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  • January 21, 2020 12:07 PM | Rebecca Storms (Administrator)

    The Women's Health Initiative: The Last Word on Breast Cancer and Hormone Replacement Therapy?

    - By Steve Goldring, RPh

    If you’ve taken any of Worldlink Medical’s CME courses with Dr. Neal Rouzier, you’ve learned about the hornet’s nest of controversy over prescribing hormones to women in menopause that’s been stirred up over the past two decades. If you haven’t attended a Worldlink course, you’re probably familiar with the landmark 2002 study, The Women’s Health Initiative.

    That study had a major impact on the prescribing of hormones and, even more dramatically, on women’s willingness to take hormone replacement therapy. The WHI was stopped early, in 2002. Preliminary results were initially announced through press release and press conferences, rather than through articles in peer-reviewed scientific journals.

    The most alarming statistic to come from the WHI was the contention that women taking HRT had a 26% increased risk of breast cancer over women who weren’t on hormones. Headlines in the lay media took hold of that terrifying number and ran with it, creating mistrust and fear in women (and healthcare providers) that has reverberated since.1

    There it was . . . the last word on HRT. 

    Hormones cause breast cancer!

    Careful evaluation of the WHI leads thoughtful practitioners to question this statement, which has become conventional wisdom in the past couple of decades. The reality is much less frightening, if equally dramatic. 

    The conclusions of the WHI are completely wrong. 

    The data in the WHI does not show HRT to increase risks for invasive breast cancer.

    We need to understand several key points regarding the WHI in order to untangle the truth from what the primary investigators have reported.

    • First, the patients chosen for the study were not the same as the patients most likely to be prescribed hormone replacement therapy.
    • Second, many of these patients exhibited signs and symptoms of some of the diseases the study concluded were caused by hormones, even before the study began.
    • Third, the study used the “Gold Standard” of hormone replacement therapy at the time. This combination of hormones has been repeatedly shown by subsequent studies to be inferior to other hormone combinations in both effectiveness at relieving symptoms and in safety.
    • Fourth, and most importantly, the risks for disease that were purportedly due to HRT were wildly overstated and, with few exceptions, not statistically significant.

    Patients Treated In The WHI

    Let’s take a look at the patient population in the WHI.

    The women recruited to complete the study were, on average, 63 years old. That’s about 12 years past the average age of menopause, 51. That means that very few of these patients were experiencing the symptoms that HRT would be prescribed for in the first place. The researchers specifically excluded patients who had moderate to severe hot flashes, on the grounds that these patients would easily see through double blinding and guess whether they were on the hormone treatment or placebo.

    Because these patients were significantly older than women entering menopause, they also had multiple health issues that are associated with advancing age. About 35% of them were overweight. 34% were obese. 36% were hypertensive. Nearly 50% reported a history of smoking.2 The health status and age of the patients may have contributed to any untoward effects of the treatment provided in the study.

    Hormones Used In The WHI

    The specific hormones used in the Women’s Health Initiative were widely accepted as the standard of care at the time of the study. 

    The estrogen used in the WHI was conjugated equine estrogens. This estrogen combination was used in menopausal women since it was developed in the early 1940s by Wyeth-Ayerst. The specific estrogens in conjugated equine estrogens are somewhat of a mystery. Wyeth (now Pfizer) has been able to keep the exact composition a ‘trade secret” for decades. The pharma giant successfully blocked a “citizen’s petition” to the FDA to clarify its ingredients in 1996.3,4. There are at least 10 distinct conjugated estrogens in the horse urine preparation.5. Several of these estrogens are not found in human females and their safety and efficacy as individual drugs has never been studied. It’s obvious that a mixture of hormones derived from horse urine would likely be contaminated with an untold number of by-products, hormones and kidney-metabolized waste.

    Wyeth also supplied the progestin given to these patients, medroxyprogesterone, a synthetic version of progesterone chosen for its potency. Medroxyprogesterone is chemically similar to progesterone except that it has an alpha-hydroxy group at position 17 and a methyl group at position 6.6 These slight chemical changes make medroxyprogesterone 10 to 20 times more potent than progesterone and have the potential to completely change its safety profile. Medroxyprogesterone has been used since the 1960s to counteract the endometrial hyperplasia caused by uterine exposure to estrogens.

    In the past all estrogens were widely considered to have the same risks and benefits. All progestins were similarly considered equivalent. The evidence accumulated after nearly 2 decades since the study points to major differences between specific hormones, both in safety and effectiveness.7,8,9,10,11,12

    Statistical Significance of Breast Cancer Risk Increase From HRT

    A single sentence, or more precisely, a single word, from the Women’s Health Initiative findings telegraphs what’s wrong with the study.

    The 26% increase (38 vs 30 per 10 000 person-years) observed in the estrogen plus progestin group almost reached nominal statistical significance and, as noted herein, the weighted test statistic used for monitoring was highly significant.13(emphasis added)

    This sentence clearly states that the “26% increase” in breast cancer incidence seen in the WHI did not reach statistical significance. It almost did.

    Study investigators chose to emphasize relative risk in their conclusions, highlighting a “26% increase” in risk that appears to be dramatic and frightening. The reality is that relative risk is just that, relative. The absolute risk is also found in the same sentence. “(38 vs. 30 per 10,000 person-years) . . .” The absolute risk of breast cancer was increased in the estrogen+progestin group by 8 breast cancer cases out of 10,000 women. That’s an absolute increase of 0.08%, much less dramatic sounding than the 26% emphasized in the study conclusions.

    Again, this 26% increase in relative risk was not statistically significant. That means there is no valid statistical argument from this study that conjugated equine estrogen plus medroxyprogesterone increases the risk for breast cancer and any increase would have to be considered coincidental. The investigators also concluded that there was an absolute decrease in breast cancer incidence in women taking only conjugated equine estrogens. Multiple evaluations of the WHI data since the original publication have confirmed the weakness of the association between HRT and breast cancer risk.

    This post is not intended as a comprehensive review of every aspect of the Women’s Health Initiative study. Many qualified scientists have rightly criticized the study and the outrageous conclusions drawn by investigators.14 Others have taken these conclusions at face value, disseminating a message that hormone replacement is something to fear. That message has had devastating results on millions of women denied safe, effective treatment for life-changing menopause symptoms over the past two decades.15,16

    If you’d like to understand more about the nuanced interpretation of The Women’s Health Initiative, you have two great options:

    First, register for Worldlink Medical’s Part I Hormone Optimization course. In that AMA accredited CME course, Dr. Neal Rouzier goes into much greater detail about the WHI and the conclusions reached by researchers. You’ll discover the controversies and the political intrigue that has cast a shadow over hormone replacement for the past two decades. You’ll also discover the benefits of hormone optimization in reducing long-term health risks, including breast cancer, as proven by hundreds of valid studies showing actual statistical significance.

    If you’ve already taken Worldlink’s Part I course, you’re eligible to become a member of the Worldlink community. Membership offers several benefits for providers who are making a difference by optimizing their patients’ hormones. A key benefit of Worldlink Level 1 and Level 2 Membership is Journal Club, where a panel of Worldlink trained practitioners evaluate relevant studies in detail, including a riveting session reviewing the Women’s Health Initiative.


    1. Haas JS, Geller B, Miglioretti DL, et al. Changes in newspaper coverage about hormone therapy with the release of new medical evidence. J Gen Intern Med. 2006;21(4):304–309. doi:10.1111/j.1525-1497.2006.00342.x

    2. Langer RD, White E, Lewis CE, Kotchen JM, Hendrix SL, Trevisan M. The Women’s Health Initiative Observational Study: BaselineCharacteristics of Participants and Reliability of Baseline Measures. Ann Epidemiol 2003;13:S107–S121.

