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Edward M. Lichten, M.D., F.A.C.O.G., F.A.C.S.

Fellow, American College of Obstetricians and Gynecologists

Fellow, American College of Surgeons

600 West Brown Street Suite #202

Birmingham, MI 48009

Office phone: (248) 593.9999  

Cellular Phone: (248) 420.8726   

Fax: (248) 593.9037

Email: [email protected]

Dr. Lichten’s focus for forty years has been the treatment of autoimmune and chronic diseases with natural, bio-identical androgenic anabolic steroids derived from testosterone.

 ABSTRACT: (532)

Submitted to:  Journal of Medical Hypothesis:


Androgenic-Anabolic Steroids (AAS)  can Stimulated Immune Recovery In Triple Negative Breast Cancer After Chemotherapy and Radiation


Edward M. Lichten, M.D.

Fellow, American College of Surgeons; Fellow, American College of Obstetrician and Gynecologists. 600 West Brown Street Suite #202. Birmingham Michigan 48009 U.S.A.

Email: [email protected]; Cell:248.420.8726; Office:248.593.9999; Fax:248.593.9037

Edward M. Lichten, M.D. consulted and is treating the patients. M. Neuman, Ph.D. has  an in-vitro laboratory

Manuela G. Neuman, M.Sc., Ph.D., FCA, July, 02CB



The complex association of endocrine ablation and breast cancer (BC) was discovered in 1896 when Beatson4 revealed that oophorectomy on an advanced cancer patient led to a pronounced and marked response.

The presumption that estradiol was linked to breast cancer was strongly influenced in 1958 by the discovery of the estrogen receptor (ER) by E.V. Jensen5; subsequent studies showed estrogen (E2) is implicated in breast cancer pathogenesis and nurtures the surge in Estrogen Receptors expressing breast cancer cells.5

Based on that presumption, two medications have become standard in the treatment/ prevention of recurrence for early estrogen receptor positive breast cancer:  anastrozole and tamoxifen. Both are not applicable to triple negative breast cancer. Both have about a 70% initial response and many hosts develop resistance predating cancer remission.

In the rewriting of the 100-year-old Endometriosis Hypothesis2 and showing the 10-year remission Case Report at the ACOG1 Annual Meeting in 2014, I and my colleague went on to develop an in-vitro laboratory that would be able to quantitate cytokines, the ‘atomic particle’ of inflammation.  Purdominici’s6 link of the estrogen receptor-beta signaling to controlling IL-6 inflammatory cytokine cascade became the next quantitative measurement for our laboratory to investigate.

It was our epiphany that the correct balance of androgenic-anabolic steroids (not testosterone) could bring homeostasis and reverse endometriosis by their action on the ERβ to control pro-inflammatory cytokines.  It is the focus of the University of Louisville I.R.B. beginning this fall 2021.



OLD BREAST CANCER HYPOTHESIS:  (same as “old” Endometriosis Hypothesis)

+Estrogen    ->      Estrogen-Receptor   ->           +Cancer


-AAS     -> +ERβ   –   +inflammatory Cytokines    ->  +cancer

Loss of Testosterone Dominance 

  • Reduces ERβ ability to signal for low levels of proinflammatory cytokines
  • high pro-inflammatory cytokines à inflammation

-> inflammation and de novo vascularisation (high VEGF)  may beget oncogenesis




 RE:  Bio-T:      Testosterone, Sex Hormone Binding Globulin, Estradiol

We in gynecology grabbed the Estradiol “cause of Endometriosis Hypothesis” and when danazol, a weak androgenic-anabolic steroid (AAS) was FDA approved in 1971, prescribed danazol for all four stages of disease. We rationalized that the drug effect was foremost driven by lowering serum estradiol levels (i.e., Estrogen Dominance”).  More danazol was prescribed for more severe disease:  menopausal symptoms were frequent at the highest dosages (200mg to 800mg/day). Based on the Cochrane review7, danazol is as effective as 5-times more expensive leuprolide acetate without the side-effect of osteoporosis. Mild hirsutism is preventable with spironolactone 100mg twice daily. However, 20 to 40% of women still have pain in their 40’s today from endometriosis. That is one of the purposes behind the University of Louisville, Department of Obstetrics and Gynecology, I.R.B. beginning this fall 2021 utilizing Lichten’s protocol and the international in-vitro laboratory.

