Vitamin D Lowers Melanoma Risk

This just in:
Ilkka T. Harvima, MD, PhD, et al., from the Department of Dermatology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland, has filed a preliminary, but significant report, titled “regular vitamin D supplements may lower melanoma risk”.

The thrust of the paper is that ” Individuals who regularly take vitamin D supplements are significantly less likely to have a history of malignant melanoma or any type of skin cancers than non-users”.

The study, published December 28 in Melanoma Research, involved almost 500 individuals attending a dermatology clinic who reported on their use of vitamin D supplements.
Regular users had a significant 55% reduction in the odds of having a past or present melanoma diagnosis, while occasional use was associated with a nonsignificant 46% reduction. The reduction was similar for all skin cancer types.

Although Dr. Harvima’s report gives neither the dosage taken by “regular users”, nor the blood levels of vitamin D in the population studied, and although a proactive study of vitamin D is role in prevention of skin cancers should be done, I take this report as supporting my recommendation that we all should supplement vitamin D3 on a regular basis (please see the page on vitamin D).

How to treat Long Covid

Long Covid is intracellular hypothyroidism

An article in “Medscape CME and education”, by Charles P. Vega, MD, Exec. Director of UCI’s Program in Medical Education for the Latino Community, reports that
(1) Long Covid can affect up to half of patients with Covid 19.
(2) 45.2% of people with Long Covid in his study met the diagnostic criteria for CFS/ME.
(3) Interestingly (an unrelated fact) among the patients he studied, long Covid was 10 times less common in those with Omicron, compared with other strains of Covid 19.

Why is this important?

This is important because chronic fatigue syndrome (CFS) is actually intracellular hypothyroidism, and if CFS/ME is chronic fatigue syndrome, then long Covid is intracellular hypothyroidism.

I conclude that about 50% of those with Covid 19 develop intracellular hypothyroidism.
That would explain the persistence of long Covid symptoms, because intracellular hypothyroidism is self-perpetuating, as long as any stress persists.

The severity of Covid infection varies

The severity of Covid infection varies markedly from person to person, being negligible in some, moderate in some and overwhelming in a few.
The degree of perceived stress produced by the infection can be expected to parallel the severity of the disease, so mild cases produce low-grade stress and severe cases cause sufficient stress to result in increased production of the stress hormone, cortisol.

Cortisol blocks intracellular T3 formation and intracellular hypothyroidism results.

Diagnosing intracellular hypothyroidism

Blood is taken, to check TSH, T4, T3 and reverse T3.
A low T3/rT 3 ratio (<20), diagnoses intracellular hypothyroidism, indicating a high liability to long Covid.

Treat long Covid by treating intracellular hypothyroidism

We can treat intracellular hypothyroidism, so we can treat long Covid.
Treatment with oral T3 eliminates intracellular hypothyroidism and thus, will prevent development of long Covid.

Therefore Individuals with new infections of Covid 19 should be tested upon diagnosis if their condition is poor, or 10–14 days following diagnosis if their infection is mild.

Proposal

New Covid Infections

Let us investigate people with long Covid by checking TSH, T4, T3 and reverse T3.
Individuals with a reduced T3/rT3 ratio (normal = > 20), which confirms intracellular hypothyroidism, can be treated effectively with slow-release T3 (Triiodothyronine).
The dose of T3 can be tapered over a 2–3 month period and the prescription may be discontinued when the circumstances permit.

To view Dr. Vega’s article, copy and paste this URL into your browser:

https://www.medscape.org/viewarticle/983265?sso=true&impID=4833519&uac=235227EV&src=wnl_tpal_221105_mscpedu
or click the link (Charles P. Vega).

To review intracellular hypothyroidism, how to diagnose it and how to treat it, click on “can be treated effectively”, above.

If you currently have Covid, or if you have developed long Covid

Please note:
(1) I am no longer licensed to give you a formal diagnosis or a prescription.
[2] However I have no objection to you showing this paper and the notes on intracellular hypothyroidism, to your doctor: perhaps he or she will be willing to test you for intracellular hypothyroidism.
(3) In the interest of my own information and that of anyone who cares to discuss this post with me later on, I would be most interested to hear from you, re. the results of your TSH/T4/T3/reverse T3, tests.
So if your doctor agrees to order the tests, please contact me, via the blog or at cbhrt@gmx.com.
(4) if necessary, email me, via cbhrt@gmx.com

TREES reduce mortality

This report shines a light on an important fact: “money may not grow from trees, but something even better does”.

In a new study led by the US Department of Agriculture (USDA) Forest Service, researchers found that each tree planted in a community was associated with significant reductions in non-accidental and cardiovascular mortality among humans living nearby.

Please go to https://www.sciencealert.com/people-in-portland-planted-trees-decades-later-a-stunning-pattern-emerged (click on “trees”).

Stress Causes Hypothyroidism

Why, Vs. How!

The tree needs to be removed: that's "why?"
How will he remove the tree?: That's complicated, like explaining how stress causes hypothyroidism

Q: Why remove this tree? A: EASY! This is only half: a storm blew the other half down.
Q: How to remove this tree? A: TOO COMPLICATED to explain!

BTW: this guy probably has Zero stress, because what he’s doing is routine, for him.

Don’t explain “how” – try to explain “why”

Once in a while, some friend asks me about the thyroid and ends up totally confused by my explanation.
For example last night, when I said “stress causes hypothyroidism”, the really smart person with whom I was speaking said “you better explain that.”
I explained how stress produces a “low thyroid” situation inside the cells, as succinctly as I could without leaving anything out: my friend missed the point entirely.

So today, I reviewed my page on Intracellular hypothyroidism: it really is complicated!

Then I realised that “why” something happens can be explained easily and quickly,
but “how” it happened is always a long story!

I should explain “why”, instead of “how”, so let’s try “why” about the thyroid.
Why thyroid hormone Is important

The thyroid gland makes a “raw-material hormone”, “Thyroxine”, nicknamed “T4”, because it has 4 iodine atoms.
Your cells absorb T4 from the blood and remove one of its iodines, to make “T3”.
T3 supercharges the cells, maximizing efficiency: your cells can’t work without T3.
If there isn’t enough T3, you get tired, like in “Long Covid”, or “CFS”, or “adrenal fatigue“,or “Burnout”.

Why Stress Makes You Weak and Tired

Why produce extra cortisol when you’re stressed?
Because cortisol saves energy, which your body might need for healing.

Why is there is a problem, from increased cortisol?
Cortisol saves energy by blocking T3 and converting T4 into a twisted molecule called “reverse T3” (rT3), which doesn’t work.

So with high cortisol, it’s like your thyroid wasn’t making any thyroid hormone at all: everything in the body loses efficiency and “Hibernates”.

Why doctors don’t know about this

Stress reduces the amount of T3 in your cells, except inside the pituitary, because it makes its T3 In a different way, that isn’t affected by cortisol.
So the pituitary does not know that the rest of the body is hibernating: it monitors T4 as usual, and puts out TSH as usual.
Doctors test for TSH only, believing that if it is normal, thyroid function is okay.
So like the pituitary, the doctors don’t realize that the entire body is hibernating.

Why don’t we have a test for cortisone-induced shutdown?

