EDUCATION
Education
High School: Southport High School
Indianapolis, IN
Diploma, 1978
Undergraduate: Indiana University
Bloomington, IN
History and Political Philosophy Major
B.A., Chemistry, 1982
Medical School: Indiana University School of Medicine
Indianapolis, IN
M.D., 1986
Residency: Family Practice
St. Francis Hospital Center
Beech Grove, IN
1986-1989
Board Certification: Diplomate, American Board of Family Practice 1989
Recertified, 1996, 2003
Additional Training:
Problem-Based Learning Conference. Scottsdale, AZ; April / May 1994
Problem-Based Learning Conference. Chicago, IL; August 1994
Psychopharmacology Two-Day Academy; Neuroscience Education Institute, 2003
Medical Licensure: Indiana, 1987 – Present (#01036126)
Hospital Appointments:
St. Francis Hospital Center; Indianapolis, IN
1989 – 2012
Community South Hospital; Indianapolis, IN
1989 – 2012
Professional Organizations:
Past member American Academy of Family Physicians
Past member Indiana Academy of Family Physicians
Past member American Medical Association
TEACHING AND CONSULTING
Below are provided examples of Dr. De Wester’s past and present research projects, lectures, consulting positions, TV appearances, etc. Due to the large number, individual items are not routinely listed after 2004, but such information is kept on file and is available upon request. Items of particular significance, however, continue to be listed after 2004.
Teaching and consulting
Positions Held:
Teaching Faculty, Family Practice Residency Program
St. Francis Hospital Center, Beech Grove, IN
1989-2012
Adjunct Clinical Professor, Butler University
Physician Assistant Program; Indianapolis, IN
1997-2002
National Teaching Faculty, Anxiety Profiles—New Perspectives for Diagnosis and Treatment
1991-1995
Physician member, AIDS Counsel
Perry Township Schools, Indianapolis, IN
1988-1991
Committee for Drug Free Schools
Perry Township Schools, Indianapolis, IN
1987-1990
Physician Member, Advisory Committee on Sex Education
Perry Township Schools, Indianapolis, IN
1988-1991
Committee Member, Philosophy Awareness Committee
St. Francis Hospital Center, Beech Grove, IN
1991
Team Physician, Southport High School Football Team
Indianapolis, IN
1987-2004
Member, National Headache Foundation
Consensus Conference: Length of Antidepressant Treatment
Sponsor: University of Minnesota, Dallas, Texas
March 1995
President/Chairman of the Board
American Health Education Foundation, Inc. Indianapolis, IN. 1996-1997
Chairman of the Board and Founder, American Health Network Education Committee(AHEC) and America Health Education Foundation(AHEF)
Indianapolis, IN. 1994-1997
National Primary Care Serzone Advisory Board Member
Bristol-Meyers Squibb Pharmaceuticals, 1997-1998
National Psychiatric Advisory Board Member
SmithKline Beecham Pharmaceuticals, 1995-1998
National Primary Care Psychiatric Advisory Board Member
SmithKline Beecham Pharmaceuticals, 1995-2001
Member, National Council of Panic Experts
Primary Care Wellbutrin Advisory Board
Glaxo-Wellcome Pharmaceuticals, 1999-2001
Faculty Trainer, Presenter, and Faculty Member of the National CME Program entitled, “Depression: Beyond Stereotype and Stigma”, supported by a grant from Glaxo-Wellcome Pharmaceuticals, 1999-2001
Visiting Professor in Family Medicine, University of Illinois; College of Medicine at Urbana-Champaign, February 24-26, 2000; Provena Covenant Hospital, Urbana, Illinois
National Androderm Advisory Board and Teaching Faculty Member (Watson Pharmaceuticals), 1999-2002
Member of the Editorial Board and author for Depression Anxiety Wellness Network (DAWN), 2001-2003.
Member of the Regional Educational Advisory Councils on Health Care-Comorbidities in Mood and Anxiety Disorders (REACH), January 2002-2003.
Member of the Pfizer International Social Phobia Advisory Board, 2002-2003.
Member of the International Depression and Anxiety Disorders Advisory Board, Pfizer Pharmaceuticals, 2002-2004.
National Depression and Anxiety Advisory Board, Pfizer Pharmaceuticals, 2002-2006.
Member of the National Sleep Disorders Advisory Board, Elán Pharmaceuticals, 2002
National Primary Care Pre-Gabalin Advisory Board, Pfizer Pharmaceuticals, 2002-2003
Xanax XR National Primary Care Advisory Board, Pfizer Pharmaceuticals, 2003-2005
Liposcience Primary Care Advisory Board Member; Special Primary Care Consultant to the Vice President of Marketing for Liposcience, 2003-2004
Member of the Personalized Medicine and Mood Anxiety Disorders Advisory Board, Pfizer CNS (Pharmacogenomics Advisory Board), 2002
Medical and Psychiatric Director and Consultant for The Family Bonding and Attachment Center,
Lennon and Associates Psychologists, Indianapolis/Carmel/Greenwood, Indiana, 2001-present
Primary Care Advisor to the Director for Flonase Marketing, GlaxoSmithKline Pharmaceuticals, and member of the training faculty for the national teaching faculty for allergic rhinitis and Flonase; 1999–2002
Editor-in-Chief, International Journal of Psychiatry in the Community, 2002-2003
Consultant Member of the Neuroscience Consultant Extranet, Pfizer Pharmaceuticals, 2004-2006
Author, Reviewer, and Consultant for Peerview of the Pri-Med Institute, 2004-2006
Steering Committee Member, Consultant, Author for the Pri-Med On-Line Condition Center – Anxiety; Pri-Med Institute, 2005
Primary Care Consultant/Advisor to Graphics Ink., 2004-present.
Primary Care Consultant/Advisor to Team Pharmaceuticals National Marketing Team, 2004-2006
Member of the National Alprazolam ODT Advisory Board for Schwarz Pharma, 2004-2006
NAPiis Advisory Board, 2006
Indiplon National Primary Care Advisory Board, 2006
Consultant on The G.O.O.D Pilot Program – investigating the utility and practicality of a compliance-enhancing program designed for use in primary care for the treatment of depression.(2006-2007)
Consulting Medical Director for Arbor Pharmaceuticals, 2007
Founding Partner, PharmaThinkTank 2007
Consultant to the Vice President of Marketing and Sales for Vilazodone (Clinical Data), 2009-2011
Consultant with Sprout Pharmaceuticals on flibanserin in the treatment of sexual dysfunction, 2014-2016
Consultant to Eiger Pharmaceuticals on the approval process with the FDA and EMA for the Progeria Therapeutic lonafarnib; 2021-present
Consultant to Eiger Pharmaceuticals on the FDA approval process for the Covid-19 therapeutic lambda; 2021-present
Consulting positions also held with: Endo, Auxilium, Wyeth-Ayerst, Eli Lilly, Valeant, Burroughs-Wellcome, Forest, and Parke-Davis Pharmaceuticals
NATIONAL CME CONFERENCE TOURS
National CME Conference Tours:
The following are a sample of the conference faculties in which I have participated. In some cases, I also acted as one of the developers and/or trainers for the conference and its faculty, as well as the Slide Kits utilized for them; these tours visited multiple cities across the United States, some visiting over one hundred sites*.
Anxiety Profiles – New Perspectives for Diagnosis and Treatment,1991-1995
Diagnosis and Treatment of Anxiety Disorders, 1992-1994
Progress in Treating Depression, A Primary Care Update, 1995-1997
Treating the Patient with Severe or Resistant Depression, 1997
Treating Depression and Anxiety in Primary Care, 1998
The Hidden Diagnosis: Uncovering Anxiety and Depressive Disorders, 1997-1998
Depression: Beyond Stereotype and Stigma, 1999-2000
The Aftermath of Trauma in the Community: Strategies to Recognize, Diagnose and Manage Post-Traumatic Stress Disorder, 1999-2000
Practical Guidelines for Managing Depression in Primary Care, 1999-2000
Challenges in Diagnosing and Managing Depression in Primary Care, 2000-2001
New Approaches to Diagnosis, Management and Treatment of Anxiety Disorders in Primary Care; Pri-Med Updates, 2003
Recognizing the Signs and Symptoms of Anxiety; Pri-Med Updates, 2003-2004
Evaluating Treatment Decisions in Depression and Anxiety Series, Pri-Med Regional/National Meetings, 2004
Utilizing of Nontraditional Dosage Forms in Treating Anxiety Series, Program Chairman, Winter/Spring/Fall, 2005, Pri-Med Regional/National Meetings
Tailoring the Treatment to Meet the Needs of Your Patient: A Case Approach; Series 2005 Pri-Med Regional Conferences
The Treatment of Anxiety Disorders: Practical Approaches for the Primary Care Practitioner; Primary Care Updates, 2004
Case studies in Anxiety and Panic Disorders; Case-based series with online format. March-August 2004
PTSD National Conference Series: The Aftermath of Trauma in the Community, Strategies to Manage Post Traumatic Stress Disorder, 1999 – 2000; CME, Inc.
2000 – 2001 Speakers Alliance: A Speakers Training Initiative, Glaxo SmithKline.
Androderm Teaching Faculty, 2000
Practical Guidelines for Managing Depression in Primary Care (National Depression CME Conference Series), 1999-2000; CME, Inc.
SPEAKING ENGAGEMENTS
*Due to volume and redundancy, individual speaking engagements are not listed except for the examples given below.
Diagnosis and Treatment of Anxiety Disorder
1992
December 2……………………………Bedford, IN
December 14…………………………..Indianapolis, IN
December 23…………………………..Ft. Wayne, IN
1993
January 4………………………………Logansport, IN
April 13………………………………..Decatur, IN
June 28…………………………………Ft. Wayne, IN
August 4………………………………Munster, IN
August 19…………………………….. Ft. Wayne, IN
October 7…………………………….. South Bend, IN
October 7…………………………….. Elkhart, IN
October 15…………………………….Ft Wayne, IN
1994
March 22………………………………Ft. Wayne, IN
April 6…………………………………Baltimore, MD
May 12…………………………………Bloomington, IN
May 29…………………………………San Antonio, TX
August 19………………………………Indianapolis, IN
November 15………………………….Avilla, IN
Differential Diagnosis of Anxiety and Depression
October 15, 1994……………………… Indianapolis, IN
Update in the Treatment of Depression
1995
May 9…………………………………..Watseko, IL
May 19………………………………….Kokomo, IN
May 25………………………………….Ft. Wayne, IN
May 25………………………………….Ft. Wayne, IN
June 6……………………………………South Bend, IN
June 12………………………………….Greenfield, IN
June 16………………………………….Louisville, KY
September 10……………………………Detroit, MI
September 23……………………………St. Louis, MO
September 24……………………………Baltimore, MD
October 15………………………………Indianapolis, IN
October 28………………………………Cleveland, OH
October 29………………………………Pittsburgh, PA
Elderly Depression/Anxiety
1993
May 26……………………………….Indianapolis, IN
August 4………………………………Munster, IN
November 30…………………………Defiance, OH
Depression
1993
June 15………………………………..Carmel, IN
September 28…………………………St. Clair, MI
September 28…………………………Detroit, MI
October 5……………………………..Columbus, IN
1994
February 3…………………………….Aspen, CO
August 1………………………………Kokomo, IN (Round table discussion)
September 13…………………………Lafayette, IN (Round table discussion)
August 15, 1995………………………Indianapolis, IN (Case discussion)
Diagnosis and Treatment of Depression
October 6, 1994………………………..Kokomo, IN
January 17, 1995……………………… Indianapolis, IN
Treatment of Depression in Family Practice Setting
October 20, 1994……………………….Evansville, IN
June 30, 1995…………………………..Lawrenceburg, IN
Primary Psychiatry
1994
July 28………………………………….French Lick, IN (IN Academy/ Family Practice annual mtg)
August 16………………………………Beech Grove, IN
1995
November 3-5………………………….Indianapolis, IN (Cutting Edge Mngmt of Anxiety/Depressive Disorders in Primary Care – CME conference)
Migraine: Diagnosis and Breakthroughs in Treatment
1993
February 16……………………………Indianapolis, IN
March 16………………………………Indianapolis, IN
April 13………………………………. Indianapolis, IN
April 21………………………………. Terre Haute, IN
April 21………………………………..Columbus, IN
April 28………………………………..Indianapolis, IN
June 9………………………………….Greenfield, IN
June 23……………………………….. Greensburg, IN
July 14…………………………………Indianapolis, IN
1994
February 15…………………………… Beech Grove, IN
March 15……………………………….Indianapolis, IN
August 9………………………………..Greenfield, IN
Hypertension
June 25, 1993……………………………St. Louis, MO
Diagnosis and Treatment of Asthma
November 5, 1993………………………Owensboro, KY
Evaluation and Management of Asthma
August 17, 1993…………………………Indianapolis, IN
March 15, 1994………………………….Indianapolis, IN
State of the Art Management of Asthma
May 21, 1994……………………………Bloomington, IN (Illinois Academy of Family Practice/
annual meeting)
Other Speaking Engagements (examples):
1991
August St. Francis Hospital Center, Indianapolis, IN
“Diagnosis and Treatment of Anxiety/Depression in Family Practice.”
September 17 St. Francis Hospital Center, Indianapolis, IN
“Primary and Secondary Prevention of Heart Disease”
Lecture 1
October 8 St. Francis Hospital Center, Indianapolis, IN
“Primary and Secondary Prevention of Heart Disease”
Lecture 2
October 15 St. Francis Hospital Center, Indianapolis, IN
“Primary and Secondary Prevention of Heart Disease”
Lecture 3
December 12 St. Francis Hospital Center, Indianapolis, IN
Lecture to joint OB/GYN Family Practice Dept. meeting
“New Treatment Prospectives in PMS”
1992
February 15 Hawaiian Family Practice annual meeting. Honolulu, HA
“The Diagnosis and Treatment of Anxiety and Depressive Disorders in Family Practice” (two lectures)
June 3 Brazil, IN
“Primary Prevention of Osteoporosis”
June 16 St. Francis Hospital Center, Indianapolis, IN
“Allergic Rhinoconjunctivitis: Diagnosis and Treatment”
June 24 Indianapolis, IN
“New Perspectives on Neurotransmitters and Implications for Treatment”
July 21 St. Francis Hospital Center, Indianapolis, IN
“Asthma: Diagnosis and Treatment”
August 18 St. Francis Hospital Center, Indianapolis, IN
“Treatment of Hypercholesterolemia”
1993
October 26, Indianapolis, IN National Headache Foundation Public Education Seminar.