Robert L. BarbieriM.D.8, former chairman of Obstetricians and Gynecologists at Brigham and Women’s Hospital in 1980 wrote that danazol had at least eight functional metabolites that needed to be investigated further. Danazol reduces Sex Hormone Binding Globulin (SBG) by 80%.

McGuire9, chairman of 3 department at Stanford, told me that Estrogen, progesterone, and testosterone: can they be used to treat autoimmune diseases. He used danazol to treat lupus erythematosus nephritis.  I used over-the-counter DHEA for my first wife’s lupus.

As a gynecologist and endometriosis microsurgeon I found a medical treatment for my surgical failures. The Realization of New Medical Alternatives to Surgery for Endometriosis reported that nandrolone and stanozolol were a 20-fold stronger-than-danazol mixture. Nandrolone was FDA approved in 1962 for wasting/ HIV, mastalgia/ breast cysts, anemia, and autoimmune diseases. Stanozolol was FDA approved in 1982 for autoimmune diseases.  Stanozolol is 20-fold stronger than its sister drug danazol and without the hirsutism side effects.   Using nandrolone together with stanozolol reduced SHBG more effectively than danazol which quadrupled the remissions from severe endometriosis.   Nandrolone was 20-fold more anti-inflammatory than any AAS and suppressed the estradiol levels below reference range. Nandrolone had a 30-fold greater affinity for the estrogen receptors than 17β estradiol or any Endocrine Disrupting Chemicals (EDCs) in environmental exposure.  Only 5% of nandrolone was bound to SHBG:  nandrolone 20mg was as anabolic as 200mg of testosterone sans hirsutism.

Burke10 and Anderson in 1972 described how the liver production of Sex Hormone Binding Globulin (SHBG) controlled bioavailability of testosterone.  SHBG is an Oestrogen Amplifier10 and we believe behind the so-called Estrogen Dominance seen in the explosion of autoimmune diseases and breast cancer since 1970. SHBG is an independent risk factor and biomarker for disease including breast cancer.  Its production is stimulated by EDCs, oral contraception, equine estrogens, pesticides, and DES (diethylstilbesterol). As little as one ug of ethinyl-estradiol will reduce bioavailable testosterone by 39%.11 Bio-available testosterone (Bio-T) is the drug-therapy measurement even though we do not use testosterone in treatment. Even the small conversion of testosterone to 17β estradiol brought back return of symptoms. The Bio-T measurement is appropriate as nandrolone displaces testosterone and is not measurable in the local laboratories.  BIO-T = [total testosterone serum]/[SHBG].

Those who doubt Endocrine Disrupting Chemicals (EDCs) influence breast cancer need only review the history of diethylstilbesterol (DES)13 prescribed to women from 1945 to 1971, it was intended to reduce pregnancy loss but increased loss 8-fold. It spawned a rare vaginal cancer and doubled the risk of breast cancer in offspring at 40-year follow up.

Fortunati13 in one of 295 articles found on PubMed search this week with the terms “SHBG” and “breast cancer” identifies some of the multiple roles SHBG is implicit it this disease: 1) regulates the bioavailable fraction of circulating estradiol, 2) direct action of SHBG in breast cancer cells, 3) specific intracellular pathway leading to cross-talk with the estradiol-activated pathway and 4) inhibition of several effects of estradiol in breast cancer cells.  (probably anabolic-anabolic Steroids (AAS) mitigated).