    3. Department of Health and Human Services Office of Inspector General -- AUDIT "Review of the Food and Drug Administration's Handling of Issues Related to Conjugated Estrogens," (A-15-96-50002) May 16, 1997

    4. Federal Register / Vol. 61, No. 217 / Thursday, November 7, 1996 / Notices

    5. Bhavnani BR. Pharmacokinetics and pharmacodynamics of conjugated equine estrogens: chemistry and metabolism. Proc Soc Exp Biol Med. 1998;217(1):6–16. doi:10.3181/00379727-217-44199

    6. Compound summary: Medroxyprogesterone | C22H32O3 PubChem

    7. Fournier A, Berrino F, Clavel-Chapelon F. Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study [published correction appears in Breast Cancer Res Treat. 2008 Jan;107(2):307-8]. Breast Cancer Res Treat. 2008;107(1):103–111. doi:10.1007/s10549-007-9523-x

    8. Regidor PA. Progesterone in Peri- and Postmenopause: A Review. Geburtshilfe Frauenheilkd. 2014;74(11):995–1002. doi:10.1055/s-0034-1383297

    9. Asi N, Mohammed K, Haydour Q, et al. Progesterone vs. synthetic progestins and the risk of breast cancer: a systematic review and meta-analysis. Syst Rev. 2016;5(1):121. Published 2016 Jul 26. doi:10.1186/s13643-016-0294-5

    10. Mirkin S, Amadioa JM, Bernicka BA, Pickarb JH, Archer DF 17-Estradiol and natural progesterone for menopausal hormonetherapy: REPLENISH phase 3 study design of a combination capsuleand evidence review Maturitas S0378-5122(15) 00314-X/dx.doi.org/10.1016 j.maturitas.2015.02.266

    11. Miller VM, Naftolin F, Asthana S, et al. The Kronos Early Estrogen Prevention Study (KEEPS): what have we learned?. Menopause. 2019;26(9):1071–1084. doi:10.1097/GME.0000000000001326

    12. Palacios S, Mejía A. Progestogen safety and tolerance in hormonal replacement therapy. Expert Opin Drug Saf. 2016;15(11):1515–1525. doi:10.1080/14740338.2016.1223041

    13. Writing Group for the Women's Health Initiative Investigators. Risks and Benefits of Estrogen Plus Progestin in Healthy Postmenopausal Women: Principal Results From the Women's Health Initiative Randomized Controlled Trial. JAMA. 2002;288(3):321–333. doi:10.1001/jama.288.3.321

    14. Critiques of The Women’s Health Initiative PubMed Bibliography

    15. Millions of women are missing out on hormone replacement therapy The Economist December 12,2019

    16. Sarrel PM, Njike VY, Vinante V, Katz DL. The mortality toll of estrogen avoidance: an analysis of excess deaths among hysterectomized women aged 50 to 59 years. Am J Public Health. 2013;103(9):1583–1588. doi:10.2105/AJPH.2013.301295

  • December 20, 2019 3:11 PM | Rebecca Storms (Administrator)

    how hormone therapy is changing lives

    BHRT and Chronic Illness

    Have you experienced the frustration of a patient who never seems to get better? You’ve diagnosed her with insulin resistance or even full-blown Type II Diabetes. You’ve counseled her on changing her diet. You’ve prescribed metformin to reduce glucose production in the liver. But on her next visit, her fasting blood glucose hasn’t changed or is even a bit higher. Her hemoglobin A1C isn’t budging. She lost a couple of pounds early on, but gained it back after a few weeks.

    You’ve asked her how she’s doing with changing the way she eats and she says, “I’m trying."

    Worst of all, your patient is clearly feeling discouraged. She’s ready to give up. "What’s the use?”

    If you’ve ever experienced this scenario, you’re not alone. This frustration comes up all the time in our discussions with providers at Worldlink Medical CME events.

    Putting A Band-Aid On Chronic Disease

    Nurse practitioner Beth York, from Nashville, TN, expressed her ongoing disappointment about her patients that never made any progress. She began to feel as though she was putting a Band-Aid on serious health issues, rather than truly moving patients toward health. She knew how to diagnose things like Type II Diabetes, but prescribing a medication and talking with the patient about lifestyle changes didn’t seem to be quite enough.

    Not Making A Difference

    Nurse practitioner Karl Lambert, from Wenatchee, WA, had been seeing 20 to 30 patients a day. He wrestled with the feeling that he wasn’t making any difference in their lives. This suspicion was confirmed when he’d see them again, 6 months to a year after, and nothing had changed. Same symptoms, same lab results.

    Here’s the Good News!

    You can make a difference.

    It’s possible to start seeing patients improve their health, even patients with chronic diseases like diabetes and obesity that don’t seem to respond well to traditional treatments.

    Providers who have trained with Dr. Neal Rouzier of Worldlink Medical have discovered a new paradigm in medical practice. 

    They’ve gone beyond the diagnosis of disease they’d been taught in medical school. They’ve started recognizing the impact that sub-optimal hormone levels can have on long-term health. These providers are looking at estradiol, progesterone, testosterone, thyroid hormones (T3 and T4, as well as TSH), DHEA, pregnenolone, melatonin, cortisol, and others.

    They’ve discovered that getting these hormones back to “optimum” levels has a profound impact on whether patients make progress toward their health goals.

    They’re also helping patients understand the benefits of diet and lifestyle changes that are much more effective when hormones have been optimized.

    These practitioners are helping patients see the big picture of wellness and helping them feel better, lose weight, regain energy, and experience a fulfilling life.

    Patient’s Body Fat Drops From 46% to 15% in 9 Months

    New Jersey physician, Johanan Rand, MD describes his experience with a morbidly obese male patient. Presenting with chronic pain issues, the patient was objectively measured at 323 pounds and 46% body fat on Dr. Rand’s body composition machine. After optimizing the patient’s hormones, based on protocols taught at Worldlink Medical courses, and providing patient education, lifestyle management, and nutritional supplements, Dr. Rand saw the patient’s body composition dramatically improve, down to 15% after only 9 months.

    Reducing Or Eliminating Medications

    Nurse Practitioner Teresa Mealy, from Springfield, MO, has experienced the power of looking at the big picture in patients struggling with diabetes, rather than simply looking at the disease process alone. In her practice, she optimizes all the patient’s hormones, deals with lifestyle issues, diet, exercise, nutritional support, and stress. She has several examples of patients who had been diagnosed with Type II Diabetes. Some of them have been able to eliminate or at least reduce the number of medications they were on after being on her holistic program for a time.

    You’ll Never Want To Go Back

    Karl Lambert would never want to go back to the “Sickness Model” of treating patients. The results he’s seeing have revitalized his passion for medicine. He’s even looking to approach companies with a proposal to help them with diabetic patients by getting them healthier. 

    Helping diabetics reverse their diabetes is something no one dreams of . . . until they find out it’s really possible.

    If you’d like to learn more about the tools of hormone optimization these providers have used to make a difference for their patients, Worldlink Medical’s Part I Hormone Optimization course is the best place to start. Click here to register for the next session of this life-changing, accredited CME course.