“Migraine Headache”
1997
July 12 Dearborn, MI
“Treating the Patient with Severe or Resistant Depression”
July 13 Chicago, IL
“Treating the Patient with Severe or Resistant Depression”
Other Speaking Engagements (examples) (cont.):
1988 to 1994 Clinton Young Grade School – Perry Township
Indianapolis, IN. Yearly Lung Dissection and Lecture Concerning
the Hazards of Tobacco Use
2004
March 12 ADAA – Anxiety Disorders of America Annual Conference
Presentation: The Continuum of Care for Anxiety Sufferers
INTERNATIONAL CONFERENCES AND LECTURES
International Conferences/lectures:
2000
April 9 Royal Palms Hotel, Bermuda
“The Impact of Allergic Rhinitis in Quality of Life: An Update”
May 12 The Atlantis Resort, Bahamas
“The Impact of Allergic Rhinitis in Quality of Life: An Update”
August 13 Royal Palms Hotel, Bermuda
“The Impact of Allergic Rhinitis in Quality of Life: An Update”
October 6 The Atlantis Resort, Bahamas
“The Impact of Allergic Rhinitis in Quality of Life: An Update”
2001
November 6 Montego Bay, Jamaica
“State of the Art Psychotropic Therapy for Anxiety and Depressive Disorders in Primary Care”
2002
April 6 Rome, Italy
“Multinational Primary Care Summit on Depression and Anxiety Disorders”
TV AND OTHER APPEARANCES
TV and Other appearances:
(For the sake of illustration, examples of other appearances are given below)
May, 1989
TV Interview with local news journalist Debbie Knox regarding the traumatic changes in the practice of medicine
February, 1993
Educational videotape presentation for Boehringer-Manheim National Sales Force
November, 1993
Appearance on television talk show Indy This Week Indianapolis, IN. “Treatment of Depression”
March 28, 1997
WTHR-TV 13, Live News Appearance as Panic Disorder expert
1989-present
Expert witness/consultant in numerous court cases
RESEARCH PAPERS AND PUBLICATIONS
Due to the large number, individual talks are not routinely listed after 1994, but such information is kept on file and is available upon request. Items of particular significance, however, continue to be listed after 1994.
Research, Papers, and Publications
(The scientific content on the Website and in this section is derived from my unpublished book, Pandora’s Medicine Box©. While this remains unpublished, those desiring more detailed information on the subjects addressed on the website and below should periodically consult our YouTube Channel for videos on these subjects. If not already available, we will be releasing more video material on an ongoing basis. Your feedback is desired and will be considered when determining the production of material.)
Research related to improving medical education through problem-based learning:
The creation of American Health Education Foundation, 1995.
In 1995, I asked a small group of my colleagues in Primary Care, to join me in the formation of AHEF. Our motivation was the obvious lack of potency in traditional models of CME to change clinician behavior, combined with widespread disillusionment and dissatisfaction among Primary Care clinicians with their CME. Our goal was to create a cost-effective CME that was optimally potent in changing clinician behavior within the context of an organization that would support the Primary Care clinician as an educator, publisher, and researcher. Researching the various methods and concepts that were shown to increase learning and behavioral change led us to center our efforts on small group case-based inter-active learning or “problem-based learning (PBL)”. Unfortunately, traditional models of PBL utilized a specialist expert facilitator meeting with a small group of learners over dinner for 1 or 2 hours of CME credit. Feeling that the cost per learner, per hour, was exorbitant with this method, we endeavored to create a large conference model that would deliver a larger number of CME credits to a larger number of learners, utilizing versatile Primary Care facilitators, while maintaining a small panel of content experts, to handle the lectures and Q&A following the case-based exercises. The result of our efforts can be appreciated by the pilot conferences and training sessions outlined below. Results of our research, thus far, have led to the creation of the AHEF Blueprint for Behavioral Change, which embodies what we believe to be the most comprehensive and potent educational mechanism for the alteration of physician behavior. A copy of this is available upon request.
AHEF Problem-based Learning C.M.E. Research
1995 – 1998
The pilot studies of a unique, case-based interactive model. The model I designed utilizes multiple typical small P.B.L. style groups but is delivered to a large group of learners at a site, and consists the whole disease management team. This model, I named P.B.L.C.M.E. trademark.
Performed:
- Pilot I, May 1995, Indianapolis, IN: F.P. Residents, P.B.L.C.M.E., Primary Psychiatry Conference
- Pilot II, November 3-5, 1995, Indianapolis, IN: A.H.N. 1st annual fall P.B.L.C.M.E. conference; “Primary Psychiatry: Cutting Edge Management of Anxiety & Depressive Disorders in the Primary Care Setting”
- Pilot III, October 31-November 2, 1996, Indianapolis, IN. 2nd annual A.H.N. B.L.C.M.E. fall conference; “Cutting Edge Management of Asthma in the Primary Care Setting”
- Pilot IV, September 19-20, 1997, Duluth, Minnesota. AHEF B.L.C.M.E. conference
“Primary Psychiatry: Cutting Edge Management of Anxiety
and Depressive Disorders in the Primary Care Setting”
Proposed:
- Pilot V, AHEF B.L.C.M.E.– Coronary Artery Disease Prevention Conf. Conference format and itinerary developed; cases have been written; C.M.E. hours have been approved by the A.A.F.P.
- Pilot VI, AHEF B.L.C.M.E.- Computer Based Model Pilot Conference. This conference would test two models of delivering P.B.L. C.M.E. at a distance from the learner. Two-prong study was been designed, and a specialist in computer medicine retained for the project. Funding/sponsorship was never found.
- Pilot VII, P.B.L.C.M.E. – Preventative Medicine Conference (5 day / 35 hour CME conference, the longest yet designed). Case writing, facility development, and deployment awaits sponsorship.
P.B.L. C.M.E. Facility Training Workshops:
1995………………………….1 workshop
1996………………………….2 workshops
1997………………………….2 workshops
Research Proposals Connected with DeWester’s Textbook of Psychiatry for Primary Care Physicians:
Usability testing for the following:
De Wester’s Psychopathologic Fingerprint
De Wester’s Primary Psychiatry Co-Morbidity Questionnaire
De Wester’s Three Part Maintenance / Surveillance Tool
De Wester’s Preventative Medicine Questionnaires
Development and utilization testing for DeWester’s Audio/Video Comprehensive Primary Psychiatry Co-Morbidity Self-Assessment Tool
ORIGINAL RESEARCH AND INTERESTS
Other original research projects and interests:
- Testosterone deficiency and physiologic replacement in men and women.
- Testosterone deficiency and metabolic syndrome in males (see papers)
- Testosterone deficiency in Type II diabetes males: implications (see papers)
- Testosterone deficiency, false negative PSAs, and delayed diagnosis of prostate cancer; a case series.
- Testosterone deficiency/replacement and effects on statin potency
- “Statin resistant” patients
- “Statin partially responsive” patients
- Implications of testosterone deficiency in adolescent males.
- Testicular functionality in testosterone deficient males with responsiveness to Beta HCG challenge: implications to our understanding of the pathophysiology of testosterone deficiency.
- Effects of sex hormones on emotional expression and emotional perception.
- Effects of sex hormones on outlook and judgment.
- Effects of sex hormones on personality.
- Effects of sex hormones on mate selection.
- Effects of
- Relationship of testosterone and sexual appetite to the sexual palate, esteem, and assertiveness in women.
- Relationship of sex hormone deficiency and fluctuations to mood, anxiety, and treatment resistance in men and women.
- Relationship of testosterone to assertiveness, confidence, socialization, and social anxiety in men and women.
- Sex hormone treatment response based on sex hormone dose and pharmacokinetics
- Sex hormone-induced diminished ovarian testosterone production and free testosterone levels and risks of breast cancer in women.
- Sex hormone(oral contraceptives and oral HRT) induced diminished ovarian testosterone production and free testosterone levels: implications of effects on mood, energy, sexual function, muscle health, and adiposity in women.
- Unexpected frequency of testosterone deficiency in adult males in the 3rd, 4th and 5th decades of life in a naturalistic family practice setting: implications.
- The concepts and practice of Primary Care in Psychiatry and Preventative Psychiatry.
- Effects of sex hormones and NMES on muscle rehabilitation and optimization.
Original research(cont.): Original hypotheses, clinical tools, and therapeutic analogies
Toward a Unitary Model of Depression:
When I was in medical school in the mid 1980’s, psychiatric orthodoxy included “The Biochemical Model of Depression”; especially at Indiana University School of Medicine, a bastion of this theory. This model divided depression in to the two subcategories of exogenous and endogenous depression. Exogenous depression was thought to result from environmental influences and to be amenable to psychotherapy, while endogenous depression was thought to result mainly from genetic influences that produce a “chemical imbalance” and that was responsive only to pharmacotherapy. Upon examination of the evidentiary basis for the theory, I became convinced that it was based on a number of inappropriate assumptions and concepts. For example, I found no compelling scientific basis for the assumption that symptoms of depression caused from environmental influences were not produced on the basis of “biochemical changes” in the central nervous system, any different from that which was purported to be associated with endogenous depression. Further, I noted that there was still extensive research data that supported the importance of environmental influences in those patients labeled endogenous depressives. Rather, it appeared to me that the best interpretation of the currently available scientific evidence suggested that all depressed patients were on a continuum, experiencing a disease both with environmental and genetic contributions to varying degrees. On the other hand, when I expressed questions and concerns to my preceptors and colleagues in medical school, I was surprised to find that these were often met with extreme defensiveness and even hostility. Of interest, as the years have passed and our understanding of depression has evolved with further research, the endogenous/exogenous terminology has quietly disappeared, and those views which once made me a heretic now find me in good, orthodox standing in psychiatry.
The Cognitive/Behavioral Wars:
One of the other fascinations beginning with my exposure to psychology in college in the late 70s was the debate between the cognitive and behavioral therapists and their relative schools of thought. Apparently, like others at the time, I found some aspects of the debate unscientific to the point of absurdity. It seemed clear from an objective examination of the evidence that only a therapy that combined elements of both schools of thought could account for the various findings in the scientific literature and provide maximal benefit. As the 80s and 90s progressed there was increasing discussion and study of concept of CBT, cognitive behavioral therapy. In fact, numerous well designed studies have now demonstrated its superior efficacy compared to other nonpharmacologic treatment in numerous psychiatric syndromes such that that CBT is now the gold standard in the nonpharmacologic treatment of the most common mental illnesses seen in primary care, including depression.
Guilt as a Psychic Pain system analogous to the Somatic Pain system:
Throughout my educational experience, guilt was presented in a negative light as something destructive to happiness and mental health. To the contrary, by the late 1980’s I became convinced that guilt arises from the conscience, a component of the psychic pain system that is functionally similar to the somatic pain system, the proper function of which is essential to health. I hypothesized that the guilt and somatic pain systems are analogous in their healthy functions, their various forms and manifestations of malfunction, their negative consequences to health when these systems malfunction, and in regard to which types of treatment will be curative, palliative, ineffective, and unhealthy. I presented this hypothesis in many lectures to health professionals and have utilized it extensively in helping patients to gain insight into their feelings of guilt, how to embrace and cultivate a healthy conscience, and practical ways to identify and address the various mental health issues stemming from dysfunctional forms of guilt.
Smashing Down the Conceptual Wall Between the Illnesses Identified as Neuroses Versus those Identified as Affective(mood) Disorders:
As I became more involved with patients suffering from psychiatric illness, I became more and more unsettled by what appeared to be the clear, neat, but apparently unscientific division between what had been labeled the neuroses versus the affective disorders in psychiatry. This was reflected in our education, where lectures were given on anxiety disorders separate from those addressing patients suffering from depression. Much to the consternation of most of the academic psychiatrists with whom I interacted as an educator and consultant, I questioned this neat division and suggested that most patients in fact have a mixture of anxiety and depressed symptoms and that these disorders are on a continuum, with most patients first experiencing anxiety that, under the right circumstances, evolves into depression. It should be noted that this once heretical view is now orthodoxy in psychiatry, especially the idea that most patients presenting to primary care physicians with depression also have anxiety symptoms, and vice versa. This is now reflected also in our education where these concepts are almost never addressed in isolation of each other.
The Concept of Primary Care in Psychiatry:
I had the good fortune to attend the St. Francis Hospital Family Residency Program under the direction of Dr. Richard Feldman, who provided an environment where psychiatry was viewed as a proper specialty to be included in primary care work, a position also embraced by my father. As I emerged from training in the late 1980’s I began to aggressively promote the concept of primary care in psychiatry. I was That is, just as the primary care physician is the primary cardiologist, primary dermatologist, primary gastroenterologist, etc. the primary care physicians should also be the primary psychiatrists. Unfortunately, while our role as the primary care physician in other specialties was accepted and clearly defined, this was not the case with psychiatry and I was to learn that there were many in psychiatry and primary care that vigorously opposed the concept. In fact, in the first paper, I submitted for publication in which the term primary care psychiatry was used, the academic psychiatrist reviewing the paper expressed vigorous opposition to the use of the term. Fortunately, the work of a small number of primary care physician educators and a significant minority of academic psychiatrists have labored over the last 10 years successfully to see this concept gain general acceptance. While there is still further work to be done to fully integrate this role into primary care medicine, the concept of the primary care physician being the primary psychiatrist is no longer in doubt.
