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Brain Cells: form and function
MENOPAUSE
Menopause, affecting more than half of our population, is easily, safely and inexpensively treatable.
As of 2022 50.9% of Canada’s population were born female, and 100% of that 50.9% will, necessarily, become menopausal, given time. Menopause, long ignored or brushed aside by mainstream medicine, finally hit the CBC news in 2023: it will continue to be a major topic for (hopefully) constructive discussion in the coming years.
Considering the rise of qualified women to key positions in government, finance, health services and every other sphere of life, it is time (truly, past time) to acknowledge women’s importance to our society. It is time to agree that these prime contributors to our civilization should no longer suffer silently in the background and should no longer be penalized for their suffering. It is time for a paradigm shift!
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Stress causes Chronic Fatigue Syndrome
WHAT CHRONIC STRESS DOES TO YOU & WHAT YOU CAN DO ABOUT IT
(1) CFS
From the point of view of a lay-person trying to make sense of an article like this, the best name for the effect of persistent stress is “Chronic Fatigue Syndrome” (“CFS“), because that name tells you what the symptoms are. CFS is well described in terms of how affected people feel, but its origin and the true reason for the symptoms, are poorly understood.
Background – how CFS develops:
1) The thyroid gland makes a “raw material” hormone with four iodine atoms (T4), which circulates in the blood so that it is available to all of your cells. The cells absorb T4 from the blood and use an enzyme called “deiodinase 1” to remove one particular iodine atom, thus changing the T4 into T3. T3 is your body’s “accelerator” and without it, no cell can function efficiently.
2) Stress causes release of cortisol from the adrenal glands and cortisol removes T3 from your cells: if the stress is mild and transient, the cortisol spike fades away quickly and there is no effect on the function of the cells, nor of the body as a whole. However if the stress is severe, or if it becomes chronic, ongoing cortisol production and continuing suppression of T3 inside the cells, produces a condition which doctors call “Low T3 Syndrome” (LT3 S).
3) This sequence of events, leading to LT3 S, is an enigma to most doctors, whose medical education does not include the “functional” aspect of metabolism. Everyone is so ignorant of the condition that it has four other names: “Functional Hypothyroidism”, “Nonthyroidal illness”, “Subclinical Hypothyroidism” and “Euthyroid Sick Syndrome”.
4) The diagnostic terms are super-confusing, because none of these names tells the whole story. To me, the best term for the syndrome is Intracellular Hypothyroidism, because that name explains the underlying problem: “Intracellular” means “inside the cells” and “Hypothyroidism” means “shortage of T3”.
5) The corollary of course is that insufficiency of T3 decimates the efficiency of every cell in the body.
Caveat
We are talking about T3, the active thyroid 3 hormone, not “T4”, the raw material hormone which the thyroid gland makes.
IH symptoms
IH produces a variable suite of “low thyroid” symptoms, depending on which organs in the body are most sensitive to “T3 starvation”. The commonest complaint is feeling “cold, weak and tired”: there is fatigue, which is worse in the afternoon, combined with anxiety, “fuzzy thinking”, loss of motivation, poor sleep, constipation, mild depression and weight gain. However prolonged IH can produce any of the 300+ symptoms associated with hypothyroidism, including the ones which women in their 20s present to the family physician: chronic hair loss, brittle fingernails, hoarseness, dry skin with itching, hives, “brain fog” and low libido.
Serious Illnesses caused by IH
Intracellular hypothyroidism doesn’t just cause CFS. Over time, chronic IH is the root cause of many “autoimmune” illnesses and often, “one thing leads to another”, as our grandmothers used to say.
An example of autoimmune illness
The most dangerous condition caused by IH is “Broken Heart Syndrome”, properly called “Takotsubo Cardiomyopathy”, or “Dilated Cardiomyopathy” (DCM).
DCM is poorly understood because doctors don’t understand IH and don’t think of it.
DCM occurs following a stressful episode, such as the death of a loved one or any condition which produces grief. In DCM, the muscle cells in the heart weaken rapidly, because they can’t get enough T3 to function properly. Since they can’t contract properly, they stretch: the heart becomes swollen and is unable to produce enough pressure to pump the blood efficiently. The result is heart failure.