    Evidence Supporting Improved Outcomes With Optimal Hormones

    1. Fifty‐two Week Treatment With Diet and Exercise Plus Transdermal Testosterone Reverses the Metabolic Syndrome and Improves Glycemic Control in Men With Newly Diagnosed Type 2 Diabetes and Subnormal Plasma Testosterone

    2. Low-Dose Transdermal Testosterone Therapy Improves Angina Threshold in Men With Chronic Stable Angina

    3. Transdermal Testosterone Treatment in Women with Impaired Sexual Function after Oophorectomy

    4. Efficacy and safety of transdermal testosterone in postmenopausal women with hypoactive sexual desire disorder: a systematic review and meta-analysis

    5. Bayesian Meta-analysis of Hormone Therapy and Mortality in Younger Postmenopausal Women

    6. Effects of Hormone Therapy on Oxidative Stress in Postmenopausal Women with Metabolic Syndrome

    7. Transdermal 17-β-Estradiol and Risk of Developing Type 2 Diabetes in a Population of Healthy, Nonobese Postmenopausal Women

    8. Lower risk of cardiovascular events in postmenopausal women taking oral estradiol compared with oral conjugated equine estrogens

    9. Effects of micronized progesterone added to non-oral estradiol on lipids and cardiovascular risk factors in early postmenopause: a clinical trial

    10. Influence of testosterone replacement therapy on metabolic disorders in male patients with type 2 diabetes mellitus and androgen deficiency

    11. The effect of different doses of micronized 17beta-estradiol on C-reactive protein, interleukin-6, and lipids in older women

    12. Testosterone and depression: a systematic review and meta-analysis

    13. The dark side of testosterone deficiency: I. Metabolic Syndrome and Erectile Dysfunction
    14. The dark side of testosterone deficiency: II. Type 2 Diabetes and Insulin Resistance
    15. The dark side of testosterone deficiency: III. Cardiovascular Disease
    16. Long‐Term Testosterone Treatment in Elderly Men with Hypogonadism and Erectile Dysfunction Reduces Obesity Parameters and Improves Metabolic Syndrome and Health‐Related Quality of Life

  • August 24, 2019 2:56 PM | Rebecca Storms (Administrator)

    A recent paper claimed that nonalcoholic fatty liver disease is an unrecognized epidemic. There is no FDA approved drug for treating and reversing NAFLD, however, sustained weight loss can reduce the risk of cardiovascular events and diabetes. Unfortunately, the article did not address how to be successful with weight loss. Weight loss attempts have obviously been unsuccessful if NAFLD is now epidemic. “Both NAFLD and CAD represent end-organ manifestations of the same systemic metabolic insult, all related to insulin resistance.” What the authors did not address is that the cause of the insulin resistance is hyperinsulinemia, and not the other way around. (Thank you, Jason Fung, for introducing this concept). In my last newsletter I described the lack of success and the increase in harm we have recently encountered with commonly prescribed diabetic medicines. Not only are we not making a dent in CVD prevention, but we now see an epidemic of NAFLD as over 70% of diabetics have NAFLD, which apparently is not being controlled by standard diabetes treatments. And I wouldn’t expect it to as I now have an understanding that diabetic meds don’t get rid of serum glucose, rather they drive the glucose into another compartment: the cell.  I believe that this increase in NAFLD is due to our inability to understand the mechanism of current medicines which increase production of, or function of, insulin that drives glucose into the cells.  Overloading the cell with glucose is not the solution. Rather, preventing intake of glucose by diet, maintaining a fasting state to provide ketosis to reduce visceral and intra-organ fat, preventing storage of glucose into glycogen and fat, increasing metabolism of fat, and increasing excretion of glucose, as opposed to sweeping it under the carpet or into the cell, is the solution. And the basic underlying problem is hyperalimentation of glucose and sugars that result in hyperinsulinemia when the cell cannot handle the increased glucose load caused by the hyperalimentation.

    Professor Samuel Klein states that 2 million people have cirrhosis caused by NAFLD.  However, the main cause of death is not liver failure but is CVD and the incidence of CVD continues to increase despite multiple drugs used to prevent DM and CVD. It’s the hyperinsulinemia that increases fat deposition in the liver and adipose tissue. Weight loss reduces visceral and liver fat, but this is difficult to implement. Well, not if you know how to do it. Jason Fung and his staff will take us through the educational process to understand how to be successful in treating ourselves and our patients. Nevertheless, not everyone can be successful as our hypothalamic set point fights us by slowing down our metabolism to maintain a set weight and body mass index, which can be difficult to overcome.  I too will demonstrate my success with patients in helping them maintain optimal metabolism, which maintains weight loss.  I will also provide all the literature support and studies demonstrating safety and efficacy of optimizing hormones, but probably different to what others are accustomed to doing. I will also provide all the studies that practitioners should be familiar with when optimizing HRT. Our focus should be on prevention, treatment, and reversal of disease which has not occurred in the majority of trials for CVD prevention using conventional medications.

    The following are excerpts from recent papers from JAMA and NEJM:

    “However, a resurgence of diabetes complications has appeared in national statistics and in the epidemiology literature. An increase in diabetes-related amputations has occurred nationally. Updated national statistics indicate that the recent increase in complication rates is occurring in middle-aged adults, among whom the risk of hyperglycemic crisis, AMI, CVA, and amputations each increased by more than 25%.” We obviously are not doing something right. “Most counties in the U.S. have seen an increase in cardiovascular disease mortality among adults.” Hmmm, just what is it that we are doing wrong that’s not working? Rather, what should we be adding that we are not? Perhaps not giving drugs that drive glucose into the cell should be a start. Other than type I diabetes, I know of no other disease entity in which there is a deficiency of glucose entering the cell.  If the cell is storing glucose as fat, triglycerides, and glycogen, then the cell is already overloaded and getting plenty of glucose on its own. If the liver, kidney, pancreas, and visceral organs are all storing excess glucose as fat, then there is plenty of glucose getting into the cells. Enter diet, exercise and life-style change. Secondly, we should be disposing of the glucose by every other means possible and keep it out of the cell. Next we should be preventing the glucose from getting into the cell by metabolizing it in muscle and liver. Enter hormones. Next we should be providing less glucose into the body in the first place.  Enter Jason Fung. (I’m currently fasting as I write this, and it really is easy.).  Lastly, we should be disposing of and excreting the glucose that enters the body.  Enter the new diabetic drugs. Perhaps we should be preventing this metabolic insult instead of just treating the disease by pushing serum glucose into the cells. That has been Dana’s goal for 20 years-establishing a medical academy that focuses on health and wellness, and promotion of that concept to physicians. This next Hormones and Beyond Cardio-Metabolic Symposium brings all this to fruition. Other medical academies attempt to reach this goal but have failed. And that’s why I am so excited about the upcoming Hormones and Beyond Symposium. 

    “This means that the future direction of diabetes complications has enormous collective implications for health and costs.” (JAMA 2019;321(19):1867-68). Yes, but why do studies show that CVD and outcomes are getting worse? And why is it that spending billions of dollars on health care and medications do not result in less CVD?  Here’s why as explained in JAMA.

    “Optimal diabetes care is predicated on balancing the immediate and long-term sequelae of the disease and its therapies and improving patient health and well-being. Professional societies have focused on HgBA1C levels to gauge the quality of diabetes care. The preferential use of HgBA1C levels in research, policy, and practice stems from the demonstrated association between lower HgBA1C levels and disease endpoints. (Observation does not prove causation and a correlate does not a surrogate make).  However, these studies did not demonstrate improvements in outcomes that are most meaningful to patients such as CVD, stroke, and mortality. Thus, HgBA1C level is a surrogate marker for a proxy of uncontrolled disease. (Remember, just because high levels portend harm does not mean that lowering HgBA1C fixes the problem. And that depends on how one lowers the HgBA1C by either driving glucose into the cell ((bad)) or metabolizing it ((good))).”

     “Similarly, for clinicians, HgBA1C level is an effective monitoring tool that is responsive to real-time changes in blood sugar control. Nevertheless, even though HgBA1C level is a valuable forewarning of future events in patients with diabetes and has an important role in reflecting the patient’s average level of glycemia, it (HgBA1C) should not be the outcome that matters most or that is prioritized at the expense of meaningful outcomes that are important to patients (and us).”

