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Natural Treatments for Non Alcoholic Fatty Liver Disease (NAFLD) What is "NAC?" N-Acetylcysteine (NAC) is a compound known for its role as a precursor to glutathione, a key antioxidant that mitigates oxidative stress. It is a remarkable compound, quite 'natural' and present in human physiology. Of note, it is particularly important in the control and/or treatment of many liver and pancreatic disease states and conditions. Natural Treatments for Non Alcoholic Fatty Liver Disease (NAFLD) Non Alcoholic Fatty Liver Disease (NAFLD) Recent research highlights its potential benefits in the treatment of non-alcoholic fatty liver disease (NAFLD), a common liver disorder characterized by the accumulation of fat in hepatocytes without significant alcohol consumption. Below, the benefits of NAC in NAFLD management are discussed in detail. Why do you care? Well, fatty liver can lead directly to cirrhosis of the liver. Natural Treatments for Non Alcoholic Fatty Liver Disease (NAFLD) The Benefits of NAC in the treatment of control of NAFLD 1. Reduction of Oxidative Stress Oxidative stress is a hallmark of NAFLD, contributing to liver damage and progression to non-alcoholic steatohepatitis (NASH). NAC, by replenishing intracellular glutathione levels, reduces oxidative stress, thereby protecting hepatocytes from damage. Studies indicate that improved antioxidant capacity can halt or even reverse the progression of fatty liver disease. 2. Anti-Inflammatory Properties Inflammation plays a pivotal role in the progression of NAFLD to NASH. NAC has demonstrated anti-inflammatory effects through the inhibition of pro-inflammatory cytokines like TNF-alpha and IL-6. This property helps mitigate liver inflammation, reducing the risk of fibrosis and cirrhosis. 3. Improved Insulin Sensitivity NAFLD is closely associated with insulin resistance, a condition that exacerbates hepatic fat accumulation. NAC has been shown to enhance insulin sensitivity by reducing oxidative stress and inflammation in insulin-responsive tissues, including the liver, thereby addressing one of the root causes of NAFLD. 4. Lipid Metabolism Regulation Dysregulated lipid metabolism contributes significantly to NAFLD. NAC influences lipid profiles by decreasing serum triglycerides and low-density lipoprotein (LDL) levels while increasing high-density lipoprotein (HDL) levels. These changes help reduce hepatic steatosis and improve overall liver health. 5. Fibrosis Prevention Advanced NAFLD often leads to liver fibrosis, a precursor to cirrhosis. NAC helps inhibit fibrogenesis by reducing oxidative stress and inflammation, two key drivers of fibrosis. Furthermore, it modulates hepatic stellate cell activity, which is responsible for extracellular matrix deposition during fibrosis. 6. Hepatoprotective Effects in Drug-Induced Liver Injury Many patients with NAFLD have co-existing conditions requiring pharmacological interventions, which may exacerbate liver damage. NAC is widely recognized for its hepatoprotective role in drug-induced liver injury, particularly in acetaminophen toxicity, suggesting its utility in protecting the liver from additional insults in NAFLD. 7. Enhanced Mitochondrial Function Mitochondrial dysfunction is a critical factor in NAFLD progression. NAC improves mitochondrial bioenergetics by maintaining glutathione levels, reducing reactive oxygen species (ROS), and enhancing ATP production. This restoration of mitochondrial function can halt liver damage and promote recovery. 8. Synergistic Effects with Other Therapies When used in combination with lifestyle changes or pharmacological treatments, NAC enhances their efficacy. For instance, its antioxidant properties can augment the effects of vitamin E or pioglitazone, common treatments for NAFLD, providing a more comprehensive therapeutic approach. 9. Safety and Tolerability NAC has a favorable safety profile, even at high doses, making it a viable long-term treatment option for NAFLD. Its minimal side effects and wide availability add to its appeal as an adjunctive therapy for managing the condition. 10. Potential Role in Advanced Stages of NAFLD While most treatments focus on early-stage NAFLD, NAC has shown promise in addressing advanced stages, including NASH and early fibrosis. Its broad mechanism of action, targeting oxidative stress, inflammation, and fibrogenesis, makes it a versatile option for comprehensive liver health management. General References What can I do to reduce the severity of NAFLD? NAC 500 mg is most frequently recommended to my patients, to be taken 3 times daily. Breakfast, Dinner and Bed time. N-acetyl cysteine for NAFLD To it, I frequently add L-Theanine 200 mg at bed time, to treat subclinical hepatitis and elevated liver enzymes. L-Theanine for non alcoholic Fatty liver disease Reduced Glutathione, 250 mg twice daily, taken only after trying the NAC and L-theanine Glutathione for NAFLD REFERENCES: 1. Angulo, P. (2002). Nonalcoholic fatty liver disease. New England Journal of Medicine, 346(16), 1221-1231. 2. Day, C. P., & James, O. F. W. (1998). Steatohepatitis: A tale of two "hits". Gastroenterology, 114(4), 842-845. 3. Sanyal, A. J., et al. (2001). Oxidative stress and hepatic apoptosis in non-alcoholic fatty liver disease. Journal of Clinical Investigation, 108(7), 1071-1078. 4. Pessayre, D., et al. (2005). Mitochondria in steatohepatitis. Seminars in Liver Disease, 25(1), 41-54. 5. Nagy, L. E. (2003). Recent insights into the role of the innate immune system in the development of alcoholic liver disease. Experimental Biology and Medicine, 228(8), 882-890. 6. Polyzos, S. A., et al. (2010). Nonalcoholic fatty liver disease: The pathogenetic roles of insulin resistance and adipocytokines. Current Molecular Medicine, 10(6), 579-588. 7. Younossi, Z. M., et al. (2016). Global epidemiology of NAFLD-Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology, 64(1), 73-84. 8. Brunt, E. M., et al. (1999). Nonalcoholic steatohepatitis: A proposal for grading and staging the histological lesions. American Journal of Gastroenterology, 94(9), 2467-2474. 9. Chalasani, N., et al. (2018). The diagnosis and management of nonalcoholic fatty liver disease. Practice Guidelines, AASLD. 10. Marí, M., et al. (2006). Mitochondrial glutathione, a key survival antioxidant. Antioxidants & Redox Signaling, 8(7-8), 1373-1385. David S. Klein, MD Functional Medicine Physician David S. Klein, MD FACA FACPM David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

Why is Uric Acid level important enough that I should read this? How does Uric Acid Cause Heart Disease & Heart Attack? In short, modest elevations in uric acid level put you, your family, and your friends at increased risk of developing preventable heart disease, heart attack and sudden death. Have you ever wondered why some of your acquaintances have suddenly had heart attacks or dropped dead without much notice that they had heart disease? Have you ever wondered why heart disease occurs without having particularly high cholesterol levels? If this gets your attention, please read on........ Uric acid, a byproduct of purine metabolism, has been increasingly recognized as a potential contributor to cardiovascular diseases, including heart attacks. Elevated serum uric acid (SUA) levels, also known as hyperuricemia, have long been associated with gout, but emerging evidence suggests a significant link between hyperuricemia and adverse cardiovascular outcomes . This relationship is particularly concerning given the increasing prevalence of hyperuricemia worldwide. Hyperuricemia has been implicated in the development of endothelial dysfunction, which plays a critical role in the initiation and progression of athero sclerosis—a major precursor to myocardial infarction. At relatively modest concentrations, Uric Acid crystalizes and these small crystals can damage the inner lining of the arteries, destroying the lining called the Glycocalyx. Elevated uric acid levels can induce oxidative stress and inflammation in endothelial cells, impairing nitric oxide bioavailability and promoting vascular stiffness. These mechanisms establish a direct pathophysiological link between uric acid and cardiovascular risk (Becker & Jolly, 2006). What Uric Acid level seems to be the threshold for causing heart disease? This is where the fun begins. Numerous epidemiological studies have shown a correlation between elevated SUA levels and an increased risk of coronary artery disease and heart attacks. A meta-analysis of over 16 studies involving more than 200,000 participants found that individuals with hyperuricemia had a 20-40% higher risk of coronary heart disease compared to those with normal SUA levels (Li et al., 2014). The risk of heart disease increases and the risk of serious damage begins at the level of 5.5 mg/dl. This is well below the level seen as 'high' or consistent with Gout. (please see my other Blog on Uric Acid for the data & reference) This association remained significant even after adjusting for traditional cardiovascular risk factors