Doctors can prescribe drugs, to strengthen the heart and keep the person alive until the stress is resolved: with the stress gone, cortisol is banished, the supply of T3 in the heart muscle cells is reinstated, the muscles recover and the heart works perfectly, as though nothing had happened. If the doctors are unsuccessful, or if some subsequent event intensifies the stress, the person literally dies of a “broken heart”!
The circumstantial proof that stress is the cause of DCM is that if the person has another stressful episode, their Cardiomyopathy recurs and they get heart failure again.
An example of “one thing leading to another”: see “40 years: the medical biography of a Doctor”, in April 2024 (Post pending).
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DILATED CARDIOMYOPATHY CAUSED BY TRUE HYPOTHYROIDISM
This is a case report, of a patient with dilated cardiomyopathy (DCM) and heart failure, caused by true hypothyroidism (not IH) and cured with T4
“Hypothyroidism-induced reversible dilated cardiomyopathy”, by P Rastogi, A Dua, S Attri, and H Sharma, J Postgrad Med. 2018 Jul-Sep; 64(3): 177–179, doi: 10.4103/jpgm.JPGM_154_17, PMCID: PMC6066629PMID: 29992912, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6066629/, which I first discussed on December 15, 2021.
It concerns a patient with dilated cardiomyopathy (DCM) and heart failure, caused by true hypothyroidism and cured with T4.
Abstract (paraphrased, for brevity)
A young female presented with heart failure and was diagnosed as having DCM. Echocardiography revealed left ventricular global hypokinesia (weak heart muscle contractions) and “severely depressed systolic function” (reduced ability of the heart to pump blood into the aorta).
The past history included hoarseness (a classic hypothyroid symptom), for two years and the Thyroid profile revealed a very high TSH (Thyroid-Stimulating Hormone) value of 313 μIU/ml. Her FT4 (free thyroxine) was very low, at 0.220 ng/dl. No mention was made of her FT3, nor of her reverse T3.
The authors state (paraphrased, for brevity):
”The heart relies mainly on Triiodothyronine (T3): there is no significant deiodinase activity inside myocytes, so the heart muscle cells (myocytes) are unable to convert T4 into T3: T3 is directly transported into the myocyte, from the blood”.
They go on, to explain that “T3 modulates inotropic and lusitropic properties of the myocardium, myocardial contractility, and vascular function” (in other words, T3 enables the myocytes to contract) and that “Hypothyroidism can cause bradycardia (slow heartbeat), impaired contractility, impaired diastolic filling of the heart, increased systemic vascular resistance, diastolic hypertension, and endothelial dysfunction.”
Further, they say, “It has also been demonstrated that Subclinical Hypothyroidism * may lead to heart failure: studies have shown that as in the sick-euthyroid syndrome,* which occurs in nonthyroidal illnesses like sepsis, patients with heart failure who have a normal thyroid gland may have low levels of FT3, with normal T4 and TSH. ** Low serum FT3 in these patients strongly predicts all-cause and cardiovascular mortality. The most consistent cardiac abnormality recognized in patients with overt hypothyroidism is impairment of Left Ventricular diastolic function, characterized by slowed myocardial relaxation and impaired early ventricular filling.”
In spite of their recognition of T3 as a prime mover in myocardial function, their appreciation of hypothyroidism as a cause of heart failure and their freely admitted realisation that this young lady’s cardiomyopathy was caused by T3 deficiency, they did not test for FT3 and reverse T3, which would have yielded a low (<20) T3/rT3 ratio, to confirm the diagnosis of LT3S.
* The following are Synonyms, for Subclinical Hypothyroidism:
– Intracellular (Functional) Hypothyroidism (IH),
– Low T3 syndrome (LT3S)
– Euthyroid Sick Syndrome(ESS)
– Non-Thyroidal Illness
Therapy, for IH (LT3S, or “subclinical hypothyroidism”)
In my opinion, prescribing slow-release T3, by itself or in addition to T4, would have corrected this young woman’s problem more certainly and more quickly. Also, the short half-life of T3 would have allowed daily reassessment, with titration of the T3 dose according to the serum concentration of T3, allowing ongoing monitoring and better control of her life-threatening condition.