    “Fallacy of the Surrogate: The rationale for using HgBA1C level as a surrogate marker for diabetes outcomes is predicated on the assumption of its direct correlation with improved outcomes that patients and doctors value like MI, CVA, and quality of life. Yet, the strength of this relationship has been called into question as the outcomes can be worse (even though the HgBA1C is lower). Meta-analyses revealed a null association between intensive glycemic control and these cardiovascular outcomes.”

    “However, the importance of glycemic control for patients with type II diabetes cannot be extrapolated from data developed among patients with type 1 diabetes.  The glucose-centric model of type 1 diabetes cannot be transferrable to the management of type II diabetes.” (In type I DM there is a deficiency of insulin and intracellular glucose whereas in type II there is excess insulin and intracellular glucose). Moreover, HgBA1C level may be misleading and its singular prioritization could lead to patient harm.” Yikes!

    “The new GLP-1 RA and SGLT-2 inhibitors were demonstrated to reduce major macrovascular events and death independent of glycemic control.” (In other words, these new meds can lower CVD disease by other mechanisms other than lowering serum glucose). Then, what parameters and outcomes should we measure and follow? “Consideration should be given to reverse the routine use of surrogate markers like HgBA1C and instead refocus on the following outcomes that are important: CVD. Encouraging clinicians to embrace patient centered care unencumbered by the constraints of the HgBA1C level could allow them to instead focus on the outcomes like CVD. To improve the quality of value of diabetes care, it will be necessary for patients and all those involved in their care to focus on what truly matters-that which improves their lives and outcomes, and not their laboratory numbers.” (JAMA 2019;321(9):1865-67). Bingo!

    I hope that the foregoing was as enlightening for you as it was for us. I’ve stopped chasing HgBA1C levels and the fruitless administration of expensive diabetic meds that lower HgBA1C but not disease outcomes. I now focus on lowering HgBA1C levels by other means. Instead I chase waist circumference, visceral fat, body weight and BMI, vascular responses, lipid levels, plaque scores, quality of life, and patient satisfaction. That’s what Hormones and Beyond is all about. Hope to see you in Austin.

    Click Here To Access Articles Referenced

  • August 14, 2019 6:21 PM | Rebecca Storms (Administrator)

    Dear Colleagues:

    The timing was perfect as it could not have happened at a more opportune time. Two articles in JAMA made claim to the fact that our treatment of diabetic patients with typical diabetic medicines increases the risk of MI and CVD. What? I thought that we needed tighter BS control to lower the risk of CVD and diabetic vascular disease? Later, the NEJM published a study that tight BS control did not improve CVD outcomes and even showed an increase in CVD events. What, how can that be?  Is everything that I/we have been teaching, preaching and doing for the last 30 years incorrect? Now, after reading Jason Fung’s book I understand why that is. It is true that the higher the HgBA1C level, the worse the prognosis and the sooner one dies from the foregoing diseases. However, just because high levels of HgBA1C are associated with increased morbidity and mortality, that does not mean that lowering the HgBA1C results in less disease, or that lowering the blood sugar is of benefit. It makes sense to lower BS and gain tighter control and lower HgBA1C levels if high levels increase the risk of disease, but the outcomes prove otherwise. Why? Maybe because what we have been doing, and falsely misled to believe, is wrong. Lowering blood glucose is correct and appropriate, however, how we lower it is the key to understanding why using one method improves but the other worsens outcomes.

    A recent TV ad for a GLP-1 analog claimed that there was no increase in MI or CVD events with this medication; their selling point was that there was no increased risk of MI? Yay, yippee, finally a drug that does not increase heart attacks! Wait. What? Why are we giving drugs to lower BS that in turn increase heart attacks, cause significant weight gain, and increase morbidity and mortality?  I thought that lowering BS was good. For years I kept increasing diabetes meds, trying to maintain tighter BS control. But the patients all gained weight and their disease got worse.  So, I added more meds and started long-acting insulin and they gained even more weight. I once bet a patient that if he lost 20 pounds I would give him $10,000. He failed.  Then I went double or nothing. Not only did he fail but he gained weight. I blamed him but little did I know and realize that it was my fault and not his. This was before I read Jason Fung’s book The Diabetes Code and learned how and why DM meds made CV disease worse. My heart sank.

    A recent video on Medscape made reference to the fact that “Cardio-Metabolic Disease” should be made a new specialty.  Based on all the GLP-1 analogs and sodium-glucose cotransporter 2 inhibitors reducing weight, disease, and MI risks, the specialty is definitely changing and gaining momentum.  So why are these new drugs any different? Although these meds work by various mechanisms to lower BS, lower HgBA1C levels, and improve CVD outcomes, the main importance is that they lower BS by different mechanisms other than increasing beta cell function, insulin levels, and driving glucose into the cell. These new wonder drugs decrease appetite, slow down glucose absorption, decrease gluconeogenesis, and increase glycosuria through the kidneys. The most important take away is the ability to decrease BS by different mechanisms other than driving glucose into the cell which all past drugs did, particularly insulin. By cramming all the excess glucose into the cell, the cell becomes overloaded with glucose which the cell must dispose of by storing it as fat and glycogen or converting it into triglycerides. Hence, the onset of fatty liver, fatty pancreas, fatty kidneys, dyslipidemia, NAFLD and NASH. I blamed all my patients for their weight gain and disease progression.  And I blamed myself for not being more vigilant in maintaining tighter BS control. I had no clue.  Mea culpa, mea culpa, mea maxima culpa.

    In June, Reaven published in the NEJM that intensive glucose control in type 2 DM patients proved just as likely to cause a MI as standard therapy. Patients also gained weight and had worse disease outcomes. Perfect. There was no better outcome in MI, CVA, CHF, CVD, death, DM complications, or QOL scores. Even after 15 years of tight control, no benefit. So, what was their suggestion to improving outcomes? The researchers recommend treating DM even sooner and much more aggressively, as though 15 years of tight BS control was not enough? (Einstein said insanity is doing the same thing over and over again but expecting different results!) Professor Simmons stated that the data from the VADT study was consistent with findings from other studies. She finally admits that perhaps we should decrease medications if the risks outweigh the benefits. The authors do note that these results are before the GLP-1 receptor agonists and SGLT2 inhibitors were available. However, their treatment suggestion was to use more and more drugs that consistently do not work.  Hmmm. Those thousands of researchers need to read and grasp Jason’s book in order to see why they, and their patients, fail.

    In the REWIND study, dulaglutide reduced MI risk by 12%. That’s relative risk and not absolute risk which was much smaller. (The RR was 12% but the absolute risk (AR) was only 1.4%, with 3.4% MI in control group and 2.0% in treatment group=1.4% AR).  It was the first major study that proved superiority over standard care, which has been consistently harmful. (An absolute risk reduction of 1.4% is quite underwhelming, but the researchers jumped for joy). So, there is less harm with the new drugs than in comparison to standard therapy (which increased risk), but what about with control groups? “In assessing the individual components of the composite outcome, Gerstein noted that there was no discernable effect observed for nonfatal MI with dulaglutide and a neutral effect observed for CV death.” You mean, no benefit? That is correct, no benefit. No benefit after spending millions of dollars on drugs and they do not work to reduce CVD? Hmmm. Their conclusion was that dulaglutide “could be considered for the management of glycemic control.” Could be? Why didn’t they state, “should be or must be?” Because the results were underwhelming and the cost $900/month!

    There are better, safer, tried and true solutions to the above. That is what Part V Hormones and Beyond is all about. Jason Fung will review his secrets and insight for success. I will review all the medical literature demonstrating what we should be doing as well as what we should not be doing. Hope to see you in October.

