ONE MORE ERRONEOUS E-NEWS ITEM

When reading medical “news items”, CAVEAT EMPTOR!

My newsfeed

My medical newsfeed is a wonderful thing: – One of these days, I really must calculate the (factual, vs. careless-ignorance-based) error rate!

This time, I received a missive from Medscape Medical News, authored by Karon Warren, a freelance journalist living in Georgia: the report details the findings of a study, in JAMA Internal Med., Published online October 23, 2023, entitled
“Be Advised: Thyroid Hormones May Increase Risk of Cognitive Disorders in Older Adults” (again, as often happens, this message fails the test of “news”: it’s dated November 02, 2023).

Let’s restate the title:

”Thyroid Hormones May Increase Risk of Cognitive Disorder in Older Adults”

It begins with “Patients age 65 and older who receive thyroid hormone therapy and experience “low thyrotropin” (TSH) are at increased risk for dementia and other cognitive problems, according to new research published October 23 in JAMA Internal Medicine.

It reports on IATROGENIC Thyrotoxicosis (see BOLD type, below)

“The study found that patients with thyrotoxicosis had a higher likelihood of incident cognitive disorder (adjusted hazard ratio (aHR), 1.39; 95% CI, 1.18 – 1.64; P < .001). Broken down between internal and external causes of thyrotoxicosis, exogenous thyrotoxicosis continued to be a significant risk factor (aHR, 1.34: 95% CI, 1.10 – 1.63; P = .003), while endogenous thyrotoxicosis did not show a statistically significant risk (aHR, 1.38; 95% CI, 0.96 – 1.98; P = .08).”

It states that females are more likely to show low TSH levels

“The study also found that women were more likely to have low levels of thyrotropin (thyroid-stimulating hormone/TSH) than men and were more likely to be overtreated.”

Then, in what seems to be an oxymoron, it says that “the signal” is present in both iatrogenic and endogenous hyperthyroidism:

“Previous studies looking at the correlation between hyperthyroidism and cognitive disorders often did not include participants who were already taking thyroid hormones, according to Jennifer S. Mammen, MD, PhD, assistant professor of medicine at the Asthma and Allergy Center at John Hopkins University School of Medicine in Baltimore and the senior author of the study” …… “The fact that we see the signal both in people who are being overtreated with thyroid hormone and in people who have endogenous hyperthyroidism is one way that we think that this supports the fact that it’s not just confounding, it’s not just bias”, Mammen said. “There’s two different sources of hyperthyroidism, and they’re both showing the same relationship.”

The study concluded that perhaps, older patients did not need treatment for their hypothyroidism

Mammen and colleagues analyzed electronic health records for patients aged 65 years and older who received primary care in the Johns Hopkins Community Physicians Network over a 10-year period starting in 2014. None had a history of low TSH levels or cognitive disorder diagnoses within 6 months of their first doctor visit.

More than 65,000 patients were included: 56% were female. Of 25,000 low TSH measurements in 2,710 patients, iatrogenic TSH comprised 14,875, endogenous TSH numbered 4,159 and those of “unknown cause“ totalled 5,833.

During the follow-up period, 7.2% (4779) patients received a new cognitive disorder diagnosis, which was dementia in 77% of cases.

Mammen concluded that primary care physicians should “carefully consider whether thyroid hormone therapy is necessary for older patients” and take great care to avoid overtreatment, saying “This is yet another reason for us to be vigilant about not overtreating people with thyroid hormone, especially in older adults. We already know that atrial fibrillation rates are increased in people who are hyperthyroid. We know that fracture and osteoporosis is affected by hyperthyroidism. And now we also have an association with higher rates of cognitive disorders.”

This report was taken seriously

According to Medscape, Jean Chen, MD, partner at Texas Diabetes & Endocrinology, who was not affiliated with the study, said “All medical providers need to be aware that the 65 and older population does not need to be treated as aggressively with their thyroid hormone. We are finding more and more complications from overtreatment, rather than benefit, in this population.”

Chen continued:
“Often, older patients may complain of symptoms such as constipation, feeling cold, or tiredness, which can be symptoms of hypothyroidism. But these symptoms could also be from anemia, vitamin deficiencies, depression, perimenopause, menopause, insulin resistance, and sleep apnea. If necessary, Chen recommends primary care physicians consult with an endocrinologist regarding a possible treatment plan and making a differential diagnosis.” ……………….
The symptoms mentioned are definitely those of hypothyroidism! – G. A. Harry

In addition, Chen said other studies have shown that treating patients with “Thyroid Hormone” (she means T4) either did not resolve the condition, or negatively impacted anxiety, muscle strength, and bone density, or it increased the risk for arrhythmia.
She concluded: “Therefore, it’s important to weigh the risks vs the benefits.”

This study was amply supported

The study was supported by the Richman Family Precision Medicine Center of Excellence in Alzheimer’s Disease, the Richman Family Foundation, the Rick Sharp Alzheimer’s Foundation, the Sharp Family Foundation, among others. The work was also supported by grants from the National Institutes of Health.
Also, Co-author Constantine Lyketsos, MD, MPH, reports personal fees from Karuna, MapLight Therapeutics, Axsome Therapeutics, GIA, GW Research Limited, Merck, EXCIVA GmbH, Otsuka, IntraCellular Therapies, and Medesis Pharma for consulting for treatment development in Alzheimer’s disease outside the submitted work. No other disclosures were reported………………. isn’t that interesting?