** The hallmarks of Intracellular Hypothyroidism are low Free T3 and elevated reverse T3, yielding a FT3/rT3 ratio of less than 20, with normal TSH and FT4: The FT3/rT3 ratio is diagnostic; but a low FT3 by itself suggests a diagnosis of IH.
COMMENTS:
(1) The authors are to be congratulated on their success: the patient recovered due to treatment with T4, thus proving the premise of the paper.
(2) The reader should appreciate that this was not Takotsubo-type DCM, which is due to stress-related intracellular hypothyroidism: the high TSH tells us that she had true hypothyroidism. (T4 and TSH are normal in Intracellular Hypothyroidism, unless there is underlying true hypothyroidism).
(3) Had this patient’s problem been due to IH, the T4 with which she was treated would have been converted into reverse T3 and she would not have recovered. Therefore the therapy she received was exactly correct, although I do think that if combination T4+T3 had been prescribed, she would have recovered more quickly.
Why a blog on this subject?
(1) This paper emphasises that Low FT3 can be responsible for heart failure.
(2) All patients presenting with CHF symptoms should have a full thyroid profile done, including TSH, Free T4, Free T3 and reverse T3, to exclude a diagnosis of Takotsubo-type DCM due to stress-related IH: Takotsubo’s DCM is due to stress-related Low T3 Syndrome and requires treatment with slow-release T3, not with T4: The FT3/rT3 ratio permits facile diagnosis of IH (Intracellular Hypothyroidism, a.k.a. the synonyms listed above), which is easily, safely treated with S-R Triiodothyronine.
Caveat
Those familiar with this SUBSTACK will have noted that Intracellular Hypothyroidism is a recurring theme in my posts: the background to this is that IH occurs in all acutely life-threatening and/or chronic conditions. It is found in 100% of people admitted to intensive care units and most people with chronic conditions, Including starvation and obesity.
So if my posts “sound like a broken record”, it is because Intracellular Hypothyroidism is so pervasive that every ill person should be investigated for IH, by checking the FT3/reverse T3 ratio.
My DISH, My Heberden's nodes, Fibromyalgia and DHEA
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HYPOTHYROIDISM: T3, Versus T4 therapy
A note from May, 2022, regarding a speech by Antonio C. Bianco, MD, PhD
May 30, 2022
Thyroid expert, Dr. Antonio C. Bianco, MD, PhD, speaking at the American Association of Clinical Endocrinology (AACE) annual meeting about T3 and T4 therapy, has acknowledged that many patients (he says 10 – 20%, but as you will agree, this percentage is much larger), treated for hypothyroidism using Levothyroxine (T4, “the number-one prescribed drug in the country”), fail to experience an improvement in their symptoms.
Of course, this isn’t news to those of you who are familiar with abnormal thyroid function and particularly, those who know about Intracellular Hypothyroidism (IH), a.k.a. Euthyroid Sick Syndrome, Low T3 Syndrome, Nonthyroidal Illness, Functional Hypothyroidism, etc..
However the salient fact is that a major player in traditional medicine is willing to admit that something is wrong with medical doctors’ usual treatment for hypothyroidism. So, it seems that our doctors’ understanding of the problem is improving and that’s REALLY encouraging!
Dr. Bianco, further to his credit, has noted that combination T3 and T4 therapy doesn’t entirely solve the problem for folks with low thyroid function (as you may know, slow-release T3 is the best way to go, if the problem is intracellular hypothyroidism: if your problem is true hypothyroidism, due to Hashimoto’s disease or some other cause, T4 is obviously best).
However it seems that the medical establishment is not yet ready to embrace the idea of investigating thyroid function with TSH, free T4, free T3 and reverse T3 (+ T3/rT3 ratio) treating Intracellular Hypothyroidism with slow-release T3.
If you would like to read about Dr. Bianco’s article, please see “Debate Continues on Combination Therapy for Hypothyroidism“, by Miriam E. Tucker, dated May 20, 2022.
If you would like to read about intracellular hypothyroidism, go to “Undiagnosed Hypothyroidism”, here on SUBSTACK.
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Iron Deficiency Anemia in Long Covid
Report on an excellent article, which leaves out an important bit
The article, titled “Iron dysregulation identified as potential trigger for long COVID” was Reviewed Mar 4 2024, by Dr Aimee Hanson, of the University of Cambridge.
