As I understand it, “functional medicine” includes:
1] EDUCATED PATIENTS: The high school curriculum includes hormonal, metabolic and microbiome health as a formal subject, so that all understand health maintainance.
2] HEALTH CARE PRACTITIONER: The healthcare professional is an MD, trained in the application of the principles of standard medicine and in the art of metabolic and hormonal maintenance. *

3] FIRST ASSESSMENT: Preferably, the first assessment should be at age 15; it can be done earlier if puberty begins before age 11 or if the child is obese, anorexic, depressed or subject to PTSD for any reason.
The patient’s physical, psychological, metabolic and hormonal status is assessed by history, physical examination and standard “checkup” tests, plus testing for neurosteroid hormone balance, microbiome status, adrenal function, vitamin D level, toxic load, thyroid function (including T3 and rT3, so as to exclude functional hypothyroidism) and other investigations as may seem necessary. **
4] INITIAL CARE: Investigation results are compared with those expected of a healthy, functionally euthyroid 15-25 year old of the same gender and the physician endeavours to correct such metabolic, or hormonal, deviations as may be discovered so as to maintain metabolic and hormonal health at youthful (age 15-25 years) levels ***.
5] HEALTH SURVEILLANCE: If all parameters are within normal limits, or when aberrations have been corrected, the assessment is repeated every five years.
Routine immunisations and “preventions” such as PAP smears, mammography, colon cancer tests, PSA etc. are provided according to accepted routine.
6] ONGOING CARE: Following each 5-yearly reassessment, deviation from normal hormonal, microbiome and metabolic balance is regarded as prodromal to illness and is managed proactively by supplementation of hormones, minerals, vitamins, antioxidants, probiotics etc, ad hoc.
7] INCIDENTAL ILLNESS: Illness presenting in spite of functional maintenance is investigated and treated as it currently is, without discontinuing supplementation.
8] ELDERCARE: At menopause or symptomatic andropause, hormone restoration tailored to the individual is provided as it is currently, utilising bioidentical preparations.

* Currently, functional, antiaging and hormone restoration medicine associations, mostly in the USA, offer training courses which culminate in formal examinations and granting of certificates of competence.
These organisations do accept non-medical candidates.
My certification acronym is ABAARM, from the American Academy for Aging and Metabolic Medicine, which is owned and operated by the TARSUS group.

** “Hormone balance tests”, done on both men and women, include DHEA, Testosterone, IGF-1 ****, Oestradiol, Progesterone, Thyroid function (TSH, T4, T3 and reverse T3), Cortisol and Allopregnanolone (when it becomes available).

*** 1] Normal hormone production rates are not a given: children subject to PTSD, severe illness, trauma or major surgery often fail to achieve normal rates in early adulthood and for example, 60-y-o DHEA levels can be found in many “20-somethings”.
2] At age 26 we all, both men and women, begin to reduce our neurosteroid hormone production, from whatever level we acheive at 25, by 1-2% per annum. Thyroid hormone, Growth hormone, Melatonin etc also decline.
3] Because of this “slide”, we should reassess all our “normal” test ranges, accepting only healthy, functionally euthyroid individuals between the ages of 20 and 25 years.
4] “Age-adjusted normal” is a misnomer: a better term would be “Age-related deficiency”.
**** 5] IGF-1 is a marker for human growth hormone (HGH), which promotes growth and maturation in youth and functions as an “anabolic” (muscle and organ maintenance) hormone throughout life.
As with most of the other hormones, HGH production falls as we age and HGH deficiency is one of the factors which lead to loss of muscle mass and progressive frailty as we age.
Please see my blog regarding HGH.

Keeping the internal millieu of the human body at youthful levels assists maintenance and repair processes, including apoptosis of new cancer cells, repair of brain tissue, optimisation of glucose and cholesterol management, fat control, (heart and skeletal) muscle maintenance, cognition and just about everything else.
Therefore hormone balance should be maintained via supplementation of deficient hormones or hormone precursors, along with vitamin and mineral balance, whether the individual remains healthy or develops some pathology, so as to ensure that the body’s repair tools are always available.


