Dr. Ali’s Course on Hormone Health


Majid Ali, M.D.

I present the subject of sex (gonadal) hormone health by raising three questions:

  • What did my professors and medical textbooks teach me about hormonal balance?
  • What did evolutionary intelligent design teach me about hormonal homeostasis?
  • What did my patients—the truest of all my teachers teach me about hormonal healing?

What Did My Professors Teach?

In 1958, my medical professors did one-hormone-one-symptom thinking. They taught us to do the same. They lectured about estrogens, progesterone, and testosterone as single entities, and seldom, if ever, talked about how these pieces fitted into the ever-changing kaleidoscope of the health/dis-ease/disease continuum. Yes, they did teach that too much testosterone is bad for women and execess estrogens are not good for men. Back then, not much was known about the hormone receptor dysfunction—most doctors still do not think of the receptors—so one cannot think unkindly of my professors then. What can one say of medical professors who still do not think of hormone receptors? Or the doctors why never attempt to restore hormone receptor health?


Hormone Receptor Restoration(RRT) 

Hormone receptors are proteins with complex and malleable structures, some traversing the cell membranes multiple times, and some anchored to cell innards. Nature conferred remarkable malleability and resilience on hormone receptors—that resilience, however, is not enough to withstand the onslaught of chemicals presently soaking human habitat. Among the consequences of that global chemicalization is the age of hormone receptor burn-out, which has brought forth epidemics of menstrual and menopausal disorders—severe menstrual syndrome, too much flow, scant flow with clots, anovulatory state, endometriosis, polycystic ovarian syndrome, and what may be designated as “pseudomenopause”—a state of presumed menopause in which menstruation resumes with robust non-hormonal integrative managment plans and remains regular for years to come.

The hormone receptors can be viewed as crank-shafts that are turned by hormone molecules working as cranks. The turning of those crank-shafts transmits information to various hormonal pathways which, in turn, activate specific enzymes, hormone response elements (pre-genes), and genes. In this context, I use the term receptor burn-out for a state of receptor unresponsiveness caused by being disfigured, twisted, jammed, clogged, or otherwise rendered dysfunctional. There is an enormous number of environmental pollutants with strong structural homology with natural hormones. Some of those compounds have a greater affinity for hormone receptors than the hormones themselves. Those compounds either jam or disarm hormone receptors. Such endocrine disruptions cause reproductive dysfunctions in humans and animals on an unprecedented scale.


Hormone Receptor Dysfunction 


What Did Evolutionary Intelligent Design Teach?

Human beings are energetic-molecular kaleidoscopes in which all pieces—hormones, hormone recptors embedded in cell membranes, and DNA response elements in the present context—sense and respond to the changing needs of all other pieces. When one thing in this kaleidoscope changes in one way, everything changes in some way.

The discussion of the roles of genes and environments in hormonal health are frivolous, since gene-environment interactions are dynamic and ever-changing. Otherwise we humans would have been microbes—at some level, it seems to me, we still are.

What Did My patients, the Truest of My Teachers, Teach?

My patients dared me to reach beyond the one-hormone-one-symptom one-dimensional thinking.
They compelled me to think five-dimensionally about hormonal health and healing . Specifically, they raise the following five questions:

* What do hormones do?
* What do hormone receptors do?
* What does the liver do?
* What does the bowel do?
* What does spiritual equilibrium do for gonadal hormonal equilibrium?

These questions force vus to think holistically and examine the essential connectivity of various ecosystems in the body.


SEX HORMONES Five Dimensional View from Majid Ali on Vimeo.


I care for my patients with menstrual and menopausal abnormalities with non-hormonal oxygen therapies. I do so because I get far superior long-term clinical results with this approach. For nearly three decades, I have not found it necessary to prescribe synthetic estrogens and synthetic progesterones for teenagers and young women with menstrual problems. During these years, I also did not find it necessary to prescribe Premarin (a synthetic estrogen) and Provers (a synthetic progesterone) for women who needed hormone therapies for peri-menopausal or menopausal symptoms. As for switching from synthetic HRT to naturally-derived hormones, I was unable to do so in three cases (less than one percent).

Estradiol from Majid Ali on Vimeo.


Say NO to Synthetic Hormones for Post-Menopausal Hot Flushes Majid Ali MD from Majid Ali on Vimeo.


Does Progesterone Protect Against Breast Cancer Majid Ali MD from Majid Ali on Vimeo.