An agrarian society where the first, full-term pregnancy (FFTP) is in the teen years followed by active nursing and multiple births can have a reduction of breast cancer risk by 90% compared to our Western civilization of hormonal contraception, induced abortion and later pregnancy with absent nursing. Early pregnancy converts breast lobules Type I and II to Type III and IV. This is associated with a dramatic change in the Estrogen Receptors in the breast. One article suggested a using hCG14 to change the menopausal breast cancer risk. However, β-hCG may increase risk14.


The concept of revisiting “Estrogen Dominance” as “loss of Testosterone Dominance” allows inclusion of mistaken observations and assumptions that are contra-productive to management of the breast cancer patient.  This is the Scientific Method:  all observations must be includable in the hypothesis for the theorem to be accepted.

The literature is prolific in these errors misdirecting from the hypothesis proposed herein. We believe the observations and literature fulfill Scientific Methodology.  Most gastroenterologists (IBD), endocrinologists (diabetes), cardiologist (heart disease and stroke) and clinical researchers have not understood the importance of environmental stimulation on SHBG, or in fact, the role of bioavailable testosterone as influenced by SHBG.  Hotz15 in 1980 showed Crohn’s patients to be hypogonadal beginning with hypothalamic-pituitary-gonadal (HPG) suppression.

We have treated a wide and diffuse group of diseases in men and women by measuring the Bio-T, adding back nandrolone and stanozolol to tolerance and following the Bio-T measurement at 6-month intervals.  For 70-years, androgenic-anabolic steroids (AAS) have been known to be anti-inflammatory.

Our research is tracing out the steps from homeostasis (Testosterone Dominance) to inflammation through the loss of bioavailable hormones effect on the T-lymphocyte nuclear membrane receptors that activate the pro-inflammatory cytokines to ‘start’ autoimmune disease and when genetically predisposed, oncogenesis.


Pierdumunici6 and the Estrogen Receptor-beta:

The breakthrough came when the Chairperson of Gastroenterology in Rome discovered that the Estrogen Receptor-beta (ERβ) on the nuclear membrane of the T-lymphocyte controlled the pro-inflammatory cytokine interleukin (IL-6).   She established that loss of signaling from ERβ allowed IL-6 to propagate and initiate the flair in Crohn’s Disease. When the patient went into remission, the IL-6 levels dropped and the ERβ levels returned upward to normal. The same reaction and inverse correlation was present in biopsied colonic mucosa.

To reduce breast cancer incidence, two socio-economic conditions would have to be met.

Considering that no one can foresee either:

1) reduction in EDCs and

2) change back to early teen multiple pregnancies, we are concerned with the proliferation of breast cancer to one in eight women.  I have prescribed nandrolone and stanozolol to an 11-year menstruating girl with severe endometriosis who remained on the medication until her 20’s.  Used by body-building women for years, there has not been even one correlated death with doses 10-fold greater than suggested here.

Our concept of an in-vitro laboratory may become a beacon for new discoveries, as its use becomes essential to analyze the hormonal pre-genetic influences and how best to augment the host’s personal, adaptive autoimmune system to naturally suppress the oncogenic and inflammatory processes, precisely. PRECISION MEDICINE

The key is to understand that nandrolone, without being aromatized to estradiol as is testosterone, produces a profound atrophy in both the endometrium and breast.  There is no need for anastrozole or tamoxifen as nandrolone with its 30-fold greater affinity for Estrogen Receptors than any other chemical, EDCs or estrogenic hormone, saturates the receptor keeping the mitogens away.

It feeds back on the HPG axis, reducing FSH/LH and menopausal symptoms of hot flushes, vaginal dryness, depression, and reduces fat cells while building muscle and bone.

Reports from Germany in 1990 showed that both nandrolone and stanozolol were effective in extending quality life in end-stage metastatic breast cancer.16,17 Nandrolone was equivalent to Tamoxifen.17 This two drug-therapy for breast cancer is unreported as is the in-vitro laboratory predetermination of effectiveness. A request has been made to the pathologist to confirm atrophy in normal breast at time of mastectomy4weeks later.  How atrophic does the breasts become in just 4 weeks of 20mg of nandrolone. Proof?