Caveat:
I have paraphrased/summarised this report, in the interest of brevity and so as not to overshadow my opinion (see “The Bottom Line”).
The article, in brief
According to Dr. Hanson, low iron levels in the blood, as a result of SARS-CoV-2 infection, could be a key trigger for long COVID. This suggestion helps to explain why symptoms similar to L COVID are common in a number of post-viral conditions and chronic inflammation. Also, it points to methods of preventing or treating the condition.
Background
As of March 2023 , an estimated 1.9 million people in the UK had self-reported Long COVID: three, out of every ten people infected with SARS-CoV-2. Long COVID, was categorized as symptoms of fatigue, shortness of breath, muscle aches and ‘brain fog’.
Shortly after the pandemic began, researchers at the U of Cambridge began recruiting and investigating, people positive for COVID-19: over 12 months, 214 participants provided blood samples, which L COVID researchers analysed: about 45% (much more than 3/10) reported symptoms of L COVID between three and ten months later.
Ongoing inflammation and low iron levels in the blood, causing anemia and disrupting red blood cell production, could be seen two weeks post COVID-19 in people who reported L COVID later: as Professor Ken Smith said, “Analysis of blood and clinical information, over the 12 months following infection, has provided insights into why SARS-CoV-2 infection is followed by months of persistent symptoms.”
Iron Deficiency Anemia
Dr Aimee Hanson, now at the University of Bristol, observed that “Iron levels, and iron regulation, were affected during SARS-CoV-2 infection and took a very long time to recover, particularly in those who developed L COVID. Although the body was trying to produce more red blood cells, it was not doing a good job of it.
“Notably, iron dysregulation was detectable, early on, in the long COVID group. This was independent of age, sex, or initial COVID-19 severity, suggesting a possible impact on recovery even when COVID-19 was too mild to need hospitalization or oxygen therapy.
Iron dysregulation was worse during and following severe COVID-19, but those with mild COVID-19 who developed L COVID later, showed similar patterns in the blood. The inflammation, iron levels and iron regulation returned to normal after a time, but symptoms often continued long after iron levels had recovered.
According to co-author Professor Hal Drakesmith, from the University of Oxford, “Iron dysregulation is a common consequence of inflammation and is a natural response to infection. When the body has an infection, it removes iron from the bloodstream, to protect against bacteria that need iron to grow. It’s an evolutionary response, but there is then less iron for red blood cells, so oxygen is transported less efficiently. This affects metabolism and energy production, so the protective mechanism ends up becoming a problem.”
According to Professor Drakesmith, “the findings help to explain why fatigue and exercise intolerance are common in L COVID, as well as in other post-viral syndromes with lasting symptoms. They suggest ways of reducing L COVID symptoms, by rectifying iron dysregulation in early COVID-19: one approach might be controlling the inflammation before it reduces iron regulation; another is iron supplementation. However this may not be straightforward, because sometimes, it’s not that individuals don’t have enough iron: the iron is trapped in the wrong place. We need a way to remobilize the iron into the bloodstream.”
Journal reference: Hanson, A. L., et al. (2024). Iron dysregulation and inflammatory stress erythropoiesis associates with long-term outcome of COVID-19. Nature Immunology. doi.org/10.1038/s41590-024-01754-8.
Caveat
This has particular interest for me, since I too developed iron deficiency anemia.
I, myself, had Covid 19, diagnosed via my own observation of classical “Covid toes”, in February 2020, just after Sophie Gregoire Trudeau was diagnosed with Covid. I was almost asymptomatic, because of my high serum vitamin D (I was taking 5000 IU of D3, daily) and apart from the bright red, extremely sensitive and tender toes, I had no significant symptoms.
I was extremely reluctant to take a Covid vaccination, since I had already demonstrated high-level resistance to the virus. However I was persuaded to have it, in view of my age (then, 81) and did so in January and August, of 2021. In late August of that year, I developed an extremely itchy neurodermatitis, which may have been from the vaccine.