Paxil for Menopausal Hot Flashes. Really!

To my great surprise, in early 2014, the Food and Drug Administration (FDA) approved Paxil by another name (Brisdelle, a brand of paroxetine) for treating hot flushes associated with menopause. What did not surprise me about this was that this approval was strongly opposed by FDA’ own advisory committee ( Reproductive Health Drugs Advisory Committee), Specifically, Committee, the Committee had concluded, by a vote of 10 to 4, that the overall benefit–risk profile of the drug did not justify its approval.

The Drugs Advisory Committee duly pointed out that the drug had taken teenagers life by inducing suicides.

Over the decades of my clinical work, I have had my share of patients whose lives were made miserable by menopausal hot flushes. Never once did I find it necessary to consider any antidepressant drugs for controlling this problem.

Causes of Severe Menopausal Hot Flushes

Severe menopausal hot flushes are heightened vascular (vaso-motor) responses to hormonal disruptions rooted in disturbances in the bowel-blood-liver axis. How do I know this? Severe hot flushes of my patients were controlled only after I addressed these problems along with a program of hormonal normalization with naturally-derived hormones, guided by blood hormone tests.

My Seven for Menopausal Hot Flushes

Following are the seven main components of my program (presented in detail in the companion article entitled “Integrrative Program for Menopausal Syndrome.”

* Insulin-reduction diet

* Optimal Hydration

* Progesterone

* Estrogen

* Folic acid

* DHEA

* Elimination or reduction of caffeine intake


Hot Flashes Return After Going Off the Diet . Why from Majid Ali on Vimeo.


How Effective is Brisdelle (a Paxil imitator) for Menopausal Hot Flushes

Minimal, even if the company data is believed. Below is text from The New England Journal of Medicine (May 8, 2014) on this subject: Doubtful. The efficacy of Brisdelle was established in two randomized, double-blind, placebo-controlled, multicenter clinical trials. Among a total of 1184 menopausal women who had a median of 10 moderate-to-severe hot flushes per day, Brisdelle was shown to provide modest relief in comparison to placebo. For example, at week 12 in one study, there was a median reduction from baseline of 5.9 moderate-to-severe hot flushes per day with Brisdelle as compared with a median reduction of 5.0 per day with placebo (median treatment difference, 0.9; P<0.01). At week 12 in the second study, there was a median reduction from baseline of 5.6 moderate-to-severe hot flushes per day with Brisdelle as compared with a median reduction of 3.9 per day with placebo (median treatment difference, 1.7; P<0.001).”


Illustrative Case Studies

Below, I include three case studies to illustrate three core aspects of the Unifying Dysox Model of Hormone Disorders. Each case sheds light on the clinical significance of the model.

Case 1: Polymenorrhea Treated With the RRT Model

In June 2006, a 43-year-old woman presented with twice-monthly periods, symptomatic autonomic intolerance, and persistent fatigue. The integrative RRT plan for her focused on robust bowel and liver detox therapies, antioxidants, redox-restorative therapies, antigen immunotherapy for IgE-mediated responses, and 15 mg of Armour thyroid extract. No synthetic hormone or phytofactor remedies with hormonal effects were included in her program between January 2007 and June 2007. Pertinent laboratory and clinical outcome data of this case are presented in Table 3. Note that she had serious hypocholesterolemia which improved modestly during the period of integrative management.

During the June 2007 visit, the patient spoke the following words, “My periods became normal in frequency and amount of flow within three months of following the treatment plan [June to September 2006]. I took 15 mg of Armour thyroid. You told me I could double up on the dose because it is a small dose. But I didn’t need to. Then in April [2007] I ran out of Armour. I did not have a period for seven weeks. This was the longest I went without a period. Can a small dose of Armour make a difference like that?” Her menstruation was restored with reintroduction of 15 mg of thyroid extract.