  • August 06, 2019 3:30 PM | Christiaan Killian (Administrator)

    Dear Colleagues,

    You will find a new level of confidence as you move from the basics of Part I to the advanced protocols in Part II. The Part II course provides the experienced practitioner with training that is essential for mastering more complex cases. The course will serve as a short refresher, but will highlight new important therapies, clinical pearls, tricks of the trade, controversies and everything that I could not cram into Part I that you still need to know. The field of age management medicine continues to grow at a rapid rate, and we only seem to get busier, making it difficult to stay abreast of all the changes. This is why we’ve condensed an inordinate amount of material into 2 ½ days—in fact, there are over 1,300 slides of information (Yikes! I’ll talk fast).

    My favorite part of this course are the informal discussions and Q&A sessions at the end of the day where we discuss anything that you want to discuss. This is one of the most interactive ways that new attendees expand their clinical knowledge by learning and sharing experiences, audience discussions, difficult cases, controversies, legal issues, suggestions, medical board issues, trials and tribulations from other seasoned attendees. I’ve yet to find anywhere else where can one go to participate in such a gathering and meeting of HRT practitioners that share their successes and challenges. This discussion is a wonderful prelude to the topics covered throughout the remainder of the weekend:

    Section A
    Antiaging, definitions of, and why we call it that. This is a review of the medical literature articles that shows us why we refer to BHRT as antiaging and provides credence for why we do what we do.

    Section B
    Longevity medicine and which hormones have a proven record of extending health, wellness, and longevity. Yes, optimization of HRT does extend life.


    Section 1 – Review and Critique of the WHI and HERS Study
    Making sense out of the many HRT studies, the critiques, and the rebuttals. Putting the pieces together will make you an expert on all the ifs, ands, and buts. It is the knowledge and command of this scientific literature (that your colleagues will never know) that makes you the expert.

    Section 2 – Bioidentical HRT: A Critical Literature Review
    The positive and negative articles on BHRT. Laying to rest estriol as the worthless metabolite it is. What the literature shows we should use and shouldn’t use, and disproving what many others are teaching without any basis.

    Section 3 -  Hormones and Cancer Protective or Causative
    “There are no studies that prove BHRT is different than synthetic HRT.” Baloney! Many studies contrast the BHRT with SHRT.  Know when it’s safe to prescribe and when

    Section 4 – Important Articles on HRT, Don’t Ignore the Literature
    A literature review proving that HGH, testosterone, estrogen, progesterone, DHEA, and melatonin protect against cancer. 

    Section 5 – Progesterone Optimization
    This section is “R” rated for language and me acting out: Optimization of progesterone and case examples, multiple studies that prove transdermal cream is worthless and harmful, and saliva testing for monitoring therapy is fraught with error. Scientific studies prove where your levels should be for maximum protection, and where they should not be if one wants to protect against cancer. Case studies with labs show the good and bad.

    Section 6 – Testosterone, New and Different Administration
    New and different methods for raising testosterone in men and women besides creams: Oral, SQ, IM, HCG, Clomid, which are the cheapest and which are the best.

    Section 7 – Oral vs Transdermal Estrogen
    Oral vs. transdermal estrogen, relative risks for both, safest vs. most beneficial. Which, when, why and how the ESTHER study guides us.

    Section 8 – Thyroid and CVD vs Osteoporosis
    A literature update of thyroid for cardiovascular protection and osteoporosis protection. So you think you know thyroid? More literature backing for why we do what we do.

    Section 9 – Cardiovascular Disease Prevention

    Cardiovascular disease protection, cardiac markers, eicosinoids, diet, EFA’s, insulin, inflammation.

    Sections 10 – Cardiology Case Management
    Cardiovascular disease protection, cardiac markers, eicosinoids, diet, EFA’s, insulin, inflammation. 

    Section 11 – Complex cases with Lab Review
    Cardiovascular case studies with management beyond statins.

    Section 12 – More Literature Review for HRT
    Diagnosis and treatment of the most common premenopausal endocrinopathy that everyone fails (misses) to diagnosis, and it’s relation to CAD, breast CA, and uterine CA.

    Section 13 – Question with Answers

    Section 14 – PCOS

    Polycystic Ovary Syndrome is the most common endocrine disorder in premenopausal women.  It’s more common than you think, learn to recognize and treat this condition

    Section 15 – Osteoporosis and Estrogen Metabolites

    Treatment of osteoporosis beyond biphosphonates: E2, D3, Vit K, strontium, & ipraflavone. Measuring and monitoring NTX & CTX. Estrogen metabolites- do they or do they not predict breast cancer and should we waste money on testing? 2OH-E1 vs. 16αOH-E1?

    Section 16 – Estrogen and Progesterone in Men
    Importance of optimization of estrogen in men too and the harm of suppression. The harm of giving progesterone to men that increases inflammatory cytokines and ED (what are they thinking)?

    Section 17 – Chronic Fatigue Syndrome and Cortisol
    Cortisol for fatigue and CFS, how and when to use it, how to monitor it, and test it with ACTH.

    Section 18 - References
    Complex cases, labs, adjustments, fun and interesting cases, and lots of WWND (What Would Neal Do?)

    Thanks everyone hope to see many of you in Indianapolis!

    – Neal

  • July 03, 2018 10:54 AM | Christiaan Killian (Administrator)

    Dear Colleagues,

    It is now time to start to prepare the lectures for Part V, which I start organizing a year in advance.  It is also time for everyone to block out October 5-7 on their calendar, so you can attend this year’s WLM symposium. My interest/focus this year will be the brain, breasts, prostate, and mitochondria. And I’m pleased to announce this conference as our 20-year anniversary event.  Dana has worked long and hard to make this reunion special. And so have I by organizing a review of the most recent profound literature that we should all be aware of. It is my annual update of literature that I can’t cram into the courses but that we should have command of to better treat our patients.

    During my toxicology fellowship we were taught that the best treatment for a poisoning was to prevent the poisoning in the first place.  The same concept applies to dementia and Alzheimer’s disease. After 30 years of failure by the pharmaceutical industry to develop a cure for Alzheimer’s disease, we still have no treatment after billions of dollars in research.  However, the best treatment still is to prevent the disease in the first place.  There is an amazing plethora of data proving loss of hormones is culpable and replacement is protective.  Our ignorance is embarrassing when it comes the research showing benefit.  “Yea but…the WHI showed…” I hope that I can cram all the articles that I want to show you into 3 hours of lecture demonstrating many different hormones affect the brain.  UCLA is one of the outstanding universities that has a special section devoted to treating dementia, with Dr. Bredesen heading that endeavor.  Unfortunately, he will not be presenting but Dr. Sharlin will review UCLA’s protocols as well as functional medicine treatments that have been shown to provide reversal of cognitive decline and improvement in symptoms.  SPECT scans demonstrate plaque reversal with BHRT but not so with SHRT.  It’s impressive. Patients can now go to you for treatment/prevention without having to travel to UCLA.

    As you know I used to run at the front of the pack.  In the last 10 years I have moved to the back of the pack, choosing not to fight the fight I used to fight, allowing the naïve specialists to have the upper hand.  The pendulum has now swung back in the opposite direction.  Patients should not have to suffer the inadequacies of their specialists nor should we have to play second fiddle.  I’m tired of dealing with physicians that don’t understand why we do what we do or ignore the literature that supports it.  It’s time to show and prove to the specialists that which they should know but don’t. Yes, I do pity them because there is no venue for them to learn this information other than WLM.  Unfortunately, it is the patient that suffers the consequences of the physician’s lack of knowledge. Thus, I’ve taken on the role of being the patient’s advocate, empowering them to understand an alternative treatment or prevention that is all evidenced based, but that which is going to be rejected by their PMD’s.  I now provide articles to patients supporting the important benefits of testosterone in prostate cancer patients, progesterone and testosterone in breast cancer patients, and the safety and efficacy in prevention and treatment of these diseases.  I will provide and review all the studies that you should have in your quiver to present to patients and their physicians that reject what we do because the physicians have not a clue.  I’m tired of letting the patients endure the consequences of physician ignorance. All new and recent evidence will be presented. Please utilize these studies to provide direction and support to your colleagues and patients.