We do. There are tests for both T3 and rT3.
If there is no stress, the test for good T3 is normal and rT3 is low.
So the blood rT3 is a valuable “marker”: a high rT3 tells us that the cells are making rT3 instead of normal T3.
However, the medical associations and the endocrinology professors, all around the world, tell regular doctors not to check T3 or rT3. **

** see “what our medical system ignores“, in the blog-page on “thyroid tests”.

Is any treatment available for stress-induced intracellular hypothyroidism?

Yes. It can be treated with slow-release T3.
(1) Preparations containing T4 don’t work well because the T4 is changed into rT3, so the T3 In the cells doesn’t improve.
(2) Quick-release preparations of T3 make the blood T3 “spike” an hour or so after you take the pills, then “crash” about 4 hours later: see the page on “thyroid tests”, under “treating functional hypothyroidism“.
(3) Slow-release capsules release T3 gradually: there isn’t a sudden rush of T3 into the blood and the treatment lasts all day.

What about TSH?

The conventional medical “system” tells doctors that they should only check how much TSH the pituitary gland is making.
They say that if the TSH is low, or normal, the thyroid must be working okay, because if it wasn’t, the TSH would be high.
So according to them, a normal TSH *** tells you that everything is okay and you don’t have to test T3 and T4.
They also tell doctors not to test for rT3: they think that rT3 is garbage and testing it is a waste of money.

But that’s not right.
First, a normal TSH only tells you that the pituitary has enough T4 to make its own T3.
It doesn’t tell you what’s happening in all the other cells.
Second, testing rT3 tells you how much rT3 the cells are making. —
If they’re making lots, they can’t be making normal T3.

*** see “regarding TSH”, in the blog-page entitled “thyroid tests“.

Why TSH stays low when cortisol prevents T3 production

As I said above, since the pituitary’s way of making T3 is different, Cortisol can’t stop its cells making T3 their own T3.
So when you’re stressed and all your other cells lose T3, the pituitary still has lots.
Therefore it doesn’t call for more T4 by making extra TSH.

Why your doctor says nothing is wrong with you

Your doctor believes what the system says: TSH doesn’t lie.
So no tests are done for “low T3 in the cells” and the doctor tells you that
Your TSH is low, so you can’t have “hypothyroidism”, or low-thyroid symptoms.
– Therefore whatever you’re complaining about has nothing to do with your thyroid.
– Your symptoms mean you’re stressed-out, “burned out”, or anxious and depressed.
– What you need is rest, or a holiday, or meditation,
– Or maybe you need some antidepressants and sleeping pills.
– in short, your MD doesn’t know / doesn’t believe that stress causes hypothyroidism.

Why your doctor has that attitude

In the old days, doctors were taught pretty much exactly as they are today, but after University no-one interfered with them.
They learned by practical experience, by trial and error (very often, they tried new medicines or procedures on themselves first, before giving them to patients) and by discussing “cases” with other doctors.
Every doctor’s experience was different and someone who did things differently from everybody else was considered at least normal, and possibly, smarter.

Nowadays, doctors are told by their “College Of Medicine” that they must all practice “evidence-based medicine”, which means that their way of diagnosing and treating must have been tested by experiments and published in a medical journal.
Not only that: the colleges send inspectors to the doctors’ offices, to make sure that the doctors are doing things in the approved manner.
Doctors are afraid that if they order a test that’s not approved, or make a wrong diagnosis, or prescribe different medicines, or even say something like “stress causes hypothyroidism”, they could be “disciplined” by the College and perhaps lose their license to practice medicine.

So when the medical “system” tells them not to test T4, T3 or rT3, and says that prescribing T3 is malpractice, most doctors feel forced to follow the rules, rather than going along with what the patient says.

Why patients should know “why” and how”

The more you know about why (or maybe even how) your body works and especially, why you have hormones and how they work, the more control you will have over your life and the better, perhaps even the longer, you will live.

Why I’m doing this

I have retired from medical practice, but it seems wasteful to jettison my learning and experience. The medical establishment disregards and ignores the hormonal aspect of our metabolic function and I feel obliged to offer my knowledge to all who wish to read these pages, in the interest of helping those who think outside the box.

So feel free to check out “how” and “why” in my pages and blog posts, and if you have any questions, please do send me an email (there aren’t any stupid questions),.

Preventive care, as it could be

Supplement your missing hormones

Abstract
Without preventive care, too many friends die because of late diagnosis, particularly of ovarian, colon, breast, lung, and pancreatic cancer.
Instead of ongoing monitoring, with the emphasis on earliest possible diagnosis, our doctors await the development of significant disease and too often, we hear dejected relatives exclaim, “by the time they found the cancer, it was stage four!”
We can do better.
We should do better.
We must do better!
Here, I explain the background of this problem and propose a protocol for relatively inexpensive, proactive preventive care which, applied across the spectrum of family medical practice, will allow comprehensive surveillance of our population’s health, in the interest of early diagnosis; the prerequisite to life-preserving medical care.

Caveat: the ideas put forward herein are my own. They represent a protocol for lifelong healthcare management of the individual citizen, as would, in my opinion, be best.
This protocol is offered in good faith as a suggestion for improvements in healthcare.
It does not imply criticism of the current paradigm, or of those who adhere to it.

The origin of this thesis
This essay was engendered by my ruminations on the medical and social “happenings” which my friends have had to, or failed to, endure, compared with my own preventive care: my complicated, but acceptably managed, course through the minefield of autoimmune and neoplastic threats with which we humans have to contend in this life.

I have had the misfortune to observe, among my friends and relatives:
A female professor’s non-Hodgkin’s lymphoma at age 74,
A female housewife’s death with Alzheimer’s disease at age 74,
A male MD’s descent into Alzheimer’s disease, beginning at age 78
A sub-genius man who became schizophrenic at 28, now struggling out of it at 50
A 16 year old male’s unmanageable schizophrenia, through age 40
Four (2 of each gender), born by Caesarean section, growing obese from age 18
Two brain tumor subjects (brother and sister) diagnosed too late at age 37 and 44
The death of an all-Canadian racket-sport champion, from ovarian cancer at 64
A brilliant university teacher, dead from colon cancer at 54
A debilitating stroke in a 75-year-old pediatric specialist
A medical professor’s wife (a nurse) who died with Alzheimer’s at age 86
Sequential, bilateral breast cancer in a registered nurse with an IQ of 160
Two deaths from pancreatic cancer
Five Doctors with prostate cancer
My favourite uncle dying of lung cancer at 55
Two prime ministers (and another uncle) dying of prostate cancer
A lethal heart attack sustained by a family doctor at 59,
A doctor, going from extra heartbeats at 65, to a bypass and pacemaker at 80
Plus many more.

Our risk Is rising
All of my friends’ conditions, excepting the two brain tumors, could have been anticipated, prevented, diagnosed and cured, or at least postponed, with suitable preventive care surveillance and timely intervention.
But the incidence of all of these conditions, in fact, all noncommunicable diseases, has been rising rapidly since the 1960s, so that now in the “2020s”, we are more and more at risk of all those missed diagnoses, which necessitate modern treatments at astronomical cost.

This thought process brought me to a consideration of preventive-care surveillance (PCS), a subject of much discussion in the medical community, which, if properly applied, would permit early diagnosis, with prevention, cure or postponement of debilitating disease.
Caveat: this treatise is not a consideration of surveillance from the public health point of view (3)

Therefore, Posit:

All citizens should be enrolled in a proactive, preventive care system at conception and followed, through birth and lifelong, so as to facilitate early diagnosis and management and so as to avoid the social and financial costs of severe, preventable illness.