Table 3. Case 1. Polymenorrhea and Dysautonomia

in a 43-Year-old Woman Treated Successfully With RRT

Laboratory Data  

                                    June 2006               June 2007  

Cholesterol                          133                       147

Estradiol                              105                       116

Progesterone                        0.3                        1.5

Testosterone                         N/A                        38

FSH                                     7.88                      22.1

Clinical Outcome*

Overall symptoms                 -3                          +2

Dysautonomia                       -3                          +2

Sleep                                    -3                         +4

 *Clinical outcome scale: -4 to +4


Case 2: Control of the Postmenopausal Syndrome With the RRT Model

A 51-year-old, six-year postmenopausal patient was seen in 2003 for severe hot flashes, myalgia, gastroesophageal reflux disorder, and chronic fatigue. Serum C-reactive protein value was 11.3 mg/L. The last menstrual period was in 1997). In 2004, she bought a bakery business, which required her to work 12 to 16 hours a day, and brought heavy exposure to flour dust and molds. The data for business stress and changes in serum estradiol levels are correlated in Table 4. She responded well to the integrative plan, and then was absent for follow-up. She returned in March 2007 with a severe relapse of postmenopausal symptoms, persistent fatigue, and myalgia. The significant rises in the serum levels of IgE antibodies with specificity for four molds are shown in Table 5. The integrative RRT plan for her focused on robust oxystatic therapies, bowel and liver detox regimens, antioxidants, redox-restorative agents, and hydrogen peroxide foot soaks. No hormone therapy was administered between January 2007 and June 2007. Her program compliance was good, and she reported a near-complete relief of her symptoms.

Table 5. Case 2. A 51-Year-Old Woman With Stress-Induced Fall in Estradiol Levels Followed by Improvement With RRT. Scale of stress: 1 to -4

                                2003             2004            2005            2006              3/2007            5/2007

Estradiol pg/mL          56.9           27.7         N/A         N/A            zero            26

Stress                          1                2             3             4                3                 1

 

Table 5. Case 2. Increased Mold Exposure between Years 2004 and 2007 Is Indicated by Rising Levels of Allergen-Specific IgE Antibodies.

 

Specific IgE               2004            2007

 

Alternaria                  127           192

Epicoccum                 163            203

Fusarium                   127            167

Penicillium                  55            132

 

 

Case 3: Treatment of Amenorrhea with the RRT Model After the Failure of High-Dose Synthetic Hormone Therapy

A 36-year-old presented with a four-year history of Type I diabetes and chronic fatigue syndrome. Following menarche at age 13, she had regular menstrual cycles for nineteen years. Within several months of the onset of diabetes and chronic fatigue, she developed oligomenorrhea for which her gynecologist prescribed combined estrogen and progesterone therapy without success. A diagnosis of “hypothalamic brain suppression” was made by her gynecologist. She was treated with large doses of Provera and Premarin without benefit. Other symptoms included troublesome memory difficulties, episodes of palpitations, abdominal bloating and cramps, and chronic constipation. Prior to the age of 32, she suffered from acne, some nasal allergy and some “food reactions.” She received multiple amalgam fillings, but otherwise considered herself an athletic individual who lifted weight and ran regularly. She developed chronic knee pain which she attributed to overexercising. She was prescribed Naprosyn and given steroid injections for pain without much benefit. She received multiple courses of antibiotics for upper respiratory infections. Her weight had been stable at 120 lbs

 

On physical examination, she appeared weak, dehydrated, and anxious. She weighed 132 lbs with a pulse of 66/min and blood pressure of 110/80. Her abdomen was bloated and deep tenderness was elicited in both lower quadrants. Multiple deeply situated myofascial trigger points were detected in soft and periarticular tissues in limbs and torso.

 

An individualized integrated management program was initiated following the general guidelines described later in this article, with a focus on restoring the bowel, blood, and liver ecosystems. Her synthetic hormone prescriptions were discontinued. Instead, she was put on initial doses of 10 mg of soybean-derived progesterone and 10 mg of pregnenolone in daily doses, and 15 drops daily of tinctures of black cohosh, licorice, dong quai, and red raspberry. Her menstrual flow resumed, first irregularly and scantily, later with increasing regularity within eight months. At fourteen months, she reported “regular” menstrual flows at 26-29 days, lasting for four to five days. Her serum hormone assay data are given in Table 6.

Table 6. Case 3. A 36-Year-Old Wman With Amenorrhea Corrected 14 Months With a Receptor Restoration Therapy (RRT) Approach. Sequential Serum Hormone Levels Obtained at 5, 8, and 11 Months Are Displayed.

Hormone*

5 Months

8 Months

11 Months

Estradiol pg/mL

365

279

89

Progesterone ng/mL

23

1.1

19.5

Testosterone ng/mL

66

56

38

LH mIU

8

6.5

8.8

FSH mIU

8.1

21

5.7

Prolactin Units ng/mL

5

15

10

* All values were determined with blood samples drawn during the early third week of the menstrual cycle.