And cured with T4: this is a case report, titledHypothyroidism-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 ,

This paper reports on a young female with DILATED CARDIOMYOPATHY CAUSED BY HYPOTHYROIDISM and cured with T4.


Interestingly, the authors state (I have paraphrased this, for brevity):
”The heart relies mainly on Triiodothyronine (T3) because there is no significant deiodinase activity inside myocytes: T3 is directly transported into the myocyte”.
They go on, to explain “T3 modulates inotropic and lusitropic properties of the myocardium, myocardial contractility, and vascular function”………….. and
Hypothyroidism can produce bradycardia, impaired contractility, impaired diastolic filling, increased systemic vascular resistance, diastolic hypertension, and endothelial dysfunction.” [6]
Further, they say ………….
“It has also been demonstrated that subclinical (intracellular) 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 normal thyroid gland may have low levels of T3 with normal T4 and TSH”.
“Low serum T3 in these patients strongly predicts all-cause and cardiovascular mortality”.[7] “The most consistent cardiac abnormality recognized in patients with overt hypothyroidism is impairment of LV 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 lady’s cardiomyopathy was caused by T3 deficiency, they still treated her with T4 instead of T3 !

MESSAGE: ** These terms are synonymous with Functional (INTRACELLULAR) Hypothyroidism and in my opinion prescribing oral, slow-release T3 would not only have corrected the problem more certainly and more quickly, but the short half-life of T3 would have allowed daily reassessment, ongoing monitoring and better control of her life-threatening condition.

Fortunately, the patient recovered due to treatment with T4, thus proving the premise of the title of their paper.

See the page on THYROID HORMONE, for details re. functional, intracellular hypothyroidism.

More about DCM

This new (August, 2021), very well-written paper, entitled
Thyroid Hormones—An Underestimated Player in Dilated Cardiomyopathy?“,
comes very close the truth of T3’s influence on heart health and function.
The authors have managed to review all the important facts on the subject, up to and including a mention of reverse T3, without coming to the conclusion that full thyroid testing might disclose functional hypothyroidism and by so doing, permit the prescription of Triiodothyronine for cure of this almost universally fatal disease (many DCM subjects, even those treated by heart transplant, die).

J Clin Med. 2021 Aug; 10(16): 3618. Published online 2021 Aug 16. doi: 10.3390/jcm10163618PMCID: PMC8397026PMID: 34441915, Karolina Zawadzka,1Radosław Dziedzic,1Andrzej Surdacki,2 and Bernadeta Chyrchel2,*

Dilated cardiomyopathy (DCM) is the most prevalent cardiomyopathy, typified by left ventricular dilation and systolic dysfunction. Many patients with DCM have altered thyroid status, especially lower levels of free triiodothyronine (T3) and elevated levels of thyroid-stimulating hormone. Moreover, growing evidence indicates that even subtle changes in thyroid status (especially low T3) are linked with a worse long-term prognosis and a higher risk of mortality. Notably, recent discoveries have shown that not only local myocardial thyroid hormones (THs) bioavailability could be diminished due to impaired expression of the activating deiodinase, but virtually all genes involved in TH biosynthesis are also expressed in the myocardium of DCM patients. Importantly, some studies have suggested beneficial effects of TH therapy in patients suffering from DCM. Our aim was to discuss new insights into the association between TH status and prognosis in DCM, abnormal expression of genes involved in the myocardial synthesis of TH in DCM, and the potential for TH use in the future treatment of DCM.

(1) A “Thyroid profile”, including TSH, T4, T3 and rT3 (with T3/rT3 calculation) should be part of the “workup” for all major diseases and conditions.
(2) When the T-profile shows functional hypothyroidism, treatment with slow-release T3, to correct the functional hypothyroidism, should be given in addition to whatever specific therapy is recommended for the condition (excepting that if T4 is recommended, T3 should be given instead).


The page on ALLOPREGNANOLONE has been updated today, to include developments re. BREXANOLONE, ZURANOLONE,
treatment of Allopregnanolone-deficiency depression and
ideas regarding treatment of the Post-Finasteride Syndrome.


