomal Vitamin C as an Adjunct to Intravenous Ascorbic Acid

INTRAVENOUS ASCORBIC ACID IN CANCER TREATMENT The rise, fall, and resurgence of high-dose IV and oral ascorbic acid not only reminds us of Ewan Cameron and Linus Paulingâ&#x20AC;&#x2122;s work in the 1970s, but illustrates how much in medicine is determined by the truth as we know it today. Although cancer patients have low plasma levels of ascorbic acid, the treatment goal is not to correct the deficiency, but rather, a two-pronged approach to directly affect the cancer cells. Chen et al. showed that high-dose pharmacologic ascorbate induces oxidative stress in cancer cells without harming healthy cells; instead of the traditional idea of vitamin C functioning as an antioxidant, at pharmacologic concentrations it functions as a prooxidant but only towards the cancer cells. The study observed sustained ascorbate radical and hydrogen peroxide formation within the interstitial fluids of tumors with a single dose in mice. Daily administration significantly reduced tumor growth rates for ovarian, pancreatic, and glioblastoma. Kuipers et al. rationalized utilizing high-dose pharmacologic ascorbate as a means to deliver sufficient ascorbate to the tumors to ensure optimal co-factor function, thereby halting tumor progression. Colorectal cancer patients whose tumors had a low ascorbate content, independent of grade and stage, did not survive in a disease-free post-surgery state as long as those patients whose tumors had higher ascorbate content. This suggests that the tumorâ&#x20AC;&#x2122;s ascorbate content is the key factor in cancer survival. Clinical data shows that high-dose IV pharmacologic ascorbate can be administered in parallel with standard anti-tumor therapy to improve chemotherapy tolerance, increase quality of life, and in some cases, prolong time to relapse, reduce tumor volume, and prolong survival. A recent review article by Cieslak et al. examined use of high-dose IV pharmacologic ascorbate in the treatment of pancreatic cancer and concluded that phase I trials demonstrated safety and potential efficacy of ascorbate. In 2018, Nauman et al. published a systematic review of intravenous ascorbate treatment in cancer clinical trials. Single arm and randomized Phase I/II trials were included and a total of 23 trials met the inclusion criteria. In one trial, patients suffering from ovarian cancer were randomized to receive standard chemotherapy with or without intravenous vitamin C (IVC); that trial reported an 8.75 month increase in progression-free survival (PFS) and an improved trend in overall survival in the vitamin C treatment arm. The authors of the review concluded that high-dose IV pharmacologic ascorbate has been shown to be safe in nearly all patient

populations, alone and in combination with chemotherapy. In a 2018 review, Klimant et al. summarized the use of highdose IV pharmacologic ascorbate in cancer care. According to the authors, use of intravenous vitamin C is a safe, supportive intervention to decrease inflammation and to improve symptoms related to antioxidant deficiency, disease processes, and side effects of standard cancer treatment. It can safely be used to treat ascorbate deficiency and could favourably affect clinical parameters such as inflammation, fatigue, and quality of life. Potential mechanisms of action of high-dose pharmacologic ascorbate in cancer and clinical studies in this field were reviewed in a 2018 article by Vissers and Das. The authors state that there is a substantial body of literature which documents potential anti-tumor effects of ascorbate in in vitro and in vivo settings, reporting cytotoxicity toward cancer cells and a slowing of tumor growth in animal models. Human clinical studies have suggested that high-dose ascorbate treatment may have a clinical benefit for patients with pancreatic cancer and other advanced cancers. According to the authors, results of these studies have expanded knowledge of the biological functions of high-dose pharmacologic ascorbate, and given its lack of toxicity, availability and low cost suggest there is a good rationale to use ascorbate as an adjunct treatment for cancer. ASCORBIC ACID INFUSIONS: LIMITATIONS & PATIENT BURDEN Despite the increasing use and promising efficacy of ascorbic acid infusion therapy in cancer patients, many unknowns, including dosing amount and frequency, timing of coadministration with conventional chemotherapy, and treatment duration, exist and hinder the establishment of a standard of care. Studies suggest that the absolute minimum treatment includes 1 g/kg administered over two hours twice a week for at least two months; increased frequency (3x/wk) and longer duration (3-4 months or longer) are highly recommended. Such recommendations involve financial, time, and convenience costs. This may place an undue burden on the patient and/ or caregiver and in turn, cause patients to abandon IV therapy protocols, especially if patients are paying out-of-pocket. Additionally, there may be no clinical trials offered within a patientâ&#x20AC;&#x2122;s geographic area. Rather than discourage patients, it is perhaps time to consider a hybrid model of intravenous and oral ascorbic acid to compliment chemotherapy and radiation. Intravenous and oral ascorbic acid have also been included in the care of terminal cancer patients. Yeom et al. assessed healthrelated quality of life following a protocol of 10g infusion twice