AAS (androgenic-anabolic steroids) can augment natural immunity after chemotherapy and radiation as observed in our pilot study of a 54-year-old woman treated for triple negative breast cancer (TNBC) 18-months after chemotherapy, radiation and bilateral mastectomy.


“Testosterone, Nandrolone, Stanozolol stimulate T-lymphocyte growth by 10 to 16.5%. Danazol stimulates cells by 40%.” Definitely not cytotoxic; cyto-prolific to natural immune system.

AAS were associated with anabolic hematologic effects:  increase in lymphocytes, red blood cells and platelet counts. Increased ferritin (phlebotomy).

AAS also decrease inflammatory serum cytokines19. The 6- month follow up of pro- and anti-inflammatory cytokines, ERβ and ERα pending.

Before prescribing the therapy to the patient Dr. Lichten  will utilized the personalized (precision) medicine approach.  This approach ensure that the individual would not present hypersensitivity syndrome or adverse effects to the prescribed therapeutic.

 In the laboratory the lymphocytes from the patients are treated with the specific anabolic steroid that Dr. Lichten would like to treat his patients. If the drug is toxic to the patient the lymphocytes will be killed either by the drug itself or by its metabolites.

The toxic effect of the drug can be quantitatively measure. In addition, the pro-inflammatory/anti-inflammatory biomarkers can be quantitatively measured. The cytokines and chemokines, cell death, and estrogen hormone receptors will give the information needed to  provide Personalized Medicine to each individual.

This month begins University of Louisville I.R.B. evaluating our protocol for Endometriosis – Stage IV (deep pelvic) women who have failed both medication and draconic surgery. Phase I: initial quantitated measurements of T-lymphocyte components, followed by Phase II where T-lymphocyte aliquot is admixed with FDA approved drug-therapy: (5) AAS, medication, or chemical over-the-counter formulations. Comparative analysis between phase I and II showed the beneficial effects in-vitro identified drug-therapy(s) had on the T- lymphocyte components: cytokines, estrogen receptors, without evidence of cytotoxicity.

The triple negative breast cancer patient’s status post chemotherapy and radiation underwent blood evaluation with the routine hormonal, metabolic, hematologic tests from our local laboratory and then 80 ml of venous blood was shipped on ice in heparin tubes to our international facility overnight.

Danazol stimulated white cell production by 40% in-vitro. This effect on normal adaptive immunity has never been reported.  Serum laboratory findings showed AAS (nandrolone and danazol) to be anabolic (increased lymphocytes, red cells, ferritin etc.), reduced inflammatory markers, and the patient reported improved quality of life.

The patient with a more common breast cancer was Estrogen+, Progesterone +, and HER2 +.; stage I-II, grade II with positive sentinel nodes (4).  She elected to have the preliminary blood drawn and with a very low testosterone to SHBG ratio to start the nandrolone/ stanozolol protocol with confirmatory testing was done at the In-vitro Drug Safety laboratory.  Her in=vitro testing supported nandrolone and stanozolol over danazol.  Minor complaints of fatigue and bloating were to be expected.  Additional nandrolone cream was applied to the inflammatory surgical line in her chest.   She elected not to use anastrozole nor tamoxifen but, did take M. Retsky’s11 protocol of 3 days of ketorolac to reduce inflammation starting the day after bilateral mastectomy surgery.

NEW HYPOTHESIS:   -AAS ->     à +ERβ -> – +Inflammatory Cytokines    ->  +Cancer



Based on our previous publications in the fields of gynecology-endometriosis and gastroenterology-Crohn’s Disease, the pattern developed that is the Hypothesis.  The literature and our pilot studies confirmed Hotz’s 1980 finding that autoimue disease was associated with HPG suppression. Anderson 1974 reported that 1 ug of ethinyl-estradiol would suppress testosterone production by more than 40 percent.  It was not until the year 2000 that the correlation between the dumping of xenoestrogens (a.k.a. 1970) was impacting autoimmune chronic diseases, obesity and the surge in breast cancer. Anderson, Hotz and then McGuire laid out the EDCsà HPG connection.  Anderson recognized the key role of increasing SHGB. SHBG increases when exposed to xenoestrogens.  Total testosterone in ratio to SHBG is the biomarker in the hypothesis: Bio-T.

