Is DHEA deficiency, and/or the LT3 S, a factor in turbo cancer? ?
I have just received, and read with great interest, Dr. Paul Marik’s “Mechanisms of Post-Vaccine Turbo Cancer”: this note, I hope, will contribute (a little) to Dr. Marik’s excellent treatise.
I do not have Dr. Marik’s training and expertise in oncology: I am a urologist, retired in the year 2000, with 14 years’ experience in family practice (following retirement) and 8 years’ experience in metabolic medicine and hormone restoration (following retirement from family practice). As such, I offer this opinion with humility.
Dr. Marik’s treatise on turbo cancer (verbatim)
Dr. Marik considers the following processes integral to the genesis of “turbo cancer”: 1. Metabolic Reprogramming: cancer cells shift into the “Warburg effect,” using inefficient glycolysis even in oxygen-rich environments. The spike protein impairs mitochondrial function, forcing this shift and favouring tumor growth.
2. Cancer stem cell propagation: Spike protein activity may fuel stemlike cancer cells that regenerate tumors, evade treatment, and spread to new sites
3. Apoptosis Resistance: by interfering with the p53 tumor-suppressor possibly, the spike protein, Lord abnormal cells through evade programmed cell death.
4. Angiogenesis & metastatic potential: Spike driven inflammation and VEGF upregulation promote new blood vessel growth to feed tumors and help them spread.
5. Immune dysfunction & tumor microenvironment disruption: vaccine -induced IgG4 antibodies, lymphopenia, and myeloid derived suppressor cells can blunt the immune system’s ability to detect and destroy cancer cells
I am convinced that Dr. Marik is correct. However I wish to expand on one aspect of his calculation: the matter of evasion of the apoptotic action of TP53 by cancer cells.
Dr J.W.Nyce’s contribution, re. TP53, apoptosis and DHEA
I hark back to a June, 2018 paper, by Jonathan W. Nyce, entitled “Detection of a novel, primate specific, “kill switch”– a tumor-suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53”. The article was published in Endocr Relat Cancer. 2018 Nov; 25(11): R497– R517. It was released online on June 25, 2018 – DOI: 10.1530/ERC – 18 –0241, PMCID: PMC 610-6910, PMID: 29941676. The URL is https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6106910/.
As noted by Dr. Marik (point #3 of his list), under normal circumstances, mutation to a cancer-type metabolism triggers conversion of TP53 into its active form, which turns on “KILLER GENES”, to arrest cell metabolism and kill the abnormal cell, by generation of ROS (“Reactive Oxygen Species”).
But when the mutation damages the TP53 gene itself, an abnormal gene is born, which activates Glucose-6-Phosphate Dehydrogenase (G6PD, present in all cells). G6PD prevents the formation of ROS by triggering production of an antioxidant, NADP (nicotinamide adenine dinucleotide phosphate). NADP prevents ROS formation by TP53, so the cancer cell survives, to multiply and metastasise.
People under 25 don’t usually get cancers: this is attributable to the liberal supply of DHEA produced in youth: DHEA blocks G6PD, stopping NADP formation: with no NADP available, ROS are produced and the cancer cell dies.
DHEA deficiency
In my practice, between 2006 and 2014, I tested 685 people for DHEA levels: the vast majority had a serum DHEAS of <6 (see Previous Post: “DHEA deficiency in family practice”). I concluded that supplementation is good for everyone, over the age of 25 (or earlier, if the serum level of DHEA is <6 µmol/L).
Therefore, re. Dr. Marik’s Treatise, re. “Turbo Cancer”:
· Turbo-cancer patients will almost certainly have DHEA deficiency; so the serum DHEA level should be verified; but regardless of the result, supplemental DHEA should be prescribed.
· The hypothalamus interprets the presence of cancer as a “stress”: ACTH production rises and cortisol manufacture increases, causing (a) reduced DHEA output (via the “pregnenolone steal”) and (b) the Low T3 Syndrome (via DIO1 inactivation and DIO3 promotion).
Assessment should therefore include, in addition to a DHEA study, a complete “thyroid profile”, including TSH, FT4, FT3, reverse T3 and thyroid antibodies. Patients with an abnormally low T3/rT3 ratio may benefit from supplementation of their T3 levels, with slow-release Liothyronine (Triiodothyronine).
An unknown: the effect of T3 on antineoplastic agents
Vis-à-vis my comment, re. Supplementation of T3: it is a “given”, that most turbo cancer subjects should be suspected of the Low T3 Syndrome, so supplementation of T3 sounds like a good idea. However many, if not most, antineoplastics cause hypothyroidism: it may be that Hypothyroidism is a major contributor to their effectiveness: if so, correction of low T3S with SRT3 would be counterproductive.
I am a Toronto-trained Urologist. I practiced in downtown Toronto, from 1977 to 1997, when I went to Saudi Arabia as chief of Urology at the Armed Forces (teaching) hospital in Tabuk.
Returning to Toronto in Y2000, I switched to family practice.
In 2007, began to prescribe Hormone Restoration Therapy and in 2012, I became a member of the American Academy of Antiaging Medicine [A4M].
I successfully wrote the A4M's written examination in December, 2013 and In May, 2016 I passed the oral examination, for accreditation as a BHRT consultant.
In 2014 I began BHRT practice in Collingwood, Ontario and in January, 2017, joined the Stone Tree Naturopathic Clinic.
Now I am 85 and retired, but it seems wasteful to jettison my learning and experience: the medical establishment knows nothing of BHRT / Functonal medicine and I feel obliged to offer my knowledge in the interest of those who are willing to think outside the box.
QUALIFICATIONS: MB, BS, (UWI), 1964. LMCC 1969. FRCSC (Urology), 1974. ECFMG 1984. Florida license [inactive], ABAARM 2016.
Affiliations: CSAMM, OMA, CMA, SUSO, CUA, RCP&S/C.
PRACTICE TO DATE:
Consultation in Functional Medicine: Chronic Fatigue Syndrome, Fibromyalgia, Andropause, Menopause, Teenage and Postpartum Depression/Panic Attacks, Thyroid Hormone malfunction, Infertility, Sexual Dysfunction and “the Undiagnosable”.
ALL ARE WELCOME to read, comment or question!
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