Type II Diabetes as a preventable disease:
When I was in medical school a large part of our education was directed to the diagnosis and treatment of type 2 diabetes. Based on what we taught then about the relationship of prolonged insulin resistance prior to the diagnosis of type 2 diabetes, and the relationship of decreased lean muscle mass and increased adiposity with insulin resistance, I became convinced that type 2 diabetes was not only preventable but that the treatment focus should be altered such that we initiate treatment when the features of insulin resistance emerge. It seemed incredible that we would wait until the islet cells of the pancreas burn out and become unable to prevent hyperglycemia before diagnosing and treating this condition. Further, I argued that what we called type 2 diabetes was actually the end stage of a chronic disease, rather than the disease itself, and that early treatment could both potentially prevent what we call diabetes and slow or reverse the progression of type 2 diabetes in those already diagnosed. My questions and speculations in this regard were often not warmly received, making it one of a number of things that marked me as a heretic in regard to the profession’s conventional approach to some of the most common medical conditions we encounter. On the other hand, the conventional view of type 2 diabetes went hand-in-hand with the profession’s medieval view of the treatment of obesity, as discussed below. Though a transition to an approach that targets insulin resistance(AKA metabolic syndrome, pre-diabetes, etc.) has required years to come about, it is exciting that we are now making amazing strides in the direction of successful prevention and optimal treatment of type 2 diabetes.
Self-Worth and the concept of Sexual Economics:
This hypothesis posits that sexual relations involve a transaction that, among other things, is both influenced by and itself influences the perceived worth of those involved. Further, it also posits that the process and dynamics of this transaction that effect the determination of worth, both initial and ongoing, are essentially the same as those of other material transactions between individuals (i.e. selling and purchasing cars, clothes, etc.).
As the science of marketing emerged and evolved over the last 150 years, certain concepts and principles have been identified that impact the way humans assess and assign worth. The validity of these “laws of marketing” is attested to by the fact that they are so successfully utilized by retailers to manipulate the public’s perception of both the worth of their products and our need for such. Further, governments and politicians have demonstrated their belief in such laws, as they are studied avidly by these same groups, who also make liberal use of experts in marketing as consultants to manipulate of voting behavior. Finally, that the application is appropriate to the assessment of worth in interpersonal relationships is indicated by the widely accepted use of such marketing principles by “experts” in their books and seminars on self-promotion and self-marketing. In fact, the hypothesis appears to accurately predict the negative findings of studies examining the influence of various aspects of sexuality on the assessment of worth in relationships, as well as illuminate many phenomena that often have seemed confusing or even incomprehensible to those involved. For example, what a seller expects in exchange for an item conveys what they perceive as its worth, a message also conveyed to the prospective buyer. On the other hand, what the buyer is willing to invest conveys their perception of the worth of the item being purchased. There is perhaps nothing more intimate and personal that one can offer to another than our sexuality, which explains why sexual abuse and crimes are so psychically devastating. Yet, current popular sexuality teaches us that bartering this part of ourselves for a date, temporary affection from another, or even for nothing in return to be perfectly healthy and without implications to relationship dynamics and outcomes. In fact, such an approach is consistent with how one markets items of little value and intended for temporary enjoyment and immediate consumption. The further one explores these concepts as they relate to interpersonal relationships, the more disturbing certain aspects of our current popular sexuality appear, leading to conclusions this old hippy never dreamed he would espouse.
In patients dealing with deficits of self-worth and as a preventive health measure, I feel exploring in detail the basic concepts of marketing as they relate to value assessments in relationships to be of inestimable value.
Sexual desire as a biologic appetite analogous to the biologic appetite for food:
As noted previously, when working with patients there are few areas associated with more confusion than what constitutes healthy sexuality. While not perfectly analogous, the similitude between the appetite for sex and the appetite for food is extensive and offers deep insight into what constitutes healthy versus unhealthy sexuality; the causes of sexual dysfunction; the effects of sexual appetite on sexual assertiveness, disinhibition, and palate; and practical approaches to optimizing sexual function. It is also useful in dismantling many of the popular myths surrounding sexuality.
Nasal Corticosteroids in the Treatment of the Ophthalmologic Symptoms of Allergic Rhinitis:
I also approached GSK with the clinical observation that, while counterintuitive, it appeared that the treatment of allergic rhinitis patients with intranasal corticosteroid monotherapy appeared, in many cases, to give significant relief from ophthalmologic symptoms as well as nasal symptoms. Fortunately, I received a grant to research this issue resulting in the publication listed previously in this document that presented evidence that supports the hypothesis.
Corticosteroids as Adjunctive Treatment for Acute Sinusitis:
As an advisor to Glaxo-Smith-Kline (GSK), the makers of Flonase, in the 1990’s I apprised them of my clinical observation that patients with sinusitis treated with antibiotics and adjunctive nasal corticosteroids improved more rapidly and that such an effect was not counter-intuitive. Others who were advising them expressed similar views and GSK funded an appropriate study which upheld the hypothesis (Dolor RJ et al. Comparison of Cefuroxime with or without intranasal fluticasone for the treatment of rhinosinusitis. The CRAFFS Trial: a randomized controlled trial. JAMA 2001;286:3097-105)
Black Pearl I: Challenging the scientific basis of the conventional definition of “normal” levels of testosterone:
At the time I entered medicine, perhaps nothing better optimized the primitive state of scientific knowledge and research in sex hormone replacement therapy, and the general lack of sophistication in a way patients with sex hormone related conditions were treated than the conventional concept of what constituted “normal” levels of testosterone. Early in my career in the mid-90s, I was serving as a member of an editorial board tasked with the responsibility to create a slide presentation for educating physicians around the country about the diagnosis and treatment of hypogonadism. While proceeding through the slides during the editing process we arrived at the slides dealing with laboratory diagnosis.
Noting that the reference range was referred to as “normal” I noted the need to clarify this to make clear to the physicians we would be teaching that such ranges were not normal in the sense of what is known to be associated with health. I did not anticipate any significant opposition but was shocked by the reaction, ranging from incomprehension to irritation. While taken aback, this response removed whatever hesitancy I might have experienced at the thought of lecturing a group of individuals whose illustrious positions and ages far surpassed my own. I proceeded to point out that the current reference ranges were simply a bell-shaped curve of testosterone levels in the general population, uncorrected for those with symptoms of the condition (hypogonadism). This statement was also challenged so we waited while our administrative staff located the appropriate studies and confirmed my statement as fact. Unmoved, the response was essentially, “so what?”. I then proceeded with a review of the basic accepted scientific concepts governing the determination of “normal ranges” and a brief history of medical clinical measurements and reference ranges for various clinical parameters, including bone mineral density, cholesterol, weight, etc. I reminded the audience that only recently a bell-curve-based reference range for cholesterol had been abandoned, prior to which that range had an upper limit of normal near 300. I pointed out that such a range included over 95% of individuals suffering from premature coronary disease and clearly not representative of health. I then noted that the reference range for bone mineral density had also utilized an age-adjusted, bell curve, a range only recently abandoned and replaced with a range reflective of healthy bone. Like in the case of cholesterol, the previous range based on the bell curve included a large percentage of the women who had poorly mineralized bone and an increased risk of experiencing a fracture. Again, clearly not representative of health, and therefore not what most practicing physicians and patients would consider “normal”. I reviewed the fact that a reference range based on a bell curve of weight in the United States would contain the vast majority of patients at risk for negative health outcomes as a consequence of their adiposity. As I presented these examples I argued that “normal levels” should be those that were not associated with negative health outcomes or quality of life, and that “optimal levels” should be those associated with the greatest health improvements. In regard to testosterone, our research indicated, consistent with the few studies that existed at the time examining this issue, that many patients experience symptoms (i.e. fatigue) and signs (i.e. excess abdominal adiposity and decreased muscle mass) associated with testosterone levels in the lower half of the reference range and that optimal health effects of testosterone were likely to be achieved with testosterone levels in the upper half -upper third of the current reference ranges. As I continued to review this issue more individuals became visibly uncomfortable, as it became apparent that neither they nor their colleagues could provide scientific evidence to defend the presumption that a bell-shaped curve of testosterone levels in the general population represents normal or healthy values.
In regards to their persistent “so what” sentiment, I indicated the seriousness of the matter by pointing out that expert panels such as the one we were currently serving on were referenced by government and insurance payors to defend their denial of coverage for testosterone replacement therapy(TRT) for men experiencing classic symptoms of hypogonadism, but whose low testosterone levels were inside this erroneously labeled “normal range”, while also denying coverage for testosterone dose increases to men who continued to be symptomatic on TRT, because their current treatment that provided meager levels of testosterone was technically inside this “normal range”. At this point, the argument was conceded, I assumed the edits I suggested would be added, and we moved on to finishing our critique of the other slides. In fact, two weeks later I received a copy of the finalized version of the slide presentation which had retained the original, unedited slide on what constitutes normal testosterone levels. Unfortunately, this area continues to be a source of error and confusion.
In regard to hormone replacement therapy(HRT), the situation is unfortunately similar. For years most HRT regimens came in one or two strengths, which constituted “the right doses” for women. While dosing options have expanded some over the years, current concepts about dosing have been based on a small number of studies examining a small fraction of the tissues that are impacted by sex hormones, for example bone mineral density and hot flashes. Even in regard to effects on bone density and hot flashes, the type of sophisticated studies that would be needed to determine the estrogen levels required to provide optimal health benefits for the average woman, and the variance in response between women, have simply not been performed. Further, our current assumption that the dose that ameliorates hot flashes will provide the hormone levels for optimal lipolysis (fat burning), body configuration, muscle health, skin health, sexual function, cardiovascular health, sleep, lower urinary tract symptoms, cognitive function, hair and nail health, etc. is without scientific basis. For 30 years we have been studying the dose-response of all the various tissues responsive to sex hormone and have formed some general impressions about this, but there continues to be a massive need for more sophisticated, properly designed dose-response studies in regard to sex hormone replacement in both men and women. In the meantime, unlike in traditional HRT, we continue to individualize treatment in all of our patients in an attempt to determine the optimal dose of sex hormone treatment within the physiologic range to achieve the patient’s treatment goals, an approach we refer to as Sex Hormone Optimization Therapy (S.H.O.T.).
Black Pearl II: Challenging the received wisdom within the medical profession that testosterone replacement therapy causes atherosclerotic cardiovascular disease (ASCVD):
There were few things presented to us within our medical education that were taught with less thoroughness and more certitude than the “fact” that testosterone treatment was associated with an unacceptable level of increased risk of cardiovascular disease, and events and mortality from such. It is unclear when I would’ve thought to even challenge something presented with such certainty if I had been forced to by my clinical work. By the time I entered practice I was having some successful cases of treating resistant depression in men with low testosterone. These men’s mood not only improves significantly, but they and their families noted a marked improvement in other things like energy, arthralgias, adiposity, and sexual function. Not surprisingly, they wanted to stay on treatment long-term and this posed a problem for me because of the way that physicians have been terrorized about the idea of exposing patients to testosterone’s risks. Therefore, though like most physicians I had little extra time for such research, I poured myself into scouring the medical literature for studies pertaining to this issue. When I began I was not even questioning whether there was a cardiovascular risk, but only wanted to understand its severity and to become familiar with any clinical factors or patient characteristics that might further increase such risk so I could present the issue competently when discussing informed consent with my patients. To my shock, what I found I can only describe as appalling.
Presenting my findings in lectures at conferences was truly one of the most fascinating experiences of my teaching career. Because of the level of negative bias present in the audience, my approach to these lectures was unique compared to other subjects, and I would come around the lectern and began by asking the audience to clear the air and give me their strongest objections to testosterone therapy. One of the two most common was the firm belief of testosterone’s cardiovascular risk we are here discussing. I would then ask the audience to share the different studies that had demonstrated this risk. While the faces on the participants started off looking quite confident, as time went on in silence things started to change. I then encouraged them to work amongst themselves to see if they could better identify such studies, and then share their thoughts. As the silence continued a crowd become visibly more uncomfortable. After was clear that we can establish that there was no response, I asked them to reflect on the fact that we had all excepted something as a fact that none of us could share having ever been exposed to any scientific evidence supporting such. I then revealed that there were no properly designed studies that demonstrated such risk, even though testosterone therapy had been available for decades. In point of fact, the only signal of risk I could locate within the medical literature globally were assertions expressed in articles touching on testosterone therapy, which were supported by references, if any were used at all, that turned out to be case reports of patients who had experienced a cardiovascular event taking what would constitute a massive overdose of the hormone. These rare papers presented events that typically were associated with clotting and a body builder or athlete using anabolic steroids, though even in these rare cases the idea that testosterone was the cause was purely conjecture. To put this in proper context, I reminded them that anabolic steroid use at 2-10 times replacement doses was utilized for years by athletes and bodybuilders legally, and at the time
was still being used on a massive scale illegally (a practice that has continued to the present). I argued that this constitutes a massive experiment by millions of men with an overdose of testosterone, and even if we excepted that these were cases were caused by such treatment, to conclusions would seem unavoidable.
First, adverse events experienced when patients consume an overdose of any hormone or medication is not relevant to the safety of consuming normal levels of such. In this case, the rare cases cited in these papers suggestive of cardiovascular risk in the context of testosterone overdose were not relevant to the safety of physiologic testosterone replacement. To illustrate the implications of this, I asked them then to imagine what would happen if we did a similar experiment with all of the hormones we use clinically every day and believe to be safe compared to testosterone; for example insulin, cortisol, or thyroid. I then presented the audience with a series of queries. First I asked if it would take 40 years to have clear evidence of serious adverse effects. The answer was no. Would we have only rare case reports of adverse events? The answer, no. I then asked if it would take 4 years; the answer was no. I then asked if it would take even 4 months, at which point the audience admitted that with any of these hormones, by 4 months emergency departments all over the country would be full of patients suffering serious side effects from each of these hormones, and certainly in the case of insulin a large number of body bags. Secondly, this data is consistent with the view that testosterone may be relatively safe compared to the hormones that we regularly utilize in clinical practice.