McGuire in 1994 suggested that hormones could be effective in treating autoimmune diseases such as women with lupus erythematosus. In private practice, individual men and women with autoimmune disorders, hypogonadism, adult-onset diabetes, Crohn’s, heart disease,  and over 50 years of age were offered hormonal replacement when symptomatic. The mixed androgenic-anabolic steroids were extremely successful at relieving symptoms and  improved the laboratory tests: this corresponded to raising Bio-T into a homeostatic range.

The connection between the androgenic-anabolic steroid drug-therapy (AAS) remained a mystery until Pierdomunici 2015 linked loss of estrogen receptor-beta to the pro-inflammatory Crohn’s flair.  When the flair cleared, the pro-inflammatory cytokines and Estrogen Receptor-beta returned toward normal The epiphany was that it must be the normal Bio-T that the host uninflamed (normal ERβ); the normal ERβ kept the IL-6 and cytokines at rest.

Therefore, we created an in-vitro laboratory to measure the T-lymphocyte cytokines, estrogen receptors (alpha and beta), and cytotoxicity on the standard drug therapies. Medications were compared in-vitro before prescribing to the patients: PRECISION medication: “it will work or it will not be prescribed.”  The initial assessment was compared to aliquots containing a single drug-therapy and repeated.

Exactly matching the literature, most autoimmune diseases and our two breast cancer patients have (as their most active) pro-inflammatory cytokines IL-06, BGFα and TNFα.  These three showed positive responses to the 3 natural androgenic-anabolic steroids: improved Bio-T corresponded t move toward normalization of the Estrogen Receptor-beta, reduction of pro-inflammatory cytokines, and increase in anti-inflammatory cytokines.

[and will return in 6-months for final ER-β proof]

While we plan to observe the breast cancer patients for 15-years. we seek a biomarker that can clinically compare initial with observations patient’s reports, and ongoing drug-treatments: 1) routine local laboratory hormonal and inflammatory biomarkers, and the in-vitro estrogen-receptor beta, inflammatory cytokines and cytotoxicity.

The hosts need energy for growth and repair. This comes from aerobic metabolism: ATP. ATP comes from anabolic steroids. The hypothesis is clearly proven: we men and women need more not less ‘free’ testosterone. What other new discoveries will be made at this intracellular level?

Discoveries in Medicine are good!



‘Early’ ER+, PR+, HER2+   Breast Cancer: PATHOLOGY REPORT

Hx:    51-year-old Caucasian Woman:  no family history of Breast Cancer

birth date 1969/12/23: G2P0 ‘miscarriages.’ Menopausal: no hormone replacement

Core Bx:          2019/06/29. Invasive ductal adenocarcinoma Stage  I-II, lymph pos

Surgery:          2021/06/29: Bilateral mastectomy; left axilla 4 sentinel nodes; removed bilateral mammary implants: create space for expanders

Final:                2019/07/05. Invasive Grade III 8/9. Size: > 2.6 cm.

3/3 architecture; 3/3 nuclear pleomorphism; 2/3 mitotic.

**Receptors:   ER positive >90%;              Progesterone positive 67%;     HER2neu  3+ positive

Consultation: Dr. Flaherty: port placement, MUGA scan, Chest x-ray

  –[Research protocol offered: EA-1181 Taxol weekly; Herceptin® & Perjeta® before OR]