Preventive care curveillance
In the words of Dr. Robert J. McCunney (1), “Prevention in medical surveillance is based on the fundamental principle of screening: that is, the administration of a test or tests at an interval such that an asymptomatic condition is recognized early in the disease process, so that intervention slows, halts or reverses the ailment.”

Applying this principle generally would guarantee ideal medical practice (2).
From the point of view of society, the overall reduction in the long-term financial and sociological costs would be a blessing (the resulting saving of fees to medico-legal lawyers, an obvious cost reduction, will not be considered here).

However from the point of view of employers, absence from work for preventive care investigations would be a short-term nuisance.
Further, from the standpoint of the “system” which would have to underwrite it, in-depth, all-encompassing, prevention-oriented surveillance for all diseases would be expensive.

Canadian healthcare thinks we can’t afford surveillance.

With these considerations in mind, Canadian politicians and medical planners have “shelved” the idea of ongoing surveillance, on the basis that doctors often order tests to increase their income, or so as not to be accused of “missing something”.
In my opinion, this is not correct. Doctors do order tests on the basis of not wanting to miss a diagnosis, but this is done in the patient’s interest, not for “CYA”, or the doctor’s financial gain.

Therefore it is reasonable to ask physicians not to order tests which are obviously unnecessary, but the decision to leave a test out of the patient’s assessment is to risk missing a diagnosis.
Anyway, surveillance has not been simply “shelved”: the ministry of health and the College of family physicians have established a protocol, by which the costs of preventive care surveillance can be avoided altogether – see the very specific directive, dubbed “choosing wisely”, which can be “googled” at: https://choosingwiselycanada.org/recommendation/family-medicine/ .
The purpose of the “choosing wisely” effort is saving costs, on healthcare.
The movement has developed into a major online campaign, a study of which entails considerable research on the Internet.
So to save you time, please see the list of instructions to family doctors, from the College of family physicians of Canada, copied verbatim from the www, below.

“Choosing wisely: 13 tests and treatments to question”, by the College of Family Physicians of Canada, last updated: July 2022

https://choosingwiselycanada.org/recommendation/family-medicine/

  1 Don’t do imaging for lower-back pain unless red flags are present. 
  Don’t use antibiotics for upper respiratory infections that are likely viral in origin, such as influenza-like illness, or self-limiting, such as sinus infections of less than seven days of duration.
  2   Don’t order screening chest X-rays and ECGs for asymptomatic or low risk outpatients. 
  3    Don’t screen with Pap smears if under 25 years of age or over 69 years of age.
  4    Don’t do annual screening blood tests unless directly indicated by the risk profile of the patient.
  5    Don’t routinely measure Vitamin D in low risk adults.
  6    Don’t routinely do screening mammography for average risk women aged 40 – 49. Individual assessment of each woman’s preferences and risk should guide the discussion and decision regarding mammography screening in this age group.
  7    Don’t do annual physical exams on asymptomatic adults with no significant risk factors.
  8    Don’t order DEXA (Dual-Energy X-ray Absorptiometry) screening for osteoporosis on low risk patients.
  9    Don’t advise non-insulin requiring diabetics to routinely self-monitor blood sugars between office visits.
  10   Don’t order thyroid function tests in asymptomatic patients.
  11    Don’t continue opioid analgesia beyond the immediate postoperative period or other episode of acute, severe pain.
  12    Don’t initiate opioids long-term for chronic pain until there has been a trial of available non-pharmacological treatments and adequate trials of non-opioid medications.
This directive has had a predictable effect on many family doctors, who now avoid doing any and all investigations unless the patient’s complaints and/or physical findings render the tests “defensible in the eyes of the ministry of health”.

This attitude, in my opinion as a retired physician and surgeon, runs contrary to the basic tenets and traditions of medicine and will lead to tremendous costs for medication, surgery and legal challenges in the long run.

The situation is unfortunate. However, here is a reasonable compromise, by which the scope (thus, the cost) of preventive care testing can be reduced, to allow lifesaving early diagnosis and treatment.

A limited number of factors underlie humans’ liability to noncommunicable diseases; these can be categorized as either
(1) age-related conditions (considered to be hormone deficiency effects), or
(2) stress-related effects, including those attributable to climate, income, social status, diet and social/recreational/occupational habit, or
(3) conditions, such as inherited gene aberrations or physical disabilities, unrelated to (1&2) (some of these, such as cardiomyopathy, can be shown to be related to (1&2).

Viewed from this standpoint, the problem of preventive care and disease avoidance becomes easier to consider, simpler to calculate and solvable In terms of cost.
I would propose the following protocol, which will avoid unnecessary office visits and “baseline” tests of questionable value:

Before conception and during pregnancy

Any maternal condition threatening to the fetus must be diagnosed and corrected before conception, or upon diagnosis of pregnancy.
Therefore the prospective mother and father, who have been educated in the principles of proactive health surveillance, request a pregnancy-planning interview (or an urgent appointment, if the pregnancy is unplanned), with their family physician.
At this visit the doctor evaluates both parents’ health history, physical condition and biochemical/hormonal status, taking their history, occupation, income, ethnicity, and physical condition into account and decides what tests should be done.

  • Of course, a part of the mother’s assessment is to check her DHEA, testosterone, estradiol, progesterone, “thyroid profile” (T3, T4, TSH and rT3), inflammatory markers and vitamin D level, along with throat, urine and vaginal tests for infection, stool tests for parasites and microbiome analysis.
  • The father is booked for such investigations as the physician may consider important.
  • A second appointment for explanation of aberrant test results is arranged, with both parents attending, if possible.
    If all results are normal, they can be advised by telephone.
The beginning of pregnancy:

Beginning pregnancy under stressful conditions or becoming stressed in the first three months of a pregnancy may may result in intracellular hypothyroidism in the mother. (7)
Intracellular hypothyroidism within the first 14 weeks of pregnancy is not just a problem for the mother: the fetus will also be hypothyroid, because it does not begin making Its own thyroid hormone until the 14th week of gestation.


Thyroid 3 hormone is essential and fetal hypothyroidism is terrible.

Major brain development occurs between the 8th and 14th week of pregnancy.
So if the T3 supply to the fetal brain is insufficient, essential brain areas may be connected incorrectly.

A significant increase in the rate of ADD/HD, dyslexia, autism, schizophrenia and gender dysphoria has been observed in children whose mothers were hypothyroid during the first 3 months of pregnancy.

Therefore it is imperative that the mother’s thyroid function be checked and signs of intracellular hypothyroidism be corrected, preferably before starting the pregnancy, but otherwise as soon as pregnancy has been diagnosed.

For the same reason, even if the mother is not conscious of stress,
her thyroid profile should be repeated at 8 weeks and 12 weeks of gestation.
Then if she develops intracellular hypothyroidism, treatment with Triiodothyronine can start immediately, to ensure that normal “nerve wiring” in the babies brain.

Other than thyroid surveillance, uterine ultrasounds and intrapartum observations and protocols are carried out as recommended.

Postpartum
Immediately after birth, the newborn and the mother are checked as usual, but in addition, the mother’s hormonal and thyroid profiles are repeated.
Special attention is given to levels of DHEA, testosterone, progesterone and Allopregnanolone and any abnormalities which may be found are corrected ASAP.
(A normal balance between these particular hormones will prevent maternal postpartum depression, which may adversely affect the newborn child).