Having gotten the audience’s as attention and cleared away some of the bias, I would then proceed to a typical lecture on the diagnosis and treatment of low testosterone in men. When I did get to the point of discussing safety issues, I noted that it would also be erroneous to assume that there were no risks associated with physiologic testosterone replacement, since the issue clearly not been studied appropriately. Every hormone and chemical thoroughly studied that is vital for life has been shown to be associated with risks in excess and/or deficiency states, or in some patient populations with special characteristics. Further, I pointed out that there were multiple mechanisms by which testosterone could cause an increase in clotting events, all of which are of much greater concern if treatment is not conducted in a competent fashion, and especially when treating patients with higher baseline cardiovascular risks. I noted that testosterone’s effect of increasing blood count, if not managed appropriately, can lead to increased blood viscosity, a change known to be associated with an increased risk of clotting. Further, testosterone is converted normally to estrogen and it had been established that estrogen stimulates the clotting system. Therefore, excessive stimulation of that system or normal stimulation in patients with predispositions to clotting could also increase the risk of such events. Lastly, testosterone uncommonly causes fluid retention, which could lead to exacerbation of heart failure, though this was a concern restricted to patients with congestive heart failure, especially in those who also suffered from kidney failure. I also noted that these risks, with competent thorough care, were mainly preventable and, when not, readily treatable even with high-risk patients, something demonstrated by our excellent safety record in treating high-risk patients for several decades. I would follow this with a presentation of all the available studies that indicate that testosterone, when administered competently, should be of benefit to the cardiovascular system. I would end with a prediction that because of the very poor standard of care in regard to the provision of testosterone treatment that future studies that included high-risk cardiovascular patients would likely show some increased risk of cardiovascular events, and that this risk would become apparent early in treatment, consistent with clotting events. In fact, studies that have been published over the intervening years continue to be consistent with my original predictions.
Black Pearl III: “Testosterone increases your risk of developing and dying from prostate cancer” … I don’t think so Tim:
I just stated that there were few things presented to us within our medical education that was taught with less thoroughness and more certitude than the “fact” that testosterone treatment was associated with an unacceptable level of increased risk of cardiovascular disease, and events and mortality from such. Well, here is another of those “few”. I noted above that when teaching on the diagnosis and treatment of low testosterone in men that I took an atypical approach and started each lecture by inviting the attendees to “give me their best shot” as to why testosterone is too dangerous to utilizes as a treatment. Along with the alleged risk of cardiovascular disease, far and away the other most common response was the “fact” that testosterone caused prostate cancer and increased ones risk of dying of prostate cancer. I also previously noted that I responded by asking the attendees to share their knowledge of the scientific evidence supporting these risks. Like the risk for cardiovascular disease, the audience was unable to produce any high-quality evidence of this supposed “fact”. I would again note how strange it was that we would believe something that had been presented to us in the absence of fact, simply because those we respected presented it to us with such certitude. I would then proceed to review the evidence available, including slide on slide containing quotations by experts and expert panels admitting that there was no definitive proof that testosterone caused prostate cancer to occur, or that one’s risk of dying of prostate cancer was increased if it was diagnosed while on testosterone therapy. Already stunned, I would further disorient the audience by proceeding to examine my hypothesis that low testosterone increased the risk of delayed diagnosis of prostate cancer by PSA screening, a perspective supported by an abundance of scientific evidence and intuitive from what we had been taught about prostate cell biology and physiology (see Silent Partner I, below)…
Black Pearl IV: “Testosterone is contraindicated in all patients with a history of prostate cancer because such treatment increases the risk of dying from prostate cancer”:
… Perhaps the most controversial aspect of my lectures in the 90s was questioning the then long-established absolute contraindication to using testosterone in patients with a previous history of prostate cancer. Specifically, I questioned whether there was any credible science to support the view that treating patients with testosterone who had received definitive therapy for prostate cancer (that is were thought to be cared) was associated with increased risk of dying of prostate cancer. Again, I would ask attendees at my lectures to share their understanding of the scientific evidence that supported this view… again, the response was typically embarrassed silence. In fact, there was no such evidence and I therefore defended the position that the choice to treat or not to treat should be left to the patient, not their physician. Throughout our years we have been treating such patients who felt that her symptoms were intolerable and were willing to accept whatever risk existed. As noted below (Silent Partner I), the only cases of prostate cancer diagnosed in such patients was immediately upon initiation of treatment, simply revealing previous residual cancer that escaped what had been thought to be definitive treatment, and hidden on PSA testing because of their very low testosterone. Over the years all of our other patients have continued to show a lack of any evidence of recurrence. Further, an increasing number of studies from around the world have been published examining testosterone treatment in such patients, with results that continue to suggest that the risks versus benefit ratio of such treatment is positive, and the choice to proceed with such treatment should be left to the patient.
Black Pearl V: “Testosterone treatment is potentially dangerous because it can cause mood instability, irritability, anger, and aggression in men” … “there is an element of truth in every lie”
The other common objection that my work was greeted with by colleagues and students alike was the assumption that testosterone treatment can have dangerous effects on mood. Like other chronically excepted myths, I came to believe that there were truths that had sustained all of the major myths in regard testosterone. For example, it is true that testosterone therapy can lead to cardiovascular events, but it is a lie to associate this with testosterone replacement therapy (TRT), because those documented cases were within the context of individuals utilizing excessive doses of testosterone, not physiologic doses of proper TRT(see above; Black Pearl II). Further, it is true that testosterone therapy increases the risk of being diagnosed with prostate cancer temporarily after the initiation of therapy, but it is a lie to conclude that testosterone leads to more diagnosis of prostate cancer, more advanced prostate cancer at diagnosis or worsening outcomes from prostate cancer. Studies of long-term TRT demonstrate that this is a temporary phenomenon related to testosterone revealing prostate cancer earlier through stimulation of PSA production by prostate cancer cells, leading to the diagnosis of earlier stage cancer in patients on testosterone, and no increase in risk of prostate cancer diagnosis or mortality in the long run (in fact, competently delivered and monitored TRT may lead to earlier diagnosis and better prostate cancer outcomes; see Silent Partner I below).
In the same way, it is true that there are case reports of men experiencing severe emotional and mood disturbance when utilizing testosterone, but it is a lie to connect these cases of mood disturbance with appropriately administered TRT. In fact, my early clinical work and research convinced me that cases of mood disturbance as a consequence of testosterone were a consequence of inappropriate treatment characterized by excessive levels and fluctuations of testosterone (i.e. conventional dosing of Depo-Testosterone TRT- see Silent Partner XVI, anabolic steroid use, or intermittent compliance by patients with their TRT) often coupled with other mood-altering substances (anabolic steroid abusers), or related to the low testosterone state, and that properly dosed and timed TRT both improved mood and emotional stability and was essential for avoiding negative mood and emotional effects related to testosterone (see silent partner XI and XVI below ) Sadly, as of 2022 regimens utilizing inappropriate 200-400mg doses and 2-4 week dosing intervals remain common, even in research studies. (Deepika F. et al. 2022)
Silent Partner I: The hidden role of testosterone deficiency in false negative PSA testing, delayed diagnosis of prostate cancer, and negative prostate cancer outcomes
Shortly after leaving training and beginning my research with testosterone, I observed the sudden elevation of Prostate Specific Antigen(PSA) after beginning testosterone replacement therapy in a patient with a long history of low PSA measurements. I stopped his testosterone and PSA immediately fell back to his original, low level. The received wisdom at that time in urology was that such behavior by PSA was consistent with benign prostate tissue(an absence of cancer). Since testosterone deprivation treatment in patients with prostate cancer was known to suppress PSA levels, I questioned this assumption. Further, upon researching the issue in the medical literature I found that it had been established that both benign and cancerous prostate cells are stimulated to release PSA under the regulation of testosterone. I approached a urology colleague and explained my concerns and requested a biopsy, in spite of the patient’s currently low PSA level off testosterone treatment. My colleague agreed. Unfortunately, the biopsy demonstrated prostate cancer and subsequent evaluation demonstrated cancer that had been present for many years, in spite of his low PSA measurements previously. It appeared clear to me that testosterone treatment had revealed his cancer, and that his previously low testosterone had led to false negative PSA screenings in the past, delaying diagnosis. When serving with urologists on expert panels in regard to testosterone therapy I shared this case with many and my concerns as to its implications but was shocked to find that there was essentially no awareness or studies on this issue. Over the years we continued to experience such cases and repeatedly documented the revelation of previously present prostate cancer by elevations of PSA upon initiation of testosterone therapy. Interestingly, in contradistinction to my profession’s view of testosterone’s risk in regard to prostate cancer, these cases, and the basic science currently available relevant to this issue support the idea that low testosterone can delay diagnosis of prostate cancer by PSA screening. Over the years I have presented this at conferences but there is still no clear position by consensus experts on the subject. This is in spite of the fact that there are now well over 55 published papers whose results are consistent with low testosterone (untreated by TRT) results in more aggressive and extensive prostate cancer at the time of diagnosis, consistent with a delay in diagnosis. Unfortunately, to date, we have been able to publish this information in the medical literature.
Silent Partner II: The hidden role of testosterone deficiency in the development of metabolic syndrome and Type II Diabetes:
As noted above, in the mid-1990’s I began treating a significant number of hypogonadal men with testosterone replacement therapy. One of the observations that emerged from this work was that one of the most common patients found to have low testosterone were those with the characteristics of metabolic syndrome. My subsequent investigation of the research concerning testosterone’s impact on the various components of metabolic syndrome, combined with my own experiences in the treatment of such patients with TRT, has led me to the view that low testosterone is an early component of the metabolic syndrome in men. As noted earlier in this document, I previously submitted a paper concerning a case series of such patients in my practice and exploring the potential implications of such but, unfortunately, this paper was not accepted for publication when submitted. On the other hand, early in 2006 and years after the failed submission of this paper, a better study was published in JAMA supporting a link between low testosterone and the development of metabolic syndrome and Type II diabetes. I continue to espouse the idea that this link not only exists between low testosterone and metabolic syndrome, but that testosterone replacement therapy early in the course of this syndrome may be one of the most potent weapons currently available to physicians in the treatment of such patients and for the prevention of Type II diabetes. As time has gone on more observational studies have linked low testosterone with metabolic syndrome and the risk of developing type 2 diabetes. At last, in 2021 the first double-blind, randomized controlled trial was published demonstrating that testosterone treatment after 2 years was associated with less development of diabetes compared to placebo. Further, a cohort of patients in the same study that already had the diagnosis of type 2 diabetes was shown to be more apt to revert to pre-diabetes status on testosterone versus placebo. We are hopeful now that this application of testosterone treatment will finally get the research attention it deserves.
Silent Partner III: The hidden role of testosterone deficiency in socialization, assertiveness, and Social Anxiety Disorder (SAD) in men and women:
Early in the 1990s, our work with testosterone revealed many unexpected findings. One such finding was obvious positive changes in a number of patients’ confidence, assertiveness, and social interactions. While this certainly applied to the patient’s sexuality, the effect was often more general impacting all aspects of social interaction. These findings were not simply reported by the patient and their mates, but also clearly evident on examination in the office. Findings at times were striking and came to include some patients with syndromal social anxiety, results that I have shared in a number of lectures around the country. At the time of our original observations, I could not find any reports of such in the medical literature globally. Ironically, I eventually found some references in the biologic literature, where testosterone’s essential effect on socialization in primates was often treated as a truism. This has become one of the longest and most important foci of research at DTRC and we have noted changes in these patients that would be typically described as aspects of personality. Fortunately, over the years there have emerged some small studies utilizing a single dose of testosterone that have demonstrated significant temporary improvements shortly after injection in social anxiety scales in both men and women with SAD. Further, we have witnessed improvement in other anxiety disorders, and there is also more emerging scientific literature confirming such.
Silent Partner IV: Allergic Rhinitis associated Nasal Obstruction induced Sleep Disorder as an unappreciated contributor to fatigue, executive dysfunction, depression, and reduced quality of life(QOL):
In the mid-1990’s I became convinced of the hypothesis that, like the nasal obstruction caused by adenoid hypertrophy, the nasal obstruction caused by allergic rhinitis could be the cause of a significant sleep disorder that can include sleep apnea. On the other hand, this hypothesis takes note of the fact that nasal obstruction from allergic rhinitis is much more common than that caused by adenoid hypertrophy. It also posits that the seemingly inexplicable negative impact on quality of life and morbidity (such as diminished energy, daytime learning, and alertness) associated with allergic rhinitis are secondary to this obstruction. Further, the hypothesis indicates a possible connection to recent findings of research studies demonstrating an association of prolonged sleep disturbance in children and adolescents to an increased risk of developing ADHD, depression, and substance abuse in adolescence and, that until proven otherwise, it should be assumed that the sleep disorder resulting from the nasal obstruction of allergic rhinitis could be the cause of the same type of morbidity. This hypothesis was presented at several conferences both inside and outside the United States at the end of the 1990s. I requested and received a grant from one of the major pharmaceutical companies for the publication of this hypothesis, and received such. However, in the midst of preparing the paper for submission, I learned that this “unrestricted educational grant” had been revoked by the pharmaceutical company following a change in management. Unfortunately, this paper remains unpublished, and to my knowledge, no other paper has since been published exploring this issue. On the other hand, there continues to be emerging data that is supportive of this hypothesis. For example, in 2004 a study was published that demonstrated an increased risk of the development of ADHD in children and adolescents who suffered from allergic rhinitis (Brawley A et al. Allergic rhinitis in children with ADHD. Ann Allergy Asthma Immunol. 2004 Jun;92(6):663-7). The authors went on to note in the discussion that nasal obstruction associated with allergic rhinitis is a possible mechanism for this association. More importantly, a study released in 2006 examined the impact of nasal obstruction caused by adenoid hypertrophy in patients who also had ADHD (reference on file). These patients were treated with surgical adenoidectomy and a majority of the patients experienced either significant or total resolution of their symptomatology after adenoidectomy and off ADHD medical therapy. It should be noted that this hypothesis has significant implications for the treatment of allergic rhinitis. Every consensus panel and expert guideline issued over recent years has recognized that nasal corticosteroids are unquestionably the best treatment for patients with nasal turbinate hypertrophy and nasal congestion and/or obstruction. If the hypothesis is accurate, patients with such symptoms not treated with nasal corticosteroids could be at risk of significant morbidity that is preventable with appropriate treatment.
