Back in 2006 two of my previously healthy, unmedicated male patients, one aged 65 and the other 66, developed “multiple extrasystoles” (random extra heartbeats, with no other problems) at the same time.
The 65YO was a light smoker (5-7 cigarettes per day), while the 66YO was not.
Both had normal blood tests (except for low DHEA levels), chest Xrays and EKGs.
I had just started prescribing DHEA.
So, I advised them both to take DHEA. The 65YO started taking it right away. The 66YO didn’t.


The 66YO continued to have multiple extrasystoles and progressed to fibrillation in 2009.
A “defibrillation” (electric shocks to his heart) was done to reset his heart rhythm, and was repeated later when the fibrillation came back.
Later on he had to have a pacemaker put in, for fibrillation in spite of multiple-drug treatment.
In 2014 three of his heart arteries plugged up and he got three stents put in.
Eventually, in Y2000, he needed a quadruple heart-artery bypass by open-heart surgery.

Now aged 83, he says that he is doing well. That sounds great, but let’s compare his experience with that of the 65YOld…..


The 65YOld started DHEA, 100mg per day, in August of 2006.
He took 100mg until the summer of 2017, when he developed the only male side-effect of DHEA: breast enlargement and tender breast cysts.
That was terrible, but the problem went away ten days after he reduced his dose to 50mg.
He has continued taking 50mg of DHEA per day ever since.*

In March of 2000, at the age of 81, he had a brief runny nose, then “Covid toes”. Then later on he developed a combination of super-itchy rash, shortness of breath and rapid heartbeat.
He seemed to improve slowly and he figured the symptoms were from “long Covid’, so he waited.
The skin itch improved with a cortisone-type cream called “Liderm”, prescribed by a dermatologist in December of 2020, but the heavy breathing and fast heartbeat continued.
In April of 2021 he saw a cardiologist and a respirologist and had an EKG, a chest xray, echocardiogram, exercise stress test with Persantine and a CAT scan of the chest with “contrast” angiogram. All tests were normal and the Cardiologist said “This 82YO’s heart is perfect, with no evidence of disease in the arteries or any other abnormality”.


So, at least based on these two cases, Restoring DHEA to more youthful levels through per-oral supplementation can protect the the heart from major cardiovascular risk factors which lead to blockage of the heart’s arteries.


In my opinion, keeping your DHEA close to “25YO level” is the best thing you can do for your body.
If acne, oily skin or hair-on-the-chin begin to bother you when you take it, reduce your intake, but don’t stop it altogether.

The other hormones, vitamins and minerals, exercise etc. are important, certainly, but
DHEA supplementation is a “must”.

The 65yo took DHEA by itself until 2014, so it is safe to say that it was the DHEA that stopped the extra heartbeats.
He started adding vitamins and other supplements in 2014. Now (2022) he takes 5000iu of VitD, 2 Grams of Vitamin C, 1mg of Vitamin B9, a multivite/multimineral pill, 200 mg of Magnesium BisGlycinate, 600 mg of NAC (a mitochondrial support molecule), Fish oil and Primrose oil pills,
50 mg of Progesterone, and 10mg of Melatonin.

He exercises in a gym and maintains a BMI of 25.5 – to – 26.
He reduced cigarette consumption from 5-7 per day, to 2-3 per day, in 2021.



Transient stress causes short-term increase of cortisol output by the adrenal glands.
Cortisol inhibits D1 (type 1, 5-deiodinase enzyme) and promotes D3, reducing conversion of T4 into T3, increasing rT3 production and increasing conversion of T3 into (inactive) T2.

By these mechanisms stress, whether physical, as in terminal illness, catastrophic infection, severe injury, major surgery, burns etc., or psychological, produces Intracellular Hypothyroidism.

We sometimes find that the adrenals no longer respond with high cortisol production and often, cortisol tests show reduced production.


Medical practitioners unfamiliar with deiodinase metabolism and intracellular hypothyroidism are at a loss to explain the low cortisol levels and the patient’s continuing complaints. They assume that the symptoms are due to low cortisol production, so they call the condition “Adrenal Fatigue”.
Many ill effects of Intracellular (Functional) Hypothyroidsm are blamed on “Adrenal Fatigue”, a fanciful label which is inappropriate, as far as I am concerned.


We don’t know the mechanism of cortisol output reduction –
Certainly, there is nothing wrong with the adrenal glands.
Certainly, the symptoms of Adrenal Fatigue are indistinguishable from those of IH.
SO, perhaps the cause is simple:
we know that metabolic slowdown due to IH affects the whole body except the Pituitary.
The adrenals are part of the body. So if, as we would expect, the adrenals respond to inadequate intracellular T3 in the same way as all our other cells, a reduction of efficiency and reduced cortisol production is inevitable and unsurprising.
Therefore the failure of cortisol production, referred to as “Adrenal Fatigue”, observed in IH
is simply a previously unrecognised manifestation of Intracellular Hypothyroidism and has nothing to do with the abilities of the Adrenal glands.