Subsequently (late in 2022) I experienced shortness of breath, tachycardia, muscle weakness, severe thigh-muscle pain with exercise and fatigue: an iron deficiency anemia was documented via blood test, in June 2023. I started taking Ferrous Fumarate (“iron pills”) and now, after 8 months, the muscle pains have stopped, I am only slightly short of breath after 2 hours of pickle ball and my pulse rate is perfect, for age 85.
A good idea
If you are fatigued and short of breath, and if exercise gives you muscle pain and fast heartbeat, make sure you get your blood tested for iron, hemoglobin and red blood cell count – maybe you’ve got iron deficiency anemia, too!
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Progesterone
Your body’s most interesting hormone
This rather long “paper” is a condensation of much information, regarding the activities and functions of Progesterone in humans. It is intended to provide “lay” persons with the basic information they need to understand the hormone, cooperate with a functional medicine practitioner and make confident decisions about their own healthcare.
If you need more information, check the other titles in this SUBSTACK, or see “you and your hormones”, an excellent site with an amazingly detailed, in-depth, all–encompassing review of the human hormones. The site is great for a scientific “take” on the subject: it’s too complicated for the casual reader, but it’s useful if you need information.
PROGESTERONE: its name and where it comes from
The hormonal action of Progesterone was discovered in 1929, following the discovery of Oestrogen in 1923. It was named thus: “PRO”, meaning for, or supportive of, “GEST”, short for “gestation”, meaning “pregnancy”and “ERONE”, a short form for “hormone”.
In the human body, Progesterone is produced from Pregnenolone, which is made from Cholesterol: the sequence is as follows.
NORMAL PROGESTERONE LEVELS
In men, and in women during the first 7 to 10 days of the menstrual cycle, the progesterone level is low (< 6 ng/ml) *. In women of childbearing age, progesterone production begins to rise at day 14 of the menstrual cycle and after ovulation it rises rapidly to 30–50 ng/mL. If no pregnancy ensues, it falls as rapidly as it rose, by the end of the cycle.
PROGESTERONE IN THE MENSTRUAL CYCLE AND IN PREGNANCY
A relatively small amount of Progesterone is made in the adrenals.
The ovary makes a lot of progesterone, starting on the 13th-14th day of the menstrual cycle, to prepare the lining of the uterus (the endometrium) for implantation of a fertilised egg. The progesterone level peaks on the 21st day and if no egg has been implanted in the uterus by then, the egg cyst shrinks and the blood progesterone level falls to baseline by the 28th day. Without Progesterone, the endometrium can’t keep going and menstruation begins.
If a pregnancy starts, a hormone called human chorionic gonadotropin (“HCG”) is released by the fertilised egg. HCG converts the egg sac in the ovary into a “corpus luteum”, which produces enough progesterone to maintain the pregnancy until the placenta begins to produce its own supply, at 8–12 weeks. The placenta keeps producing large amounts of progesterone (enough to keep the blood level up to 100–200 ng/ml) until a day or two before the baby is born. ** Then the blood progesterone level falls to its baseline level *** and stays down while the mother is breastfeeding.
* It has been suggested that women have better memories than men do because they make more progesterone. I agree; my memory improved when I started taking it.
** The sudden drop in Progesterone availability is the trigger for “parturition” (birth).
*** If the progesterone goes low enough to cause Allopregnanolone deficiency, serious postpartum depression may ensue, needing treatment.
Progesterone is Indispensable in Human Body Systems
So: progesterone is the pregnancy hormone, but it’s much, much more than that. Progesterone is in many ways the body’s most interesting hormone: certainly, it is the second-most-surprising hormone (the most surprising is vitamin D, a hormone made by the skin).
A quick list of progesterone’s activities
Progesterone is converted into Allopregnanolone, the “king of the brain hormones” and “mineralocorticoids”, which control salt output by the kidneys.
It normalizes the menstrual cycle and is necessary for pregnancy.
It puts us to sleep, via Allopregnanolone production.
It improves memory, also by increasing Allopregnanolone.
It supports kidney function and controls mineral levels via the mineralocorticoids.
It acts to prevent breast cancer.
A high progesterone/oestrogen ratio prevents oestrogenic weight gain on the hips, the breasts and the “tummy”.
A low progesterone/estrogen ratio, referred to as “estrogen dominance” is the reason for the classic “Heavy-breasted, Saddlebag-hipped” female figure seen in some young women.