Silent partner V: Low testosterone associated with oral estrogen treatment(contraceptives and HRT) and the potential effect on sexual function, energy, muscle health, athletic performance, adiposity, and mate selection:
One of the most underdiagnosed and undertreated conditions in health care is a low sexual desire in young women. Further, for those that do suffer such, there is typically the assumption that the impact of sex hormones on sex is something that is confined to older women. In the late 80s while still in training, we repeatedly documented extremely low free testosterone in patients on oral contraceptives who also suffered from sexual dysfunction, commonly low libido, diminished arousal, and difficulty achieving orgasm and/or diminished intensity orgasm. We also came to identify similar cases among women on oral estrogen HRT. Upon researching the issue, I found support for this relationship and papers identifying low free testosterone as a consequence of oral estrogen’s effect on dramatically increasing sex hormone binding globulin, and the application of oral contraceptives for acne in light of this phenomenon. On the other hand, many of our patients noted that they had complained to the gynecologist about their diminished sexual function after starting oral contraceptive pills (OCPs), and yet were told, “it’s not related” or “they don’t do that” or “your problem isn’t medical”. The response of many of these patients was truly astounding. Many of these couples had severe issues with relationship dynamics and multiple identified sources of conflict that were not improving in therapy by the time they consulted with me. In fact, sometimes these issues were so severe that I doubted the significance of their low testosterone as a contributing factor to their sexual problems. On the other hand, such patients often, in spite of my doubts, not only responded robustly in regard to their sexual function but in the context of a more nurturing relationship were able to work out practical solutions to their other differences. This has been an ongoing focus of research, and besides impaired sexual function, many of these patients also have exhibited diminished muscle mass and strength, fatigue, and increased adiposity that correlated with the onset of their sexual complaints and that also improved upon treatment with testosterone. Further, we have observed changes in relationship dynamics and marital outcomes that are supportive of the view that this impact of OCPs may be impacting mate selection. Over the years other studies have been published that support many of our findings in relation to oral contraceptives, including negative effects on energy, muscle mass, and athletic performance, and with a particularly interesting number of studies documenting changes in women’s perception of the OCP that would be indicative of a potential effect on mate selection.
Silent partner VI: The unperceived effects of sex hormone fluctuations and deficiencies on mood and migraine expression and treatment resistance:
Perhaps the most fascinating branch of our research began while I was still in training, the effect of sex hormones on mood, anxiety, and migraine. I soon became convinced that in women most if not all such deleterious effects were a consequence of sex hormone fluctuation. In what little medical literature existed on the subject, this was thought to be likely the basis for PMS. On the other hand, upon researching the subject and ongoing study in our own patients it appeared that any clinical situation in which significant sex hormone fluctuation occurred was associated with deleterious effects on mood and/or migraine in some women; new mood or migraine symptoms, exacerbation of their previously diagnosed mood or migraine disorder, and/or emergent resistance to their current antidepressant or migraine therapy. Further, as an advocate of the view that anxiety and depression commonly occur together, we examined patients more closely and became convinced that these same clinical circumstances were often associated with new symptoms of anxiety, exacerbation of previously diagnosed anxiety disorders, and/or emergent resistance to their antianxiety treatment. Consistent with that, we have utilized sex hormone treatment and seen improvement of symptoms in patients experiencing increased anxiety or depression in the following clinical circumstances: monthly before the menstrual cycle (premenstrual dysphoric disorder), postpartum, ongoing during irregular periods, during the menopausal transition, and during infertility treatment. All of these clinical circumstances are associated with increased sex hormone fluctuation. We have continued to study this phenomenon and our findings indicate that there are a large number of women experiencing significant mood and anxiety symptoms related to sex hormone fluctuation, that such is a common cause of resistance to antidepressant and antianxiety treatment, and that this is one of the most neglected areas within psychiatry, and is an area of huge opportunity for improvement of the care of women suffering from anxiety and depressive symptoms.
In regard to men, fluctuations of the magnitude that would cause mood, anxiety, or migraine do not appear to occur naturally, as they do at certain times over the life cycle in women. On the other hand,
as my career progressed and the emphasis on diagnosing and treating psychiatric disorders in my practice increased, I became concerned as both a practitioner and educator with the significant number of patients who did not significantly respond to psychotropic medications. While comorbidities such as occult sleep apnea and hypothyroidism were well described as possible causes of such non-response in some patients, there were clearly other male patients for which such non-response was currently inexplicable. This led me in the mid 1990s to examine the possibility of low testosterone in such patients. In fact, not only was low testosterone frequently found in men with poor or partial response to psychotropic medication, it was also not infrequently found in men in their 20’s, 30’s, and 40’s, and treatment of such deficiency frequently produced a marked improvement in such patients’ response to antidepressants. Further, while significant sex hormone fluctuations do not occur naturally in men, it soon became clear that testosterone treatment-induced fluctuations had the potential of causing the same kinds of issues as we had witnessed in women. Since that time there has been an increasing amount of data, especially from Great Britain and Australia, but also more recently in the United States that supports the importance of diagnosing comorbid hypogonadism in male patients with depression. On the other hand, research and discussion of the effects of testosterone on migraine in men and the common phenomena of suboptimal testosterone treatment-induced exacerbation of mood, anxiety, and migraine remain grossly underrepresented in our literature and education. I continue to advocate both the need for further research as well as improved education of clinicians on these issues.
Silent partner VII: The unperceived effects of sex hormone fluctuations and deficiencies on emotional expression, perception, judgment, and outlook:
Some of our most interesting and yet troubling cases over the years have involved patients whose symptoms in the context of sex hormone fluctuations or deficiencies and subsequent response to sex hormone treatment indicate the potentially profound effect on emotional IQ, perception, and judgment. On reflection, these symptoms should not have been unanticipated or a subject treated with a mixture of silence and contempt by the medical profession. The disturbing effects of hormone fluctuations are clearly well recognized, and such is frequently utilized as a source of humor in sitcoms featuring a woman experiencing PMS. In such cases there is the presence of extreme mood disturbance and irritability in the context of the woman not perceiving their own symptoms, but rather perceiving such symptoms in the person they are interacting with. In point of fact, such symptoms and their impact on a patient’s life and relationships are anything but humorous. Fortunately, skilled treatment to deliver therapeutic, smooth sex hormone treatment can resolve such symptoms. Further, though at the time studies were lacking in the medical literature, the same kind of emotional irritability and mood disturbance in the context of disturbing emotional perception was exhibited not infrequently in men with low testosterone, or who were being treated with testosterone treatment regimens that inappropriately create testosterone fluctuations. Tragically, a number of DTRC patients, once successfully treated, have concluded that previous relationships could have been saved had they found appropriate treatment sooner.
Interestingly, many women during their mate’s initial evaluation have described changes regarding their outlook, often noting that their mate used to be a “glass half-full” optimist, who has turned into a “glass-half-empty” pessimist while denying any such change in perspective. On multiple occasions, this latter phenomenon has demonstrated potentially tragic consequences. In one case the male patient involved presented with typical symptoms of hypogonadism, but was also refusing treatment for a highly curable cancer, something the spouse insisted would have never been the case with her previously optimistic husband. Impressively, once treated with testosterone the spouse noted that the patient was back to his old, optimistic self and had aggressively pursued treatment for his cancer, which was subsequently cured. In another case, a patient with a similar history of pretreatment mood and outlook disturbance and excellent response to TRT subsequently refused treatment in the hospital for severe hyponatremia. His family contacted me emergently and noted that he had returned to his old, pre-TRT pessimistic demeanor after stopping his testosterone treatments the month previous. In fact, when I examined him in the hospital he continued to refuse treatment and was requesting DNR status. Fortunately, he did agree to restart TRT, and by the next day had morphed back into his positive, pre-hypogonadal self, and enthusiastically signed permission for treatment. Such cases continue to be a focus of research at DTRC and raise many disturbing questions that await more thorough and comprehensive research.
Silent Partner VIII: Cardiovascular disease, obstructive sleep apnea, and risk of dementia:
While I was in training I was surprised to learn that neither cardiovascular disease (CVD) nor obstructive sleep apnea was considered risk factors for dementia. I found this incomprehensible and raised the issue with my instructors, again risking heresy. I pointed out that it was then currently believed that for diagnostic symptoms of dementia to occur requires about a 30% loss of brain cells, leading researchers to search for potential causes that would produce global brain insult, neuron loss, and atrophy gradually over years prior to diagnosis. Further, atherosclerosis was posited to result in a gradual buildup of plaque over years, clogging up tiny blood vessels first, and potentially causing damage in tissues throughout the body, including the brain. From the standpoint of apnea, sleep experts were asserting that millions of people had undiagnosed sleep apnea, experiencing repeated episodes of low oxygenation nightly, insulting the brain globally. Hence, it was my contention that both of these diseases provided just such a mechanism of gradual neuron loss over years. I was shocked to find out that there were no properly designed studies examining this theory at that time. Once in practice, I continued to present this hypothesis when relevant during lectures and while serving on consulting boards. Over recent years both cardiovascular disease and sleep apnea have received more attention with respect to a possible role in dementia. Specifically, CVD has recently been included in the risk factors for dementia and apnea is under investigation as such. This is very good news as both are modifiable risks for a condition that has long been viewed as both untreatable and unpreventable.
Silent partner IX: Sleep apnea as a cause of resistant depression:
As noted previously, while I was in training I became increasingly concerned about the effects of sleep apnea. In light of the fact that studies indicated that the vast majority of patients with apnea were undiagnosed and because of its documented effects on energy, mood, and memory, I became suspicious about its role in resistant depression. Because of my medical background, I have referred patients with treatment-resistant depression and did a thorough workup based on the typically known things that can cause such. Unfortunately, a subset of these patients demonstrated an absence of any such conditions. I began testing such patients for occult sleep apnea and was surprised by the number that had significant apnea on testing. Further, the results of CPAP treatment were often impressive, with some patients being restored to a full response to their antidepressant, while a minority were able to stop antidepressant therapy and maintain full remission from symptoms. As a medical educator who frequently spoke at conferences on the treatment of depression, I began including a discussion of apnea as a cause of treatment resistance in the early 1990s. Unfortunately, at that time I had never seen that issue discussed either in a lecture or journal article devoted to the treatment of resistant depression, though my primary care colleagues who were experts in the treatment of depression also felt that the contribution of OSA to resistant depression significant. Therefore, we began using our participation on the various expert psychiatry advisory and editorial boards to which we belonged to advocate the need for screening for sleep apnea in patients with treatment-resistant depression and to include a discussion of such screening in continuing medical education (CME) journal articles and lectures to physicians around the country. Though progress was frustratingly slow, over the years this eventually became a standard component of the discussion of the causes of resistant depression, and screening for sleep apnea in that context has become much more common.
Silent Partner X: A tale of three tissues; low testosterone and the seemingly paradoxical lack of improvement in menopausal-related sex drive, muscle mass, and incontinence on traditional HRT:
The incidence of both urinary and fecal incontinence increases after the loss of sex hormones associated with menopause. Therefore, it was hoped that HRT would help prevent the development of such. While conventional oral HRT improved many other pelvic-related symptoms associated with menopause, studies have demonstrated that this is not the case with urinary incontinence. In fact, the risk for such may actually be increased on HRT. This seemingly paradoxical effect of conventional oral HRT has remained unexplained.
Another paradox is the seemingly contradictory effect of menopause and conventional HRT respectively on muscle mass. The loss of sex hormones at menopause has been associated with an increased risk of adiposity, loss of muscle mass and tone, and diabetes. Currently available scientific evidence was exhaustively reviewed (Mauvais-Jarvis F) and a clear positive effect of conventional oral HRT on the postmenopausal risk of adiposity and diabetes. On the other hand, it was noted that there was a lack of consistent evidence of a clear improvement in muscle tone and mass.
A third seeming paradox is the apparent contradictory effect of menopause and conventional HRT respectively on sexual desire. Sexual function is also known to deteriorate at menopause, particularly with decreases in libido and lubrication and increase in pain with intercourse. Conventional oral HRT consistently improves lubrication, while many women continue to complain of diminished or absent libido. Numerous trials of testosterone replacement have shown efficacy in correcting this complaint.
My research in testosterone treatment in women convinced me that testosterone deficiency holds the key to unraveling these seeming paradoxes. It must be remembered that what we commonly call “hormone replacement” is actually partial replacement. That is, the ovaries make 3 hormones: estrogen, progestogen, and testosterone, and when the ovary stops working after menopause the levels of all 3 hormones dramatically drop. However, conventional HRT only replaces estrogen and progestogen, leaving the patient with only the testosterone that is produced from the adrenal gland and thereby lowering testosterone levels from premenopausal levels. To make matters worse, not only does conventional HRT not replace the testosterone produced by the ovary, but the estrogen in conventional HRT also stimulates the liver to produce more binding proteins. Importantly, only testosterone which is free from protein binding is biologically active. Hence, this effect of estrogen treatment on binding proteins predictably lowers free testosterone even further, an effect more strongly associated with oral estrogen preparations. In fact, in our experience, some patients on conventional oral HRT have extremely low levels of free testosterone.