Like Medical Reviewer Jessica Rodriguez CNP, from “Endocrine Web”, on July 02. 2021, at
And Dr. Lam, from AGRINEWS.NET, on 09 April 2020
And Dr. Shawn Greenan, DACM, CFMP, from RUPA HEALTH, in “A Functional Medicine Approach”, |June 23, 2021 https://www.rupahealth.com/post/hypothyroid-vs-adrenal-fatigue-know-the-signs-and-symptoms

Do have a look at these and any other sites you find, and send me a note on the subject.

Funny ! …… The big guys haven’t caught up yet !

Dr. Harry.



Cardiomyocyte-specific inactivation of thyroid hormone in pathologic ventricular hypertrophy, by Christine J. Pol,Alice Muller, and Warner S. Simonides, was published in Nov. 2008.

It proves Deiodinase-3 activity in ventricular hypertrophy, causing heart failure, associated with severe impairment of cardiac T3 signaling.

If you have an interest in heart failure, especially cardiomyopathy, have a look at this paper (the abstract is not a difficult read and the article as a whole isn’t bad from the point of view of readability).

DHEA and cancer prevention

TP53 and DHEA

This note was inspired by a very well-written, easy-to-read, but very long and complicated dissertation on the anticancer function of DHEA, entitled “DETECTION OF A NOVEL, PRIMATE-SPECIFIC ‘KILL SWITCH’ TUMOR SUPPRESSION MECHANISM THAT MAY FUNDAMENTALLY CONTROL CANCER RISK IN HUMANS: AN UNEXPECTED TWIST IN THE BASIC BIOLOGY OF TP53″,
by Jonathan W Nyce, In: Endocr Relat Cancer. 2018 Nov; 25(11): R497–R517., Published online 2018 Jun 25. doi: 10.1530/ERC-18-0241, PMCID: PMC6106910, PMID: 29941676 , at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6106910/   


Our cells are constantly exposed to a variety of cellular stressors and are prone to DNA damage, which can lead to mutation, formation of abnormal genes and eventually, cancer.
Therefore, to protect cells from malignant transformation, the cells’ nuclei carry a special gene called TP53.

TP53 activates other genes, “KILLER GENES”, which can arrest cell metabolism and kill the cell.
This is a natural process called apoptosis, which is good because cells with cancerous potential are destroyed.
However the cells only carry tiny quantities of TP53 and it exists in a dormant, inactive form.

When DNA is damaged, TP53 is induced to accumulate in the cell nucleus and is converted into an active form, which triggers the killer genes to induce cell cycle arrest and/or apoptosis, depending on how much DNA damage has occurred.

If the damage is mild, cell metabolic slowdown permits DNA repair, but if the situation is bad enough, TP53 triggers the killer genes to destroy the cell.
In this way dangerously damaged cells are prevented from cloning themselves and producing daughter cells with damaged DNA and cancer potential.
This idea is supported by the fact that TP53-deficient mice develop spontaneous cancers.


The background point is that TP53 blockade by mutant TP53 depends on an enzyme, glucose-6-phosphate dehydrogenase (G6PD):
G6PD facilitates production of NADP and
NADP inactivates any normal TP53, keeping the abnormal cell alive.


(1) Many years ago (BACK IN THE ’80S), DHEA, the “mother hormone” made by our adrenal glands and our brains, was observed, in mice, to inhibit spontaneous breast cancer and chemically induced tumors of the lung and colon.
In mice it also stopped tumour formation by a carcinogen named DMBA and another called TPA.
In fact it was proved to be effective in stopping cancer formation generally, excepting that it promoted liver cancer in rats. This action of DHEA remained a mystery for decades, but recently (2018) there has been a breakthrough: now we know that DHEA potently blocks G6PD, thereby stopping NADP formation.
Without NADP, there is nothing to stop TP53 from working and it is free to trigger killer genes.
Therefore effectively, DHEA has the potential to discourage new cancer initiation.
(Of course, DHEA may not be effective against all cancers and as yet there have been no human trials, so what we are talking about here is a potential use in prevention of cancer, not about curing someone with an existing tumour).

(2) Many of us fail to produce normal amounts of DHEA ab initio, perhaps as a consequence of PTSD suffered in childhood, so when we all begin to lose 1% of DHEA production at age 26, high DHEA producers start from normal and low producers, from whatever they had in their teens.
Thus by age 80, the highest DHEA producers at age 25 are down to 10-20% of their original level and poor producers at 25 are down to zero.

(3) I have no certifiable answers, but I do have a lot of obvious questions, like
Do we make cancers because we don’t make enough DHEA?
If I take DHEA as a supplement, will it prevent cancer?
If I have a cancer, will DHEA stop it?
Why don’t all doctors know about this ? …… Well actually, I myself only just found it, 3 years after publishing !