I am still getting occasional queries re. the PFS.

Please see ….. the salient section is under “CONSTRUCTIVE ANALYSIS”.

Please note that, as for all else in this site, this is my opinion only and statements entered here are for discussion with a currently licensed metabolic (“functional”) medicine practitioner.

Please do not solicit my opinion regarding your “case”.

Please realise that I cannot write prescriptions: I offer my opinion as a basis for your www research and to empower you in discussions with an appropriate MD.



Currently, our “system” says that to figure out whether a person’s thyroid balance is satisfactory in terms of keeping our cells working at maximum efficiency, all we need to check is the Thyroid Stimulating Hormone. However TSH is a signal sent by the Pituitary gland, to tell the Thyroid how much T4 to make.

THIS HAS NOTHING TO DO WITH THE REST OF THE BODY: the pituitary is merely ordering Thyroxine, to satisfy itself.


Since FT3 is rarely, and rT3 never, measured, Physicians are unaware of the state of thyroid hormonal balance in the cells and organs: the body has no way of expressing its state of satisfaction, and other than T4/FT3 /rT3 we don’t have a dedicated test for thyroid balance.We can, however resolve the dilemma with minimum civil disobedience: let’s see FT3 and rT3 results and figure it out!


T4 is converted preferentially to T3 rather than rT3 under normal circumstances, but when Cortisol output rises due to fasting or any other stress [1,2], FT3 production falls and rT3 increases, while TSH and FT4 are only minimally affected.

If rT3 goes up when T3 goes down, we can estimate the “strength” of the shift by dividing the T3 value by that of rT3; the ratio thus derived is a measure of the severity of the process and the depth of pathological deviation from normal T3/rT3 balance.

It has been observed that when the FT3/rT3 ratio is less than 20.0, hypothyroid symptoms appear; we differentiate this from true Hypothyroidism with a new term: “Functional Hypothyroidism”.

Clinical observation confirms that Hypothyroid symptoms coincide with this logic and that therapy with slow-release Triiodothyronine reliably relieves those symptoms.


If the patient takes T3 (slow-release,”SR” Triiodothyronine *), serum FT3 rises, rT3 falls and the ratio goes up.

Usually, FT3/rT3 exceeds 20.0 when the serum FT3 rises above 4.5, but a FT3 of 5.0-6.0 is the target of choice.

Treatment with SR T3 is safe and side effects (SE) are minimal.

The mildest SE is a feeling of being “high”, with enhanced vision and other sensory abilities, but some subjects have noted a hyper-reactive state, irritability, “antsiness” or increased pulse rate.

Therapy begins with 5mcg daily, increasing weekly by 5mcg/day, to a maximum 25mcg or until SEs occur: if SEs are noted, the dose is reduced to the previous level. TSH, FT4, FT3 and rT3 are repeated at a dose of 25mcg, or the dose which does not cause SEs and the dose is modified accordingly, to yeild a FT3 between 5.0 and 6.0.

Reverse T3 usually falls to less than 13 Nanograms/Decilitre when T3 exceeds 5.0 pM/Litre.


The endpoint of therapy is elimination, or suppression, of hypothyroid symptoms, as judged by the patient.
Successful therapy reduces the perception of stress, whether or not the individual’s stressors are lessened and relapse is unlikely as long as treatment continues.
SRT3 can be discontinued if the stress is eliminated, but hypothyroidism will relapse if the stress recurs.


Iodine and Selenium supplements may help, but successful prescription of Triiodothyronine does not affect the patient’s requirement for other supportive hormone replacements or prescribed medications, excepting that drugs for Glucose and Cholesterol control, hypotensives, cognitive support, soporifics and psychoactive drugs can often be eliminated or minimised.


The normal level of Reverse T3, nominally 5 to 25, is difficult to assess. Similarly to T3 and TSH, it has been subject to error due to the inclusion of functionally hypothyroid subjects in the cadre of “normal” people whose thyroid profiles have been used to calculate the reference ranges.