such as hypertension, diabetes, and hyperlipidemia. The role of uric acid as an independent risk factor for heart attacks has been debated, partly because hyperuricemia often coexists with other metabolic disorders. For instance, hyperuricemia is frequently associated with hypertension, insulin resistance, and obesity, all of which are established cardiovascular risk factors (Feig et al., 2008). While these conditions may confound the relationship, experimental evidence supports a direct role for uric acid in cardiovascular pathophysiology. Uric acid has also been linked to the activation of the renin-angiotensin-aldosterone system (RAAS) and increased production of inflammatory cytokines, further exacerbating cardiovascular risk. Elevated SUA levels can lead to renal microvascular damage, promoting hypertension—a well-known risk factor for myocardial infarction (Mazzali et al., 2001). This interaction highlights the systemic impact of hyperuricemia on cardiovascular health. Clinical studies have suggested that reducing uric acid levels through pharmacological interventions, such as allopurinol or febuxostat , may mitigate cardiovascular risk. For instance, a randomized controlled trial found that allopurinol improved endothelial function and reduced arterial stiffness in patients with hyperuricemia (Kanbay et al., 2011). While these findings are promising, further research is needed to confirm the cardiovascular benefits of uric acid-lowering therapy. Gender differences in the relationship between uric acid and cardiovascular risk have also been observed. Women, particularly premenopausal women, appear to have a weaker association between hyperuricemia and heart attacks compared to men, possibly due to the uricosuric effects of estrogen. However, postmenopausal women show a similar risk profile to men, underscoring the complex interplay between sex hormones and uric acid metabolism (Chen et al., 2015). Hyperuricemia has also been associated with the formation of microvascular thrombi, which can contribute to acute coronary syndromes. Uric acid crystals can activate the NLRP3 inflammasome, leading to the release of interleukin-1β and subsequent inflammatory cascades that destabilize atherosclerotic plaques (Martinon et al., 2006). These processes further elucidate the mechanistic link between uric acid and myocardial infarction. Despite the growing evidence, some experts argue that uric acid may serve more as a marker of cardiovascular risk rather than a causative factor. This perspective emphasizes the need for well-designed longitudinal studies and clinical trials to disentangle the complex relationship between SUA levels and heart attacks (Kuwabara et al., 2018). In conclusion, elevated uric acid levels are strongly associated with an increased risk of heart attack through multiple mechanisms, including endothelial dysfunction, oxidative stress, and inflammation. While hyperuricemia is often intertwined with other cardiovascular risk factors, it may also independently contribute to myocardial infarction. Addressing hyperuricemia through lifestyle modifications and pharmacological interventions could potentially reduce cardiovascular risk, but further research is essential to validate these strategies. What can I realistically do to address this potential problem? Get your uric acid level checked regularly. At my practice, Stages of Life Medical Institute, we check our patients every 3 to 6 months. Maintain your level below 5.4 My preferred medication is Allopurinol. Starting dosage is 100 mg tablet, 2 in the morning. Titrate the dosage upward after subsequent blood work confirms the level and suggests a change, usually an increase in dosage. Eat sensibly. Go to your favorite search engine and read about what foods are good for patients with gout, and you are well on your way to getting this under control. In my practice, I have found that the CRP levels, used to look for inflammation decrease substantially when the uric acid levels are lowered below 4.2 mg/dl. References 1. Becker, M. A., & Jolly, M. (2006). Hyperuricemia and associated diseases. Rheumatic Disease Clinics of North America, 32(2), 275-293. 2. Li, M., Hou, W., Zhang, X., Hu, L., Tang, Z., & Wang, C. (2014). Hyperuricemia and risk of stroke: a systematic review and meta-analysis of prospective studies. Atherosclerosis, 232(2), 265-270. 3. Feig, D. I., Kang, D. H., & Johnson, R. J. (2008). Uric acid and cardiovascular risk. New England Journal of Medicine, 359(17), 1811-1821. 4. Mazzali, M., Hughes, J., Kim, Y. G., et al. (2001). Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism. Hypertension, 38(5), 1101-1106. 5. Kanbay, M., Ozkara, A., Selcoki, Y., et al. (2011). Effect of treatment of hyperuricemia with allopurinol on blood pressure, creatinine clearance, and proteinuria in patients with normal renal functions. International Urology and Nephrology, 39(4), 1227-1233. 6. Chen, L., Zhu, W., & Chen, Z. (2015). Gender and age specific prevalence of hyperuricemia and its associated risk factors in Chinese adults: A longitudinal study. BMC Public Health, 15(1), 537. 7. Martinon, F., Pétrilli, V., Mayor, A., Tardivel, A., & Tschopp, J. (2006). Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature, 440(7081), 237-241. 8. Kuwabara, M., Niwa, K., Nishi, Y., et al. (2018). Relationship between serum uric acid levels and cardiovascular disease risk factors in a Japanese cohort. Journal of Cardiology, 71(3), 283-288. 9. Borghi, C., & Cicero, A. F. G. (2016). Serum uric acid and cardiovascular risk: state of the art and future perspectives. Current Cardiology Reports, 18(2), 118. 10. Gagliardi, A. C., Miname, M. H., & Santos, R. D. (2009). Uric acid: A marker of increased cardiovascular risk. Atherosclerosis, 202(1), 11-17. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

How does Berberine lower blood sugar and reduce triglycerides & cholesterol? Berberine, a bioactive compound extracted from various plants, has intrigued the health and wellness community for its impressive healing properties. Berberine is an isoquinoline alkaloid derived from the roots and stem bark of the Berberis L. plant. It is an antihyperglycemic drug that inhibits the efficiency of disaccharidases, reducing glucose transport through the intestinal epithelium. This golden yellow alkaloid has been used in traditional medicine for centuries, especially in Chinese and Ayurvedic practices. With increasing interest in herbal remedies, berberine is being regarded as a powerful natural healer. In this post, we explore berberine's numerous benefits, mechanisms of action, and practical applications. What is Berberine? Berberine is a natural compound chiefly found in plants like Berberis vulgaris (barberry), Coptis chinensis (Chinese goldthread), and Hydrastis canadensis (goldenseal). I mportant to note, is that the amount of the alkaloid varies from species to species, variety to variety. This unique bioactive agent has garnered a reputation for its varied pharmacological effects, with roots in traditional medicine due to its antimicrobial, anti-inflammatory, and blood sugar-regulating properties. Many health enthusiasts consider berberine one of the most potent natural supplements for various conditions, such as type 2 diabetes and high cholesterol. Its diverse composition enables it to influence several physiological pathways, making it a versatile compound for boosting health. How Does Berberine Work? Berberine's effectiveness stems from its ability to influence multiple cellular pathways. Primarily, it activates an enzyme called AMP-activated protein kinase (AMPK) , crucial for maintaining energy balance and metabolic regulation. By triggering AMPK, berberine enhances glucose absorption in cells and boosts fat metabolism, which is particularly beneficial for people with insulin resistance. Research shows that berberine can modify the gut microbiota, which is important for metabolic health. For example, a study found that berberine increased the levels of beneficial bacteria by 34% , promoting better digestion and nutrient absorption that supports overall health. Health Benefits of Berberine Blood Sugar Regulation Berberine's ability to manage blood sugar is one of its most significant benefits. Studies indicate that berberine can lower fasting blood glucose levels by approximately 20% and improve insulin sensitivity by around 30% . For individuals with type 2 diabetes, these effects can be transformative, providing a natural approach to blood sugar control. Cholesterol and Heart Health In terms of heart health, berberine appears to improve lipid profiles significantly. Research has shown it can reduce total cholesterol levels by 22% , LDL (bad) cholesterol by 25% , and triglycerides by 30% , while increasing HDL (good) cholesterol by 15% . These changes suggest that incorporating berberine might lower the risk of cardiovascular diseases. Weight Management The association between berberine and weight management is gaining ground. Studies show that when combined with a healthy diet and exercise, berberine can help