Case 4: Estrogen Abuse Prevented with the RRT Model

In April 2004, a 58-year-old woman was seen for incapacitating fibromyalgia, tachycardia, episodes of hot flashes, sweating, anxiety, multiple soft tissue trigger points,and episodes of vaginal spotting. In 2002, her gynecologist prescribed 0.625 mg of Premarin and 10 mg of Provera for control of hot flashes. Her symptoms recurred after an initial period of relief. The hormone doses were increased progressively when her symptom recurred after each increase. Despite incremental doses, her symptom-complex worsened. An endometrial biopsy showed endometrial hyperplasia with atypical changes. Table 7 shows sequential changes in serum estradiol levels establishing the existence of a serious and persistent estrogenic overdrive that caused endometrial hyperplasia during 2004. A robust integrative program addressing all relevant issues of the Dysox Model was implemented in April 2004 while the doses of synthetic hormones were decreased until such therapies were discontinued. A dose of 30 mg transdermal progesterone and 1.25 mg estradiol was included in her program. Her symptom-complexes were markedly relieved by year 2006 when her serum estradiol levels was 71 pg/mL.

 

Table 7. Case 4. A 58-Year-Old Woman With Fibromyalgia, Tachycardia, Severe Menopause Syndrome and Endometrial Hyperplasia Caused by Estrogenic Abuse. Her Symptom-Complexes Were Markedly Reduced With the Clinical Application of the Dysox Model. Scale of Overall Symptom Score 0-4+

Date

Estradiol pg/mL

Symptom Score

Date

Estradiol pg/mL

Symptom Score

2002

129

4+

5.2004

12.32

1+

2003

60.94

1+

9.2004

65.63

1+

1.2004

257.02

3+

2.2005

65.89

1+

3.2004

408.89

4+

4.2006

71

1+

4.1.2004

408.01

4+

3.2007

20

4+*

4.13.2004

218.5

4+

4.2007

7**

2+

     

7.5.2007

26

1+

*Stress caused by husband’s hospitalization for a serious illness.

** Note a rapid drop in serum estradiol level following that stress.

This case illustrates a crucial clinical aspect of the Dysox Model: large doses of synthetic hormones—notwithstanding the symptom relief with each increment in dose—not only fail to yield long-term benefits but also set the stage for the development of endometrial hyperplasia and cancer. What is required in such cases is an intelligent application of the Dysox Model.

Oxygen Orchestrates the Biosynthesis of Cholesterol and Steroidal HormoneA brief outline of the cytochrome P450 system is necessary to show how oxygen orchestrates the biosynthesis of cholesterol and of gonadal hormone derived from cholesterol. Cytochrome P450s (CYPs, P450s, or CYP450s) are a superfamily of iron-containing proteins found in bacteria, archaea and eukaryotes (more than 6400 distinct CYP sequences as of October 2006). A measure of the genetic diversity of this superfamily is that humans have 57 genes and more than 59 pseudogenes divided among 18 families of cytochrome P450 genes and 43 subfamilies.9-12

In general, members of this family occur as components of multicomponent electron transfer chains, called P450-containing systems, which are involved in metabolism of a wide range of exogenous and endogenous compounds, including drugs, industrial compounds, synthetic hormones, and xenohormones. The main importance of the CYP450 family in the present context is that the most common reaction catalyzed by them is monooxygenase reaction (insertion of one atom of oxygen into an organic substrate while the other oxygen atom is reduced to water).

Animal CYPs are primarily membrane-associated enzymes found either in the inner membrane of mitochondria or in the endoplasmic reticulum of cells. P450s play central roles in the biosynthesis of cholesterol, steroids (including estrogen and testosterone), and vitamin D metabolism. These enzymes are equally involved with further metabolic processing of both natural and synthetic estrogens and progestins.

According to the prevailing CYP nomenclature, genes encoding for CYP450 enzymes, and the enzymes themselves, individual member enzymes are given the designation of CYP, followed by an Arabic numeral indicating the gene family, a capital letter indicating the subfamily, and another numeral for the individual gene. For example, CYP11A1 (also known as P450scc) is involved with cholesterol side chain scission). CYP19A (P450arom, aromatase) occurs in the endoplasmic reticulum of ovaries, testes, brain, and fat catalyzes aromatization of androgens to estrogens.