Progesterone and the brain
In the brain, in a process driven and supported by PEA (Palmitoyl Ethanol Amide), Progesterone generates Allopregnanolone. Allopregnanolone * does brain maintenance, promotes normal sleep patterns, repairs demyelinated nerves, helps to control pain, enhances self-image, elevates mood and improves cognition and memory.
Allopregnanolone is anti-anxiety, prosocial and antidepressant **. It cancels the effects of stress (including stress-related intracellular hypothyroidism) and thus prevents high blood pressure.
* Allopregnanolone deficiency causes depression.
** See “Allopregnanolone” in Wikipedia.
Caveat:
1) The synthetic Allopregnanolone, Zulresso, is very expensive. Progesterone is not and PEA is available over-the-counter in health food stores. If you find it is difficult to get a prescription for progesterone, you can take pregnenolone with PEA at bedtime, and depend on conversion of Pregnenolone – to Progesterone – to Allopregnanolone: that works quite well.
2) A new, oral form of Zulresso, “Zuranolone”, has been approved (2023), but the best supplement for Allopregnanolone is bioidentical progesterone cream, prescribed along with PEA (Palmitoylethanolamine), which is available in health food stores.
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Alzheimer's Might Not Be a Brain Disease
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About Myself
I should have posted this in December, 2023, when I started with SUBSTACK, but better late than never!
Gervais A. Harry, MB, BS (London), LMCC, FRCSC, ABAARM (A4M)
I’m a (Toronto) Urologist (1974) and an A4M functional medicine specialist (2016).
Studying at the University College of the West Indies, in Jamaica*, I earned the MB, BS (MD) certification from London University (England) in 1964. After internship in Kingston, I joined my father, G. Valentine Harry, FRCS (Edinburgh), as the sole assistant at his 164 Bed Hospital in Port Maria, Jamaica. Following that, I became the sole MD for a 65-bed hospital at Ulster Spring (pop. 4,000), in the “cockpit country”, in Jamaica.
There were no other MDs in the area, so the experience was “interesting” and professionally satisfying: however I soon received notification from the UWI, that I had been accepted for training in surgery:
In 1967, I returned to the UWI Hospital, intending to study for a British surgical degree, but revised my plans in 1968 and relocated instead to the U. of Toronto, for training in Urology. In “first year, as a designated research assistant, I won the Canadian Urological Association research prize (1972) – thanks, in large part, to my mentor, Dr Gerald Ranking.
Returning to Jamaica in 1974, I spent 2 years as the sole Urologist for the Montego Bay area (population 600,000). Professionally, I was “in heaven”; but social factors beyond my control led me back to Toronto in 1976.
After 20 years of freelance practice in urology, based at the Doctors Hospital and (also) operating at the Wellesley and Central hospitals, in Toronto, my career was effectively terminated by the golf instructor Michael Harris, then premier of Ontario, who included my 3 workplaces in a province-wide, “money-saving” closure of small hospitals, in 1997.
So my wife, two sons and I relocated to the Kingdom of Saudi Arabia, with me as chief of Urology for the Northwest Armed Forces teaching hospital in Tabuk, in North-West KSA and my wife as an operating room nurse (later, manager of the endoscopy unit).
My duties in Tabuk were supervision and instruction of Dr. Mahmoud Zakaria, a highly professional, excellent senior resident with superb diagnostic and surgical skills, plus two junior residents. Collectively, we provided consultation and surgery for Urological diseases and presentation of unusual cases, to the medical/surgical staff.
My time in KSA was worthwhile and enjoyable, but not as hectic as the Toronto practice had been, so I had time to write the first 200 pages of my science fiction opus, “XCRATH”.
Returning to Ontario in Y2000, I quit Urology and joined a family practice in Etobicoke, rather than opening a new surgical practice at the age of 60 years.
Bio-Identical Hormone Restoration in Family Practice
In 2006, I became aware of the progressive loss of DHEA production which begins at age 26 in both male and female humans. After studying DHEA, including experimentation by taking it myself, I began to prescribe DHEA and then progressed to bioidentical Estrogen and Progesterone, for some of my patients, in 2006.