Why am I suggesting that this resolves the 3 apparent paradoxes discussed above associated with conventional HRT? In fact, it is known that the main anabolic effects on muscle mass in women is also from testosterone, though normal levels are about a 15th of what is typical in men. Further, sexual desire and arousal are strongly impacted by testosterone in women, and the striated muscle of the pelvic floor and urinary and rectal sphincter would also be expected to be responsive to testosterone. Hence, since conventional HRT lowers free testosterone, in some women dramatically, in those patients experiencing low free testosterone loss of muscle mass and strength, loss of sexual desire and arousal, and urinary and fecal incontinence would be expected possible side effects of treatment. Certainly, one would not expect this regimen to correct these problems that are a natural consequence of the menopausal transition and its associated loss of estrogen, progesterone, and testosterone. Results from our research of adding testosterone to the HRT regimen in patients that would otherwise be low in testosterone, along with the available relevant studies addressing this issue, strongly support that this is the key to avoiding these paradoxical effects of conventional HRT.
Silent Partner XI: Sex hormone treatment (SHT) induced hormone fluctuations as the cause of mood, anxiety, and mood symptoms:
As noted previously, hormone fluctuations can exacerbate mood and migraine syndromes in women, leading to our use of hormone treatment and subsequent discussion of such treatment in my lectures to physicians addressing the treatment of mood disorders. One of the most common objections I was confronted with by the physicians attending such conferences was the well-known paradox that many women experience worsening migraine and/or mood phenomena with sex hormone treatment, rather than improvement. This fact had previously disturbed me as well when I was a resident in training. Hormone products (such as HRT and oral contraceptives) were once-a-day treatments that many of us supposed were associated with smooth, 24-hour delivery. The paradoxical effect on some women caused me to form the hypothesis that these treatments were not actually delivering smooth levels of hormones. To pursue this hypothesis I petitioned two of the pharmaceutical manufacturers of these products to obtain their pharmacokinetic data (the behavior of the blood level of the hormone over 24 hours). In fact, this data confirmed my suspicion that these products, contrary to the common impression in the medical profession at the time, do not have a smooth 24-hour delivery system, but create a hormone fluctuation similar to the natural fluctuation causing the patient’s migraine and/or mood phenomena. I further hypothesized that in women whose metabolism of hormones is more rapid than average, the level of fluctuation created would worsen rather than improve their symptoms. To test this I improvised to create regimens that would be expected to eliminate these fluctuations, which in fact relieved the patient’s migraine and mood on treatment, confirming the hypothesis. Over the years this view has come to be more generally accepted and a few contraceptive and HRT products have even been created in an attempt to minimize and/or eliminate these fluctuations.
Silent Partner XII: Invisible in the shadows of Science; the hidden physiologic derangements of obesity and the silent suffering of millions:
OR
Auto de Fat: The medical profession’s medieval attitude toward the treatment of excess adiposity and obesity:
As I entered medical school there was no condition that was met with more contempt and ridicule than obesity. This was true both inside the profession and in society generally. One of the most disturbing observations I made early in medical school was the discrepancy of fact between what we were taught about the causes of excessive adiposity and the regulation of body composition and what one actually observed in the patients we were treating. It became clear that, like many outpatients we treated, many of our hospitalized patients under direct observation failed to lose weight on diets designed by our dietitians. Further, interviewing such patients revealed recurrent components in their history that did not conform to our current understanding. When I asked my teachers about these discrepancies my questions were often met with a dismissive, even hostile attitude. Repeatedly it was emphatically expressed that if a patient’s history did not conform to our current concepts, that history must be fabricated. That is, if the patient’s labs did not confirm hypothyroidism and yet they maintained that they were unable to lose weight utilizing prescribed diet and exercise programs, the patient was diagnosed as either being in denial or a liar! Other preceptors responded by informing me that obesity “isn’t a medical problem, but a behavioral problem”, and therefore had no place in medical education. This view was popular in spite of the fact that beyond smoking, few conditions rivaled obesity in the magnitude of their negative effects on health. Further, this ideology assumed that current science had delineated all of the causes of low metabolism and obesity and, therefore, if their condition didn’t make sense to us, it couldn’t be real. The only problem was that this assumption was without a scientific basis.
Though I found support from my father on this issue, generally speaking, my rejection of my profession’s medievalism caused me to be viewed as a heretic. My continued work with patients once in practice only reinforced my conviction that our current understanding of obesity was woefully inadequate, and led to my hypothesis that there were endocrinologic and other physiologic derangements beyond traditionally defined hypothyroidism that explain the severe resistance to conventional weight loss measures experienced by so many of our patients. Our work with sex hormones quickly demonstrated that sex hormone deficiencies in men and women were one such cause, observations confirmed by a multiplicity of published studies in the medical literature. On the other hand, sex hormone deficiencies did not explain the resistant adiposity of many of our patients, so I theorized that some patients have peripheral resistance to the thyroid, similar to the peripheral resistance to insulin experienced by patients with prediabetes and diabetes. Further, I was unable to find research that had disproven such, peripheral thyroid resistance would explain a lot of what we were observing in patients, and there were published scientific studies confirming that many patients did not experience remission of their hypothyroid symptoms with conventional thyroid replacement.
Interestingly, in a subset of patients experimentation with higher levels of thyroid lead to dramatic long-term improvement in weight loss and other hypothyroid symptoms without any symptoms of toxicity. Unfortunately, these have proven to be a small minority of obese patients. The large number of patients remaining with resistance to weight loss led me to the conclusion that there must be other endocrinologic disturbances that remained unidentified. On the other hand, I was convinced that these derangements would be quickly delineated by appropriate research if the profession and the FDA would reverse their opposition to such treatment and open the flood gates of pharmaceutical research investment. As the years passed I became increasingly pessimistic about whether I would ever see the day when this would happen. Fortunately, it eventually became accepted by the government that obesity-related health problems would bankrupt the entitlement programs (Medicare, Medicaid, VA) if this epidemic of obesity was not addressed. The FDA reversed its position and as predicted, the subsequent massive investment in research by the pharmaceutical industry has led to rapid advancement in our understanding of the causes of obesity, confirmed the veracity of those much-maligned histories provided by our obese patients, resulted in the ongoing development of a multiplicity of effective treatments, and opened a new era of vindication, respect, and hope for those suffering from obesity. On the other hand, the history of the medical profession’s approach to obesity will serve as a poignant example of how bias and bigotry can subvert the greatest of intellects and dangerously retard the progress of medical science.
Silent partner XIII: The unappreciated impact of sex hormone-induced alterations of perception, emotional competence, outlook, and judgment on clinical assessment in the office and on the outcomes of research studies focused on psychiatric conditions influenced by sex hormones:
As dramatic distortions in judgment, outlook and expression, and perception of mood and emotion continued to be documented in our research, the need for analyzing the implications of such became obvious. One of the consequences of such ongoing analysis resulted in the hypothesis that these distortions had serious potential implications in regard to the accuracy of clinical assessment in the office and in research studies. The marked discrepancy in these parameters between the patient and reality (as represented by the perceptions of those intimately associated with them) suggested studies relying on the perceptions of such individuals could significantly compromise the findings of such. For example, studies of premenstrual dysphoric disorder (PMS) examining the incidence of the disorder and/or the response of the disorder to treatment typically rely on self-rating symptom scales, which, based on our research, could clearly lead to errors. These errors span the spectrum from a gross underestimation of the severity of the symptoms to complete denial of the existence of such symptoms, phenomena that we have commonly documented in our patients. In fact, this phenomenon is so common that standard procedure at DTRC assumes that the patient’s assessment of their symptoms of mood and emotion may be inaccurate, and that accurate assessment of mood and emotional symptoms requires feedback from both the patient and their mate (or someone else who has intimate contact with them), as well as objective direct assessment by the physician. The same can apply to studies in hypogonadal men in regard to the assessment of the frequency and severity of mood and emotional derangements, and the response to treatment of such. This is an area in great need of further, in-depth research.
Silent partner XIV: The distortions in our understanding of the pathophysiology, clinical course, and responsiveness to the therapeutic intervention of Social Anxiety Disorder (SAD) related to the lack of early primary care-based intervention and treatment:
One of the most fascinating odysseys of my career has been the exploration of the effects of testosterone on confidence, assertiveness, and socialization. But even prior to that time, social anxiety disorder was one of the primary examples I utilized in making my case the need for primary psychiatry or psychiatry in the primary care setting. A case that I became involved with early in my career and later published (Dumb and dumber … see below under papers) because of its implications on this issue, and on our understanding of the clinical course and potential effectiveness of treatment for social anxiety disorder (SAD). I still had a primary care practice along with my other clinical research work and came into contact with this young woman because I was her primary care physician and she was needing referral from her “gatekeeper” for neurocognitive testing because of progressive decline of her performance on national standardized testing over recent years. She was 17 at the time of this interaction and her performance had declined to the point where colleges were not wanting to admit her. She did see a neurologist who was investigating the source of her neurocognitive problems. Having cared for her for a number of years none of this made much sense and so I asked to evaluate her before I approved of the testing.
In point of fact, on taking an extensive history it became clear that she had experienced the emergence of social anxiety around the time of puberty, with progressive worsening of severity of the symptoms which had eventually become associated with depression. Though no one at her school, among her doctors, or her family had made any observation in regard to social anxiety at this point, and though the patient herself did not make a connection, on routine family history 2 aunts were identified that lived as recluses because of severe aversion to social settings. She was no longer attending social settings and spent most of her time in her bedroom. Also of interest was the fact that the patient had been an excellent student prior to puberty, still performed excellently in homework assignments on all of her subjects, but could not present in class and was progressively failing in her performance on observed testing. I diagnosed her with social anxiety disorder associated with test-taking anxiety and comorbid depression, the latter surely a consequence of her observing the possible outcome of her future life as exemplified by her aunts. With talk therapy and pharmacologic intervention, she improved rapidly and was soon able to stop pharmacologic treatment. She not only got into college but prior to graduating she gave a speech in the auditorium of her college to her classmates about her condition. She proceeded to a career as well as marriage and children and only intermittently has utilized medication.
In light of the fact that the current view of SAD treatment typically has very modest benefits, this case had apparently led to an invitation to serve on Pfizer’s International Social Phobia Board, a great honor that I was perplexed at receiving. There were perhaps a dozen of us from different countries serving on this board, requiring that we use headphones and interpreters. Among us was Michael Lieberman, one of the foremost experts on social anxiety disorder in the United States. It wasn’t long before it became obvious from questions directed at me that I was there because of the paper I had published on this case and the fact that it challenged our view of how responsive this disorder was to treatment. Frankly, the participants found her clinical course somewhat unbelievable.
In responding to their interest, I took the opportunity to ask the group what was the average number of years patients suffer from SAD prior to diagnosis and participation in clinical trials. Without hesitation Michael Lieberman stated that it was around 22 years, slowing down to a pause as the words left his mouth, apparently already grasping where I was headed. I pointed out that chronic social anxiety patients have been documented to commonly go on to develop other comorbidities like depression and substance addiction, and that those conditions typically lead to the diagnosis of social anxiety. That is, patients have severe disease complicated by other severe conditions before we diagnose and treat them for their SAD. I suggested that this delay in diagnosis, it’s associated development of serious comorbidities, and their cumulative degradation of the patient’s quality of life and future prospects was the key difference between the response of my patient and the response of those patients typically treated in psychiatric settings and in clinical trials. I noted that the only reason that I was able to diagnose her early was that I was a primary care physician that reviewed psychiatry as a part of primary care practice and routinely screened for such conditions.
Since that time things have both progressed and regressed. It has become accepted that psychiatry is an integral part of primary care. On the other hand, because of the drastic changes in healthcare over recent years and the greatly reduced amount of time primary care physicians are allowed to spend with their patients, this, from a practical standpoint, is of much less benefit in regard to optimal primary care screening for psychiatric illness.
Silent partner XV: The unacknowledged role of declining sex hormones in sarcopenia, cachexia, frailty, and loss of muscle and bone mass associated with an activity as we age and the serious implications of such:
Early in my work with testosterone in the 1990s, the effects on muscle mass and many patients led me to become intrigued with other possible applications of testosterone treatment in regard to some of the most common problems that physicians confront. I began to speculate about whether sex hormone treatment, in combination with exercise and protein supplementation, might be an effective intervention to help prevent and treat the loss of muscle mass and function in patients with age-related muscle loss left (sarcopenia), muscle loss associated with disease (cachexia), muscle loss associated with frailty, and muscle loss associated with disuse atrophy. While I speculated, a case forced my hand. An 86-year-old patient was to present the foremost intriguing cases of my early career (see YouTube channel for a video presenting more details of the case). He was previously independent but experienced a spinal fracture that landed him in the hospital. He had failed physical therapy and continues to be unable to ambulate without assistance. The orthopedic surgeon approached his daughter about DNR status and placement in a long-term care facility. The patient was in fact, so I informed the daughter that she did not feel a burning about this decision, as it wasn’t hers or the physician’s decision, but only her father’s. I told her I could try some experimental treatment if her father was interested and she soon presented to my office with her father in a wheelchair. He had clearly experienced significant muscle atrophy and weakness and I explained the basis of our approach using testosterone and protein supplementation in combination with calcitonin to improve both his muscle and bone mass and the need to send him back through physical therapy on treatment. He made clear that he would not consent to a long-term care facility under any conditions and was eager to try experimental therapy regardless of the risks. Point of fact, his response to physical therapy was markedly different and shocked his therapist. He was within a few months able to write with his walker down the hall, even though I did not encourage this. He resumed gardening and other activities, and his daughter noted he also had resumed his interest in the ladies. He lived happily at home for the next couple of years with an excellent quality of life until his sudden death by the long-anticipated rupture of his long-standing aortic aneurysm at the age of 89. This case lead to many others, developing into one of the most intense areas of research at DTRC as discussed more in detail below (“In my time of dying” … Experimental protocols for muscle health optimization to promote muscle function, quality of life, and independence to achieve optimal health while we age and prevent and treat deconditioning and frailty in elderly patients. See also: Experimental protocols for muscle health optimization for developing, protecting, and rehabilitating elite athletes).