The resting state of the P450 protein is as oxidized Fe3+. In the first step, the binding of a substrate initiates electron transport and oxygen binding—availability of functional oxygen, in the current context, brings to life the union of the enzyme and its substrate. It is noteworthy that electrons are supplied to the CYP by other proteins (cytochrome P450 reductase, ferredoxins, or cytochrome b5 to reduce the heme iron). Molecular oxygen (again in the prevailing view) responds to the then reduced iron. To complete the cycle, an iron-bound oxidant oxidizes the substrate to an alcohol or an epoxide, regenerating the resting state of the CYP.

My focus on oxygen here was drawn by my clinical observations. Specifically, I needed to understand the scientific basis of how bowel and liver detox procedures correct menstrual and menopausal disorders when the treatment plans do not include gonadal hormone therapies. Later I realized that the validity of my view is equally well supported by the utter simplicity of the model. I offer the following analogy of a shepherd and his sheep dogs and flock to illustrate my central point here.

Pro-inflammatory Roles of Estrogens and the Dysox Model

Oxygen governs the inflammatory response and adjudicates man-microbe conflicts. That was the title of my column of May 2005.13 Synthetic estrogens and xenoestrogens are potent pro-inflammatory agents. A clear understanding of the pro-inflammatory roles of synthetic estrogens, progestins, and androgens is key to understanding the Unifying Dysox Model of Hormone Dysfunctions. The following are major mechanisms by which synthetic estrogens, xenoestrogens, and synthetic androgens evoke and perpetuate pathologic inflammatory responses, and thereby set the stage for dysoxic hormonal disorders 14-18:

Postmenopausal hormone therapy (PHT) is associated with raised blood levels of a protein called CRP, a well established marker of inflammation.

PHT is also associated with raised blood levels of another well established marker of inflammation called IL-6.

PHT is associated with raised blood levels of a class of proteins found in the matrix—materials that hold cells together in tissues—called MMP-9. The increased levels of these proteins indicate an accelerated breakdown of the matrix substances.

PHT is associated with raised blood levels of a substance that anchors cells together called sICAM. Again, the raised levels of this substance indicate the presence of molecular inflammation and increased stress on normal cohesion among cells .

The case for pathologic proinflammatory effects of synthetic hormones becomes even stronger when the effects of controlled ovarian hyperstimulation (COH) caused by potent synthetic hormones used for in vitro fertilization (IVF) are carefully examined.

Oxygen, Hypoxia Inducible Factors, and Hormone Receptors

Protein systems in living tissues are dynamic. Proteins fold and unfold in response to cues in their molecular environment to assume various functions.19-21 Though well-protected by chaperons (which are proteins and so require their own chaperons), proteins misfold with excessive stress and become dysfunctional. The protein biosynthesis is closely matched with proteolysis to replace the disfigured or broken down units. The proteins that make up hormone receptors are not an exception to this protein order of human biology. It is well established that for a large number of proteins, proteolysis occurs in response to changes in the prevailing conditions of oxygen. In the following paragraph, I present some information about one family of proteins that display a high degree of responsiveness to oxygen signalling, which is of evident relevance to the Unifying Dysox Model of Hormone Dysfunctions.

Hypoxia-inducible factors (HIF) are a large family of proteins that display a high degree of responsiveness to oxygen signalling. I include here brief comments about one member of this family, hypoxia-inducible factor 1a (HIF-1a1) to shed light on one important aspect of the Unifying Dysox Model of Hormone Dysfunction. (HIF-1a is a basic helix-loop-helix transcription factor of the PAS superfamily. It plays a central role in cellular adaptation to diminished reduced oxygen availability.22,23 It senses and responds to oxygen deficit (becomes activated) and strives to restore oxygen homeostasis by:

  • inducing glycolysis, and angiogenesis to maintain cellular energetics
  • inhibits cell proliferation and DNA repair to limit energy consumption
  • activating a sleuth of its target genes, including those that encode erythropoietin, vascular endothelial growth factor, PGK1, and ARNT (also known as HIF-1ß)24)
  • recruiting the transcription co-activator p300/CBP25,26
  • binding to the hypoxia-responsive element in the promoter27
  • functionally antagonizing the oncogene Myc via protein-protein interactions
  • up-regulating the CDKN1A/p21cip system
  • down-regulating MSH2 and MSH6 down-regulation.28

For all those, and probably others as yet unrecognized roles, HIF-1a has been designated as a master regulator of oxygen homeostasis for cell survival. Disruptions of all the above genetic and signaling pathways create the dysoxic conditions that set the stage—directly or indirectly—for the development of menstrual and menopausal disorders.