The “Pediatric Years”
Thus, the newborn enters the world with the advantage of a carefully managed pregnancy in a fit and healthy, happy mother and presumably, in the best of health.
The pediatrician observes the child’s progress and administers immunizations and other care as recommended.

The pediatrician should ensure that each child has acceptable vitamin D levels, but otherwise need not check for hormonal aberrations.
It must be remembered however, that children who are abused, or otherwise “psycho-shocked”, may develop PTSD.
PTSD results in “up regulation” (increase)of cortisol and “down-regulation” (reduction) of thyroid 3: in other words, intracellular hypothyroidism.
Further, under these circumstances, aberration of other hormone levels is inevitable.

Frequently, stressed children begin their teen years with severe hormone imbalances.
Therefore it is important to make sure that any shocked child Is checked for intracellular hypothyroidism (easily diagnosed with T3/rT3 Calculation) (7).
If the tests show a low T3/rT3 ratio, the child should be referred to a metabolic medicine professional, for careful management and special attention should be paid to that child’s hormone balance in the teen years.

The pubertal and early “Teen” years: baseline adult assessment at age 15.

In the female, Hormonal balance is assessed at menarche, to establish a baseline: ongoing testing is scheduled if abnormalities are found.
In particular, Progesterone deficiency (tested on the 21st day of a female’s menstrual cycle) and DHEA deficiency should be noted, reassessed on an ongoing basis and treated (or referred to an appropriate specialist), if necessary.
The first adult “baseline” test panel is done at age 15.

In the male, hormonal aberrations found at puberty are corrected if necessary, pending adult baseline testing at age 15.

For both males and females, vitamin D, DHEA, Testosterone, Estradiol, Progesterone and Thyroid balance should be assessed at age 15 and as necessary, especially if there has been abuse, psychological upset, excessive weight gain, anorexia or poor performance at school.
However, in the absence of symptoms, abnormal results or “troubled teen” events, hormonal assessment at 15 years of age can be done virtually: a doctor’s visit can be arranged if aberrant results are flagged.
If all test results are normal, they need not be repeated until age 20.

The young adult: 3rd – 4th decade

(1) Neurosteroid (DHEA, Testosterone, Estradiol, Progesterone), thyroid hormone balance with T3/rT 3 ratio, vitamin D levels* and general “checkup” testing should be done at age 20 and if all is well, repeated at age 25 and 30.
“Virtual” reporting is fine: if no abnormality is found, there is no need for a doctor’s visit. However if aberrant results are “flagged”, a face-to-face visit with the doctor should be arranged so as to sort the question out.

* Vitamin D, a hormone of cutaneous origin, is chronically deficient in a majority of the population, resulting in increased susceptibility to viral, and other, infections, osteoporosis and many metabolic aberrations.

(2) A machine-readable questionnaire regarding symptomatology (with particular reference to hypothyroid symptoms), subjective assessment of health status including changes in appetite, weight, sleep, bowel and urinary habits, libido and mood, is filled out yearly by the patient and a doctor’s appointment is arranged to discuss any flagged items.
(3) Routine surveillance, usual in family medicine practices, might be automated (5), with a doctor’s visit for flagged items: for example,
– fecal PCR tests for colon cancer,
– a self-administered PCR “Pap” test,
– hepatitis and other routine blood tests,
– microbiome assessments,
 – breast thermography,
– PSA,
– urinalysis
– hormone balance testing.
(4) In-depth reassessment, with questionnaire, EKG, chest x-ray, hormone balance and abdominal ultrasound, is done every 5 years to age 40.
The patient is seen for reevaluation, at a formal “doctors appointment” at age 30 and 40.

The established adult (5th – 6th decade)


(1) In-depth reassessment, including the questionnaire and a doctor’s visit, plus PSA for men and hormone balance for women, should be repeated every 2 years from age 40 to age 66 and ad hoc: if all tests remain normal and there are no symptoms, the patient should visit with the doctor at age 45, 50, 55, 60 and 65.

The older adult

Healthy persons over 65 years of age should plan for an in-depth reassessment yearly, including a questionnaire, repeat laboratory tests and a doctor’s visit, “In person”, from age 66, onwards.
Specific investigation, with a doctor’s visit, should follow discovery of hormonal, symptomatic or test result aberrations observed at any age.

The system, our citizens and the ministry of health

The above suggestions are intended as a guideline for the granular management of the individual citizen’s healthcare, not as a criticism of, instruction to, or proposed management of our central, supervisory institutions.
Proactive healthcare monitoring would not survive without central surveillance (6): therefore this treatise, its principles and its propositions is intended to apply the basic principles of good medicine and the tenets of our central colleges and associations, and not as a substitute for central, overall surveillance of the health system.

Summary: proactive, preventive medical care includes

Routine assessment of the mother and father, for conditions which might adversely affect the fetus and later, the child.
Postnatal blood testing of both mother and baby, to exclude threatening abnormalities.
The child is followed as usual by a pediatrician, but special attention is paid to thyroid hormone balance and vitamin D.
The teenager is observed for aberrations of socialization, plus neurosteroid and thyroid hormone balance.
Surveillance in the 3rd, 4th and 5th decades is minimized by concentration on neurosteroid and thyroid balance: additional investigations are done remotely and visits to the doctor are arranged as necessary, based on a 5-yearly reassessment to age 40, a 2-yearly reassessment to age 66 and thereafter, yearly follow-up.

References

(1) Medical Surveillance: The Role of the Family Physician, by ROBERT J. MCCUNNEY, M.D., Massachusetts Institute of Technology Medical Department Cambridge, Massachusetts, Am Fam Physician. 2001;63(12):2339-2340, https://www.aafp.org/pubs/afp/issues/2001/0615/p2339.html

(2) “Quality in primary care./System performance.”, Editorial in Can Fam Physician. 2011 Oct; 57(10): 1219–1220.

PMCID: PMC3192094. PMID: 21998241,

https://www.hqontario.ca/System-Performance/Specialized-Reports/Primary-Care-Report

(3) “Canadian Primary Care Sentinel Surveillance Network, a developing resource for family medicine and public health.”, by
Richard V. Birtwhistle, MD MSc CCFP FCFP, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192094/
The Canadian Primary Care Sentinel Surveillance Network (CPCSSN—pronounced sipsin) started in 2008, with a grant from the Public Health Agency of Canada (PHAC), to study the feasibility of developing a network to collect health information on patients with chronic diseases across the country. This information is intended to be a resource for monitoring chronic disease in Canada, as well as for primary care research. The Canadian Primary Care Sentinel Surveillance Network has been organized as a network of networks, and its board is made up of network directors. As a sub-entity of the College of Family Physicians of Canada (CFPC), CPCSSN is partnering with the PHAC and the Canadian Institute for Health Information. The CFPC has been instrumental in both the support and the development of this network. The central office for CPCSSN is at the CFPC’s national office, where its project management, financial oversight, and privacy and knowledge transfer take place.