Silent partner XVI: The contribution of improper dosing frequency with injectable testosterone-based TRT to many of the common myths regarding the efficacy and safety of TRT … An ongoing Odyssey:
When I began clinical work with testosterone replacement in training, the small number of physicians utilizing such provided treatment with depotestosterone injections, dosed 200-400mg every 2-4 weeks, with monthly injections the most common regimen. What little literature existed on the subject advocated this regimen, but without providing scientific evidence for such a dosing interval. Further, the few patients treated in this fashion relayed a history consistent with a week of improvement followed by a “crash”. Uncomfortable with this situation, I requested the relevant data from the manufacturer (pharmacokinetic data). This data was revealing and consistent with a peak effect within 24 hours, followed by decreasing levels of testosterone until returning to pretreatment levels in 10-12 days. It explained the temporary benefit followed by a “crash” described by the patients and their mates, and the mood irritability component of this “crash” indicated that men also can experience mood instability in response of sex hormone fluctuations(What my female patients have referred to as “Male PMS”). This time course for testosterone levels also made clear that one would predict that achieving smooth, therapeutic levels throughout the dosing cycle would require at least weekly dosing. I proceeded to study weekly dosing, though my patients often informed me that their urologist, endocrinologist, or PCP thought I was making treatment unnecessarily inconvenient, expensive, and/or excessive, even though such comments were without scientific basis and inconsistent with how we determine dosing with other treatments. Once teaching at conferences, I was fortunate to finally have the opportunity to confront and expose such unscientific nonsense. As time wore on, weekly dosing has become more of the accepted standard. However, during the same period of time, by utilizing mate feedback during reevaluation it became clear that a large percentage of our patients were still exhibiting a Jekyll to Hyde transformation at the end of each dosing cycle, though, like females with PMS, the patient often minimized their symptoms or even blamed their mates as the guilty party. On the other hand, men often did note on careful questioning that they noted a significant change in their workouts at the end of each week, with some even declining to work out the day before their next shot. On lab testing performed the day after their shot and immediately preceding their next shot it was confirmed that weekly dosing was still associated with large fluctuations in T levels, with levels often dropping >400 points and completely consistent with the patient’s clinical history. We then proceeded to twice weekly shots, which resulted in smooth symptom improvement (without “PMS-ing”) in 95% of patients. We could never have advanced to optimal dosing without our own research into the pharmacokinetics of testosterone and ongoing thorough re-evaluation of the patient’s sex hormone-influenced symptoms that included feedback from their mate on mood symptoms, a practice we have maintained and advocated ever since.
Another consequence of this inappropriate dosing that has characterized conventional Depo-Testosterone TRT for decades is the creation of some of the most commonly held myths concerning the dangers of testosterone treatment. As noted above, this dosing can create fluctuations associated with significant aggression, depression, and emotional instability (see Black Pearl V above). In point of fact, these symptoms are produced by fluctuations caused by the inappropriately timed dosing frequency of conventional TRT or by partial compliance with testosterone treatment by patients. It has also contributed heavily to the myth that competently prescribed TRT commonly causes high red blood cell counts and thick blood (polycythemia), and the view that if this occurs an appropriate response by the treating physician would be to lower the dose to where the excessive elevation in blood count no longer occurs. Interestingly, at the same editorial board meeting mentioned above (see Black Pearl I) I was engaged in another intense debate surrounding this very issue. When we came to the slide noting side effects of TRT, it listed polycythemia and recommended lowering the dose as an appropriate response. No other action was recommended. Since no one else spoke up, I challenged my distinguished colleagues about the scientific accuracy of this statement. Though my challenge was met originally with incredulity, I persisted and requested appropriately designed studies supporting this view. In fact, as I already was aware, there were none. The only “studies” that could be found were reports of patients experiencing polycythemia on the conventional Depo-Testosterone treatment of the time, 200–400 mg every 2-4 weeks. I reviewed the known property of testosterone to stimulate red blood cell production and the known pharmacokinetics of Depo-Testosterone, the latter demonstrating that this dosing regimen was well documented for producing excessive peak levels of testosterone markedly above the physiologic range that would be expected to excessively stimulate RBC production leading to polycythemia. Therefore, I noted that this left us without any properly designed studies or other credible scientific evidence supporting the conventional view. On the other hand, I noted that we had been studying the issue for years, managing testosterone strictly within the physiologic range and that patients experiencing polycythemia on physiologic levels of testosterone were worked up for another cause of their polycythemia. More importantly, this approach documented other causes of polycythemia in 95% of these patients, including genetic mutations known to cause polycythemia and conditions associated with hypoxia-related polycythemia, such as chronic lung disease (COPD) and obstructive sleep apnea (OSA). Further, I pointed to the inconsistency of suggesting that normal levels of testosterone delivered via TRT cause polycythemia, when any patient presenting for evaluation of polycythemia who is not on testosterone treatment is assumed to have some other cause and appropriately evaluated to identify and treat such. In light of these facts, I asserted that all scientific evidence available indicated that our slide should state that polycythemia on TRT either indicates inappropriately excessive TRT outside the physiologic range or another cause of polycythemia and that all patients with persistent polycythemia with testosterone levels in the normal range should be evaluated for other conditions known to cause such. Finally, I concluded that teaching physicians to respond to this situation by ignoring what is clearly a signal of undiagnosed disease and simply lowering the testosterone level constitutes malpractice. Though it was clear that they originally believed they would be able to mount a defense, after thorough discussion and appeal to the literature through our administrative staff it was conceded that they had no such defense. Pathetically, when I received my final edited copies of the slides, no changes had been made to correct this dangerous misconception, which has continued to be conveyed in lectures and publications around the country since.
(Sadly, as of 2022 regimens utilizing inappropriate 200-400mg doses and 2-4 week dosing intervals remain common, even in research studies. Deepika F. et al. 2022)
Exploring the utility of subcutaneous implanted sex hormone pellets in patients with conditions caused or exacerbated by sex hormone fluctuations:
As noted repeatedly in this section, the adverse effects of sex hormone fluctuations and deficiencies have constituted some of the most important foci of my research for over 30 years. Conditions affected by such include disorders of mood, anxiety, and migraine. Other symptoms documented in our research include impairment of emotional perception and expression, outlook, and judgment. I quickly realized that sex hormones were not commonly in use to treat such symptoms in clinical practice and that there was minimal, if any, research to guide such treatment. As I embraced the therapeutic concept of the superiority of treating the underlying cause of a disease or symptoms whenever possible, I became determined to study how to utilize sex hormones effectively to address such conditions. The goal in the treatment of such conditions was to utilize sex hormone treatment that would replace these fluctuations or deficiencies with smooth, therapeutic blood levels of sex hormone. Surprisingly, though initially I didn’t realize it, achieving this was one of the greatest obstacles I confronted in my attempts to determine how to use sex hormones effectively to treat such conditions. In women, as noted in the previous section, I soon became familiar with the well-known paradox in medicine that many women experienced worsening migraine and/or mood phenomena when treated with sex hormones, rather than improvement. In fact, my own clinical experience quickly came to confirm the reality of this seeming paradox. My odyssey in researching this issue and unraveling the reason for the seeming paradox (discussed above) led me to improvise with available products to custom design regimens that attempted to achieve smooth, physiologic sex hormone levels. While this led to an improved rate of success, the results were still far from ideal. As time went on, FDA-approved products came on the market designed to address this issue, including transdermal formulations of contraceptives and HRT, though transdermal patches continued to demonstrate considerable peak/trough fluctuations in some patients, as well as fluctuations caused by poor adherence of the patch to the skin. More importantly, missed doses by patients remained a very common cause of sex hormone fluctuations and their related symptoms.
With men, the situation was very similar. At the time that I entered practice the most common form of TRT was Depo-Testosterone injections, which were routinely prescribed to be given every 2-4 weeks. Because the pharmacokinetics of Depo-Testosterone demonstrated that a dose only lasted 10-12 days, marked hormone fluctuations followed by periods of hormone deficiency occurred as a matter of course with this dosing regimen. We significantly reduced such fluctuations by requiring patients to dose injections once-twice weekly. However, this made this approach considerably less attractive to patients, multiplied the opportunity for missed doses, and was treated as a radical deviation from normal treatment by many of those few specialists who prescribed testosterone at the time. Daily testosterone gel and patch formulations were associated with fewer fluctuations, but all of these treatment approaches were plagued with fluctuations related to missed doses, a common phenomenon associated with symptoms severe enough for some mates to request discontinuation of treatment. As so much of our work was focused on conditions associated with hormone fluctuations, I continued to search for a better treatment approach for these patients. Through a small number of published studies I became aware of sex hormone pellets for subcutaneous insertion. I was impressed by the slow, gradual release of the hormone as the pellets slowly dissolved. Further, they could be placed through a brief minor procedure every 3-6 months and, when properly timed, had clearly the smoothest delivery of any sex hormone treatment currently available, closely approximating the body’s natural delivery of hormone in the bloodstream. Finally, this approach had the potential of eliminating the most common cause of fluctuation, missed doses, with the ability to objectively verify the patient’s compliance with treatment, and intervene to ensure appropriate compliance. With rare exceptions, we continue to utilize all the various hormone formulations available, but this form of treatment has been an excellent option for those with conditions related to sex hormone fluctuations and/or struggle with compliance with taking medications.
There have been criticisms of utilizing sex hormone pellets for HRT, including by The Endocrine Society and the North American Menopausal Society, recommending they not be used, based on a number of objections stemming from the fact that they are produced by compounding pharmacies, and not FDA-approved products. Ironically, I voiced many of the same criticisms regarding compounding pharmacies long before these organizations expressed such, but do not agree with their blanket disapproval of all compounding pharmacies. Certainly, the lack of FDA approval raises the concern about product quality, purity, and consistency, which is why I argued that compounding pharmacies seek FDA certification. In point of fact, some compounding pharmacies have gone through the expensive and extensive process to do so. Such pharmacies should be commended for doing so, rather than lump them together with others who have not. Further, I raised concerns about sterility based on the lack of an adequate methodology to ensure pellet sterility by nearly all compounding pharmacies when I started to practice. Again, some compounding pharmacies have adopted the appropriate and expensive methodology of ionizing radiation to sterilize sex hormone pellets and should be recognized for doing so instead of being lumped in with other pharmacies that have not. Some have objected to the fact that different patients experience different levels of sex hormone to the same pellet dose, and it is unclear how much variation is experienced in the same patient over time on the same dose. It is argued that this creates unnecessary costs due to more need of monitoring blood levels with this form of treatment. In point of fact, based on data presented to the FDA by all currently available FDA-approved sex hormone products, interpatient variability in regard to blood levels achieved on any given dose of the product is a shared characteristic by all currently available sex hormone treatments. Further, what data exists for FDA-approved products, consistent with our own long-term research, indicates considerable intrapatient variability on these products. Therefore, the only way to know the level of hormone a patient is being exposed to when utilizing any of these treatments is to monitor their blood levels. Some have inquired why we do not use the FDA-approved testosterone pellets, Testopel. Unfortunately, this product only comes in 75 mg doses, which leaves little flexibility in dosing. More importantly, it means that to achieve the doses that are typically optimal for patient symptom response one would have to use a massive number of these pellets compared to compounded pellets, increasing the risk of complication, the likelihood of wound discomfort, and dramatically increasing the cost of treatment. Until this situation changes we believe that testosterone pellets from an FDA-certified compounding pharmacy that provides a vast variety of dosing options to be the superior choice. Finally, a large amount of research over many years has demonstrated that compliance is one of the strongest determinants of safety and efficacy of medical treatments and, as noted previously, subcutaneous pellet delivery both facilitates compliance while also allowing such compliance to be monitored and documented. Therefore, at DTRC we continue to feel that subcutaneous sex hormone pellets continue to be an excellent option for sex hormone treatment.
De Wester’s Defense System Model of Anxiety:
As a result of my work with anxiety patients in the 1990s, I became convinced that the anxiety system of the brain was essentially analogous to currently available complex, computer-enhanced defense/security systems designed to prevent and counter threats. One component of this hypothesis suggests that the various components of complex defense/security systems are analogous to the components of the anxiety system of the brain and that the various types of malfunctions experienced by such components, and the manifestations of such, are analogous to the various types of anxiety disorders and their corresponding symptoms. This model accurately predicts the kind of traumas and life circumstances that have been shown to be risk factors for developing anxiety disorders. Further, this model not only appears to predict accurately what therapies are effective in the treatment of anxiety disorders, but it also provides a mechanism for anxiety’s perplexing and hotly debated relationship with a number of chronic medical diseases. Finally, I found this model not only practical in helping physicians to understand the disease and its treatment, but also therapeutic for patients in their struggles to not only understand their disorder, but also to embrace and execute effective treatment. This hypothesis has been presented at numerous CME regional and national conferences since the year 2000.
Preventive Psychiatry:
As the concept of primary psychiatry has become more accepted, there emerged another need within the practice of primary care psychiatry. I have espoused the idea that there is also preventative care in psychiatry and that such care can only be rendered by effectively integrating primary care physicians into the practice of such. As noted previously, I have published a case report, “Dumb and Dumber” that highlighted the potential for this concept in regard to preventing a lot of the morbidity currently associated with late diagnosis and treatment of psychiatric disorders. Like the concept of primary care psychiatry before it, preventive psychiatry may be one of the next great frontiers in clinical psychiatry.
Streams from the Heart:
Two of the primary functions of our emotions are a) to motivate us to act, and b) to communicate to others our needs, desires, values, and state of mind. Unfortunately, my study of human emotions and my work with patients struggling with emotional problems suggest that emotional expression is one of the greatest sources of compromised mental health and dysfunctional communication in relationships. In fact, it is uncommon to find patients who feel comfortable and competent in dealing with emotions; both their own and/or the emotions of others.