As mentioned earlier, oxygen seldom enters in descriptions of the biosynthesis and metabolism of cholesterol and steroidal hormones. Here is an interesting quote from Medical Biochemistry: “The exact mechanism by which this is achieved [reduction of HMG CoA reductase activity] remains unclear but may involve intracellular oxygenation of cholesterol to more potent enzyme inhibitors.29 In light of the facts of steroidal chemistry, pro-inflammatory effects of synthetic hormones, and oxygen-sensing molecular moieties presented above, below are the three analogies mentioned in the opening paragraphs of this column.

The Farmer With His Dogs and Sheep

A farmer’s dogs sleep in front of his ranch house. His sheep stay in the shed at the rear of the house. In the morning he makes his breakfast. The smell of his cooking wakes his dogs. Minutes later, the farmer appears at the door with food for his dogs. The dogs eat and then walk to the shed. The sheep get ready to be herded by the dogs, just as they have done for years.

Who starts the sheep? The farmer’s cooking? His appearance at the door? The dogs? Or the morning light? It is simply a case of Pavlovian conditioning, someone might say. Yes. That is true at one level. At another level, the sun created the conditions to form the planet Earth. The earth created the conditions to make farming possible. Now the earth spins to give the farmer its morning clues. The farmer creates the conditions for the dogs and the dogs for the sheep.

The sun created the oxygen conditions on the Earth which, in turn, created the conditions in which life began, differentiated, and grew into diverse life forms. The primordial cells evolved in the highly reducing ambient conditions on the Earth’s surface about three billion years ago when the atmosphere did not have appreciable amounts of free oxygen. The defining event in biology occurred when the primordial cells learned the ability to harness solar energy to split water into hydrogen and oxygen—hydrogen for chemical bond energy and oxygen to provide the organizing influence for the evolutionary surge that built highly complex energetic and metabolic molecular systems. Among the most sophisticated of those systems are thousands of P450 enzymes. Indeed, the P450 enzyme systems seemed to have evolved not only to provide for highly efficient electron transport protein systems for serving the growing energetic needs of cells but also to protect primordial cells from direct oxygen toxicity. So, today we have the oxygen-driven respiratory ATP generation system. I present this subject at length in Darwin, Dysox, and Oxystatic Therapies, the third volume of The Principles and Practice of Integrative Medicine. 30

Returning to my oxygen/monooxygenase hypothesis, ambient oxygen appeared on planet Earth long before the family of P450s did. The enzyme evolved in response to oxygen signaling, rather than the other way around. Thus, in the evolutionary context it is not tenable to hold that oxygen responds to enzyme signals.

Simply stated, the sheep farmer analogy allows us to consider the oxygen/mono-oxygenase dynamics at a deeper level. It illustrates the role reversal I saw in my eureka moment: oxygen is the principal actor and the enzymes respond to its cues on the stage of human biology, notwithstanding the traditional teaching in which the enzyme handles oxygen—inserts oxygen into organic compounds—to exert its enzymatic role. The core clinical point here is this: the oxygen view of enzyme functions in health and disease compels the clinician to recognize and address all relevant oxygen issues, regardless of the diagnostic label used in chronic illness.

Cytochrome Steal

I introduce the term cytochrome steal in this column to refer to a functional deficit of P450 enzyme systems required for the biosynthesis and breakdown of estrogens, progesterone, and testosterone. Such a deficit occurs in the body because the normal functions of these enzymes are being impaired by:

  • synthetic chemicals in the air, food, and water
  • drugs
  • industrial pollutants
  • synthetic hormones
  • industrial pollutants with hormone-like activities (xenohormones).

Since P450s are also recognized and important players in cellular energy generation, it should not come as a surprise that menstrual and menopausal syndromes are frequently associated with energy deficit states—the clinically observed phenomena that led me to the oxygen signaling hypothesis in the first place.1,2 The best known examples of energy deficit states are fibromyalgia, chronic fatigue syndrome, following chemotherapy for malignant diseases, and environmentally-induced disorders (9/11-related chronic illnesses and others).

The phenomenon of cytochrome steal—in my view—provides the scientific basis for the clinically-observed benefits in the menstrual and menopausal syndromes when the gonadal hormonal functions are restored with bowel and liver detox measures.