(4) Governments in several European countries equip all primary care practices with interoperable, ambulatory care-focused electronic health records (EHRs) ………. From “A new vision for Canada: Family Practice—The Patient’s Medical Home 2019” (4), a vision of a high quality, coordinated pan- Canadian health care system, by the College of Family Physicians of Canada.
Mississauga, ON: College of Family Physicians of Canada; 2019. https://patientsmedicalhome.ca/files/uploads/PMH_VISION2019_ENG_WEB_2.pdf

 (5) How Medical Practices Can Succeed At Remote Patient Monitoring: sponsored by by Accuhealth – “Once mastered, the remote patient monitoring platform gives the practice a pathway to establishing meaningful care management.”
https://mhealthintelligence.com/news/how-medical-practices-can-succeed-at-remote-patient-monitoring

(6) European primary care surveillance networks: their structure and operation, by Joan GM Deckers, W John Paget, François G Schellevis, Douglas M Fleming, in Family Practice, Volume 23, Issue 2, April 2006, Pages 151–158, Published 07 February 2006, https://doi.org/10.1093/fampra/cmi118

(7) Intracellular Hypothyroidism & Thyroid Hormone, by GA Harry, https://wordpress.com/page/cbhrt.ca/91

 

Finasteride Warning (France)

France just Issued a “red box warning”, with a QR code to facilitate complaints, to be attached to Finasteride Products by April 2023.

5 Dec., 2022: I just got the note below, from the “post-finasteride syndrome foundation”:

France Orders ‘Red-Box’ Warning—and QR Code Linking to PFS-Awareness Dossier,
on all Finasteride 1 mg Products by April, 2023.

you can see the details at
https://www.google.com/search?client=firefox-b-d&q=REGULATORY+UPDATE++France+Orders+%E2%80%98Red-Box%E2%80%99+Warning%E2%80%94and+QR+Code+Linking+to+PFS-Awareness+Dossier%E2%80%94Slapped+on+all+Finasteride+1+mg+Prod-ucts+by+April++Dec.+4%2C+2022++Dear+Friends%3A++

Psychotherapy Tax

Your therapist must collect GST/HST 

One of my sons, who has qualified as a registered psychotherapist after 5 years of study, just told me about something which I find most distressing:
Counselling therapists and psychotherapists must collect GST/HST.

Psychiatrists and family doctors do not have to charge the GST/HST: they are paid by the various provincial insurance systems without having to submit a GST/HST tax report to the government.

Most people don’t get adequate, satisfying counselling from their family doctor anyway, because MDs are not taught how to listen: medical school training does not include in-depth psychotherapy instruction, so the doctor is not as well qualified to supply what the psychotherapy patient needs.
Secondly, the doctor doesn’t have enough time to listen: time and patience are essential to an adequate psychotherapy session and the family doctor falls short on both prerequisites, as compared with a trained and certified psychotherapist.
Thirdly, the MD has been trained to prescribe psychoactive drugs as treatment for psychological upset: if you refuse drugs, the doctor may be less inclined to deal with you.

Think about it – the usual psychotherapy course takes 5 years and the MD course, 3 years: who would you expect to provide psychotherapy to your satisfaction – an MD, who hasn’t had the same in-depth training, may not be a good listener and who only has 10 – 20 minutes to talk to you, or a psychotherapist, trained to listen and responsive to your story, who will dedicate an hour to your concerns?


The family doctor might refer you to a psychiatrist (but
)

(1) Psychiatry training does not include the intensive study, instruction from experienced psychotherapists, personal experience of psychotherapy and ongoing supervision, which the psychotherapist has to go through as a prerequisite to registration.
(2) The psychiatrist’s MO is to make a diagnosis as to what sort of mental illness the complainant has and to write a prescription, for treatment of that illness.
This is counterproductive, because the psychotherapist’s clients are simply upset, confused, or having difficulty with modern life: they are not mentally ill, they don’t need psychotropics and the side effects of psychoactive drugs can make their situation worse.
(3) Even if the psychiatrist is an exceptionally good listener and is willing to spend the time (some are), he or she is a government servant, subject to and fearful of the rigid regulations which govern civil servants. ***
(4) As with all other branches of medicine, there has been a chronic shortage of psychiatrists for 30 years and an immediate appointment for assessment is almost unheard of.

*** see Choosing wisely: 13 tests and treatments to question”, by the College of Family Physicians of Canada, last updated: July 2022, in the page entitled “preventive care, as it could be”.

The therapist’s fee …… plus tax?

The (average) $150 psychotherapist’s fee is reasonable (in fact, inexpensive, in view of their training) and there is a saving in drug costs, which psychotherapists don’t prescribe.
However several visits may be necessary, so adding a $22.50 tax to the fee for every visit can make the difference between affordability and unsustainable cost.

A tax on distress?

A mandatory GST/HST tax on necessary healthcare makes it seem as though our government is taxing citizens for their distress.

An anti-efficiency tax?

What is the cost to society when a worker is too upset to concentrate on the job ?
(see addendum, below) and why should our government tax the upset worker’s psychotherapy healthcare, making it difficult for stressed-out persons to get the help they need to return to normal function?

Petition

Now the good news!  A petition has been started, to convince the government to discontinue taxation of the disadvantaged: see https://www.taxfreetherapy.ca/.

Addendum

For an understanding of the sort of “troubles” which your psychotherapist may be able to steer you away from, please see the paragraph on stress and its effects, in “intracellular hypothyroidism and thyroid hormone

DHEA cures cancer: one case.

 BACKGROUND

DHEA was first discovered as a urine metabolite in 1934 by Adolf Buteiiandt and Hans Dannenbaum from Germany. It was reaffirmed as a urinary metabolite in 1943 and isolated from serum in 1954. Basically, the actions of DHEA oppose those of cortisol, but in addition it is used as raw material for production of a long list of “neurosteroid” hormones.


Figure 1, Synthesis and metabolism of DHEA

DHEA, a lipophilic prohormone, is pluripotent.
In Humans, it is manufactured in the adrenal glands and the brain (the brain is the sole source of DHEA in lower animals) and to a lesser extent by the testes, ovaries and skin. (1)
The adrenal supply is delivered to the serum in its hydrophilic, sulfated form, “DHEAS”, which is not bound by SHBG. It is utilised internally by all cells of the body, after removal of the Sulfur moiety, to produce that mix of “downstream” hormones which is necessary for each particular cell.
Human DHEA output by the adrenals begins to fall, 1%-2% per annum, by age 26 (humans original life expectancy) and production reaches zero by age 80, at which point the brain is the only source of the prohormone (figure 1).
As the level drops to less than 6 µmol/Litre, we begin to see progressive deterioration of functions dependent on DHEA. (2, 2a).

Figure 2: This graphic explains the Human Lifetime cancer risk of 38.4% and compares it with the cancer risk of most long-lived mammals (= 4%,)….. For detail, regarding human cancer statistics, click here.