**Serum Lab Assays



WBC 7.2 x10E3/uL 6
Hemoglobin 13.0 g/dL 13.6
platelet 329 x10E3/uL 345
neutro 58.3% 50.5
lymph 31.1% 33.3
Lymph absolute 2.24 1.99
Mono 7.5% 10.1
glucose 83 mg/dl 85
Protein/alb ?/ 4IU/L  
BUN/Cr 8/ 0.73  16/1.1
HgB A1c 5.6%  
AST/ALT 19/ 16 26/17
DHEAs 127 ug/dl  
Chol 156.2mg/dL  
Immun G/A/M normal  
Homocysteine 10.1 umol/L  
FSH 87.5mIU/mL  43/ 29
TSH 2.8 uIU/mL
No antibodies  T3    
Estradiol ? pg/mL 52
Insulin ?  uIU/ml  pending
SHBG 65 nmol/L 17.2
Testosterone 25.22 ng/ml 32
Progesterone 0.2ug/mL  
Vitamin D3 L(ow) 23ng/mL
IGF-1 153ng/mL  
RF/ ANA/ sed (8) negative
CRP 0.2 mg/dL  
Ferritin 30 ng/dl 7

The lymphocytes extracted from the blood sample have been exposed to several anabolic steroids in-vitro. The results of toxicity/proliferation study and the interpretation of the results are shown in the table.

Sample + drug Toxicity% -interpretation

Estrogen receptors

Alpha/beta (pg/mL)


7.5%  –

5.5%  – (normal 0-15%)

Stimulate the cells 10%

4% ((normal 0-15%)

1% toxicity ((normal 15%)

Not ne





Stanozolol stimulates the cells to grow 10%.

None of the other drugs can lead to drug adverse events.

Patient’s lymphocytes have been exposed to the therapeutics. Viability/toxicity of the drug is represented in % toxicity/proliferation. The medium in which the cells grew was use to quantitate the levels of cytokines and estrogen receptors.


Levels of serum cytokine/chemokine before therapy #1LE.

Normal values

(500 individuals)

IL-1beta  (pg/mL) -Interleukin 26 30± 12
TNF-alpha (pg/mL)-Tumor necrosis factor 46 42± 16
IL 6 (pg/mL) 38 35± 10
VEGF (pg/mL) vascular endothelial growth factor 30 80± 30
IL -8 (pg/mL) 23 25±15
IL 2 (pg/mL) 24 45± 20


The cytokines in sera are in the normal limit.

Serum Estrogen receptor 0.052 pg/mL

Serum Estrogen receptor beta 0.78 pg/mL

Oxandrolone Stanozolol Donazol
IL-1beta 20 22 16 20
TNF-alpha 40 38 24 39
IL 6 36 28 22 18
VEGF 38 30 25 26
IL -8 24 28 16 28
IL 2 18 20 20 25

All the cytokine levels in response to the drugs used are in the limit of normal. The levels of TNF and VEGF are much lower in Stanozolol treated cells.

Since TNF is a pro-inflammatory cytokine and VEGF is a pro-angiogenic cytokine, we can interpret Stanozolol reduces the inflammation of the cells and angiogenesis.


Triple Negative Breast Cancer: PATHOLOGY REPORT

Hx:    54-year-old Caucasian Woman:  no family history of Breast Cancer

birth date 1967/05/21:   G1P1 19-years old. Menopausal: no hormone replacement

Core Bx:          2019/06/29. Invasive ductal adenocarcinoma Grade III, lymph ??

Final:                2019/07/05. Invasive Grade III 8/9. Greater than 0.6cm.

3/3 architecture; 3/3 nuclear pleomorphism; 2/3 mitotic.