Oxygen: The Master Membrane Detergent

A cell membrane separates the internal order of a cell from external disorder. In 1987, I proposed the model of the oxidative leaky cell membrane state to draw attention to the clinical manifestation of cell membrane dysfunction and injury caused by incremental and cumulative oxidative stress.31 In 1998, I proposed that model of cell membrane dysfunction as a major pathogenetic component of menstrual and menopausal syndromes.1,2 In my May 2007 column, I wrote that I consider the abnormalities of insulin functions in hyperinsulinemia, the so-called metabolic syndrome, and Type 2 diabetes as the consequences of plasticized (chemicalized) and hardened cell membranes which immobilize the insulin receptors embedded in them.32 The image of oxygen as the “master membrane detergent” arose as I searched for an analogy to explain the expected consequences of chemicalized, hardened and “greasy” cell membranes. Specifically, how cell membranes in such states might interfere with the functionalities of hormone receptors embedded in them. And in the context of the Dysox Model, how oxygen-induced proteolysis (digestion and breakdown) of the membrane proteins might restore receptor functions. In an earlier section, I described the wide range of protein-modulating roles of oxygen mediated through altered dynamics of hypoxia-inducible factor 1a.

Simply stated, oxygen serves as a cell membrane detergent and restores hormone receptor function in menstrual and menopausal disorders. Just as oxygen is the keeper of white sand on a beach—it degrades and eliminates organic matter in it—so it is the keeper of cell membrane and degrades and clears up the greasy, proteinaceous materials on them.

I recognize there are elements of speculation in all three analogies described above. However, I believe the analogies are valid for their essential message when seen in light of the enormous body of available clinical, epidemiologic, and experimental data on the subject.

Clinical Implications of the Unifying Dysox Model of Hormone Dysfunction

Models in clinical medicine are put forth for two reasons: to enhance the understanding of complex issues and to offer workable simplicities in therapeutic efforts. Within these columns, and the eleven volumes of The Principles and Practice of Integrative Medicine, I continue to offer dysox models of various clinicopathologic entities because I believe they meet these two criteria. Specifically, I have attempted to show how the Unifying Dysox Model of Hormone Disorders sheds light on:

  • delineation of the links between the oxygen-driven enzymatic systems and detoxification pathways
  • potent pro-inflammatory effects of synthetic estrogens and xenoestrogens
  • the pathogenesis of menstrual and menopausal disorders within the context of oxygen signalling
  • furnish sound scientific basis for the observed clinical superiority of the hormone receptor restoration (RRT) over the traditional hormone replacement therapy (HRT)
  • provides clear scientific rationale for treating hormone dysfunctions with nutritional and detox therapies.

In past columns, it has been explained how therapies that address issues of acid-alkali imbalance, oxidant/antioxidant regulation, and clotting-unclotting equilibrium serve as oxystatic (oxygen homeostatic) therapies.33-36 Such therapies focus on issues on the central roles bowel and liver detox therapies to address the matters of altered gut microbiota, mold allergy and mycotoxicosis, increased bowel permeability, and impaired liver detox. For additional information, I refer readers to Integrative Nutritional Medicine, the fifth volume of The principles and Practice of Integrative Medicine.37

Adjunctive Gonadal Hormone Therapies

I consider supplemental gonadal regimens for menstrual and menopausal disorders as adjunct therapies, and not the primary treatment . Such therapies are optimally used for limited periods of time only when nutrient, phytofactor, and detox measures fail to offer relief within weeks. It must be recognized that in a minority of patients with menstrual and menopausal disorders, the use of hormone replacement therapies becomes necessary despite the best efforts to address all relevant issues addressed in the Dysox Model. Those therapies are discussed at length in various articles in this issue of the Townsend Letter.

Closing Comments

In closing, I present a unifying Dysox Model of Hormone Disorders that has strong explanatory power for: (1) patterns of abnormal hormonal levels in various “non-hormonal” disease; (2) altered oxygen signalling that underlie those hormonal shifts; and (3) documented clinical superiority of RRT over HRT; and (4) improved clinical results in control of menstrual disorders when oxystatic, nutritional, and detox measures. I hope that the proposed model will be considered and put to test by others.

 



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Healing Seminar 1 – Introduction
Life is growing and growing is learning. In his course, he offers simple and low-cost natural remedies to preserve health and reverse chronic disease.