CAVEATS, re. Figure 2:
(1) Figure 2 implies a normal serum DHEAS maximum of 9.2 µmol/L in men and 2000 ng/mL (5.428 µmol/L) in women (9). This is different from my experience, in that the CML healthcare, the Laboratory I used in Toronto, quotes DHEAS in micromoles/L, with a maximum of 14.14 in males at age 40 and 11.04 in females at age 30.
(2) An excellent study, “Low Levels of Dehydroepiandrosterone Sulfate in Younger Burnout Patients”by Anna-Karin Lennartsson et al, showed that in chronically stressed individuals, there is a 25% reduction in serum DHEAS in the 3rd decade of life. (3)
(3) My experience is that most disease presents to the family doctor when the serum DHEAS falls below 6.0 µmol/L (2a). Therefore
(4) Dr. Nyce’s upper limits of normal seem low, although that fact does not affect the importance, nor the veracity, of his excellent graphic.
(5) The “endmemo” unit conversion website (9) provides a Ng/mL-to-NanoMole/L table, from which I have calculated as follows:

Figure 3

DHEAS, nanograms/mLDHEAS, nanomoles/LDHEAS, micromoles/L
3400
1000
100
1
9227.6
2714
271.4
2.714
9.2276
2.714
0.2714
0.02714
  Conversion: multiply Ng/mL by 0.02714

(6) Long-term-stressed individuals in the 3rd decade of life constitute a particular, important group, because a 25% lower serum DHEAS (10) translates into an enhanced liability to neoplastic disease, in contrast to the nonstressed population.
In these individuals, circulating DHEAS (blue and grey lines in figure 2), necessary for targeting G6PD, may never reach optimal levels.
Especially in the presence of overt or unrecognized childhood PTSD, the at-risk age may lie within the 2nd decade. However that situation may be masked, because such children tend to maintain their DHEA levels as a hedge against depression. (11)

When serum DHEAS attains optimal levels, maximum production is maintained only until age 25 years (the original life expectancy of humans). From age 25, production falls by 1% – 2%, each year in all humans, except in some females with polycystic ovaries (the Stein- Leventhal syndrome), many of whom overproduce it.
As human DHEA production progressively falls, there is an exponential rise in cancer risk with increasing age (Figure 2, red line).
However in species such as the elephant, moose and naked mole rat, which use tumor suppression systems that do not decline with age, (4) there is little or no increased risk of cancer with age (Figure 2, green line). (4)

Note:
(1) Extremely low levels of DHEA, permissive of organ malfunction, are pervasive in severe, critical illness. (5)
(2), As suggested with regard to long-term-stressed individuals(above), the age group 0–24 years has experienced the greatest increase in cancer risk since 1990.
(3) It would be interesting to find out whether DHEA levels in the 0–24 year group have been maintained, or fallen, since 1990,


TP53 and DHEA

I am indebted to Dr. Nyce for his superlative (2018) explanation of the anticancer effects of DHEA (6), which inspired me to write this paper and to Ozaki and Nakagawara, whose excellent (2011) article on p53 (7) was cited in Dr. Nyce’s paper.


DNA DAMAGE AND MALIGNANT TRANSFORMATION

Our cells are constantly exposed to a variety of cellular stressors and are prone to DNA damage, leading to mutation, with production of abnormal genes and eventually, cancer.
Therefore, to protect our cells from malignant transformation, the cells’ nuclei carry tiny quantities of a special gene, TP53, which exists in a dormant, inactive form.
When DNA is damaged or mutated, one, of three, scenarios may obtain:
(1) If the damage is mild and the TP53 gene is intact, the cell repairs itself.
(2) If the damage is severe enough, TP53 is “promoted”. It accumulates in the cell nucleus and converts to an active form. Active TP53 triggers rapid production of “ROS” (reactive oxygen species), which kill the cell.
This natural process, called apoptosis, ensures that cells with cancerous potential are destroyed before they can clone themselves and produce a cancer.

(3) If the mutation includes an abnormality of the TP53 gene itself, no ROS is produced, because mutant TP53 malfunction supports an enzyme, glucose-6-phosphate dehydrogenase (G6PD), which neutralises ROS and facilitates production of NADP.
NADP inactivates any existing normal TP53, allowing the abnormal cell to grow, clone itself and start a cancer. (7)
This idea has beenconfirmed by studying TP53-deficient mice, who develop spontaneous cancers.

HOW DOES DHEA PREVENT CANCER?

Many years ago, DHEA was observed to inhibit both spontaneous breast cancer and chemically induced tumors of the lung and colon, in mice.
It also stopped tumour formation when mice were given a cancer-promoting drug called DMBA, or one called TPA.
DHEA was generally effective in stopping cancer formation except in rats, in whom it promoted liver cancer (we don’t know why).
This anti-cancer action of DHEA remained a mystery for decades, but Dr. Nyce’s (2018) breakthrough proved that DHEA works by blocking glucose-6-phosphate dehydrogenase (G6PD), allowing a rapid rise in ROS and by stopping NADP formation.

To put it another way,
under normal circumstances G6PD keeps reactive oxygen species low within normal cells: without G6PD, reactive oxygen species would kill them.
So when a cell goes “wild”, normal TP53 shuts off G6PD, ROS accumulates and the cell dies.
But when a mutation includes damage to the TP53 gene, G6PD function continues, keeping the ROS low and allowing the abnormal cell to grow, multiply and produce a cancer.
That’s where DHEA comes in: DHEA shuts off G6PD, allowing a lethal rise of reactive oxygen species inside the cell, which kills it.

THE HUMAN PROBLEM

Our DHEA production falls by 1% every year* from age 26. So as we age, there is less and less DHEA to prevent cancer.
Consequently, our protection from cancer-producing mutations falls as we age.
Therefore I, Dr. Nyce and other MDs of like mind surmise that supplementing DHEA should prevent cancer (review Fig 2, see Fig 4),

Figure 4, “the potential for pharmacologic extension of the DHEA kill switch”, is also from Dr. Nyce’s paper.
It shows that normally, Humans are protected by their adrenal DHEA-mediated “kill switch” up to age 30.
However I observed, in my 15-year experience of treating DHEA deficiency syndromes,
high-stress individuals are protected only as long as their circulating DHEAS exceeds 5.0 – 6.0 µmol/L, which is slightly less than 2000 ng/mL. (2a).

What Figure 2 does not show, is that some individuals’ serum concentration of DHEA is reduced to less than 6 µmol/L before age 25. (3)
In these people, who become DHEA-deficient earlier in life, the exponential increase in cancer risk depicted in figures 2 and 4 begins earlier and progresses more rapidly.

The bottom line is that we can elevate serum DHEAS Immediately upon diagnosis and we can maintain it at normal levels into old age (Figure 4: dashed blue and grey lines).
Doing so will, hopefully, reduce the age-adjusted cancer risk, hopefully holding it to 4%.

How much DHEA should one take, and when should one start taking it?

The dose of DHEA needs to be tailored to the individual. For females, 25 to 50 mg per day is sufficient to achieve a high-normal testosterone level while avoiding testosterone side effects such as facial hair, oily skin and acne.
For males, 50 to 75 mg per day is enough to improve self-confidence and muscle (including heart muscle) maintenance.
Some males do quite well with 100 – 150 mg of DHEA per day, but many develop gynecomastia when taking 100 mg or more:
Therefore, The recommended dosage is 50 mg, taken at 8 AM

DHEA CURES PROSTATE CANCER: ONE CASE

A small, quiet and unassuming, but intelligent gentleman with a good family history, born in 1947, was admitted to our clinic in January 2006, after his family doctor retired.
He attended fairly regularly, usually accompanied by his adult son, who translated to and from his native language.
He was semiretired, a drug-free non-smoker and an occasional user of alcohol.

He had a prior history of hypercholesterolemia and hypertension, for which he had been prescribed 40 mg of Simvastatin, Coversyl 2 mg and HCTZ, 25 mg daily: he took his medications faithfully and both conditions were in satisfactory control.
He had no other medical conditions and when first seen, had no symptoms.
His family history was excellent.