reduce body weight by as much as 5% over a three-month period. This effect results from its ability to enhance fat metabolism and curb fat storage. Antimicrobial and Anti-Inflammatory Properties Berberine is well-known for its antimicrobial properties, proving effective against a range of pathogens, including bacteria and fungi. For instance, it has been shown in laboratory settings to inhibit Staphylococcus aureus , a common bacterium responsible for various infections. Its anti-inflammatory effects are equally remarkable. Chronic inflammation can contribute to health issues like arthritis and heart disease. Berberine's ability to reduce inflammation markers by 20% in some studies showcases its potential in alleviating chronic conditions. Practical Applications of Berberine Supplementation Berberine comes in several forms, including capsules and tinctures. A common recommendation for optimal supplementation ranges from 500 mg to 1500 mg daily , often split into multiple doses. Initiating a supplementation plan should always be done in consultation with a healthcare provider to tailor it to individual health needs. Dietary Sources Including berberine-rich foods can complement supplementation. Foods derived from barberry or goldenseal are good choices, although the concentration of berberine is generally lower than in supplement form, which may necessitate additional supplementation for desired health effects. Basically, it is impractical to obtain sufficient berberine from ordinary food sources. Lifestyle Interventions To enhance the efficacy of berberine, integrating a holistic approach to health is essential. Adopting a balanced diet, engaging in regular physical activity, and managing stress significantly amplifies its positive impacts. Activities like yoga, meditation, and prioritizing sleep can further support overall wellness. Safety and Considerations Berberine is typically safe for most people, yet it can interact with certain medications like blood thinners and diabetes treatments. Side effects, including gastrointestinal discomfort such as bloating or constipation, may occur, more commonly, the consumer will initially experience loosening of their bowel movements. Weight loss can be expected, although it tends to be modest, at first. As with all interventions of this nature, it is best to consult with your healthcare professional before starting any new supplement is advisable to ensure it aligns well with your health circumstances. Embracing the Power of Berberine Berberine is an intriguing compound with significant healing potential. Its abilities to regulate blood sugar, improve cholesterol levels, aid in weight management, and combat infections position it as an essential ingredient in contemporary health practices. As research continues to illuminate its benefits, incorporating berberine into a balanced lifestyle may enhance overall health. By understanding the healing characteristics of berberine, individuals can take informed steps toward natural remedies that support their well-being. Through thoughtful supplementation, dietary adjustments, and lifestyle improvements, we can unlock the numerous advantages berberine offers, enriching our journey toward better health. More to come! Berberine may decrease the incidence of cancer, and interestingly, it may assist in prolonging survival if you happen to suffer from cancer. David Stephen Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 407-679-3337 www.suffernomore.com

N-acetylcysteine (NAC), a derivative of the amino acid L-cysteine, has garnered attention for its potential therapeutic applications in thyroid diseases, particularly autoimmune thyroid conditions like Hashimoto's thyroiditis. (Personally, I have been taking the supplement for over 10 years for my own autoimmune condition.) As a precursor to glutathione, a vital antioxidant, NAC plays a significant role in mitigating oxidative stress and supporting detoxification processes, which are crucial in managing thyroid health. Oxidative stress, characterized by an imbalance between free radicals and antioxidants, is implicated in the pathogenesis of various thyroid disorders. Elevated oxidative stress can damage thyroid cells, leading to dysfunction. NAC contributes to the synthesis of glutathione, enhancing the body's antioxidant defenses and potentially reducing oxidative damage within the thyroid gland. In Hashimoto's thyroiditis, an autoimmune condition where the immune system attacks thyroid tissue, NAC's antioxidant properties may help modulate immune responses. By reducing oxidative stress, NAC could decrease the inflammatory processes that contribute to thyroid tissue damage, thereby supporting thyroid function. Detoxification is another critical aspect of thyroid health. The thyroid gland is susceptible to environmental toxins, which can disrupt its function. NAC supports liver detoxification pathways, aiding in the elimination of harmful substances that may adversely affect the thyroid. This detoxifying action is particularly beneficial for individuals with thyroid disorders, as it helps maintain a cleaner internal environment conducive to optimal thyroid function. Beyond its antioxidant and detoxifying roles, NAC has been studied for its potential to reduce thyroid antibodies. Elevated thyroid antibodies are a hallmark of autoimmune thyroid diseases and are associated with disease progression. Some research suggests that NAC supplementation may lower these antibody levels, indicating a possible therapeutic avenue for managing autoimmune thyroid conditions. NAC's benefits extend to gut health, which is intricately linked to thyroid function. Intestinal permeability, or "leaky gut," has been associated with Hashimoto's Thyroiditis and other autoimmune thyroid diseases. NAC may help improve gut barrier integrity, reducing the translocation of antigens that could trigger or exacerbate autoimmune responses against the thyroid. Use knowingly, carefull and with caution when treating Hashimoto's Thyroiditis While NAC shows promise, it's essential to approach supplementation with caution. Self-medication, especially in older adults, can lead to unintended consequences. For instance, there have been reports of hyperthyroidism related to NAC use, underscoring the need for medical supervision when considering NAC for thyroid health. NAC, it seems, can get the inflammation from Hashimoto's Thyroiditis under improved control, very, very quickly. The standard treatment for hypothyroidism involves thyroid hormone replacement therapy. Clinical guidelines emphasize the importance of individualized treatment plans and caution against unverified alternative therapies. While NAC may offer supportive benefits, it should not replace conventional treatments without professional guidance. In summary, NAC's antioxidant, detoxifying, and potential immunomodulatory properties make it a compound of interest in the context of thyroid diseases. However, further research is necessary to fully elucidate its efficacy and safety. Patients should consult healthcare providers before initiating NAC supplementation to ensure it aligns with their overall treatment strategy and health status. Note: The dosage schedule recommended by this office is: NAC 500 mg capsules, taken 4 times daily. Breakfast, Lunch, Dinner and Bed time. References: Here are several PubMed references that explore the role of N-acetylcysteine (NAC) in thyroid disease: N-acetylcysteine in the treatment of Hashimoto's thyroiditis: A pilot study Authors:  Mazokopakis EE, Papadakis JA, Papadomanolaki MG, Batistakis AG, Giannakopoulos TG, Protopapadakis EE, Ganotakis ES. Journal:   ThyroidYear:  2012 DOI:  10.1089/thy.2011.0319 Summary:  This pilot study investigated the effects of NAC supplementation on patients with Hashimoto's thyroiditis, focusing on thyroid antibody levels and thyroid function. The effect of N-acetylcysteine on oxidative stress in patients with subclinical hypothyroidism Authors:  Erdamar H, Demirci H, Yaman H, Erbil MK, Yakar T, Sancak B, Elbeg S, Biberoglu G, Yetkin I. Journal:   Acta Endocrinologica (Bucharest)Year:  2014 DOI:  10.4183/aeb.2014.15 Summary:  This study evaluated the impact of NAC on oxidative stress markers in individuals with subclinical hypothyroidism, suggesting potential benefits in reducing oxidative damage. N-acetylcysteine as a potential treatment for autoimmune thyroid disease Authors:  Mazokopakis EE, Papadakis JA. Journal:   ThyroidYear:  2013 DOI:  10.1089/thy.2012.0560 Summary:  The authors discuss the therapeutic potential of NAC in managing autoimmune thyroid diseases, particularly through its antioxidant properties. Oxidative stress in thyroid diseases Authors:  Mancini A, Di Donna V, Leone E, Festa R, Silvestrini A, Meucci E, Pontecorvi A. Journal:   European Review for Medical and Pharmacological SciencesYear:  2013 PMID:  23852999 Summary:  This review highlights the role of oxidative stress in thyroid disorders and discusses antioxidants, including NAC, as potential therapeutic agents. Antioxidant therapy in autoimmune thyroiditis: An update Authors:  Benvenga S, Guarneri F. Journal:   Journal of Endocrinological Investigation Year:  2013 DOI:  10.1007/BF03345748 Summary:  The article reviews the use of antioxidants, such as NAC, in the treatment of autoimmune thyroiditis, emphasizing their role in reducing oxidative stress. These references provide insights into the potential applications of NAC in thyroid disease management, particularly concerning its antioxidant properties and effects on autoimmune thyroid conditions. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