Oral Liposomal Vitamin C as an Adjunct to Intravenous Ascorbic Acid

with a 3-day interval and 4g orally every day for a week. Patients reported improved physical, emotional, and cognitive function, and less fatigue, nausea, vomiting, pain, and appetite loss. This suggests that despite mixed results and controversial research on vitamin C over the decades, therapeutic use of ascorbic acid is safe and improving quality of life in terminal patients is not simply aspirational, but realistic. Currently, patients under the care of an integrative physician are more likely to receive any type of “natural” infusion therapy, and so, a physician’s receptivity, or lack of, to nutritional intervention may be a limitation itself. LIPOSOMAL VITAMIN C Traditional vitamin C supplements are convenient yet have extremely low bioavailability and can cause extreme stomach discomfort when consumed in large doses. Vitamin C-rich foods have similar drawbacks, and patients undergoing chemotherapy may find eating difficult in general. Low bioavailability is due to the transit through the digestive tract as the ascorbic acid encounters oral enzymes, digestive juices, and bile salts that essentially “use up” most of the antioxidant capacity. The challenging view is the usage of liposomal vitamin C, a more bioavailable form of ascorbic acid that is encapsulated in liposomes comprised of a phospholipid bilayer containing phosphatidylcholine. Liposome encapsulated vitamin C is capable of reaching the liver non-oxidized and is 10 to 20 times more bioavailable than non-encapsulated vitamin C. Although more bioavailable than non-encapsulated vitamin C, liposome encapsulated vitamin C produces lower circulating concentrations than IV administration. With a superior form of oral vitamin C available today, Cameron and Pauling’s IVoral vitamin C combination therapy is worth reconsidering. 1. Carr AC, Maggini S. Vitamin C and Immune Function. Nutrients. 2017 Nov 3;9(11). 2. Huijskens MJ, Wodzig WK, Walczak M, Germeraad WT, Bos GM. Ascorbic acid serum levels are reduced in patients with hematological malignancies. Results Immunol. 2016 Jan 12;6:8-10. 3. Carr AC, Rosengrave PC, Bayer S, Chambers S, Mehrtens J, Shaw GM. Hypovitaminosis C and vitamin C deficiency in critically ill patients despite recommended enteral and parenteral intakes. Crit Care. 2017 Dec 11;21(1):300. 4. Hager DN, Hooper MH, Bernard GR, Busse LW, Ely EW, Fowler AA, Gaieski DF, Hall A, Hinson JS, Jackson JC, Kelen GD, Levine M, Lindsell CJ, Malone RE, McGlothlin A, Rothman RE, Viele K, Wright DW, Sevransky JE, Martin GS. The Vitamin C, Thiamine and Steroids in Sepsis (VICTAS) Protocol: a prospective, multi-center, double-blind, adaptive sample size, randomized, placebo-controlled, clinical trial. Trials. 2019 Apr 5;20(1):197. 5. Hwang SY, Park JE, Jo IJ, Kim S, Chung SP, Kong T, Shin J, Lee HJ, You KM, Jo YH, Kim D, Suh GJ, Kim T, Kim WY, Kim YJ, Ryoo SM, Choi SH, Shin TG; Korean Shock Society (KoSS) Investigators. Combination therapy of vitamin C and thiamine for septic shock in a multicentre, double-blind, randomized, controlled study (ATESS): study protocol for a randomized controlled trial. Trials. 2019 Jul 11;20(1):420. 6. Chen Q, Espey MG, Sun AY, Pooput C, Kirk KL, Krishna MC, Khosh DB, Drisko J, Levine M. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11105-9. 7. Kuiper C, Vissers MC. Ascorbate as a co-factor for fe- and 2-oxoglutarate dependent dioxygenases: physiological activity in tumor growth and progression. Front Oncol. 2014 Dec 10;4:359. 8. Kuiper C, Dachs GU, Munn D, Currie MJ, Robinson BA, Pearson JF, Vissers MC. Increased Tumor Ascorbate is Associated with Extended Disease-Free Survival and Decreased HypoxiaInducible Factor-1 Activation in Human Colorectal Cancer. Front Oncol. 2014 Feb 4;4:10.