Routine investigation was entirely normal excepting for a blood sugar of 6.3, but his HbA1C was consistently normal and a glucose tolerance test done in November 2009, was normal.
PSA and hormone balance tests were not done in 2006.

  • In November 2009, when he was 62 years old, a routine PSA was 3.56 (almost 4.0, the upper limit of normal).
    His DHEA was 5.0, which was “Normal for age 65”, but low as compared with the normal serum level at age 25:
    I considered it suspicious.
  • He then complained of “LUTS” (Lower Urinary Tract Symptoms) and an ultrasound in January 2010 showed benign prostate enlargement, with incomplete emptying of the bladder and also, a 1 cm nodule in the right side of the prostate.
    He was referred to an urologist, who diagnosed BPH, with a benign nodule, recommended against a needle biopsy and prescribed Flomax and Dutasteride.
  • Despite Dutasteride, his PSA rose to 4.57 in January 2010 and 5.09 in August, 2011.
    Because of this, the prostate ultrasound was repeated and a second nodule was found. He was referred for a biopsy.
  • A transrectal prostate biopsy, done in December, 2011, produced eight specimens, of which one showed a small, but unequivocal, Gleason 6 Carcinoma of the Prostate.
Discussion with the patient.

I showed the biopsy report to this cooperative patient and his son.
I explained the demographic evidence for “watchful waiting” and the possibility that DHEA would either advance or retard the progress of his prostate cancer (we had previously discussed Neurosteroids, Steroidopenia and the role of DHEA in cancer prevention).

The patient and his son expressed an interest in a trial of treatment with DHEA and Pregnenolone, providing that it would be discontinued if there was a rapid rise in his PSA.

He stopped taking Flomax and Dutasteride and began DHEA, 150 mg and Pregnenolone, 50 mg on 19 January, 2012.

Figure 5. Case report: summary of observations, November 2009, to November 2022.
“PSA” = prostate specific antigen.
PSAr = free PSA/PSA ratio (normal = >0.25).

DATEPrescriptionPSAPSArDHEAComments/notes
Nov ’09 3.56 5.0Ultrasound: BPH, 1 nodule
14 Jan ‘10Flomax, Dutasteride3.42  Urologist reported BPH, benign nodule
3 Mar ‘11 4.57  US: 1 nodule on the right
16 Mar ‘11 4.57   
23 Jun ‘11 5.09   
1 Sep ‘11 3.840.27 US: 2 nodules found
4 Dec ‘11DHEA 150mg, preg. 50 mg4.1  US with biopsy: Gleason 6 Ca
3 Feb ‘12 4.66 25.5 
17 Feb ‘12 4.030.2  
3Mar ‘12 5.01 30.0 
16 Mar ‘12 4.04 21.7 
10 Apr ‘12 4.47 27.1 
8 Jun ‘12 3.98 23.6 
5 Jul ‘12 3.96   
7 Aug ‘12 4.0   
4 Dec ‘12 4.1  US: no nodule. No biopsy.
12 Dec ‘12    Urologist stopped DHEA
May ‘13 4.31   
23 Dec ‘13 3.73   
3 Jul ‘14DHEA 100 mg, preg 50 mg4.240.3 Biopsy: high-grade PIN
3 Jul ‘14    Plan: continue DHEA
12 Nov ‘14DHEA,7KDHEA, Preg,50mg3.73   
4 Jan ‘15 5.25 17.2 
3 Mar ‘15 4.860.2 DRE: 30 g BPH, no nodule
26 May ‘15 4.29 4.2 
3 Jul ‘15 3.86   
15 Sep ‘15 4.26 4.2 
18 Dec ‘15 4.76 4.2 
31 Oct ‘16 5.1   
3 Jan ‘17 4.87   
15 May ‘18 4.77   
Nov ‘19 5.47   
Aug ‘22    Prostate resection: no cancer.
Sept ‘22    Repeat resection: no cancer.
CONCLUSION

In summary, this patient presented with a suspicious PSA result in 2009 and was proven to have a Gleason 6 cancer of the prostate. In November 2011.
He was treated with DHEA 50 mg and pregnenolone 50 mg until December, 2012, at which point his urologist discontinued DHEA on the grounds that it would accelerate the progress of his prostate cancer.

Despite discontinuation of DHEA, serial tests showed no further increase of his PSA, apart from slight increase to 5.25 and 5.47 in January 2015 and October 2016: both of these elevations were most likely due to prostatitis.

He was unable to urinate in July,2022 and prostate resection in August showed no evidence of prostate cancer.
Complications of the surgery led to repeat resection of the prostate, In September 2022 and again, no cancer was found in the prostate tissue which was removed.

I conclude: this man’s prostate cancer was cured by a one year course of DHEA.

REFERENCES

(1)     Sexual Hormones in Human Skin, Zouboulis CC et al. Horm Metab Res 2007; 39: 85–95 Horm Metab Res 2007; DOI 10.1055/s-2007-961807 https://d-nb.info/1179576837/34

 (2)     Review of Age-Related Dehydroepiandrosterone Decline and Its Association with Well-Known Geriatric Syndromes: Is Treatment Beneficial?, Nikolaos Samaras,1,2 Dimitrios Samaras,2,3 Emilia Frangos,4 Alexandre Forster,1 and Jacques Philippe5 Rejuvenation Res. 2013 Aug; (4) 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/

(2a) Personal series of 600+ individuals: to be reported.

(3) Low Levels of Dehydroepiandrosterone Sulfate in Younger Burnout Patients
Anna-Karin Lennartsson, 1 , 2 ,* Töres Theorell, 3 Mark M. Kushnir, 4 and Ingibjörg H. Jonsdottir, Onno C Meijer, Editor PLoS One. 2015; 10(10): e0140054. Published online 2015 Oct 6. doi: 10.1371/journal.pone.0140054 PMCID: PMC4595129, PMID: 26441131

(4) Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans, Lisa M Abegglen  1 Aleah F Caulin  2 Ashley Chan  1 Kristy Lee  1 Rosann Robinson  1 Michael S Campbell  3 Wendy K Kiso  4 Dennis L Schmitt  4 Peter J Waddell  5 Srividya Bhaskara  6 Shane T Jensen  7 Carlo C Maley  8 Joshua D Schiffman JAMA  2015 Nov 3;314(17):1850-60, doi: 10.1001/jama.2015.13134. https://pubmed.ncbi.nlm.nih.gov/26447779/

(5) Decreased levels of dehydroepiandrosterone sulphate in severe critical illness: a sign of exhausted adrenal reserve? Albertus Beishuizen,1 Lambertus G Thijs,2 and István Vermes3 Crit Care. 2002; 6(5): 434–438.
Published online 2002 Jul 9. doi: 10.1186/cc1530 , PMCID: PMC130144, PMID: 12398784, Crit Care. 2002; 6(5): 434–438.