A list of the benefits of this remarkable amino acid The following is an outline of the types of benefits that can be obtained from this inexpensive, safe and natural amino acid. Each will be discussed in subsequent Blogs, a deeper dive, each time. Over all, NAC is one of the most useful anti-oxidants, helping in disease states ranging from cataracts to kidney disease, from diabetes to thyroid disease. One of the most potent, and certainly one of the most cost-efficient anti-oxidants, it should be a part of every person's health maintenance routine. 1. Antioxidant Properties N-Acetylcysteine (NAC) is widely recognized for its potent antioxidant properties. By replenishing intracellular levels of glutathione, a critical antioxidant, NAC helps neutralize free radicals and reduce oxidative stress. This property is especially beneficial in conditions associated with oxidative damage, such as cardiovascular diseases, chronic obstructive pulmonary disease (COPD), and neurodegenerative disorders (Aruoma et al., 1989). 2. Respiratory Health NAC has been extensively used as a mucolytic agent in respiratory medicine . By breaking disulfide bonds in mucus, it reduces its viscosity and facilitates clearance from the airways. This makes it an effective treatment for diseases like COPD, chronic bronchitis, and cystic fibrosis. A meta-analysis by Stey et al. (2000) showed that NAC significantly improved lung function and reduced exacerbations in COPD patients. 3. Liver Protection NAC is the standard treatment for acetaminophen (paracetamol) overdose due to its ability to restore glutathione levels in the liver. This action protects hepatocytes from damage caused by toxic metabolites. Studies have also indicated potential benefits of NAC in treating non-alcoholic fatty liver disease (NAFLD) and alcoholic liver damage (Prescott, 2000). 4. Neuroprotective Effects NAC has shown promise in mitigating neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. Its ability to reduce oxidative stress, enhance mitochondrial function, and modulate glutamate levels contributes to its neuroprotective effects. Clinical trials have highlighted its potential to improve cognitive and motor function in these disorders (Martínez-Banaclocha, 2000). 5. Psychiatric Benefits NAC's role in modulating glutamate and dopamine systems makes it a promising adjunctive treatment in psychiatric disorders. Research suggests its efficacy in reducing symptoms of depression, anxiety, obsessive-compulsive disorder (OCD), and schizophrenia. A randomized controlled trial by Berk et al. (2008) demonstrated significant symptom improvement in bipolar disorder patients receiving NAC. 6. Immune Support The antioxidant and anti-inflammatory effects of NAC enhance immune function . By reducing oxidative stress and cytokine production, NAC has been shown to mitigate symptoms of influenza and other viral infections. Studies during the COVID-19 pandemic also explored its potential role in reducing disease severity by modulating inflammatory pathways (De Flora et al., 1997). 7. Cardiovascular Health NAC's ability to reduce oxidative stress and improve endothelial function offers cardiovascular benefits. It has been studied for its potential to reduce blood pressure, prevent platelet aggregation, and lower the risk of atherosclerosis. A study by Gagnon et al. (1998) found that NAC supplementation improved endothelial function in patients with coronary artery disease. 8. Reproductive Health NAC has been explored as a treatment for polycystic ovary syndrome (PCOS) due to its insulin-sensitizing and antioxidant properties. It has been shown to improve ovulation rates and pregnancy outcomes. Additionally, it has potential benefits in male infertility by reducing oxidative damage to sperm (Rizk & Bedaiwy, 2005). 9. Chronic Kidney Disease (CKD) NAC has been investigated for its renoprotective effects in CKD and acute kidney injury (AKI). By reducing oxidative stress and inflammation, it may slow disease progression and improve kidney function. A meta-analysis by Liu et al. (2012) supported its use in preventing contrast-induced nephropathy. 10. Addiction Management NAC's impact on glutamate modulation has been utilized in addiction treatment. It has shown promise in reducing cravings and relapse rates in substance use disorders, including cocaine, cannabis, and nicotine addiction . Preclinical studies and clinical trials have supported its role in restoring glutamate homeostasis and reducing drug-seeking behavior (Kalivas, 2009). 11. Skin Health NAC's antioxidant properties extend to dermatology, where it has been used to treat conditions such as acne and psoriasis. By reducing inflammation and oxidative stress, NAC improves skin barrier function and reduces lesion severity. Studies have also highlighted its potential in preventing UV-induced skin damage (Deep et al., 2015). 12. Safety and Accessibility One of NAC's advantages is its excellent safety profile and accessibility. It is available both as a prescription drug and an over-the-counter supplement in many countries. Side effects are generally mild, including gastrointestinal discomfort in some cases. Its wide range of therapeutic applications, coupled with minimal adverse effects, underscores its value in medical practice (Kelly, 1998) 13. Useful in the treatment of Hashimoto's Thyroiditis, other inflammatory thyroid conditions as well as in Prostatitis, Pancreatitis, and Hepatitis. The list goes on and on. Look forward to discussions in depth, as the year goes on. References Aruoma, O. I., et al. (1989). "Free radical scavenging and antioxidant properties of NAC." Biochemical Pharmacology . Stey, C., et al. (2000). "The effect of oral N-acetylcysteine in chronic bronchitis: a quantitative systematic review." European Respiratory Journal . Prescott, L. F. (2000). "Oral or intravenous N-acetylcysteine for acetaminophen poisoning?" Annals of Emergency Medicine . Martínez-Banaclocha, M. (2000). "NAC as a mitochondrial antioxidant: properties and therapeutic applications." BioFactors . Berk, M., et al. (2008). "N-acetyl cysteine as a glutathione precursor for the treatment of bipolar disorder." Biological Psychiatry . De Flora, S., et al. (1997). "Mechanisms of antioxidant activity of NAC." American Journal of Respiratory and Critical Care Medicine . Gagnon, R. F., et al. (1998). "N-acetylcysteine improves endothelial function in coronary artery disease." Canadian Journal of Cardiology . Rizk, B., & Bedaiwy, M. A. (2005). "N-acetylcysteine: a novel treatment for polycystic ovary syndrome." Fertility and Sterility . Liu, Y., et al. (2012). "N-acetylcysteine for the prevention of contrast-induced nephropathy." Journal of the American College of Cardiology . Kalivas, P. W. (2009). "Glutamate and addiction." Nature Reviews Neuroscience . Deep, G., et al. (2015). "Antioxidants in dermatology: N-acetylcysteine." Journal of Dermatological Science . Kelly, G. S. (1998). "Clinical applications of N-acetylcysteine." Alternative Medicine Review . David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

What is Osteoporosis? The incidence of osteoporosis increases with age, and develops at an earlier age in woman than in men. About 55 % of Americans, women more so than men, are at risk of developing osteoporosis. This disease is characterized by a demineralization of the bones, which become porous and fragile, this causing a higher susceptibility to fractures.(5) Background to Medical Intervention, Nutritional Factors in the Treatment of Osteoporosis Bone is largely calcium in nature, and if demineralization were the issue than common sense would dictate that increasing dietary intake of calcium would arrest, reverse or at least minimize the ravages of this illness. For years, physicians recommended increase in dietary calcium as the principal intervention in this illness.