    The diagnosis and treatment of prostate cancer continues to evolve yet remains controversial.  Dr. Bernadette Greenberg from Desert Medical Imaging will present the update in diagnosis and treatment as well as the use of genomics to predict outcomes. This will be the most captivating lecture you will ever hear as I have never experienced any lecturer as dynamic as this lady. Be prepared to be blown away by her knowledge and presentation.

    We at WLM are pleased to now have a 2-hour presentation before Part I to help attendees “figure me out.”  This is presented by Dr. David Kern who has the same sarcasm and insight as I do.  He will be presenting all the data on how glucose affects the brain, dysglycemia, and protein glycation.

    A new addition to WLM is a separate course on PRP, injection techniques, and the latest literature by Dr. Nacouzi.  Unfortunately, the PRP course sells out due to the popularity of this new and easy treatment.  We’ll learn why it is so popular and how to incorporate this procedure into your practice.

    We have tried to introduce new and promising concepts that we can incorporate into our practices. I know nothing about genetic testing, epigenetics, when to test, and what to do with the results. What I have read in JAMA is confusing and perhaps political. Dr. Stickler will enlighten us as to what, when, and why to test and then what to do with the results.

    I also know little about cannabis, cannabinoids, CBD, etc.  Are they a safe and effective alternative to opiates now that we suffer from opiate paranoia?  I have had many patients request it with excellent results.  Now that it is legal in California and other states, pot shop owners know more about cannabis than physicians. So, we have chosen Dr. Felice to enlighten us about what we should know about this alternative for pain and sleep management.

    Our resident attorney and business consultant that teaches the WLM business course will provide an update on practice management, compliance, and how to avoid hassles with insurance and regulatory agencies. As far as hormones are concerned I have focused in this course primarily on breast cancer, prostate cancer, and mitochondrial dysfunction. 

    I would like to focus on the recent literature as it pertains to my personal situation and how HRT has helped me in this regard as well as the medical literature as it pertains to pain. After 30 joint surgeries, joint sepsis, 5 back surgeries, and over 20 IV antibiotics that have played havoc with my gut that resulted in significant inflammation, I’m an expert in pain management and gut dysbiosis.  Pain can affect our psyche and sleep cycles.  I’ll review the recent literature as it pertains to opiates effects on hormones. Concurrently, hormones have been shown to have a significant impact on multiple nociceptive pathways that result in significant pain improvement.  Unfortunately, do to my snips, opiates and cannabis don’t work for me but I’ll present literature and as to what does work and why.

    Lastly, and most disturbingly, is a topic that I must address but with grave reservation and frustration, and that is our legal environment.  It is a complete system failure, from the process of medical board complaints, to medical board handling of complaints, to reliance on completely inappropriate endocrine guidelines as if they were case law.  I will review all the cases (with fake names, case scenarios, and circumstances of course) that I have had to deal with so that history doesn’t repeat itself. More importantly, I will discuss my solution to the issues and how everyone can help.  This will be an audience participation time, Q & A, discussion by Dr. Kadambi (esteemed endocrinologist that totally gets it), and how we can all help each other through this process.  Number one on my current bucket list is to educate the medical boards to the literature as well as stop using worthless and outdated guidelines to sanction physicians that only make their patients better. WLM attendees should be the experts that review these cases, not a specialty that has no understanding of the literature and current studies. I will enlist everyone’s assistance in doing so.  We will spend an entire evening addressing these issues and concerns.

    Last year’s Beyond Hormones conference at the Lied Lodge will be hard to beat.  However, we are going to try to make this anniversary celebration better than last year with great food and entertainment at a fabulous resort in Tucson.  I’m looking forward to a great reunion this October and hope to see everyone there. 

    Kindest regards, Neal


    Neal Rouzier, M.D.
    Faculty Chairman

    Course Details & Registration

  • April 02, 2018 6:33 AM | Taylor Hill (Administrator)
    Dr.Nacouzi, M.D.

    Dear Doctors and Practitioners,

    When planning a weekend-long course to learn and incorporate a significant clinical advancement such as PRP, it should be thought of carefully. The presented material and exercises need to be clinically relevant, succinct, and applicable.

    After attending many PRP-specific conferences, I recognized that the same contents and formats were endlessly being recycled. The hands-on exercises often left me wanting and in the worst cases, left me questioning the clinical experience of the instructors. As presented, to try and apply these experiences the next day in my own practice would be unreasonable, if not unsafe.

    There needed to be a format that would allow attendees to easily apply the information they were presented. Thus, after performing over 2500 procedures in our office, I decided to put together a course summarizing the up-to-date thinking on PRP along with a way to establish confidence in those performing some of the most common procedures encountered.

    As a result, my colleagues and I have summarized the majority of our experience thus far with PRP. We have read and abridged hundreds of articles regarding preparation, dosage, activation, and implementation of PRP into an easily applicable format. We then developed a system of reference for each step of implementation, including: functional diagrams, planning methods, safe zones, dosing, adjunct product use, pearls of injection, caution zones, follow-up, and discussion of relevant challenges encountered.

    In addition, we will share the intricacies and important modifications needed for PRP preparation. The latest recommendations and reasoning proposed by leading European and international researchers.

    In order to make the most of our time together, we will substitute more long-winded pathway lectures with hands on need to know material, and the complete reference material will be distributed to attendees in advance for their conference.

    Every slide in our program will be relevant material aimed to benefit attendees in their own practice. As such, we will have two one-hour open discussion periods based on the questions asked at registration. The hands-on-lab will offer over ten live cases to participate in and will include the application of neuromodulators (Botulinum A toxins), Hyaluronic filler injections, facial volumetric remodeling, and other relevant procedures. In addition to our hands-on-lab, 5 conference attendees will be able to volunteer for 5 independent procedures guided by myself and my colleague.

    We welcome you to our conference.

    Dr. Nacouzi, MD

    Course Details & Registration
  • October 02, 2017 4:12 PM | Christiaan Killian (Administrator)

    Dear Colleagues,

    Over the past 12 years of teaching HRT courses I have tried to modify the content to be what I thought best as far as practicing HRT.  Part I begins with the didactic, evidence-based approach to demonstrate what we do and why we do it, based on the medical literature.  Day two is designed to get you started on prescribing, monitoring and adjusting hormones based on symptoms and laboratory data.  When I ran out of time and space, then Part II was developed to complete the Part I course.  Part II consisted of finishing what I thought to be important facts, papers, and labs that I felt you should know but could not cram into Part I.  Finally, we reviewed chronic fatigue, PCOS, hair loss, skin, osteoporosis and new lab markers. The most important section of Part II was demonstrating the anti-cancer benefit of our hormones, which most physicians and academicians have never read or seen. I had hoped to lay the groundwork for everything there is to know, based upon our literature, to have a firm understanding of preventive medicine.  Unfortunately the sections on clinical pearls, tricks of the trade, and difficult and interesting cases I've accumulated were eliminated.  Hence, Part III.