(1) Role of p53 in Cell Death and Human Cancers: Toshinori Ozaki1 and Akira Nakagawara , Cancers (Basel). 2011 Mar; 3(1): 994–1013.Published online 2011 Mar 3. doi: 10.3390/cancers3010994, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756401/

(2) Detection of a novel, primate-specific ‘kill switch’ tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53, Jonathan W Nyce,
2018 Nov;25(11):R497-R517., oi: 10.1530/ERC-18-0241. Epub 2018 Jun 25.
PMID: 29941676, PMCID: PMC6106910, DOI: 10.1530/ERC-18-0241, https://pubmed.ncbi.nlm.nih.gov/29941676/

Request for donations

Hi All,

I just found an Article in JAMA (the Journal of the American Medical Association), dated June 21, 2021, by WK Silverstein and D. Grady, entitled “Overuse of Levothyroxine in Patients With Subclinical Hypothyroidism: Time to “Leve”-Out-Thyroxine“.
The abstract (the summary) of this article reads as follows:
“Recent clinical trials and a meta-analysis demonstrate no symptomatic benefit from treatment with levothyroxine among nonpregnant adults with subclinical hypothyroidism ……. Contemporary evidence-based clinical practice guidelines strongly advise against levothyroxine (ELTROXIN or SYTHROID) supplementation for subclinical hypothyroidism …. (and) …. older guidelines from professional societies generally do not recommend treatment for subclinical hypothyroidism.”

This sort of information is very important to many of you, especially the people who are unhappy about being treated with Eltroxin or Synthroid and I would love to write a post about it.

So here’s the problem: JAMA, like many journals, especially those which belong to big online “libraries”, charges fees to allow access to articles. If I were working at a teaching hospital or a university, my institution would pay these fees, but I am not.

As a “standalone” researcher I could buy the article for US$40, or I could join an outfit called “DeepDyve” for US$499 per year.
That doesn’t sound like such a lot, but here, I am talking about one single article! If I am going to do that sort of thing, I would need to join four or five other libraries so as to access articles which I should read so as to give you the cogent information which I would like to provide.
Frankly, such sums are not available to me.

Funds donated to this website will be applied to cover the costs involved in acquisition of information you need.
So …… ?
With my thanks, in advance, and with my best wishes, for 2022 !
Gervais A. Harry.


Here is one more anecdotal story.

In February of 2020, my wife went to London for a conference, returning on the 5th of March.
On the return trip she had a mild sore throat, which she reported to the border officer at the airport: she was advised that since she was feeling fine, there was no need for a covid-19 test.

On the news two days later we heard that Sophie Trudeau had returned from London with a covid-19 infection, the night before my wife’s flight.

We did not develop any respiratory symptoms and we decided not to worry about it, but five days later I developed classical “Covid toes”, involving my right foot and the inflammation, with swelling, burning, pain and tenderness, lasted about five days.

In June of 2020, I began to experience extraordinarily itchy, little spots, of different sizes, symmetrically positioned on my legs (right and left), then my back (at the tip of each scapula), then my arms (usually at the elbows, or over the triceps muscles).

I unsuccessfully searched the web for causes of dermatitis in an 80-year old and consulted with a family physician friend, then with a dermatologist, online: the consensus was that I had nummular neurodermatitis. 

Treatment with “Liderm”, a corticosteroid cream, stopped the itching about 20 minutes after application, but next day I would have another crop of itchy spots, always symmetrically placed, right and left.

The problem continued, getting very slowly better until it stopped in October of 2021.

I had my first Covid vaccinations (Pfizer) on 13th March, and my second in July, of 2021.
My booster was scheduled for 11th January 2022.

On the 7th of January 2022, I had a sniffly nose. The dermatitis began again and on 9th January my Covid toes recurred, milder this time. 
Neither the itch nor the inflammation of the toes is as severe as it was in March of 2020.
I have not redone the home Covid test because it is currently not easily available.

On the 11th of January, I went for the booster shot anyway.

I began applying Liderm to the itchy spots, but this time it did not work well, so my wife suggested taking primrose oil capsules, by mouth: I am taking one, twice per day.
The primrose oil stopped the itching in two days and I have no “spots”.


  • It is uncertain as to whether or not I had Covid in March 2020, and it is even less certain that I have got it again now, but the circumstantial evidence suggests that I did.
  • Although I am 82 years old, my hormone balance and vitamin levels are those of a 30 or 35 year-old and I take 5,000 iu of Vitamin D daily, which might explain the fact that I did not develop a severe covid infection in March, 2021, or Jan, 2922. 
  • Regardless of the answers to these questions, it is fair to say that primrose oil has relieved my itch within two days.

Primrose oil contains GLA (Linoleic Acid), an omega-6 essential fatty acid that has anti-inflammatory effects in the body, so it is not surprising that it has helped my dermatitis.

According to the “WEB MD” site, it is used for the nerve damage of Diabetes and for Osteoporosis.


So, come to your own conclusions, but I think that if you have dermatitis from long Covid, you should give primrose oil a try!

If you have further information, comments or objections to this post, please do send me a note.


(1) Web MD:


(2) Evening primrose oil: Bryan Bayles 1 Richard Usatine: Am Fam Physician, 2009 Dec 15;80(12):1405-8. https://pubmed.ncbi.nlm.nih.gov/20000302/

(3) Review Article karger.com/Article/Fulltext/512932#

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