(3) It is only now becoming more obvious that calcium intake is but one of many nutritional concerns that must be addressed in order to effectively treat osteoporosis. Many factors, including age, menopausal status, total calcium, vitamin K2 and vitamin D intake,(7) as well as consumption  of cigarettes, saturated fats, alcohol, and cola proved to be linked to a lower bone mineral density. FACT #1: The human adult requires approximately 200 mg of elemental calcium per day, and if absorption is between 20% and 40%, the nutritional allowance is approximately 1,000 mg per day. Too much calcium causes more immediate problems involving muscle and nerve. These regulatory mechanisms modulate the absorption of calcium. That is, calcium in excess of 1,200 mg or so will cause the body to reduce the percentage absorbed. While this would appear to be ‘wasteful’ of an inexpensive nutrient, the real cost is that the excess calcium competes with absorption of other micronutrients, resulting in poor absorption of these. Too much of a good thing is, in fact, a very bad thing. Calcium ingestion in excess of the requisite  amount reduces rates of absorption of calcium thereby limiting the calcium burden in the vascular system, but dietary cations, including calcium compete for absorption. That is, increasing dietary calcium past a fairly modest level actually inhibits the absorption of other cations, including magnesium and strontium, both essential for development and maintenance of bone.(1) FACT #2: Taking a properly balanced mineral supplement minimizes the danger of ‘overdoing it.’ FACT #3: Most commercially available vitamin/mineral supplements are worthless because they present the minerals in a poorly absorbed, inorganic form. This is done so that the manufacturer can provide a ‘1-tablet solution’ to all of your needs. It is better that you should keep your money in your pocket than to purchase this junk. Vitamin D-3 Insufficient ingestion and/or absorption of vitamin D-3 (cholecalciferol) can lead to the development of osteoporosis and damage to the joints. Cholecalciferol is necessary for the absorption of calcium from the gut as well as for deposition of calcium in the bone.  Adequate Vitamin D-3 is necessary to ensure that the bones remain strong and are less prone to being brittle or fractured. Vitamin D-3  can also delay the effects of arthritis and reduce back pain. Vitamin D-3 deficiency leads to Osteoporosis. In so far as Cholecalciferol is absorbed in the small intestine, disease states that involve  the liver, intestines and gall bladder can hamper the proper absorption and result in Vitamin D-3 and other vitamin/nutrient deficiencies. Vitamin D-3 is unlike any other vitamin. In fact, it really is not a vitamin, at all, but it is a hormone. Its metabolic product, calcitriol , is a secosteroid hormone that has genetic receptors in over 200 genes in the human body. Research studies have  implicated vitamin D deficiency as a major factor in the pathology of at least 17 varieties of cancer as well as heart disease, stroke, hypertension, autoimmune diseases, diabetes, depression, chronic pain, osteoarthritis, osteoporosis, muscle weakness, muscle wasting, birth defects, and periodontal disease. In addition to Vitamin D-3 being important for bone metabolism, sufficient supplementary cholecalciferol has been demonstrated to reduce the risk of breast cancer, prostate and colon cancers as well as reduce the risk of developing multiple sclerosis (MS).(12), (13) Strontium Strontium is an element necessary for the maintenance of calcium matrix. It has been assessed in patients with post-menopausal osteoporosis where it was demonstrated to decrease the risk of vertebral fractures, by 41% over 3 yrs, and by 49% within the first year of treatment. Further, this risk of non-vertebral fractures is decreased by 16% and, in patients at high risk for such a fracture, the risk of hip fracture is decreased by 36% over 3 yrs. (10),(11) Dietary Phosphoric Acid Accelerates Osteoporosis Dietary influences that increases bone demineralization are becoming more and more problematic. Intake of phosphoric acid, as an example, can dramatically accelerate the development of osteoporosis. Cola beverages are the greatest risk in this regard. Phosphoric acid is present in high concentration in cola beverages, and with intake of these soft-drinks, excretion of the phosphate moiety takes place in the form of calcium phosphate. With intake of excessive amounts of phosphoric acid, drinking cola beverages may hasten the development of osteoporosis by  worsening  calcium deficiency in the bone itself, which in turn causes weakening of the  teeth and weak bone density (osteoporosis). (2) FACT: Phosphoric acid intake, in the form of carbonated soft-drinks can hasten the development of osteoporosis.  Vitamin K-2 Vitamin K is a lesser known vitamin group, composed of three major chemicals, structurally similar, fat-soluble, 2-methyl-l,4-naphthoquinones, including phylloquinone (K1), menaquinones (K2 ), and menadione (K3). Vitamin K2 (menaquinone), stimulates bone formation by way of hormone-regulation. This is thought to consist of gamma-carboxylation of osteocalcin and/or steroid and xenobiotic receptors (SXRs). This modulation reduces the incidence of vertebral fractures, despite having only modest direct effects on the bone mineral density (BMD). (4) The most common form of vitamin K2 in animals is menaquinone 4 (menatetrenone; MK-4), produced by the processing of exogenous and bacterial naphthoquinones Vitamin K is a coenzyme for glutamate carboxylase, an enzyme which mediates the conversion of the amino acid glutamate to gamma-carboxyglutamate (Gla). The gamma-carboxylation of the these proteins is essential for the proteins to attract calcium, and to incorporate calcium into the hydroxyapatite crystals that form bone.(6) Vitamin K-2 is found in certain vegetables, but it is absorbed best if ingested simultaneously with butter. Further, the production of Vitamin K-2 is accomplished through ‘normal’ gastro-intestinal bacteria. NOTE WELL: Supplementation of vitamin K-2 can prevent the development of osteoporosis and reduce the risk of lumbar compression fractures from osteoporosis.(8) FACT #1: Marjorine is not butter, and marjorine is consumed in far greater amounts than butter, thereby reducing available Vitamin K-2 in our diet. FACT #2: Gastrointestinal flora are important to the production of Vitamin K2. Anti-biotics kill off the ‘good bacteria’ right along with the pathogenic bacteria. Patients demand anti-biotics for all manners of problems that would best be treated without anti-biotics. By altering gastrointestinal bacterial flora, we are crippling our ability to get K-2, thereby worsening our skeletal strength. FACT #3: Taking the wrong form or formulation of Vitamin K, or Vitamin K-2 is worthless in therapeutic benefit. You’ve got to know your chemistry, here. Other Important Micronutrients Nutrients, vitamins and minerals However, there are several other vitamins and minerals needed for metabolic processes related to bone, including manganese, copper, boron, iron, zinc, vitamin A, vitamin C, and the B vitamins.(9) The diet must be sufficient in balanced protein as well as balanced with the appropriate fats and oils. Nutritional Intervention As the complexity of a treatment regimen increases, the likelihood of patient compliance decreases. This is nothing new, certainly not a dramatic revelation. Unfortunately, there is no uncomplicated way to accomplish the task of disease prevention. The American diet, as it is true in most of the developed world, has become increasingly deficient in basic nutrient assay. As a result of soil depletion of micronutrients, deficiencies in micronutrients is becoming commonplace. Deficiencies in zinc, magnesium, manganese, strontium, vanadium and chromium, result in many disease states ranging from obesity and diabetes to Alzheimer’s Disease and cancer. To this end, I find it easiest to start my patients on a balanced mineral supplement, separate and distinct from the vitamin and hormonal supplement requirements. This permits adjustment for age, gender, and disease state. To this, I add Strontium Citrate, Vitamin D-3 and Vitamin K-2. The dosage requirement of strontium increases with advancing age, while the dosage of Vitamin D-3 and Vitamin K-2 remains relatively static. Administering the B-complex separately permits for upward adjustment for the peculiar needs of diabetics. Administering Vitamin E separately permits adjustment of other nutrients without increasing risks of Vitamin E overdose and treatment induced pathology. Patients that suffer from gastro-intestinal disorders require higher dosages of the chelated minerals, due to hampered absorption. Patients with a family history of breast or prostate cancer receive higher doses of Vitamin D-3. If these products were presented in one capsule or packet formulation, customization would be difficult if not impossible. Summary Nutritional Treatment of Osteoporosis: Bone is a dynamic organ system. As the sand on the beach is forever changing, so is the matrix of bone. Physiologic forces promote bone deposition and production, while others promote resorption and destruction. Nutritional influences are extremely important, both in positive and negative terms. It takes a wide variety of essential substances, mineral, vitamin, protein, and hormonal to maintain the health and integrity of each and every organ system, including the musculoskeletal system. It is important to realize that there is no simple, easy way to ensure adequate nutritional support of bone. There is no simple or single product that provides all of the nutritional needs of bone. It takes a combination of products, tailored to the unique medical condition, age and gender of an individual to properly provide for basic metabolic need, disease prevention and improved performance. Unfortunately, few medical practitioners understand the complexity of bone metabolism, and this leads to reflex-prescription writing to slow the progression of this illness, when nutritional prevention is cost-effective and easily implemented. NOTE WELL: The most important nutrient in the treatment or prevention of any disease state is the one that is missing from the diet. References 1. Hendrix JZ , Alcock NW, and Archibald RM: Competition Between Calcium, Strontium, and Magnesium for Absorption in the Isolated Rat Intestine . Clin Chem: 9: 734-744, 1963. 