Chemotherapy:  Opdivo® – Yervoy®

Mastectomy/ left lumpectomy: bilateral /: 2020/01

**Receptors:   ER negative                 Progesterone negative           HER2 negative


**Serum Lab Assays 2021/05/03 2021/09/15
WBC 3.7 x10E3/uL 4.5
Hemoglobin 13.8 g/dL 14.8
Platelet 181 x10E3/uL 194
Neutro 62%  
Lymph 27% 27
Lymph absolute 1 1.2
Mono 8% 7
Glucose 89 mg/dl 85
Protein/alb 6.7/ 4.6IU/L  
BUN/Cr   10/ 0.92
HgB A1c 5.6%
AST/ALT   27/ 20
DHEAs 127 ug/dl 144
Chol 212mg/dL 212
Immun G/A/M Normal  
Homocysteine 10.1 umol/L 18.4
FSH 70.5mIU/mL 62.7
TSH 1.53 uIU/mL 1.44
No antibodies T3   3.6 (border)
Estradiol 7.7 pg/mL 94pg/mL
Insulin 13.4 7
SHBG 50.3 nmol/L 17.2
Testosterone 1.2 pg/ml 362ng/dL
Progesterone 0.2ug/mL  
Vitamin D3 L(ow) 28.2ng/mL 39.6
IGF-1 153ng/mL 171
RF/ ANA/sed(7) Negative Sed(15)
CRP <1 mg/dL 1 mg/L
Ferritin (High) 242ng/mL 559;Iron 170ug/dL
Dihydrotestosterone   1.8ng/dL
Cortisol AM   6.3ug/dL


Serum estrogen receptor alpha    0.050 pg/ml

Serum estrogen receptor beta        0.095 pg/ml


Drug & Sample Toxicity/Proliferation
Testosterone 16.5% – (normal 1-12.5%)
Nandrolone 16.5% (normal 1- 15%)
Stanozolol 10%  (normal 1- 15%)
Danazol Proliferation 40%**
Oxandrolone 6% (normal 1- 12.5%)
Taxol-Tamoxiphen 46% toxicity (normal 1- 15%) *

* Tamoxiphen was very efficient in killing the cancer cells, however produced side effects (muscle pain).

**The best stimulator and the drug recommended therapeutic is Danazol that stimulates cell proliferation 46%


pg/mL Nandrolone Oxandrolone Stanozolol Danazol
IL-1β/ 18 24 16 22
TNF-α 48 44 24 19
IL-6 36 28 22 18
VEGF 48 32 25 26
IL-8 28 24 18 25

All the cytokine levels in response to the drugs used are in the limit of normal.

The levels of TNF. VEGF and IL 6 are much lower in Danazol and Stanozolol treated cells. The interpretation is that both Danazol and Stanozolol reduce the inflammation and contribute to repair of the cells.




Cytokine K. Z.

Normal values

(500 individuals)

IL-1beta  (pg/mL) -Interleukin 20 30± 12
TNF-alpha (pg/mL)-Tumor necrosis factor 50 42± 16
IL 6 (pg/mL) 40 35± 10
VEGF (pg/mL) vascular endothelial growth factor 120 80± 30
IL -8 (pg/mL) 32 25±15
Adiponectin (g/mL) 10 8.1±3.3
Resistin (ng/mL) 118 124±22
IL 2 (pg/mL) 28 45± 20


 All the proinflammatory cytokines (IL-1 beta; IL-6; IL8; TNF-alpha) are in the limit of normal.

VEGF- (pro-angiogenic cytokine) is higher vs. normal. The interpretation is that KZ has a possible re-vascularization. IL-2 an anti-inflammatory cytokine is normal. Adiponectin and Resistin are cytokines/hormone involved in nutritional/lipid/ obesity and metabolism. Both are normal. 


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TABLE I. Science Magazine. 2021

Goal: Author: Natural Physiology: Scientific Observation in using MAAS: End Point/ side-effects:
Cost and availability Nusinovich Y.1 MAAS inexpensive and readily available “More work is needed to overcome this increasingly prevalent disease with the eventual goal of prevention or a cure.”
Childhood: prevent the islet specific auto-antibody Dayan CM.2 MAAS not applicable to children “…is recent successes in using immunotherapy to delay the progression.” Editor adds ‘although MAAS may not bev applicable to those who have not reached adult height”
Immunotherapy could reduce insulin needs: cyclosporin was toxic Bluestone JA3 if immunotherapy reduced inflammation/ cytokines

Individual MAAS11 may have different effects on pro- inflammatory cytokines (IL-01, TNFα) IL-6, etc.)