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TurboCancer: Dr. Paul Marik’s treatise, DHEA and T3

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.

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Certain omissions are ever-present in scientific medical reporting

Alzheimer’s treatments, this time: there’s always something missing!

The latest report: Donanemab for Alzheimer’s disease

I continue to receive reports on various and sundry scientific papers, purporting to present “breakthrough” scientific studies to the medical profession.
Usually, the “breakthrough” study being reported turns out to have been done in the absence of any attempt to ascertain, let alone to include, the effects of hormonal or metabolic aberration on the patient’s diagnosis, response to therapy or outcome.

The one I received today, “Donanemab in Early Symptomatic Alzheimer Disease”, ClinicalTrials.gov Identifier: NCT04437511, is no exception.

The report is huge and apart from the omission, very well done.

It is an absolutely monumental report on a trial of Donanemab (an immunoglobulin), a G1 monoclonal antibody, which is “directed against insoluble, modified, N-terminal truncated form of β-amyloid present only in brain amyloid plaques”.

Donanemab “binds to N-terminal truncated form of β-amyloid and aids plaque removal through microglial-mediated phagocytosis”.

The authors tried their best

In deference to the authors, John R. Sims, MD1; Jennifer A. Zimmer, MD1; Cynthia D. Evans, PhD1; et al, I must say that this monumentally expensive study appears to have been intelligently designed, carefully supervised and meticulously executed.
It was a Multicenter (277 medical research centers/hospitals in 8 countries), randomized, double-blind, placebo-controlled, 18-month phase 3 trial that enrolled 1736, 65–85-year-old participants, with early symptomatic Alzheimer disease (mild cognitive impairment/mild dementia) with amyloid and low/medium or high tau pathology based on positron emission tomography imaging from June 2020 to November 2021.

The paper is a masterpiece.

The paper gives clear evidence that Donanemab, prescribed by itself and without correction of pre-existing hormonal/metabolic aberrations, has beneficial effects on humans with early Alzheimer’s disease. I read it in its entirety, and am impressed with the authors’ attention to detail: I could find nothing to criticise, excepting for one omission which in truth, seems to be present in every clinical trial, nowadays.

The ever-present omission

Clinical trials, perhaps because they are almost always initiated by pharmaceutical companies or by individual physicians who are interested in a drug, procedure or intervention as it applies to a narrow, “specialised” aspect of disease, investigation or therapy, tend to focus sharply on the diagnosis, investigation or therapy being investigated, with little consideration for pre-existing disease, or metabolic aberrations.

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Why DHEA and T3/rT3 Testing Matters, & why everyone should be aware of DHEA deficiency and Intracellular Hypothyroidism

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Big Pharma, Big Medicine and the grassroots MD

It is time, for logical thought!

Preamble

This is not a new post: I originally wrote it some time ago, as a “thread” in “chat”. I came across it just now, while reviewing “Aging and Your Hormones”.
I think it’s valid, even though not new and now that I seem to have persuaded a few doctors to subscribe to the blog, it strikes me as important enough to resubmit (it’s very lightly paraphrased and I’ve tried to make it readable!).

The idea is to remind MDs that they are licensed, independent professionals, able to think for themselves and that at least nominally, they should remain unfettered by official “guidelines”, which so often, are illogical.

So here is “IN SUPPORT OF LEARNING BY EXPERIENCE” (“chat”, from16th February, 2025):

IN SUPPORT OF LEARNING BY EXPERIENCE

I wish to express my thanks to, and to laud, the unfettered online journal, “ResearchGate”, which accepted and published my two articles, “Intracellular Hypothyroidism” and “T3/rT3 diagnoses the low T3 syndrome” back in 2022, even though I declared myself non-academic, un-attached to any hospital or other ”institution” and to boot, retired and hence “de-licensed”!

Career researchers and overgrown pharmaceutical companies are not the be-all and end-all of logic and discovery. As a general class, they are rendered myopic by the necessity to publish and the urge to profit. Their success in infiltrating “mainstream medicine” has resulted in a transfer of that myopia to the “omni-potent”, but hardly “omni-scient” Medical Colleges and Ministries of Health, which have the power to “defrock” the lowly MD (speaking of which, to my consternation and chagrin, the lowly MD’s consciousness has been invaded by the “defrocking” threat to the extent that he (she), in fear of fine and slander and rejection, literally cowers (as a colleague of mine did, back in 2012) at the mere mention of my practice of “Hormone Restoration Therapy”! – “You can’t do that! You’ll be delisted”, he said.

How’s that, for a run-on sentence?

Medical Doctors have been disenfranchised

His degree is the least – the smallest – segment of his experience (“freepik”)

MDs have been disenfranchised and rendered apathetic and un-inventive, by an insistence on “evidence-based medicine”, which is forced upon the working professional by the “establishment” under threat of termination-of-license if they dare to contravene the one-size-fits-all “guidelines”, laid down by their Medical College. **

**see “Ode, to the medical profession, as it was

Doctors’ capacity for original thought and the Initiative to apply experience-based learning in the care of their patients, have been ground to dust, by the heavy boots of modern-day, Capitalistic Academia and its bedfellow, “Big Pharma”!

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