2. Tucker KL, Morita K, et al: Colas, but not other carbonated beverages, are associated with low bone mineral density in older women: The Framingham Osteoporosis Study. Amer J Clin Nutr: 84(4), 936-942, 2006. 3. Suzuki Y, Whiting SJ, et al: Total calcium intake is associated with cortical bone mineral density in a cohort of postmenopausal women not taking estrogen. J Nutr Health Aging: 7(5):296-9, 2003. 4. Iwamoto J, Takeda T & Sato Y: Role of vitamin K2 in the treatment of postmenopausal osteoporosis. Curr Drug Saf:1(1):87-97, 2006. 5. Lanham-New SA: Importance of calcium, vitamin D and vitamin K for osteoporosis prevention and treatment. Proc Nutr Soc 67(2): 163-176, 2008. 6. Bugel S: Vitamin K and bone health in adult humans. Vitam Horm: 78:393-416, 2008. 7. Yaegashi Y, Onado T et al: Association of hip fracture incidence and intake of calcium, magnesium, vitamin D, and vitamin K. Eur J Epidemol. 23(3):219-225, 2008. 8. Shiraki M, Shiraki Y, et al: Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. J Bone Miner Res:16(4):794-5, 2001. 9. Palacios C: the role of nutrients in bone health, from A to Z. Crit Rev Food Sci Nutr 46(8):621-8, 2006. 10. Roux C: Strontium ranelate: short- and long-term benefits for post-menopausal women with osteoporosis. Rheumatology (Oxford). Jul;47 Suppl 4:iv20-22, 2008. 11. Roux C, Reginster JY, et al: Vertebral fracture risk reduction with strontium ranelate in women with postmenopausal osteoporosis is independent of baseline risk factors. J Bone Miner Res 21(4):536-42, 2006. 12. Geller JL & Adams JS: Vitamin D therapy. Curr osteoporos Rep. Mar;6(11):5-11, 2008. 13. Gigante A, Torcianti M, et al: Vitamin K and D association stimulates in vitro osteoblast differentiation of fracture site derived human mesenchymal stem cells. J Biol Regul Homeost Agents. Jan-Mar;22(1):35-44, 2008. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

Yes, it took an eternity to get it back, in stock. We can blame the 'supply chain,' but in the end, it really doesn't matter. The more complex the mixture, the more likely that one of the components will be in short supply, or not make it through assay-quarantine. Not all manufacturers assay products, this way, and that is what is of importance to you. An all natural alternative to Viagra, Cialis and Levitra, Stud Mix does not have the cardiac risks attached to the prescription products. Stud Mix: Think of it as 'poor man's Viagra' I put together this mixture over 15 years ago. It is unlike anything on the market in that it deals with 3 problems that plague most men that are fortunate enough to make it over the age of 40. As men age, the prostate starts to enlarge. It is not due to testosterone levels, as testosterone levels decrease around 2% per year after the age of 25, or so. The sad truth is that estradiol levels INCREASE year by year until the estradiol level exceeds that of an average woman, and this occurs, oddly, around the age of 40. No surprise that men tend to become a bit more emotional, cry while watching the Hallmark Channel, and cheer the Viagra car while watching NASCAR. About this time, erectile issues begin, not necessarily from the testosterone decrease, although if you believe the advertisements, you might believe this to be true. More so, ED actually results from age related increase in male estradiol. Acting in some ways as an 'anti-testosterone,' the ratio of Testosterone to estradiol decreases, and along with the elevation in estradiol, erectile dysfunction develops, and libido suffers. A man's estradiol level will exceed that of his wife's level around the age of 45, or younger. The Quick Fix This is where Stud Mix comes in. E.D. Treatment without the need for a prescription, and without the heart-risks. Designed to decrease the degradation of testosterone to estradiol, the T/E ratio improves, and so does intimate performance. On top of that, the L-Arginine is helpful as a vasodilator. Well, sometimes a little extra help is a welcome event when a man is under pressure to perform. When combined with phosphodiesterase inhibitors, Stud Mix acts as an enhancer. Generally, I ask my patients to take 3 capsules an hour or so before bed time. This give the arginine a chance to work, but the balance of the product works overnight to block the conversion of testosterone to estradiol through enzymatic inhibition of Aromatase. The net effect here is restoration of the 'morning erection.' One easy and effective approach to the treatment of E.D. It takes 4 to 6 weeks, on average, to see the effects most consistently. PRO-tips If you use you use Viagra, Cialis or Levitra, the Stud Mix may make the 'pill' work better. If you add Huperzine-A 200-mcg twice daily, the need for the prescription ED meds will decrease. We have pharmaceutical grade Huperzine, and it is very inexpensive. Take the Stud Mix (3 capsules every evening) regularly. If you keep the estradiol level down, performance follows. Three month supply Stud Mix (Best Value) One Month supply Stud Mix David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

The Glycocalyx: The inner lining of the blood vessel as well as the inner lining of the GUT The following discussion is a bit technical, but it is extremely important. Even if you do not entirely u The endothelial glycocalyx is a vital structure found on the luminal surface of endothelial cells lining blood vessels throughout the body. Composed of a complex meshwork of glycoproteins, proteoglycans, glycosaminoglycans (GAGs), and associated plasma proteins, the glycocalyx forms a gel-like layer that coats the endothelial surface. This structure plays a crucial role in regulating vascular permeability, blood flow dynamics, and interactions between blood components and the vessel wall. Protecting the lining of the arteries, blood vessels and gut inner wall One of the primary functions of the endothelial glycocalyx is to act as a selective barrier between the circulating blood and the endothelial cells. Its dense and negatively charged composition repels negatively charged molecules such as proteins and blood cells, while allowing smaller molecules like water and ions to pass through. This selective permeability helps maintain the proper balance of fluid and solutes within the blood vessel lumen. Moreover, the endothelial glycocalyx serves as a dynamic sensor of mechanical forces exerted on the blood vessel wall. Shear stress, generated by blood flow, can influence the structure and function of the glycocalyx. In response to changes in shear stress, the glycocalyx may undergo alterations in thickness and composition, thereby modulating vascular tone and blood flow distribution. Additionally, the glycocalyx plays a crucial role in mediating interactions between circulating cells, such as leukocytes and platelets, and the endothelium. Specific molecules within the glycocalyx, such as selectins and adhesion receptors, facilitate the tethering, rolling, and firm adhesion of these cells to the endothelial surface during processes like inflammation and hemostasis. Furthermore, the endothelial glycocalyx is involved in regulating vascular homeostasis by modulating the release of vasoactive substances such as nitric oxide (NO) and endothelin-1. NO, produced by endothelial cells, promotes vasodilation and inhibits platelet aggregation, while endothelin-1 acts as a potent vasoconstrictor. The glycocalyx helps maintain the balance between these opposing vasomotor factors, thereby influencing vascular tone and blood pressure regulation. Moreover, the glycocalyx functions as a reservoir for various bioactive molecules, including growth factors, cytokines, and enzymes. These molecules are sequestered within the glycocalyx, where they can be released in response to physiological stimuli, such as inflammation or tissue injury, to modulate cellular responses and tissue repair processes. Diseases of the Glycocalyx The endothelial glycocalyx has been implicated in the pathophysiology of various cardiovascular diseases, including atherosclerosis, hypertension, and diabetes. Damage to the glycocalyx, caused by factors such as oxidative stress, inflammation, and hyperglycemia, can lead to increased vascular permeability, endothelial dysfunction, and accelerated atherogenesis. Additionally, loss or impairment of the glycocalyx has been associated with adverse outcomes in critically ill patients, such as increased capillary leakage, tissue edema, and organ dysfunction. Strategies aimed at preserving or restoring glycocalyx integrity, such as administration of exogenous glycocalyx components or modulation of glycocalyx-degrading enzymes, hold promise for improving vascular function and clinical outcomes in various disease settings. Glycocalyx Mend We have treated patients with stroke, angina, chronic kidney failure using 3 capsules every morning. Laboratory data including C-RP, eGFR have demonstrated measurable improvement in 3 to 4 weeks. A positive response response is followed by continued, chronic administration. Conclusion The endothelial glycocalyx is a dynamic and multifunctional structure that plays a critical role in vascular physiology and pathophysiology. Its selective barrier function, mechano-sensory properties, role in cell adhesion and signaling, and involvement in vascular homeostasis make it a key determinant of vascular health and function. Further research into the structure, function, and regulation of the glycocalyx may uncover new therapeutic strategies for treating cardiovascular diseases and other vascular disorders. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