In-vitro lab can checks cyto-toxicity.  Drug-resistance does not usually develop to MAAS.  Results with 3-hr OGTT observable in lab confirm reduced insulin needs.


Cyclosporin immunotherapy was cytotoxic.

MAAS is cyto-protective of anti-inflammatory cytokines [EML]

Reduce insulin needs

Brusko TM4;

if β-cell transplant

NIFT can reduce insulin requirements


Β-cells subject to blood-mediated inflammatory reaction. Transplant increases risk for infection & cancer.  Tregs suppressà immune-regulatory cytokines.

MAAS reduces proinflammatory cytokines, reduces insulin required.


Prevent hypoglycemia Perkins BA5 non-insulin facilitated transport (NIFT)

  mixed androgenic anabolic steroids (MAAS)

prevention of Somogyi effect: hypoglycemia


AAS Class III Aromatize to E2 Reductase to DHT Receptor affinity SHBG
Testosterone ü ü ü 10-fold E2 98% bound
Nandrolone ü 30-fold E2 5% bound
Danazol ü Reduces SHBG 80%
Stanozolol ü Reduces SHBG 80%
Oxandrolone ü Reduces SHBG41
DHEA Over-counter
  • TRT offers reductions in insulin resistance, total cholesterol, LDL cholesterol and triglycerides and improvement in glycemic control and anthropometric parameters.24
  • Danazolincreases the sensitivity of pancreatic insulin and glucagon secretion to glucose. Danazol-induced insulin and glucagon resistance could be due to receptor down-regulation resulting from hypersecretion of insulin and glucagon.25
  • Pharmacological doses of testosterone or 19-nortestosterone to normal men is not associated with increased insulin secretion or impaired glucose tolerance 26
  • Stanozolol reduces insulin requirements initially 27
  • DHEA supplementation has no effects on blood glucose levels.30

TABLE III.  Types of Diabetic Medications

Regular Insulin 30 minutes 3 to 6 hours >>Insulin regular Novolin R®
Intermediate- acting insulin 1 to 2 hours 12 hours


Novolin N®

Long lasting insulin 2 to 4 hours 24 hours

>>Insulin detemir/ Levemir®

>>insulin glargine/Lantus®, Basglar®

Ultra-long-lasting insulin 6 hours 36 to 42 hours

>>Insulin degludec Tresiba®

>>Insulin glargine U300 Toujeo®

Non-insulin drugs
(GLP-1) Glucagon-like protein Releases more insulin from pancreas

Semaglutide/ (Ozempic)®; Lixisenatide/ (Adlyxin)®;Dulaglutide (Trulicity)

Exenatide ER (Bydureon);Exenatide (Byetta)

Liraglutide (Victoza)

Dipeptidyl peptidase-4 inhibitors  (DPP-IV)

Releases more insulin from pancreas Sitagliptin (Januvia®) saxagliptin (Onglyza®) linagliptin (Tradjenta®) alogliptin     (Nesina®)
(SGLT2)  Sodium-glucose co-transporter 2 inhibitors release more sugar through kidneys Canagliflozin (Invokana®), dapagliflozin (Farxiga®), empagliflozin (Jardiance®)


Biochemical Patterns of Increasing Metabolic Syndrome >> Diabetes Mellitus

Pattern I: Glucose < 100 insulin <20 at 60min NORMAL
Pattern II: Glucose >140 insulin >40 at 60min Delay and increased peaks (In&G) at 60min
Pattern III; Glucose< 140 insulin <40 at 60min Delay and increased peaks (In&G) at 120min
Pattern IV: Glucose< 140 insulin <50 at 60min Hyperinsulinemia -Insulin >50
Pattern V: Glucose< 100 insulin <20 at 60min Insulin never rises above baseline
Reference Keys: Insulin (In) and Glucose (G): both (In & G)




24-hr (Lantus®)



Testosterone serum mg/dl

SHBG nmol/ml

#/ week injections


14 units







30 units





40 units





50 units





60 units






70 units






80 units




75 units






75 units





88 units





  1/ 27/2007

100 units