Based on observation of approximately 300 cases and in line with their responses to therapy, my opinion is that especially since rT3 is a nonfunctional “waste” metabolite, the level is significant only because it gives laboratory evidence of excessive conversion of T4 to rT3. Ergo, estimation of “normal” for rT3 is unnesessary and perhaps obfuscatory.

Having said which, I would suggest a nominal “Normal” of 5-13 Ng/DL.


Patients given Eltroxin or Synthroid during an episode of functional hypothyroidism, while T4 is being preferentially converted to rT3, experience marked worsening of their hypothyroid symptoms. This is because the T4 is converted to rT3, which has the effect of reducing T4 conversion to normal T3. Therefore their T3 level falls even further and the hypothyroid symptoms are exacerbated.

Patients who experience a stressful episode while on treatment for pre-existing true hypothyroidism, may suffer the same fate.

Dessicated Thyroid should not be used to treat stress-related functional hypothyroidism, because it is 70% T4 and 30% T3 and therefore may increase symptoms just as Eltroxin does.

Patients taking T3 (in a slow-release format) often reduce rT3 production to < 9 Ng/DL.

Since T3 usually penetrates the Pituitary and since the Pituitary actually uses its level of T3, not T4, to guage its TSH output, TSH often falls to <<1.0.

Reduced TSH output by the pituitary results in reduction of T4 production by the thyroid, so a T4 of 8 or less is often seen during SRT3 treatment. THIS IS NOT A CAUSE FOR CONCERN.

Most often, exogenous T3 enters the pituitary easily and TSH falls to a minimum. However in a small precentage of cases a high TSH is seen, in the face of high-normal T3 and very low rT3: this shows exclusion of exogenous T3 from the Pituitary and requires therapy with T4 …… This is the only scenario in which a prescription of T4, as Eltroxin or Synthroid, is appropriate.

NOTE: In 2014, two of my patients presented to an ER with FT3 of 1.7: both had cardiac failure of myxoedema.

TSH should be tested as an indicator of the Pituitary’s need for T4, but not for T3 balance.

The Normal for T3/rT3 being > 20, the optimal level should arguably, be 24-50.

The T3 range, currently skewed because a large, unrecognised percentage of our population is functionally hypothyroid, should be reviewed, reverted to the original 3.4 – 6.2 (or more) pMol/L


2.8(newLo N)181.81018.2Mild FHIncludes endemic hypothyroidism
3.2 (old Lo N)207.81118.9Mild FHNeed rT3 <11,
to be Euthyroid
5.0 (Optimal Lo N)324.725 (Lab High N)13.0Severe FHNeed rT3 < 16
to be Euthyroid
5.0324.720 (Lab High Mid)16.2Moderate FHNeed rT3 < 16
to be Euthyroid
5.0324.717 (Lab Low Mid)19.1Mild FHNeed rT3 < 16
to be Euthyroid
5.8(New Hi N376.61919.8Mild FHNeed RT3 <19
to be Euthyroid
6.2 (Opt Hi N)402.621 (Lab Mid-High)19.2BorderlineNeed rT3 < 20
to be Euthyroid
6.2 (Opt Hi N)402.625 (Lab High N)16.1Moderate FHNeed rT3 < 20
to be Euthyroid
7.6 493.52519.7Still has FHIf rT3 = 25, Need T3 > 7.6 to be Euthyroid
rT3 corresponds to T4 level and state of stress. there is no “normal” rT3.


In 2005 Leonard Wartofsky and Richard A Dickey wrote, (paraphrased, for brevity): “It has become clear that our reference ranges are no longer valid. We have more sensitive TSH tests and also, we now realise that previous reference populations included people with (low) thyroid dysfunction, whose high TSH levels led to a spuriously high reference range for TSH in the group. Recent laboratory guidelines from the National Academy of Clinical Biochemistry indicate that more than 95% of normal individuals have TSH levels below 2.5 mU/liter.”

In 2007 Martin I. Surks and Joseph G. Hollowell said as follows (paraphrased, for brevity)……
“The TSH median, 97.5 centile and prevalence of subclinical hypothyroidism (SCH) increase progressively with age.
Age-adjusted reference ranges would include many people with TSH greater than 4.5 mIU/liter.” *
They continued: (”Without thyroid disease”), 10.6% of 20- to 29-yr-olds had TSH greater than 2.5 mIU/liter. *
In the 80+ year-old group “without thyroid disease”, 14.5% had TSH greater than 4.5 mIU/liter. *
TSH frequency distribution curves of the 80+ year-old group showed higher TSH.
The 97.5 centiles for the 20–29 and 80+ year-olds were 3.56 and 7.49 mIU/litre, respectively.
70% of older patients with TSH greater than 4.5 mIU/liter were within their age-specific range (up to 7.49)**. In spite of these findings (almost 100% of) our medical doctors preferred to think like Surks and Hollowell and the reference range for TSH has remained unchanged.

However to me, the implications are clear:
· Wartofsky and Dickey were correct and the upper limit of normal TSH should be 2.5, but they should have realised that 10.6% of their 20-29-year-olds were in fact, hypothyroid and should have excluded them. ****
· Surks and Hollowell would have done better to label the older folks hypothyroid, rather than concluding that “high TSH is normal for the older population”: what their findings mean is that a large percentage of the 80+-year-olds were hypothyroid and should have been excluded from calculations of normal.·

* AGE-SPECIFIC NORMAL, or “NATURAL NORMAL” makes no sense. “Normal” should be understood to mean the status of healthy humans aged 20-25 with no abnormal results for any test: any abnormal finding should disqualify the candidate for all estimates of “normal”.
These findings should not have been included in a calculation of “normal”.

** Any result >2.5 suggests hypothyroidism, so this implies that more than 14.5% of the
80+ year olds were hypothyroid: including them in the “normal” group means that 15+% of 80-yr-olds won’t get the treatment they need !

*** I dare suggest that one should apply fair logic to every scientific paper, so as to exclude glaring errors and prejudices like these from your belief systems.

**** Think about it – if I am right, since the thyroid hormone dictates the efficiency level of every cell and system in the body, and if 10.6% (or more) of the thyroid test study population should have been excluded from the calculation of “normal” thyroid hormone levels, then the parameters for all our other tests could be wrong and maybe a lot of tests might be invalid !


· Many other hormones suffer the same fate as DHEA: Melatonin, Progesterone, Allopregnanolone, Testosterone and Thyroid hormone all go down over time, mostly by slow, gradual loss of production.

· In some people several hormone levels can “crash” suddenly, causing various symptoms of deficiency depending on which hormones are involved. This can happen with Melatonin in the “teens”, Progesterone and Allopregnanolone in the twenties, Testosterone in the thirties or earlier and particularly Oestrogen, which disappears in the early fifties but can fall to zero in the late thirties or early forties.

· Thus assesssment of “normal” in the presence of “natural age related hormonal change” is very difficult.

· To give medical investigators their due, a concerted effort is always made to include only the fittest individuls in the group evaluated. However there are instances in which unknown or ignored factors lead to a “curve ball” situation and consequent unreliability of an accepted “normal” range.

· IN SUMMARY, aberrations of hormonal production are pervasive and the interdependence of hormonal systems is delicate: test subjects should be BETWEEN AGE 20 AND 25 YEARS and ALL THEIR OTHER RESULTS SHOULD BE 100% NORMAL, for inclusion in studies to calculate a “normal” reference range for whatever test is to be evaluated.


[1] Opposite effects of dexamethasone on serum concentrations of 3,3′,5′-triiodothyronine (reverse T3) and 3,3’5-triiodothyronine (T3),I J ChopraD E WilliamsJ OrgiazziD H Solomon, J Clin Endocrinol Metab, 1975Nov;41(5):911-20, doi: 10.1210/jcem-41-5-911, PMID: 1242390. DOI: 10.1210/jcem-41-5-911,

[2] Diversion of peripheral thyroxine metabolism from activating to inactivating pathways during complete fasting, A G VagenakisA BurgerG I PortnaryM RudolphJ R O’BrianF AziziR A ArkyP NicodS H IngbarL E Braverman, PMID: 1150863, DOI: 10.1210/jcem-41-1-191 J Clin Endocrinol Metab, 1975 Jul;41(1):191-4. doi: 10.1210/jcem-41-1-191.

(3) The evidence for a narrower thyrotropin reference range is compelling
Leonard Wartofsky 1 Richard A Dickey, J Clin Endocrinol Metab, 2005 Sep; 90(9):5483-8
PMID: 16148345 DOI: 10.1210/jc.2005-0455 .

(4) Age-Specific Distribution of Serum Thyrotropin and Antithyroid Antibodies in the U.S. Population: Implications for the Prevalence of Subclinical Hypothyroidism:
Martin I. Surks, Joseph G. Hollowell, The Journal of Clinical Endocrinology & Metabolism, Volume 92, Issue 12, 1 December 2007, 4575–4582, 01 Dec. 2007.

(5) A new prognostic index in surgery and parenteral feeding: the ratio of triiodothyronine to reverse triiodothyronine in serum (T3/rT3 ratio) H.D. Calvey, W.J. Marshall, P.D. Marsden M. Davis
Front Endocrinol (Lausanne). 2018; 9: 97.Volume 5, ISSUE 3, P145-149, August 01, 1986:OI: Published online 2018 Mar 20. doi: 10.3389/fendo.2018.00097 PMCID: PMC5869352 PMID: 29615976

(6) Higher Prevalence of “Low T3 Syndrome” in Patients With Chronic Fatigue Syndrome: A Case–Control Study
Begoña Ruiz-Núñez,1,2,* Rabab Tarasse,1 Emar F. Vogelaar,3 D. A. Janneke Dijck-Brouwer,1 and Frits A. J. Muskiet1 Front Endocrinol (Lausanne). 2018; 9: 97, Published online 2018 Mar 20. doi: 10.3389/fendo.2018.00097, PMCID: PMC5869352 PMID: 29615976

(7) Opposite effects of dexamethasone on serum concentrations of 3,3′,5′-triiodothyronine (reverse T3) and 3,3’5-triiodothyronine (T3) I J ChopraD E WilliamsJ OrgiazziD H Solomon, PMID: 1242390, DOI: 10.1210/jcem-41-5-911

(8) Effect of 3:5:3′-L-triiodothyronine in myxoedema, GROSS J, PITT-RIVERS R, TROTTER WR. Lancet. 1952 May 24;1(6717):1044–1045.

(9) A radioimmunoassay for measurement of 3,3′,5′-triiodothyronine (reverse T3). Chopra IJ. J Clin Invest. 1974 Sep;54(3):583–592. [PMC free article] [PubMed] [Google Scholar]

(10) Diversion of peripheral thyroxine metabolism from activating to inactivating pathways during complete fasting.Vagenakis AG, Burger A, Portnary GI, Rudolph M, O’Brian JR, Azizi F, Arky RA, Nicod P, Ingbar SH, Braverman LE. J Clin Endocrinol Metab. 1975 Jul;41(1):191–194.

(11) Concentrations of 3,3′,5′-triiodothyronine (reverse T3) and 3,3’5-triiodothyronine (T3) I J ChopraD E WilliamsJ OrgiazziD H Solomon, PMID: 1242390, DOI: 10.1210/jcem-41-5-911

(12) Diversion of peripheral thyroxine metabolism from activating to inactivating pathways during complete fasting, A G VagenakisA BurgerG I PortnaryM RudolphJ R O’BrianF AziziR A ArkyP NicodS H IngbarL E Braverman, PMID: 1150863, DOI: 10.1210/jcem-41-1-191 J Clin Endocrinol Metab, 1975 Jul;41(1):191-4. doi: 10.1210/jcem-41-1-191.

G. A. Harry, MB, BS (London), LMCC, FRCSC (urology), ABAARM (A4M, 2014).

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