In 2012, I became a member of the American Academy of Antiaging Medicine (A4M) and started their two-year course of study. I wrote their examination successfully in December of 2013 and began a Bioidentical Hormone Restoration Therapy (BIHRT) practice in December, 2014: at about that time, I became aware that a major part of our “aging” symptoms are the result of combined DHEA, Progesterone and Thyroid Hormone insufficiency.
Vindication, by observation, of the imortance of DHEA
The majority of my patients benefited from hormone balancing, so in October of 2015, I stopped accepting new family practice patients and concentrated on BIHRT, utilising DHEA & Pregnenolone supplementation for all, estrogen and progesterone for my menopausal patients and desiccated thyroid, or thyroid 3 hormone, for thyroid insufficiency.
In May, 2016, I passed the A4M’s oral examination, receiving their “ABAARM” certification as a BIHRT/ Metabolic Mesicine consultant
In January of 2017 I relocated from the West Etobicoke Medical Centre, to the Stone Tree Naturopathic Clinic, in Collingwood, Ontario.
Specialising in BIHRT
MY PRACTICE, from 2015 TO July 2021, was dedicated to consultation in Functional and Metabolic Medicine, including management of Chronic Fatigue Syndrome, Fibromyalgia, Andropause, Menopause, Depression with or without Panic Attacks, the “Troubled Teen”, Thyroid Hormone Malfunction, Failed Treatment of Hypothyroidism, Infertility, Sexual Dysfunction and “the Undiagnosable”.
I RETIRED in 2021
I retired from medical practice in July of 2021 and cancelled my medical license. However it seems wasteful to jettison my learning and experience. Particularly, since the medical establishment disregards and ignores the hormonal aspect of human metabolic function, I feel obliged to offer my knowledge to anyone who wishes to read my blog, in the interest of helping those who think outside the box.
JUST TO REMIND YOU
My Qualifications:
MB, BS (MD), London, via the University of the West Indies, 1964,
LMCC (Canadian medical license exam), 1969,
FRCSC (Urology), via University of Toronto, 1974,
ECFMG 1984 …… Florida license 1998 [inactive],
ABAARM Certification [A4M], 2016.
My memberships: OMA/CMA, RCP&S, SUSO, CUA and CSAMM [Canadian Society of Aging and Metabolic Medicine].
Florida license, 1999: never utilised.
My website
I started a website in August, 2020, to provide background information regarding hormone deficiency and its management, but my efforts were un-remunerated and the costs were significant, for a retired Canadian MD. So in December 2023, I began my journey on SUBSTACK: new posts go into SUBSTACK only and most of the old ones have been transferred.
If you wish to see the website, “go” to cbhrt.ca.
CAVEAT
The “flavour” of this blog, its content and the opinions expressed are my own.
At times, my attitude and opinion differ from those of official, mainstream, allopathic medicine, since they are based on “extracurricular” knowledge and my experience of 18 years, in the practice of hormone assessment and restoration. Therefore, much of the information offered in my posts may be rejected by family doctors (the link goes to a post, which explains why doctors don’t innovate), who are constrained by the official “guidelines” set by the medical establishment.
Should there be conflict between my opinions and those of your family doctor, please accept the family doctor’s advice, but seek a second opinion from a metabolic medicine (functional medicine) professional *.
* (1) Click this link to see an explanation of Functional (or “Metabolic”) medicine. The page to which it leads explains it well. Note: the page is provided by the IFM, but the link does not constitute a preference for the IFM’s professional certification, compared to those of the A4M or other metabolic medicine training organizations.
(2) For a further explanation of functional medicine, click here.
I must emphasise:
I provide functional medicine and hormone balancing information via my blog and I will be happy to answer any questions you may have. However having cancelled my medical license, I am no longer legally entitled to order tests, diagnose your problem officially, give my opinion regarding diagnosis, or prescribe medicines.
Therefore, armed with the information you glean from these pages, you should consult with both your family doctor and a “Functional”, or “Metabolic”, medicine practitioner (a medical doctor, certified as a specialist by the A4M, the IFM, or other accredited “functional” or metabolic medicine organization), for diagnosis and ongoing treatment (by all means, if you consider it advantageous and if you are sure that our MD if calm enough to accept it, you may print any of my posts, to show the origin of your “odd ideas” to your MD.