Healing Seminar 2 – Cellular Fermentation Forms the Foundation of Disease
Professor Ali defines disease in two ways: (1) disease is a state of separation from one’s nature; and (2) disease is evolution in reverse. In this second of 8 seminars of “Dr. Ali’s Course on Healing,” he explains what he means by evolution in reverse.

Healing Seminar 3 – Oxygen Model of Inflammation
Professor Majid Ali recognizes and describes two modes of inflammation: (1) healing physiologic inflammation and (2) disease-causing pathologic inflammation. He explains how no healing is possible without inflammation and how there is no disease in which inflammation does not play a crucial role.

Healing Seminar 4 – Breakfast Shake
In this 45-minute video seminar, Professor Majid Ali, M.D. presents his own breakfast taken four to five days a week. It consists of organic 12 ounces of vegetable juice and water, two tablespoons each of a protein powder and freshly ground flaxseed, one-and-half tablespoon of lecithin, and 12 ounces of water.

Healing Seminar 5 – Top Seven Natural Remedies
Professor Ali describes his top seven natural healing remedies as follows: (1) Limbic Breathing ; (2) Dr. Ali’s Breakfast; (3) Exercise; (4) Bowel-Liver Detox; (5) Castor Oil Rub Therapies; (6) Peroxide Oxygen Therapies; and (7) Ethical-Spiritual-Energy healing. He found these therapies to be safe and highly effective for all chronic disorders.

Healing Seminar 6 Natural Anti-inflammatory Remedies
In this 45-minute video seminar, Professor Majid Ali, M.D. presents his choices of most effective natural remedies for various inflammatory disease and how most people can avoid drugs for diseases, such as asthma, eczema, acne, psoriasis, arthritis, trigger points, fibromyalgia, lupus, interstitial cystitis, polymyalgia, sarcoidosis, Crohn’s colitis, ulcerative colitis, and others.

Healing Seminar 7 – Bowel Detox –
In this DVD video seminar, Prof. Ali describes his guidelines for gentle daily bowel detox and colon cleanse. He explains the advantages of this approach over intense one-week to 3-week programs which, notwithstanding their temporary benefits, often create adverse effects programs bowel.

Healing Seminar 8 – Liver Detox
In this DVD video seminar, Prof. Ali describes his guidelines for gentle daily liver detox. He explains the advantages of this approach over intense one-week to 3-week programs which, notwithstanding their temporary benefits, often create adverse effects. The guardian angel of the liver is the bowel. Please view Dr. Ali’s Bowel Video Detox Seminar for a deeper understanding of this subject.

Healing Seminar 9 – Oxygen Model of Health and Disease
Professor Majid Ali presents his Oxygen Mode of Health and Disease and Oxygen Model of Disease. He speaks about his journey of a surgeon-turned-pathologist-turned-immunologist-turned-nutritionist-turned-ecologist-turned-“energy physician.” His unifying oxygen models are based on his evolutionary perspective of health, disease, and healing.

Healing Seminar 10 – Acid-Alkali Balance
Professor Majid Ali explains the importance of acid-alkali balance in health preservation and the reversal of chronic disease. In his evolutionary perspective, he recognizes oxygen as the ultimate regulator of this balance. He cautions against too much reliance on the values of pH (acidity indicator) in blood, urine, and saliva samples, since these samples reflect the body’s responses to threats to the balance.

Healing Seminar 11 – Oxidant – Antioxidant Regulation
Professor Majid Ali presents the scientific facts of oxidant-antioxidant regulation, beginning with definitions of terms and simple explanation of natural processes called oxidation (loss of electron energy) and reduction (gain of electron energy) with simple analogies. Next he shows how oxygen regulates oxidant-oxidates reactions and why oxidant therapies are more important than antioxidant therapies.

1. Ali M. The unifying dysox model of hormone disorders and receptor restoration therapy. Townsend Letter-The examiner of Alternative Medicine. 2007; 291;145-151.

2. Ali M: Amenorrhea, oligomenorrhea, and polymenorrhea in CFS and fibromyalgia are caused by oxidative menstrual dysfunction (OMD-I) J Integrative Medicine 1998; 2:101-124.
3. Ali M: Oxidative menopausal dysfunction (OMD-II):hormone replacement therapy (HRT) or receptor restoration therapy (RRT)? J Integrative Medicine 1998;2:125-139.

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