    All 3 courses are in constant evolution.  New to this Part III is the importance of SHBG, which is the most important and least recognized serum protein for predicting cardiovascular disease in both men and women.  The literature demonstrates the importance of optimizing this protein.  The literature also weighs in on which estrogen is best for long term health and it’s the opposite of what most are doing.  Recent literature purports that testosterone has a longevity effect on men with treated prostate cancer.  Unbelievably, some doctors are now treating men that have active prostate cancer with testosterone with no ill effects except improvement in longevity and well-being.  We will also look at prevention and treatment of prostate cancer with estrogen, completely the opposite of what other academies are teaching.  We’ll review how SHBG protects against cancer and how testosterone raises SHBG?

    Part III involves new material and studies to further shape why we do what we do.  However I have the most fun when we utilize the medical literature to debunk what other groups commonly teach and believe which is why I focus so much on evidence based teaching. Even though many theorize that estrogen is harmful in men, the literature entirely supports the opposite.  In fact, recent literature supports estrogen’s role in treating and preventing prostate cancer, CAD, DM, osteoporosis, and dementia.  We will review the literature to decide which estrogen to use in men, when, how much, and which ones to avoid. I will present the many cases of active prostate cancer that I have been treating for 15 years with only estrogen! Many practitioners are still being taught that estrogen causes prostate cancer despite estrogen having antiangiogenic and proapoptotic properties against prostate cancer.  As for women, we will also review which vaginal estrogen to use, which ones to avoid, how much, when and why, which ones are absorbed systemically and which ones are not.  In addition, the new treatment of choice for prostate cancer is HIFU and the best diagnostic test is the MRI-S.  We should only biopsy the prostate after we produce a mapping of the prostate under MRI guidance.  And if no tumor is seen, then no biopsy should be done.

    At what level should a man’s serum estradiol level be maintained for optimal health?  What estradiol level should be maintained to suppress the growth of active prostate cancer?  This is counter to the teaching of A4M and AMMG, yet they have no scientific evidence to back up their unsupported claims that estrogen causes prostate cancer which is contrary to the studies showing the success of estrogen in treating prostate cancer.  Let’s see who wins in this court of medicine.  The pendulum now swings in the direction that optimal testosterone levels, with the resulting optimal estradiol levels, may be protective against prostate cancer.  Lastly we will look at the literature supporting estrogen in the treatment of prostate cancer and review the cases where I have successfully treated prostate cancer with estrogen administration throughout the last 15 years.

    The local osteoporosis expert can't get NTX levels below 50.  He is baffled as to how I get them below 20, then raise vitamin D levels to above 60, and get all DEXA scans to improve.  He believes that I use toxic levels of vitamin D whereas studies prove what levels are toxic and the side effects associated with these toxic levels.  The cardiologist wonders how I can lower cholesterol, triglycerides, lipoprotein and CRP levels, and get HDL up that high.  And a local fertility expert is frustrated that I have made two of his patients pregnant whereas he could not (don't go there!).   It was simply due to the effect of Femara in blocking excess estrogen, maintaining adequate progesterone, thyroid, and metformin levels throughout pregnancy in patients with PCOS. The literature tells us how to prevent and treat post-partum depression.  Fun and interesting cases will be reviewed that I did not have time to review in Parts I & II.  There will be many cases involving “what to do when this happens,” that we couldn’t cover in the prior courses. Let’s see how you do with the 50 menopausal cases that review every type of problem you could possibly encounter in a menopausal woman.  The amount of data and study that is available to support this therapy is amazing and I love to share and decipher these studies that are so important yet missed by most physicians and academies.  As you know by my passion, this medicine is absolute fun!

    The prescribing of HRT is relatively straightforward and that was very repetitiously covered in Parts I & II.  However, it is that 10% of patients that have problems and complications that will challenge your knowledge and expertise.  So, Part III is designed as a course that reviews tricks of the trade as it relates to problem cases, many ifs, ands, or buts, complications, and what to do and say to patients and their doctors when they challenge you.  As in keeping with our tradition, more supportive and interesting articles from our literature will be analyzed to support our unique style of medicine.  Following this letter will be a small sampling of questions that may pique your interest.  After completing Part III you should feel confident in calling yourself an expert in preventive medicine and hormone replacement therapy.

    So bring the Provigil and coffee and get ready for an intense 2.5 day board review type of course. Past attendees have commented that it was the most fun course of the three because of the discussions.  If you have signed up for the certification, WLM will present the third part of the certification test upon completion of Part III.  In preparation for this we will review 500 questions and cases of clinical pertinence to understand the most difficult, interesting, fascinating, and controversial cases.  In addition there will be an hour potpourri of interesting articles that don’t fit into any particular topic yet are so pertinent to our science.  I hope to see you all soon in Fort Worth, TX!




    Neal Rouzier

    Course Details & Registration

  • February 13, 2017 4:14 PM | Christiaan Killian (Administrator)


    Dear Neal,

    Has there been any progress on new reference ranges on progesterone? My patients are coming back with levels of 2-5 ng/mL which was confusing to me until I read on the forum about the reagent. I’d appreciate any update.

    Based on looking at many recent tests, I think the new range should be at least >2. Still working on that with LabCorp.  Again it is completely arbitrary and nebulous. Unfortunately the manufacturer of the new reagent, nor LabCorp Executives, have recommended a certain level of normal or optimal to shoot for. Just goes to show how these numbers are picked and how they should be used as only a guide.

    The consensus meeting of OB/GYNS in Europe last year felt that a level of 10 ng/dl was adequate for endometrial protection.  Unfortunately that number was established using the old reagent but has now been discontinued.  Ultimately the number that will be decided on will be based on negotiations between me and a few pathologists at LabCorp.  Now how scientific is that?  Hard to believe that LabCorp would suddenly start using a new reagent without reference ranges and without alerting the public as to their doing so.

    Use the number as a guide but keep an eye on bleeding or spotting.  Based on doing this for 20 years, I still feel that the doses we prescribe (100mg SL or 200mg PO) should be adequate for most women.  The OB/GYN community does not follow levels like I do, so a lot of their dosing is based on the studies that show 200mg PO is protective, which in our experience results in P4 levels of at least > 10ng/dl.  In my experience, about 20% will require more progesterone to prevent endometrial proliferation.  Use your clinical judgement as well as inform the patient to be alert for any abnormal bleeding/spotting which would then require an endometrial ultrasound/biopsy and dosage increase of progesterone.  So we never will truly know the exact or best level to shoot for, however with time and experience we will eventually come to know what level to shoot for in most women, with a few outliers requiring more.  Remember all women are like snowflakes, all are different and will respond differently depending on cellular sensitivity to progesterone and intestinal absorption.

    We hope this preliminary information is helpful, please comment as we all work collectively to resolve this issue.  Thanks to many of you for reaching out with your initial concerns, it has helped us to better figure out what is happening as we reach out to LabCorp to re-establish some starting guidelines.  As soon as we have more definitive information Dana will send along an update.


    – Neal

  • August 19, 2016 4:15 PM | Christiaan Killian (Administrator)


    Dear Fellow Colleagues,

    In addition to learning about dysbiosis and all the effects that probiotics play on health and wellness, I thought that it would be interesting to learn and review from an expert all that we should know about gut flora, health and wellness.  I personally have been on 8 different potent IV antibiotics since January and have completely messed up my intestines, only to be saved by gut healing supplements and probiotics.  Dr. Dirk Parvus will review how he assisted me in recovering.  Eric Serrano sent a care package to my home with all of the necessary elements to heal my leaky gut and put me back to normal.  What a tough road it’s been, but I’m finally back to normal thanks to these docs.  I’ll review their treatments that led to my healing when nothing conventional worked.  And I’m sure you’re interested in hearing where I’ve had stem cells injected, why, and the results.  Although you may never administer stem cells, we feel it is extremely important that you become aware of the modality, what it can be used for, and when you should utilize it. Dr. Herman Pang will enlighten us with everything you should know about stem cells and where to refer your patients for the various treatments with PRP and stem cells, as well as where I sent my own patient that had an ejection fraction of 15% with class IV CHF.