In the 1980’s I began an odyssey that originated in an attempt to understand my own emotional make-up and, in the process, came upon an intriguing analogy. This analogy compares the flow of water in nature with the flow (expression) of emotion and is alluded to in many ancient sources, including the Bible. While I could not locate any detailed application of this analogy to test the limits of its application, my own meditations upon it soon pointed to the possibility that it possessed both broad and deep application in illuminating human emotion.
Like a large, mountainous island, we each possess an emotional landscape with an easily visible exterior and a deeper, less visible interior. Further, the storms and showers from where all water flow originates, correlate to events in life from which all negative emotions originate. Further, water gradually coalesces into larger and larger individual bodies of flow that are called rivers. These rivers correspond to individual emotions which, like rivers of water, have been given names. Importantly, like the process by which water forms streams, emotions also flow based on a principle I refer to as The Law of the Path of Least Resistance of Emotional Flow (Expression). Interestingly, in regard to natural water flow, the occurrence of controlled flow has always been that flow associated by man with peace, happiness, and life. Conversely, the two polarities of drought and flooding correlate to danger, fear, the barrenness of life, and death.
Man’s attempts to alter the flow of water, healthy and unhealthy, constructive and destructive, and for benevolent or malevolent motivations, along with their associated results, correlate with amazing similitude to man’s various attempts to alter the natural flow of emotion.
This brief overview hopefully illustrates why I have utilized this analogy extensively in both one-on-one and group therapeutic situations. The analogy helps patients better understand the following:
- Their own emotional landscape, its origins, and its consequences in regard to relationship dynamics and mental health.
- Grasp what measures and resources must be employed if dysfunctional flow patterns are to be restored to normal patterns of flow.
- To comprehend and navigate more effectively the emotional landscapes of those with whom they relate.
The ongoing utilization and self-application of this analogy by patients have been accompanied by the ongoing emergence of new observations and insights that continue to illuminate the full extent of its application.
“In my time of dying” … Experimental protocols for muscle health optimization to promote muscle function, quality of life, and independence to achieve optimal health while we age and prevent and treat deconditioning and frailty in elderly patients.
One of the biggest threats to elderly individuals in regard to dying or losing their independence and quality of life is the development of severe deconditioning, weakness, or frailty. As people are living more commonly into their 70s, 80s, 90s, and beyond this is becoming a massive problem. This has not only become one of the greatest concerns of the elderly but has increasingly caught the attention of middle-aged individuals as we observe a very disturbing picture as our parents struggle to navigate this part of life. Even the medical profession and government health care agencies are increasingly recognizing the disastrous consequences of these conditions on medical and surgical outcomes, the number of people requiring long-term care, life span, and the enormous associated financial costs of such. Unfortunately, there are few proven, effective interventions. Over the years, DTRC has done some preliminary research involving the addition of sex hormone treatment to conventional rehabilitative care to improve the patient’s response to such, with impressive results. More recently we’ve added some other experimental treatments to design a unique protocol that we are currently studying in a pilot case series in the hopes that the results of such will lead to a randomized controlled trial. Access to the details of this protocol are currently restricted to those involved directly in the research. Those who have an interest in participating in the research should contact us to discuss such.
Experimental protocols for muscle health optimization for developing, protecting, and rehabilitating elite athletes
Another major opportunity for improvement in muscle health optimization is in regard to creating more effective rehabilitation regimens for elite athletes; regimens to minimize loss of muscle mass and strength, speed recovery, and make a return to competition both quicker and safer after injury and/or surgery. Past research at DTRC and currently available relevant scientific studies support the view that sex hormones clearly impact muscle health in ways that could potentially impact the risk of injury, muscle mass and strength, athletic performance, and response to conventional rehabilitation treatments in injured patients. On the basis of these considerations, we developed the hypothesis that both natural and induced sex hormone deficiency states negatively impact these issues, while optimal sex hormone physiology has the potential to improve such. Further, we have recently designed an experimental protocol combining uniquely designed sex hormone regimens with other experimental treatment modalities to test this hypothesis. Access to the details of this protocol is currently restricted to those involved directly in the research, but those who have an interest in participating directly in the research should feel free to contact us directly to discuss such.
ORIGINAL PAPERS
Original Papers:
Efficacy of Vitamin B6 Therapy in the Absence of Obvious Deficiency; A Review of Literature. Residency Research Project. Presented at St Francis Hospital Residency; May, 1989. Unpublished.
De Wester, JN. Against Assembly Line Sports Physicals. American Family Physician. 40 (3): 53, 1989 Sept.
De Wester, JN. Taking a Long-term View of Depression, A Special Report. Postgraduate Medicine;1995: 21-35
Length of Antidepressant Therapy – Consensus Conference Statement
(Letter – University of Minnesota publication), Fall, 1995. Sent to Primary Care providers nationwide
Length of Antidepressant Therapy – Consensus Conference Monograph.
Univ. of Minnesota in conjunction with Health Learning Systems, Inc.
Spring, 1996; Sent to Primary Care providers nationwide
De Wester JN. Primary Psychiatry at the Crossroads.
The Journal of Family Practice. Volume 43, No. 6 (supplement), 1996. Pages S1-S3.
De Wester JN. Recognizing and Treating the Patient with Somatic Manifestations of Depression. The Journal of Family Practice Volume 43, No. 6 (supplement), 1996. Pages S3-S14. (republished in 3 European medical journals)
De Wester, JN. Silent Partner I: The hidden role of testosterone deficiency in false negative PSA testing, delayed diagnosis of prostate cancer, and negative prostate cancer outcomes. 2009. (unpublished – see Hypotheses section for comments).
De Wester, JN. Silent Partner II: The hidden role of testosterone deficiency in the development of metabolic syndrome and Type II Diabetes; A Pilot Study Examining the incidence and implications of testosterone deficiency in obese, hyperinsulinemic males with a Family History of Type II Diabetes; 2001 (unpublished – see Hypotheses section for comments).
De Wester, JN. Silent Partner III: The hidden role of testosterone deficiency in socialization, assertiveness, and Social Anxiety Disorder in men and women. 2008. (unpublished – see Hypotheses section for comments).
De Wester, JN, et al, The Efficacy of Internasal Fluticasone Propionate in the Relief of Ocular Symptoms Associated with Seasonal Allergic Rhinitis. Allergy and Asthma Proc 2003; 24 (5): 331-337.
De Wester, JN. Dumb and Dumber – A Case of Social Anxiety Presenting as Declining Academic Performance: Implications for Primary Care, Primary Psychiatry. 2001;8(12):68-69.
De Wester, JN. Adding Bupropion to Eliminate Venlafaxine Induced Sexual Dysfunction: A Case Report. 2001 (presently unpublished)
De Wester, JN. Mehle, M. E., Nathan, R. A., Internasal Corticosteroids in Allergic Rhinitis: Comparisons with Oral Non-Sedating Antihistamines and Leukotriene Antagonists. Monograph, April 2001.
De Wester, JN, Mehle, M. E., Nathan, R. A., Pharmacotherapy for Allergic Rhinitis: Leukotriene Antagonists Compared with Internasal Corticosteroids and Non-Sedating Antihistamines. Monograph, January 2002
De Wester, JN. Motor Vehicle Accident Associated with Nefazodone-Induced Side Effects: Implications for Clinical Practice: A Case Report. 2002 (presently unpublished)
De Wester, JN. Silent Partner IV: Allergic Rhinitis Induced Sleep Disorder and Quality of Life: A New Perspective on an Old Problem. 2002 (unpublished)
De Wester, JN. Expression of Mania After Initiation of Testosterone Replacement Therapy: A Case Report. 2004. (currently unpublished)
De Wester JN. AHEF(American Health Education Foundation) Blueprint for Behavioral Change; 1997.
Drossman DA, De Wester J.N. Irritable Bowel Syndrome: A Multicomponent Approach to a Heterogeneous Syndrome. 2001. (unpublished).
De Wester, JN, Primary Psychiatry at the Crossroads. The International Journal of Psychiatry in the Community. Volume 1, No. 1, 2002: 2-3
De Wester, JN, Why Primary Care Psychiatry. The International Journal of Psychiatry in the Community. Volume 1, No. 1, 2002: 4-12
De Wester JN, Wise D, Metabolic Syndrome. American Academy of Family Practice. CME Bulletin. Feb. 2004
Rapaport, M.H., Skrky, S.B., Katzelnick, D.J., De Wester, J.N., Harper, J.M., and McCrary, E.E.; Time to Response in Generalized Anxiety Disorder in a Naturalistic Setting: Combination Therapy with Alprazolam Orally Disintegrating Tablets and Serotonin Reuptake Inhibitors Compared to Serotonin Reuptake Inhibitors Alone.
Psychiatry; Volume 3 No. 12, 2006:50-59
Chung H, Culpepper L, De Wester J, et al, Defining the challenge: Recognizing and treating bipolar disorder wherever patients present. The Journal of Family Practice 2007; 56(11) (Suppl): S3-S4.
Chung H, Culpepper L, De Wester J, et al, Recognizing and understanding bipolar disorder. The Journal of Family Practice 2007; 56(11) (Suppl): S5-S10.
Chung H, Culpepper L, De Wester J, et al. Clinical management of bipolar disorder: Role of the primary care provider. The Journal of Family Practice 2007; 56(11) (Suppl): S11-S18.
Chung H, Culpepper L, De Wester J, et al. Treatment by phase: Pharmacologic management of bipolar disorder. The Journal of Family Practice 2007; 56(11) (Suppl): S19-S27.
Chung H, Culpepper L, De Wester J, et al. Recognizing bipolar disorder on initial presentation: A case study with decision points. The Journal of Family Practice 2007; 56(11) (Suppl): S28 – S32.
De Wester, J. N., et al, Comprehensive Review of the Evaluation and Pharmacologic Management of Hypoactive Sexual Desire Disorder. 2016 (unpublished)
BOOKS/WORKBOOKS
Books/ Workbooks:
American Roulette: The Risks and Consequences of Sex Outside of Marriage
(Currently for office distribution and patient education only)
De Wester’s Textbook of Psychiatry for Primary Care Physicians. (Unpublished).
In the mid-1990s I endeavored to recruit a number of my primary care and psychiatry colleagues who were leaders in the field of the practice of psychiatry in the primary care setting to bring about something we felt was essential to firmly establish and maintain the practice of primary care in psychiatry. The first of its kind, this was to be a textbook devoted to the practice of psychiatry in the primary care setting supported by an ongoing, comprehensive educational support system for those physicians engaging in such. To this end, a professionally designed proposal was prepared for soliciting grant support for the development of this endeavor which contained the following: table of contents for the textbook; detailed outline of the content for each chapter; associated clinical diagnostic, screening, and monitoring tools; list of prospective authors who had agreed to contribute chapters and/or serve as ongoing educational faculty; and website for ongoing interactive support, including CME accredited case-based lectures and videos. Unfortunately, the necessary funding was not forthcoming and this need remains largely unmet.
The Foundations of Mental Health, 1st edition, 1991, 2nd edition, 1997
Text and workbook designed for psychotherapy performed in a Primary Care
setting. The contents are geared toward problems relating to depression and/or anxiety associated with insecurity and deficits of self-esteem. (Currently, its use is reserved only for the author and is under continued development.)
Testosterone Replacement Therapy: Making An Informed Choice – A patient education booklet, April 2004
Pandora’s Medicine Box. 2018.
Contents compiled over the last two decades with chapters featuring patient cases that highlight various effects of sex hormones on various tissues and conditions that have inspired the various foci of DTRC research. (Currently unpublished; It is anticipated that the contents of various chapters will be featured in Vlogs on DTRC YouTube Channel. Much of the material above under “Other research. Original hypotheses, clinical tools, and concepts, and therapeutic analogies:” constitute the material forming many of the chapters of this work.).
ACKNOWLEDGEMENTS
Acknowledgments:
I could never have experienced the various things I’ve been blessed to participate in without the help of so many others. First and foremost growing up in the nurturing environment of two loving and encouraging parents, and a father who was the model of what a physician should be. He taught me the importance of thinking independently and standing apart, if necessary, for what is right. On the other hand, even with such advantages, I doubt I could’ve taken all the various paths I have explored without the encouragement and support of many others. I had the good fortune to attend the St. Francis Hospital Family Residency Program under the direction of Dr. Richard Feldman, who provided an environment where psychiatry was viewed as a proper specialty to be included in primary care work. He also encouraged us to explore our special interests and concerns within the vast scope of specialties that comprise medicine, an environment that encouraged me to become involved in clinical research. Further, I was greatly impacted by his foresight in having a Ph.D. psychologist, Dr. Don Fleener, as a member of his faculty. Don provided regular lectures (referred to by the residence as “donference”) on nonpharmacologic treatment of psychiatric conditions and gave us the opportunity to explore providing basic talk therapy in a primary care setting. Further, Dr. Fleener also provided clinical support and encouragement in regard to my concerns about what I perceived as the imbalances contained within what had been presented as the biochemical theory of psychiatry. Dr. Feldman also ensured that we were surrounded by an impressive clinical teaching faculty that included some of the finest physicians I’ve ever known, ensuring that I would leave training optimally prepared. My father was a clinician who saw it important to also spend time teaching other doctors, and Dr. Feldman shared his view that, in spite of the prevailing attitudes in medical education of the time, clinicians make the best teachers of clinicians. Without question, this greatly influenced my future commitment to being a medical educator. In my early years traveling as a teacher, I had the good fortune of being taken under the wing by Dr. Joseph Lieberman, who served for many years as the Head of Family and Community Medicine at Delaware School of Medicine. He was a great role model and friend, and I consider him to have been the country’s finest primary care medical educator of his time. Last but not least, I have been blessed by having a long-suffering mate who has put up with all of the challenges and frustrations of living with an idealist.