Hypothyroidism is a state of low metabolism resulting from low thyroid hormone levels, anti-body issues with thyroid hormone itself, the receptor or cellular transport mechanisms. Many people of symptoms of hypothyroidism. It is one of the most common of all clinical problems encountered in primary care. It can also be one of the most challenging. Why is that? Diagnosing hypothyroidism There is no single blood test that is useful to diagnose or treat the majority of patients. In spite of what we were taught, TSH alone is not even close to being a 'gold standard.' Fools gold is more like it. A normal TSH only suggests that your pituitary thinks that things are 'normal.' Euthyroid Sick is the medical diagnosis for clinical hypothyroidism given a 'normal TSH level. Conversion of T-4 to T-3 is necessary for secreted thyroid (and orally ingested thyroid hormone, like levothyroxine, to become the active form of the hormone. Sixteen percent (16%) of the population has some difficulty making this conversion. One person in 6 is thereby metabolically challenged, consistent with a normal TSH. Presence of thyroid peroxidase antibody, anti-thyroglobulin or thyroid receptor antibody will also give you a 'normal' TSH with a very different clinical picture. Symptoms of hypothyroidism evaluation should include TPA and ATG titers, Cortisol levels, and gonadotropin (sex hormone) levels. There are many ways to become hypothyroid. Hypothyroidism is a medical condition where the thyroid gland doesn't produce enough thyroid hormones to meet the body's needs. It's typically treated with synthetic thyroid hormone medication, such as levothyroxine (Synthroid), to replace the missing hormones and restore normal thyroid function. This medication is usually effective and well-tolerated when prescribed and monitored by a healthcare professional. Levothyroxine is cheap, available and works MOST of the time. What if it does not help you? Natural Approach to Treating Hypothyroidism If you do not respond to the typical prescription of levothyroxine, you likely need something else. My preferred approach is to use a natural thyroid hormone preparation, containing T-4 as well as T-3, with T-2 and T-1, as well. It is what your body produces and it is likely what you need to regain your health. Complementary actions that may provide some clinical benefit However, some people may be interested in complementary or natural treatments to support their thyroid health alongside conventional medical treatment. I have found an interesting product available without a prescription. It contains the glandular thyroid hormone, but it is not assayed as a traditional prescription medicine. It could be used as an adjunct to or in addition to prescription thyroid medications in situations where a prescription for natural thyroid hormone is otherwise unavailable. It's essential to consult with a healthcare provider before making any changes to your treatment plan. Here are some natural approaches that may complement hypothyroidism treatment: Diet: Iodine: Ensure you have sufficient but not excessive iodine intake, as iodine is a crucial component of thyroid hormones. Common dietary sources of iodine include iodized salt, seaweed, fish, and dairy products. Iodine deficiency is very rare in the Western Diet. Ingestion of Iodine in excess of dietary needs can adversely affect the immune system, resulting in worsening of autoimmune issues. Selenium: Selenium is important for the conversion of T4 (inactive thyroid hormone) to T3 (active thyroid hormone). Good dietary sources of selenium include Brazil nuts, fish, and organ meats. Supplements are useful, but excessive selenium is toxic. Balanced diet: Maintain a well-balanced diet with a variety of nutrients to support overall health. Lifestyle changes: Stress management: Chronic stress can affect thyroid function, so stress-reduction techniques like meditation, yoga, or deep breathing exercises may be beneficial. Regular exercise: Engaging in regular physical activity can help improve metabolism and overall health. Herbal supplements: Some herbs may have potential benefits for thyroid health. Ashwagandha and guggul are examples of herbs that have been studied for their potential thyroid-supporting properties. However, the use of herbal supplements should be discussed with a healthcare provider, as they can interact with medications and may not be suitable for everyone. Gluten-free diet: Some individuals with hypothyroidism and autoimmune thyroid conditions like Hashimoto's thyroiditis may benefit from a gluten-free diet, as gluten may trigger inflammation in these cases. Consult with a healthcare provider before making dietary changes. Nutritional supplements useful in the natural approach to treating hypothyroidism: Some people with hypothyroidism may have deficiencies in certain vitamins and minerals, such as vitamin D and B12, magnesium, zinc and ot6hers. Your healthcare provider can assess your nutrient levels and recommend appropriate supplements if necessary. Often, a little attention to the nutritional deficiencies that can cause hypothyroidism will pay off in control, weight loss and improvement of your general physical condition. First and foremost, you must get adequate zinc and selenium into your supplement regimen. This product, 2 capsule twice daily, provides enough zinc and selenium to satisfy most clinical situations. Additionally, it contains other mineral micronutrients providing an excellent, rounded approach. Remember, too much zinc and too much selenium can be dangerous. Do not frivolously add more minerals on top of this. Too much of any good thing can rapidly become a bad thing. If you need a rounded multi-vitamin and mineral regimen, you can use MAGIC MINERALS in a reduced daily dosage of one capsule twice daily. A good choice, and great value is our DOWN to BASICS product, which is taken two capsules twice daily. (Add 1 magic mineral capsule to it, twice daily, and you have done it. Unless you are anemic or a heavily menstruating female, use the 'without iron' selection. Iron, ingested in amounts exceeding your metabolic needs can make you constipated. Both of these products are gluten and soy-free. Both of them are manufactured to the highest industry standards. Assayed to be within tight tolerances and free of heavy metals and toxins, the are remarkably inexpensive. They are stronger than most things you may have tried. Take them with meals, or your tummy might get a little upset. Limit goitrogenic foods: Goitrogens are compounds that can interfere with thyroid function. Common goitrogenic foods include cruciferous vegetables (e.g., broccoli, cabbage, kale) and soy. Cooking these foods can reduce their goitrogenic effects. Note Well: Avoid all soy-containing products, food and otherwise. It is best to avoid peanut, peanut butter and garbanzo beans. See my post on 'Death by Soy.' Remember that natural treatments should not replace prescribed thyroid hormone medication if you have hypothyroidism. These natural approaches are meant to complement conventional treatment and support overall thyroid health. Always consult with a healthcare professional to determine the most appropriate and safe approach for your specific condition. Regular monitoring of thyroid function is essential to adjust treatment as needed. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