    The administration of growth hormone has always been complex and confusing, and many practitioners and zealots still try to convince everyone that growth hormone is illegal to prescribe based on their misinterpretation and misunderstanding of some law they say applies to growth hormone.  Fortunately,  it’s up to the law makers to enact laws and the courts to interpret them, and NOT the FDA or pundits that claim to.  We’ll review case law on legalities of HGH and put the false claims to rest that are intended to scare practitioners away from prescribing HGH.  If it is illegal to prescribe HGH, then I know about 10,000 doctors that are breaking the law.  Really?  Are all of us breaking the law?  Nope, not to worry, I’m not going to turn you in because you prescribed HGH.  However, I will discuss the various cases that I’ve had to defend (medical board cases), issues regarding the use of HGH, and how to prescribe and document so that you will never have any concern with prescribing growth hormone for medical reasons.  Don’t make the mistakes that others are making.

    We will review 100 studies on diagnosing, prescribing, monitoring and troubleshooting HGH.  Old landmark articles will be reviewed, as well as the most recent literature showing benefits.  We’ll review tricks to maximize response and raise IGF-1 levels.  We’ll also review various types, costs, where to go to prescribe for best cost, alternatives to HGH, and the important facts that you need to document when you prescribe growth hormone for off-label use.  Ever hear of ipramoralin, tesamorilin, or ibutamorin?  We’ll review both injectable HGH and PO secretagogues, which ones work and for how long. The use and clinical utility of pharmaceutical secretogogues and the lack of efficacy of non-pharmaceutical secretogogues will be reviewed. Recent evidence proves significant protection against Alzheimer’s disease by HGH and various secretagogues.  Just how illegal is it to prescribe growth hormone?  I’ll review the reasons why I don’t prescribe growth hormone, as well as the reasons why I DO prescribe growth hormone.  We’ll review supply and demand, cost and availability, andeverything else you need to know before prescribing growth hormone, including the necessary verbiage for documenting and defending its use.  It may take me several hours to get through the material, but I hope to cover everything of importance that I feel you should know about HGH. And of course, it goes without saying:  WWYLYLTB?

    Five years ago, I put together a lecture on the brain that I gave at AMMG.  Three years later I added a second lecture that consisted ofnewer articles not included in the first lecture.  Earlier this year I put together a third lecture from all recent data that addresses the various treatments for dementia and Alzheimer’s disease.  It is thoroughly amazing that the experts who write the articles on Alzheimer’s disease and dementia have no understanding of the pathophysiology of hormones on the brain.  They just don’t get it.  However, you will by the time I finish the third lecture.  I will convince you of how bad estrogen is for the brain, and the same goes for testosterone.  Then, in my usual style, I will show you all the bad effects of not using hormones to protect the brain. Recently there have been several studies proving the harm of estrogen in older women, as well as demonstrating the harm in having high baseline levels of estradiol that have been associated with an increase in Alzheimer’s disease and dementia. That is absolutely true as you can’t argue the results, only the extrapolation. But in fact, their conclusion couldn’t be further from the truth.  Unfortunately, researchers still don’t understand that association does not prove causation.  We will review the medical literature that demonstrates protection of the brain with various hormones for both men and women.  After 20 years and billions of dollars of research we are no better off in treating Alzheimer’s disease.  Aricept and Namenda have been disappointing in treating symptoms, and no drug reverses the disease process as it progresses. We will review all the EBM that medical academies and pharmaceutical companies ignore, which instruct us on how to prevent dementia as opposed to treating once the disease becomes established. Can/should we treat Alzheimer’s disease with estrogen?  Yes, absolutely, if you want to reverse the disease process. Unfortunately, the pharmaceutical industry fails to read and appreciate all the data for the various hormones in preventing the disease in the first place.  There is definitive evidence that CEE≠E2 and MP≠MPA, particularly when it comes to the brain and this is demonstrated in SPECT scans.  Finally, there is only one drug that reverses (removes) beta amyloid plaque from neurons, which is what the pharmaceutical industry has been searching for to treat AD.  Well, we found it, but we are going to keep it a secret!  It doesn’t make me any less sarcastic, but it does make me think clearer so that I can be even more sarcastic.

    Recently while in China, I read about another promising Alzheimer’s disease drug that failed to improve AD or reverse beta-amyloid plaque deposition.  After 50 years and billions of dollars spent, there is no successful treatment or preventive drug therapy for AD.  And now we have good data to show the harm of HRT which logically calls for yanking out ovaries, heuvos, and your pituitary gland.  Fortunately, those are all observational studies that suggest harm of hormones, in contrast to RCT’s that show and prove protection.  This then leads us to another section where we will learn how to evaluate medical journal articles and interpret their results, which are usually the opposite of what the real data shows.  We will review a multitude of studies whereby the ultimate results are different than what the authors originally claimed.  I hope to make you better students by teaching you how to interpret and review studies for bias, political correctness and economic agendas.

    I have also invited two hormone experts, both internationally recognized, that have completely opposite opinions on HRT.  You will find their debate on hormones enlightening and be amazed how two experts can have  completely different views of HRT.  Listening to them both will give you a new perspective on life.

    Lastly, I have found the most profound article on BHRT that I have ever seen or read.  Finally, someone has published exactly what I have been teaching and preaching on thyroid administration for the last 20 years. In spite of the fact that it’s in the bible of endocrinology not to suppress TSH, endocrinologists, ENT surgeons, and psychiatrists suppress TSH with impunity, but you can’t.  Regardless of this right of certain physicians to suppress TSH, a landmark study reviewed why and how we came to fear suppression of TSH.  Unfortunately,  all of the studies that showed harm of TSH suppression were from extrapolation from Grave’s disease which causes harmful effects due to an autoimmune disorder and not from elevated levels of thyroid hormone.  Years of studies of suppressing TSH by endocrinologists, psychiatrists using high doses of T3 for depression, and ENT surgeons suppressing TSH for treatment of DTC, none showed any harm.  We will review this study and recent other studies showing the benefits of thyroid optimization and lack of harm with TSH suppression. In fact, proper treatment involves TSH suppression. I could not sleep after reading this article and I’m sure that you will feel the same.

    We’ll review all the articles that review PCV vs erythrocytosis, as well as review outcome studies. High hematocrit is predictive of stroke and heart attacks but only in patients with PCV, not erythrocytosis.  Got that?  Well most don’t got it and here’s why.  Fifty years of study prove no harm to physiologic erythrocytosis.  Don’t assume and don’t extrapolate but everyone does because they don’t get it. However you’ll get it.  Need studies, documentation that erythrocytosis is harmless, need to understand why checking a CBC is in the endocrine guidelines? No I don’t go by (incorrect) endocrine guidelines.

    We’ll review the physiology of erythrocytosis that the hematology world doesn’t comprehend, and look at how and why they confuse PCV with erythrocytosis.  The mechanism and physiology of erythrocytosis is thoroughly amazing and none of my hematologists know or understand the physiology behind normocytosis, erythrocytosis, and extreme erythrocytosis, as well as when, and when not, to phlebotomize each.   I’ve saved interesting cases of PCV with lab reviews.

    How to analyze a medical study:  Examples of studies that state one thing and prove another.  Review and critique a study before even reading it.  DBRCT’s, RCT’s, prospective studies, retrospective studies, observational studies and confabulation.  How to design a study to prove or disprove anything that you want by using sensitivity, specificity, relative risk vs. absolute risk, number to treat, underdiagnose and overdiagnosis.  We’ll make it fun!

    Hope to see you in October!

    Sarcastically yours, Neal

    P.S.  I just heard from Einstein and he’s coming all the way from Tokyo.

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