LIPOSOMAL VITAMIN C: BEYOND CANCER & SEPSIS Vitamin C status can be affected by various environmental conditions (i.e., air pollution, tobacco smoke), chronic diseases (i.e., diabetes, alcoholism), infections, and advancing age. These conditions are characterized by excessive and sustained inflammation in the body, which begs the question, should daily oral liposomal vitamin C be included in the standard of care? Vitamin C’s immune-modulating effects suggest yes. Furthermore, prophylactic use to prevent infections is advisable. Millions of Americans take vitamin C supplements or multi-vitamins with vitamin C every day, but the majority of it is of low quality and low bioavailability. A liposomal form may be a little more expensive, but provides the anticipated benefits. In other words, a little goes a long way, and stomach discomfort is not an issue. CONCLUSION Vitamin C therapy, whether administered intravenously or orally, is not without disagreement among cancer specialists. The one attribute that everyone can agree upon is its safety. Along with an obligation of “do no harm,” it is also the medical community’s duty to explore all potential options, even if that includes a biohack. For the time being, oral liposomal vitamin C may be a biohack, but that could change in the future. One day, we may refer to liposomal vitamin C as the truth as we know it today, especially if we keep an open mindset in the present.

10. Cieslak JA, Cullen JJ. Treatment of pancreatic cancer with pharmacological ascorbate. Curr Pharm Biotechnol. 2015;16:759-770. 11. Nauman G, Gray JC, Parkinson R, Levine M, Paller CJ. Systematic review of intravenous ascorbate in cancer clinical trials. Antioxidants 2018 Jul;7:89.   12. Ma Y, Chapman J, Levine M, Polireddy K, Drisko J, Chen Q. High-dose parenteral ascorbate enhanced chemosensitivity of ovarian cancer and reduced toxicity of chemotherapy. Sci Transl Med. 2014 Feb 5;6:222-18.  13. Klimant E, Wright H, Rubin D. Intravenous vitamin C in the supportive care of cancer patients: a review and rational approach. Curr Oncol. 2018 Apr;25:139-148. 14. Vissers MCM, Das AB. Potential mechanisms of action for vitamin C in cancer: reviewing the evidence. Front Physiol. 2018 Jul 3;9:809. 15. Shenoy N, Creagan E, Witzig T, Levine M. Ascorbic Acid in Cancer Treatment: Let the Phoenix Fly. Cancer Cell. 2018 Nov 12;34(5):700-706. 16. Yeom CH, Jung GC, Song KJ. Changes of terminal cancer patients’ health-related quality of life after high dose vitamin C administration. J Korean Med Sci. 2007 Feb;22(1):7-11. 17. Milne, RD. (2004). PC Liposomal Encapsulation Technology. Henderson: Life’s Fountain Books. 18. Davis JL, Paris HL, Beals JW, Binns SE, Giordano GR, Scalzo RL, Schweder MM, Blair E, Bell C. Liposomal-encapsulated Ascorbic Acid: Influence on Vitamin C Bioavailability and Capacity to Protect Against Ischemia–Reperfusion Injury. Nutr Metab Insights. 2016 Jun 20;9:25-30. 19. Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: Prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A. 1976 Oct;73(10):3685-9.

9. Fritz H, Flower G, Weeks L, Cooley K, Callachan M, McGowan J, Skidmore B, Kirchner L, Seely D. Intravenous vitamin C and cancer: a systematic review. Integr Cancer Ther. 2014 May 26;13:280-300. 



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