Berberine, a natural alkaloid found in various plants like goldenseal and barberry, has been extensively studied for its diverse medicinal properties, showcasing potential benefits across several health domains. One prominent area of interest lies in its role in metabolic health. Berberine has demonstrated significant efficacy in managing diabetes and metabolic syndrome by improving insulin sensitivity, reducing blood sugar levels, and regulating lipid metabolism(1). These effects make it a valuable adjunct therapy for individuals with diabetes or those at risk of developing metabolic disorders. Moreover, berberine exhibits notable anti-inflammatory properties (2). This attribute extends its potential therapeutic applications to conditions characterized by chronic inflammation, such as arthritis and inflammatory bowel disease. By modulating inflammatory pathways, berberine offers a natural alternative for alleviating symptoms associated with these ailments, potentially complementing existing treatment strategies. Berberine's antimicrobial activity further enhances its medical utility (3). Research indicates its effectiveness against various pathogens, including bacteria, viruses, and fungi. This broad-spectrum antimicrobial action suggests berberine's potential in treating infectious diseases and underscores its role as a natural antimicrobial agent. In addition to its metabolic and anti-inflammatory properties, berberine has emerged as a promising cardioprotective agent (4) . Studies have shown that berberine can help lower blood pressure, reduce cholesterol levels, and inhibit plaque formation in arteries, thus reducing the risk of cardiovascular diseases such as hypertension and atherosclerosis. Berberine's neuroprotective effects have also garnered attention (5). Research suggests its potential in mitigating neurodegenerative disorders like Alzheimer's and Parkinson's diseases. Its ability to modulate neuronal function and protect against neurotoxicity makes it a compelling candidate for further investigation in the realm of neurological health. Furthermore, berberine has shown promise in cancer therapy (6). Preclinical studies have demonstrated its ability to inhibit cancer cell growth, induce apoptosis, and suppress tumor metastasis. While further clinical research is needed, berberine's multifaceted anti-cancer mechanisms present exciting prospects for its inclusion in cancer treatment regimens. Weight management and obesity treatment represent another area of interest for berberine research (7). Studies have indicated its potential to reduce body weight, visceral fat accumulation, and improve metabolic parameters in overweight and obese individuals. These findings suggest berberine's role in addressing the global challenge of obesity and its associated health complications. In summary, berberine exhibits a wide array of medical benefits, including its effects on metabolic health, inflammation, antimicrobial activity, cardiovascular health, neuro-protection, cancer therapy, and weight management. While much of the evidence supporting these benefits comes from preclinical studies, the accumulating research underscores berberine's potential as a versatile natural compound for promoting health and treating various diseases and conditions. Further clinical investigations are warranted to validate its efficacy, safety profile, and optimal therapeutic applications in clinical settings. Note Well: The preferred genus and specie to get the most alkaloid per gram, best effect and best value, is Berberis Vulgaris. The Aristata Specie is not nearly as effective, although it is easier to find in most preparations. The real value is to look for the Vulgaris Specie. Our typical regimen for Berberine: For Diabetes and/or insulin resistance syndrome, we start with 500 mg twice daily, taken with food. Check blood sugar levels and adjust the dosage by an additional 500 mg until the blood sugar drops to the desired range. Many patient experience loose bowel movements for the first few weeks, until the insulin and blood sugar levels equilibrate. Anticipate weight loss during this period to average 2-3 pounds per month, if you get the insulin below 10 and blood sugar below 90. References: Yin, J., Xing, H., & Li, D. (2008). Antidiabetic activities of aqueous extract from Berberis holstii and berberine in vivo and in vitro. Journal of Ethnopharmacology, 118(3), 479–484. Xu, D., Hu, M.-J., Wang, Y.-Q., & Cui, Y.-L. (2019). Antioxidant Activities of Quercetin and Its Complexes for Medicinal Application. Molecules, 24(6), 1123. Imenshahidi, M., & Hosseinzadeh, H. (2019). Berberis Vulgaris and Berberine: An Update Review. Phytotherapy Research, 33(3), 504–523. Kong, W., Wei, J., Abidi, P., Lin, M., Inaba, S., Li, C., Wang, Y., Wang, Z., Si, S., & Pan, H. (2004). Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. Nature Medicine, 10(12), 1344–1351. Ahmed, T., Gilani, A.-u.-H., & Abdollahi, M. (2015). Berberine and Neurodegeneration: A Review of Literature. Pharmacological Reports, 67(5), 970–979. Wang, N., Feng, Y., Zhu, M., Tsang, C.-M., Man, K., Tong, Y., & Tsao, S. W. (2019). Berberine Induces Autophagic Cell Death and Mitochondrial Apoptosis in Liver Cancer Cells: The Cellular Mechanism. Journal of Cellular Biochemistry, 120(4), 6616–6626. Zhang, H., Wei, J., Xue, R., Wu, J.-D., Zhao, W., Wang, Z.-Z., Wang, S.-K., Zhou, Z.-X., Song, D.-Q., Wang, Y.-M., & Pan, H.-N. (2018). Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. Metabolism, 59(2), 285–292. 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

Molds survive by creating chemicals called beta glucans. These protect the mold from being eaten by bacteria. These same chemicals can help protect us from infection, in exactly the same manner. Think about the history of Penicillin, a mold derivative. Beta-glucans are a type of polysaccharide found in the cell walls of certain fungi, yeast, bacteria, and grains like oats and barley. They have gained attention for their potential health benefits, including their ability to modulate the immune system and potentially help with infections. Here's how beta-glucans may be relevant to infection: Immune system modulation: Beta-glucans are known as immunomodulators. They can activate various immune cells, such as macrophages, neutrophils, and natural killer (NK) cells, which play essential roles in the body's defense against infections. By enhancing the activity of these immune cells, beta-glucans may help the body respond more effectively to pathogens. Beta Glucans derived from mold helps fight infections! Antimicrobial properties: Some studies suggest that beta-glucans may have direct antimicrobial effects against certain pathogens, including bacteria and fungi. They can inhibit the growth of these microorganisms, making it harder for them to cause infections. Best use of Beta Glucans may be in the treatment of viral upper respiratory tract infection, including the common cold and influenza. Remember, COVID is a 'common cold virus.' Respiratory infections: Beta-glucans have been studied in the context of respiratory infections, such as the common cold and influenza a. Some research suggests that beta-glucan supplementation may reduce the incidence and severity of respiratory infections, potentially by enhancing the immune response in the respiratory tract. Wound Healing may be improved with beta glucans derived from Mold! Wound healing: Beta-glucans may also have a role in wound healing by promoting tissue repair and reducing the risk of infection in wounds. It's important to note that while beta-glucans have shown promise in some studies, their effectiveness can vary depending on factors such as the specific source of the beta-glucans, the dosage, and the type of infection. Additionally, beta-glucans are typically considered as part of a broader approach to supporting immune health and infection prevention, rather than as a standalone treatment. If you are considering using beta-glucans to support your immune system or for infection prevention, it's often advisable to consult with a healthcare professional. They can provide guidance on the appropriate dosage, potential interactions with medications, and whether beta-glucans are a suitable option for your specific health needs. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246

What do you need when you injury your ankle or foot? What do you need if you are having or expecting to have surgery? Less pain during your recovery time. If you wait until you are being driven home from the hospital, sorting through how you are going to feed yourself, get the mail and function as an adult, you are going to find yourself in trouble. lf you anticipate the need, get this ahead of your scheduled surgery! Do not wait until the last minute to find the essentials that you need to survive. The surgeons may not be particularly helpful, here. The physical therapists, vocational rehabilitation specialists and family physicians may not be aware of what you need. The pillow above, is not the only way to keep your foot elevated, but it is extremely practical and cost-effective. Reduce swelling by elevation, protect the foot from blankets and sheet 'pulling your foot the wrong way.' For acute injury, this includes fracture and surgery, keeping the extremity elevated results in reduced swelling, and reduced pain. Reducing swelling reduces recovery time! Worth a try, available to be delivered to your door. David S. Klein, MD, FACA, FACPM 1917 Boothe Circle Longwood, Florida 32750 Tel: 407-679-3337 Fax: 407-678-7246