(6) 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 TP 53, 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/,

(7) 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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756401/

(8) Dehydroepiandrosterone sulfate (DHEA-S) ng/mLnmol/L Conversion Table
http://www.endmemo.com/medical/unitconvert/Dehydroepiandrosterone_sulfate.php

(9) Clinical correlates of DHEA associated with post-traumatic stress disorder, R Yehuda  1 S R BrandJ A GolierR-K Yang, Acta Psych. Scand, 2006 Sep;114(3):187-93. doi: 10.1111/j.1600-0447.2006.00801. PMID: 16889589, DOI: 10.1111/j.1600-0447.2006.00801.x  https://pubmed.ncbi.nlm.nih.gov/16889589/

(10) Cortisol and DHEA in development and psychopathology, Hayley S.Kamin, Darlene A.Kertes, Hormones and Behavior, Vol 89, Mar2017, P69-85, https://doi.org/10.1016/j.yhbeh.2016.11.018, https://www.sciencedirect.com/science/article/abs/pii/S0018506X1630215X

(11) Influence of DHEA administration on 24-hour cortisol concentrations , by Patricia D Kroboth,   Janet A Amico, Roslyn A Stone, Maggie Folan, Reginald F Frye, Frank J Kroboth, Kristin L Bigos, Tanya J Fabian, Ana M Linares, Bruce G Pollock, Charles Hakala, J.Clin.Psychopharmacol,2003Feb;23(1):96-9,PMID:12544381,DOI:10.1097/00004714-200302000-00014
https://pubmed.ncbi.nlm.nih.gov/12544381/

(12) Double-blind treatment of major depression with dehydroepiandrosterone, by Wolkowitz OM, Reus VI, Keebler A, Nelson N, Friedland M, Brizendine L, Roberts E, in Am J Psychiatry. 1999;156:646-9. https://pubmed.ncbi.nlm.nih.gov/10200751/

(13) Testosterone therapy in men with prostate cancer, Alan L Kaplan  1 Jim C Hu  2 Abraham Morgentaler  3 , :John P Mulhall  4 Claude C Schulman  5 Francesco Montorsi, Eur Urol. 2016 May; 69 (5): 894–903. DOI: 10. 1016/J.eururo.2015. Epub 2015 Dec 21. PM ID: 26719015, PMC ID PMC 5000551 . DOI: 10. 1016/J.eururo. 2015. 12. 005.

(14) Species-specific mechanisms of tumor suppression are fundamental drivers of vertebrate speciation: critical implications for the ‘war on cancer’.
Nyce JW. Endocr Relat Cancer. 2019 Feb;26(2):C1-C5. doi: 10.1530/ERC-18-0468. PMID: 30400061 Free PMC article.

(15) A lex naturalis delineates components of a human-specific, adrenal androgen-dependent, p53-mediated ‘kill switch’ tumor suppression mechanism.
Nyce JW. Endocr Relat Cancer. 2020 Feb;27(2):R51-R65. doi: 10.1530/ERC-19-0382. PMID: 31815681 Free PMC article.

(16) In Vivo and In Vitro Evidences of Dehydroepiandrosterone Protective Role on the Cardiovascular System, Int J Endocrinol Metab. 2015 Apr; 13(2): e24660, by Tiphaine Mannic,1,2,* Joanna Viguie,3 and Michel Florian Rossier1,4, Published online 2015 Apr 30. doi: 10.5812/ijem.24660, PMCID: PMC4389253, PMID: 25926854, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389253/

(17) Dehydroepiandrosterone sulfate (DHEAS) secretion in early and advanced solid neoplasms: selective deficiency in metastatic disease, by P Lissoni  1 F RovelliL GianiM MandalaS MeregalliS BarniG ConfalonieriA Bonfanti, in Int J Biol Markers, . Jul-Sep 1998;13(3):154-7, PMID: 10079390,  https://pubmed.ncbi.nlm.nih.gov/10079390/

(18) Cancer prevention with DHEA: has the day arrived ? https://cbhrt.ca/2022/01/24/dhea-and-cancer-prevention/

(19) Testosterone therapy for men at risk for or with history of prostate cancer: Abraham Morgentaler  1  Curr Treat Options Oncol. 2006 Sep:7(5):363-9. PMID:16904053, doi: 10.1007/s11864-006-0004-y.

CANCER TREATMENT WITH FAECAL TRANSPLANT

December, 2022:
This note is from my newsfeed: I have no comments to make, but it seems important.

The cancer–microbiome connection

Zion Levi’s melanoma went into remission thanks to a powerful immunotherapy drug called nivolumab. Then he donated his faeces — and the microbes inside — to help others who had failed to respond to the treatment or whose cancers had become resistant to it.

It was a small trial — it involved only 26 people — but one in three of them benefited from the faecal microbial transfer (FMT).
Today, at least 30 FMT trials are under way around the world.
They hint at a new era of ‘ecological oncology’ and aim to uncover how the gut microbiome influences the progression of tumours, the effectiveness of treatments and the organisms that live in tumours themselves.

Antioxidants lower dementia risk (pseudo-news)

The note below is from a report by Sharon Reynolds, dated 2022-05-24, on the NIH website (I have paraphrased it, for brevity and clarity).

In “Antioxidants and DementiaMore Than Meets the Eye“, J. Neurology May 24, 2022, Babak Hooshmand and Miia Kivipelto report on blood levels of antioxidants in more than 7,000 people, aged 45 to 90, enrolled in the NHANES study of nutrition between 1988 and 1994. These people were followed for an average of 16 years to see who developed Alzheimer’s disease or other dementias.
The compounds analyzed included carotenoids, a large group of antioxidant pigments found in plants, and some vitamins.

The team found that people with generally higher blood levels of all kinds of carotenoids were less likely to develop dementia, but when lifestyle factors such as smoking and diet, and socioeconomic factors like education and income, the benefit of higher blood carotenoid levels disappeared.

The team then looked at individual carotenoids and found that lutein and zeaxanthin, found in green, leafy vegetables, and β-cryptoxanthin, which is found in some orange-colored fruits definitely reduced the risk of dementia, even when other health, lifestyle, and social factors were taken into account (the size of the effect was reduced to some extent by these adjustments).

In contrast, according to the authors, blood levels of the antioxidant vitamins A, C, and E weren’t individually associated with dementia risk. Also, their analyses suggested that high levels of vitamin A and E might actually counteract the effects of other antioxidants.
The findings suggest that the protective effects of some antioxidants may depend on the presence of other molecules in the body.

None of this is new; so what’s the point of mentioning it?
The point is that those of us who follow newsfeeds are inundated with “grabber headlines”, which make us think that some brand-new research has come up with amazing scientific facts, although the coverage by the “report” is incomplete at best and often, inaccurate.

For example, a look at the Wikipedia entry re. Antioxidants yields a quick list: vitamin C, glutathione, lipoic acid, uric acid, carotenes, vitamin E and CoQ10 (ubiquinone).
However your body’s best anti-oxidants are Vitamin D and Melatonin ** and although brightly coloured fruits and vegetables are extremely important in our diet, perhaps the best supplement is NAC (N Acetyl Cysteine), which generates glutathione.

** For melatonin, see “Antioxidant properties of melatonin–an emerging mystery”, by
C E Beyer  1 J D SteketeeD Saphier, in “Biochem Pharmacol”, 1998 Nov 15;56(10): 1265-72, doi: 10.1016/s0006-2952(98)00180-4.
For vitamin D, see “Vitamin D is a membrane antioxidant. Ability to inhibit iron-dependent lipid peroxidation in liposomes compared to cholesterol, ergosterol and tamoxifen and relevance to anticancer action”, by H Wiseman, in FEBS Lett, 1993 Jul 12;326(1-3):285-8, doi: 10.1016/0014-5793(93)81809-e.

So once again, what’s the reason for this blog entry?

The reason for this blog entry is to remind you to take newsfeed headlines with a grain of salt and always, double-check them on the web, for yourself.


%d bloggers like this: