THYROID TESTS

SHOULD OUR THYROID HORMONAL ASSESSMENT BE REVIEWED?

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.

WHAT OUR MEDICAL SYSTEM IGNORES

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!

 METABOLISM OF THYROXINE, THE “T4” HORMONE

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.

TREATING FUNCTIONAL HYPOTHYROIDISM

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.

EFFECT OF THERAPY WITH TRIIODOTHYRONINE

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.
CAVEAT: weight loss may occur, but SRT3 MUST NOT BE PRSECRIBED FOR WEIGHT CONTROL !

ANCILLARY PRESCRIPTIONS

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.

REGARDING THE “NORMAL” RANGE OF REVERSE T3

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.

NOTES

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

THIS TABLE WAS DEVISED FOR A PREVIOUS ITERATION: I INCLUDE IT HERE, “JUST FOR FUN”

If T3 in Pm/L  T3,Ng/DL rT3,Ng/DL T3/rT3 DIAGNOSISCOMMENT
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.

REGARDING TSH

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 !

MESSAGE

· 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.

  REFERENCES

[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. https://pubmed.ncbi.nlm.nih.gov/1150863/

(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 .https://pubmed.ncbi.nlm.nih.gov/16148345/

(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, https://doi.org/10.1210/jc.2007-1499 01 Dec. 2007.
https://academic.oup.com/jcem/article/92/12/4575/2596923?login=true

(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:https://doi.org/10.1016/0261-5614(86)90003-8 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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869352/

(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
https://pubmed.ncbi.nlm.nih.gov/1242390/

(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]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC301591/

(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. https://pubmed.ncbi.nlm.nih.gov/1150863/

(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 https://pubmed.ncbi.nlm.nih.gov/1242390/

(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. https://pubmed.ncbi.nlm.nih.gov/1150863/

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

HIGHER PREVALENCE OF “LOW T3 SYNDROME” IN CHRONIC FATIGUE SYNDROME: A CASE-CONTROL STUDY

by Begoña Ruiz-Núñez, Rabab Tarasse, Emar F Vogelaar, D A Janneke Dijck-Brouwer, Frits A J Muskiet PMID: 29615976, PMCID: PMC5869352, DOI:10.3389/fendo.2018.00097, Front Endocrinol (Lausanne), 2018 Mar 20;9:97. doi: 10.3389/fendo.2018.00097. 2018.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869352/

CFS symptoms resemble a hypothyroid state.

ABSTRACT (I paraphrased this abstract, for brevity and clarity)

Chronic fatigue syndrome (CFS) is a heterogeneous disease with unknown cause(s). CFS symptoms resemble a hypothyroid state, secondary to chronic inflammation.
We studied 98 CFS patients and 99 age- and sex-matched controls.
We measured parameters of thyroid function, (metabolic) inflammation, gut wall integrity and nutrients influencing thyroid function and/or inflammation.
Remarkably, CFS patients exhibited:
Similar TSH,
Lower free T3 (FT3),
Lower total thyroxine (TT4),
Lower total T3 (TT3),
Lower %TT3 (4.7%),
Lower activity of deiodinases,
Lower secretory capacity of the thyroid gland (14.9%) and
Lower 24-h urinary iodine (27.6%).

The % of reverse T3 (rT3) was higher (13.3%), among the patients and FT3 below the normal range, consistent with the “low T3 syndrome,” was found in 16/98 CFS patients vs. 7/99 controls.

We also found evidence of low-grade metabolic inflammation (ferritin & HDL-C).
FT3, TT3, TT4, and rT3 correlated positively with hsCRP in CFS patients and controls. TT3 and TT4 were positively related to hsCRP in controls.
Low T3 and the shift from T3 to rT3 may reflect more depressed tissue T3 levels.

The findings in patients agree with studies suggesting a hypometabolic state.
They resemble “non-thyroidal illness syndrome” and “low T3 syndrome” experienced by a subgroup of hypothyroid patients receiving T4 monotherapy.
Our study needs confirmation by others: trials with,T3 and iodide supplements might be indicated.

Keywords: chronic fatigue syndrome, thyroid, “low T3 syndrome”, triiodothyronine, reverse triiodothyronine, urinary iodine, inflammation, high-sensitive C-reactive protein

My COMMENT REGARDING THIS ARTICLE:

This is a truly excellent paper.
It tends to agree with me, confirming that CFS symptoms resemble a hypothyroid state, or at least that there is a relationship between CFS and “Functional Hypothyroidism“, and it raises the obvious question: is therapy available?
My answer is as follows:
(1) CFS is “Low T3 syndrome” and “CFS” a manifestation of Functional (Intracellular) Hypothyroidism (IH).
(2) Those presenting with CFS, or other symptoms of Intracellular Hypothyroidism, should have Thyroid Profile tests, including TSH, free T4, free T3 and reverse T3:
(3) If the FT3/rT3 ratio is less than 20, all patients, male or female of whatever age, should be treated with T3 (Triiodothyronine), using a protocol of upward titration of the T3 dose * to achieve a serum T3 between 5.0 and 6.1 Picomoles/Litre.
(4) Treatment with slow-release T3 can be expected to be successful: if it is, the IH will be eliminated, “low thyroid” symptoms will be gone and the CFS will be CURED. **

  • * Monitored with weekly retesting of FT3 and rT3, at 3-4 hours post-dose: since the half-life of Triiodothyronine is just 2-3 hours, there is no need for a 6-week dose-test interval, as is done with Levothyroxine.
  • ** Weaning off Triiodothyronine can be attempted 3-6 months after confirming the curative dose. However IH is a stress-dependent condition and will quickly recur, with relapse of CFS, if and when the patient is subjected to stress.
    In such cases, T3 therapy can be continued, with dose adjustment ad hoc, indefinitely.

IMAGINE TWIN CHIMPANZEES:

A PARABLE ON HEALTHY AGING

ONCE UPON A TIME THERE WERE TWO CHIMPANZEES: they were twins, but one was smart and the other, not so very.

On their third birthday each was given a toolbox, with a fat-handled screwdriver, pliers, a hammer, a saw, a crowbar and a big knife.

The smart Chimp opened his toolbox and found that he could use the tools, lifting stones to find delicious worms, getting termites from their nests, opening walnuts, cutting coconuts, peeling oranges, squeezing things and generally making life easier for himself. He kept the toolbox in a dry spot inside his cave, took it with him everywhere and used the tools often, always cleaning and returning them to the box after use.

The unsmart brother loved his toolbox because it was the first birthday present that he could remember, but he never opened it and often left it out In the rain.

When they were about 26 years old, each somehow, on the same day, got caught in a trap set by a trapper who suffered from carpenteric dyslexia: he made all his traps with autolocking doors, but he put the hinges on the inside.

The smart Chimp immediately noticed that his screwdriver would fit the screws which held the hinges and couldn’t keep his amusement down.
He sat for a while, giggling, then opened his box, disconnected the door with his screwdriver, put the ‘driver back into the box and walked out, taking his toolkit with him as usual.

He tried to set his brother free, but couldn’t reach the hinges, the cage was made of steel, the crowbar wasn’t strong enough and the spaces between the bars were too narrow to let the screwdriver through, so he gave up trying.

The smart Chimp took his toolbox back to his cave and lived happily ever after, using his tools often and keeping them oiled and in good condition.

The unsmart Chimp was sold to a zoo, where he died at 33 from Alzheimer’s disease.

Q: WHAT’S THE POINT OF THIS IDIOTIC STORY ?

A: LOSS OF OUR HORMONAL “TOOLS” MAY BE NATURAL, BUT KEEPING THEM HAS BENEFITS

Due to hormone loss, we humans do not maintain perfect control over our functions permanently.

Kept healthy by our hormonal tools, we are fine up to age 25 or so, but thereafter we begin losing hormone production at a rate of about 1% per year, overall: by age 80 most of our hormone production is gone.

This produces a slowly accelerating decline in the efficiency of our metabolic management systems, which become “skewed” to a greater or lesser degree in one or another direction, depending on how our individual internal organs respond to reduced hormone levels.

Each individual, male of female, responds to hormonal loss with his or her own pattern of symptoms: depending on the individual organ’s sensitivity to lowered hormone availability there may be hair loss, weight gain, recurrent acne, dry skin, thin finger nails, allergies, high blood pressure, diabetes, autoimmune diseases, psychological change, cancer, neurological disease or other problems.
In addition stress, endemic to our modern lifestyle, can trigger suppression of thyroid function as an energy-saving reaction. When this happens all systems lose efficiency: muscles (including heart muscle) weaken and ache, the metabolic rate falls and we gain weight, loss of self-confidence leads to anxiety/depression and any pre-existing effects of hormonal reduction are accentuated.

In the opinion of Functional Medicine afficionados, our progressive loss of hormone production, though naturally occurring and 100% pervasive, is a disease and the resulting deviations from perfect health should be considered to be ill-effects of a pathological process.
From the Metabolic Medicine point of view, natural aging due to hormone loss is modifiable, if not truly treatable: hormonal balance is safely and easily achieved and with intuitive, inexpensive surveillance, can be perfectly timed.

While most people begin their disabilities at 26 (or earlier), many appear to be unaffected until much later. There is such a wide spectrum of “aging” effects that the majority are able to “carry on as usual” and the ones who fall by the wayside early in life are regarded as poor eaters, unhealthy due to bad habits or simply “unlucky”.
Nevertheless one thing is clear: no-one escapes the trap into which we are born and our “slide down the razorblade of life”, whether fast or slow, is inevitable.

As we age, most of the parameters by which our health professionals measure health remain stable and reasonably constant until some major system fails: tests for the function of the heart, blood vessels, kidneys, liver, lungs, intestines, endocrine glands, brain, bones etc remain sufficiently stable that hardly anyone shows obvious evidence of deterioration.

Unfortunately however, errors are built into our surveillance plan:
[1] The hormonal balance, the measurable parameter which affects the function of all organs, changes steadily and can be monitored to give some indication of the general state of affairs, is ignored: decreasing test results are labeled “age-related” and considered “natural and normal for age”, thereby being relegated to the “interesting, but unimportant” file.

Let’s think about what we lose as aging progresses:
– Consider DHEA – it is the precursor for Testosterone, Progesterone, Oestradiol, Cortisol and a host of microhormones which keep our parts working: all our cells, including heart, brain and thyroid cells, need it to maintain perfect function, but in Canada it is on the “dangerous drugs” list.
– Consider Testosterone: quite aside from the well-known “low T” difficulties in the male, “low T” (normal = 20-30 picomoles/Litre) is a huge problem for our females. In fact even ZERO “T” is often found in young women (I had a patient aged 23 with zero testosterone). It is easily and safely treated with DHEA or “T” cream, but is usually ignored.
– Consider Progesterone: it rules the menstrual cycle, prevents PMDD, promotes sleep, counteracts fat-making Oestrogens and is raw material for Allopregnanolone (Q.V., Infra). Deficiency of Progesterone is the usual cause of dysmenorrhoea, but most practitioners don’t test for it.
– Consider Allopregnanolone, darling of neuropsychiatry, which prevents and treats depression, ensures good sleep, is essential for memory, and maintains / repairs the brain (12): Allopregnanolone deficiency is the main reason for depression, especially postpartum, but we don’t even test for it.
– Consider Oestradiol: it maintains the female “parts”, keeps the skin young and makes bones stronger, but we strongly recommend against prescribing it.
…None of this is news, yet the progressive loss of all these hormones is accepted as “normal for age” and unremarkable. The ill-effects of hormone deficiency are accepted as inevitably due to “normal” aging and we are told to “live with it”!

[2] One hormonal system, the thyroid, is not tested accurately because TSH, which the pituitary gland sends out when it needs T4, is considered to be the only necessary thyroid test, although it only speaks to the pituitary’s need for T4 and has nothing to do with the body as a whole.
Consider the following:
– T3, your efficiency accelerator, is hardly ever measured and its so-called “normal range” is impossibly wide.
– Reverse T3, produced when the metabolic brake is applied and whole-body efficiency falls, is virtually never measured.
– Many anticancer drugs work by blocking T3, because cancer cells need it (all cells need T3).

[3] Mainstream doctors don’t test for vitamins and minerals, excepting Electrolytes, Vit B12, Iron, Calcium, Magnesium and Phosphorus. Although we know that an overload of Lead, Mercury and many other metals can be deleterious, tests for metal poisoning are almost never done and chelation treatment for metal overload is regarded as “quackery”.

WE CAN DETECT THE START OF HORMONE LOSS AND WE CAN REMEDY THE PROBLEM

A PLAN FOR HEALTHY AGING:

Age 5-15: Hormone information / awareness courses are taught in high school, to improve basic knowledge of the subject among the general population, facilitating the health practitioner’s surveillance and instruction of patients.

Age 15-25: A “wellness assessment questionnaire” and a short list of tests, most of which are inexpensive and easily available, are assessed by the family physician at age 15, 20 and 25. If and when symptoms of hormone loss begin, the tests are repeated and the doctor discusses the results with the patient.

Age 25-35: The wellness questionnaire and tests are repeated every 3 years.
The onset of symptoms, an abnormal test result, or the individual’s concern triggers a brief explanation by the family doctor and referral to a health education professional (a well-paid paramedic, or nurse).
The the HEP reviews all aspects of hormonal balance, to ensure the patient’s understanding of the diagnosis and possible therapy, then the person returns to the MD to discuss a plan for management and possible prescription.

If the person concerned needs, and is ready to embark on (necessarily lifelong) hormone restoration, they themselves request a trial of therapy: this request is a mandatory prerequisite to prescription.
Refusal of advice or postponement of surveillance and/or therapy, is the individual’s prerogative, to be accepted without question by healthcare professionals and garnering no consequences.

FAQ

Q: WHAT’S THE POINT OF ALL THIS?
A: To reduce and delay body-system deterioration due to hormone deficiency. (1)

Q: WON’T IT BE EXPENSIVE?
A: It is a lot cheaper to prevent, than to cure. (2)

Q: HOW CAN WE AVOID OVERTREATMENT?
A: Repeated tests show the effect of therapy and the dose of hormone is adjusted accordingly.

Q: WHAT ABOUT HORMONE – DEPENDENT CANCER, LIKE HER-2 BREAST CANCER?
A1: These cancers need the hormones to grow, but are not caused by the hormones.
A2: Maintainance of DHEA, Melatonin, Progesterone, NAC, MTHF, Magnesium etc deters cancer formation (4)

Q: PEOPLE WITH PCOS HAVE HIGH DHEA – WILL YOU CAUSE PCOS, BY INCREASING DHEA?
A: PCOS causes the high DHEA; not the other way around. (5)

Q: SUPPOSE TESTOSTERONE PRODUCES A PROSTATE CANCER?
A1: That idea is wrong. Testosterone opposes Prostate Ca formation & low Testosterone promotes it.
A2: The Mayo Clinic still endorses the idea that P cancer should be treated by blocking T, (9), but
DHEA, or Testosterone, prevents Prostate cancer and can be used as a treatment, in some cases. (6,7,8).

Q: DON’T HORMONES PREVENT PREGNANCY?
A: Only artificial hormones in birth control pills do, not hormones made by human glands. (10)

Q: AMD IS CAUSED BY THYROID HORMONE – CAN Thyroid Hormone MAKE YOU BLIND?
A: There is a link between higher levels of T4 and spontaneous AMD, not with Rx of T3 and T4. There must be some other factor that we have not as yet found: why would an essential hormone ruin vision? (11)

Q: WHAT ABOUT THYROID CANCER?
A: The story is the same as for other hormone-sensitive tumours: the cancer cells need thyroid hormone to grow,  but TH does not cause the cancer.

REFERENCES

For brevity, only a few are listed. Many more are available through NCBI.

(1) The “multiple hormone deficiency” theory of aging: is human senescence caused mainly by multiple hormone deficiencies? T Hertoghe 1 Ann N Y Acad Sci 2005 Dec;1057:448-65. doi: 10.1196/annals.1322.035. https://pubmed.ncbi.nlm.nih.gov/16399912/

(2) The Healthcare Imperative: Lowering Costs and Improving Outcomes: Workshop Series Summary (Book)

(4) Hormone-sensitive cancer: Wikipedia, the free encyclopedia, https://en.wikipedia.org/wiki/Hormone-sensitive_cancer

(5) Adrenal Androgen Excess and Body Mass Index in Polycystic Ovary Syndrome, Carlos Moran, Monica Arriaga, Fabian Arechavaleta-Velasco, Segundo Moran The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 3, 1 March 2015, Pages 942–950, https://doi.org/10.1210/jc.2014-2569 https://academic.oup.com/jcem/article/100/3/942/2839480

(6) Does Testosterone Cause Prostate Cancer? Stephanie Watson — Healthline, September 18, 2018

(7) Testosterone as a Drug, Johns Hopkins 05/01/2018 Dr Denmeade https://www.hopkinsmedicine.org/news/articles/testosterone-as-a-drug

(8) Bipolar androgen therapy in men with metastatic castration-resistant prostate cancer after progression on enzalutamide: an open-label, phase 2, multicohort study Benjamin A Teply 1 Hao Wang 2 Brandon Luber 2 Rana Sullivan 2 Irina Rifkind 2 Ashley Bruns 2 Avery Spitz 2 Morgan DeCarli 2 Victoria Sinibaldi 2 Caroline F Pratz 2 Changxue Lu 3 John L Silberstein 3 Jun Luo 3 Michael T Schweizer 4 Charles G Drake 5 Michael A Carducci 2 Channing J Paller 2 Emmanuel S Antonarakis 2 Mario A Eisenberger 2 Samuel R Denmeade 6 Clinical Trial, Lancet Oncol. 2018 Jan;19(1):76-86, doi: 10.1016/S1470-2045(17)30906-3. Epub 2017 Dec 14. https://pubmed.ncbi.nlm.nih.gov/29248236/

(9) Hormone therapy for prostate cancer is a treatment that stops the male hormone testosterone from being produced or reaching prostate cancer cells MAYO CLINIC, April 9, 2021 https://www.mayoclinic.org/tests-procedures/hormone-therapy-for-prostate-cancer/about/pac-20384737

(10) Birth Control Pills https://www.webmd.com/sex/birth-control/birth-control-pills

(11) Exploring the link between thyroid hormones and vision loss https://blogs.biomedcentral.com/on-medicine/2015/04/30/exploring-link-thyroid-hormones-vision-loss/

(12) Allopregnanolone, the Neuromodulator Turned Therapeutic Agent: Thank You, Next? Graziano Pinna*Department of Psychiatry, The Psychiatric Institute, University of Illinois at Chicago, Chicago, IL, United States. Front. Endocrinol., 14 May 2020 | https://doi.org/10.3389/fendo.2020.00236
https://www.frontiersin.org/articles/10.3389/fendo.2020.00236/full

THINK ABOUT NORMAL

"NORMAL" = pristine pure product of honorable nature, like banana, or lovely HIBISCUS !
“NORMAL” = pristine pure product of honorable nature, like banana, or lovely HIBISCUS !

Before we begin, please remember that I am not a professorial-level expert on this subject, so what I have to say here is merely my opinion, which I think is worth adding into the discussion of this complicated subject, but which, I must admit, cannot be the last word.

WHAT DOES “NORMAL” MEAN?

In health-related fields, “normal” is not a single number. It is a reference range or reference interval, against which a health professional can compare urine, blood or other test results in order to decide whether they are within “normal limits”.

This dissertation is regarding “normal” and TSH is a good example.
This paper mentions, but does not discuss, Hypothyroidism.

Calculation of a “normal” curve is simple for mathematicians, but complicated for most of us: see Fig. 1:

Figure 1: “NORMAL” is the 95% in the middle.

The statement below is from a statistician’s explanation of “NORMAL”.
I have included it so that readers who are familiar with statistics won’t complain about me.

When we assume a normal distribution, the reference range is obtained by measuring the values in a reference group and subtracting a “standard deviation” on each side of the curve. This leaves the values found in ~ 95% of the test population.
The 95% interval can be estimated by assuming a normal distribution of the measured parameter, in which case it can be defined as the interval limited by 1.96 (often rounded up to 2), standard deviations from either side of the mean (the expected value).”
Be that as it may, in the real world neither the population mean nor the population standard deviation are known.
They both need to be estimated from a sample, of size designated n.
The population standard deviation is estimated by the sample standard deviation and the population mean is estimated by the sample mean (also called mean or arithmetic mean).
To account for these estimations, the 95% prediction interval (95% PI) is calculated as: 95% PI = mean ± t0.975,n−1·√(n+1)/n·sd.”

  THE BOTTOM LINE, re. CALCULATING “NORMAL”

……… If that sounds complicated, don’t look at me: ask your favourite math genius for his/her usual facile explanation!
……… Suffice it that the reference range includes results found in 95% of a reference group from a healthy population.
……… There are also optimal ranges (ranges that we think indicate optimal health) and
……… There are ranges for particular conditions or situations (such as pregnancy reference ranges for hormone levels).
……… My preference is for optimal ranges. I have doubts about the accepted “normal” ranges of quite a few tests.
……… Caveat: the blithe idea that 95% of a “healthy” population will have “normal” levels for all test results is unrealistic unless the term “healthy” is rigorously defined and conscientiously applied. To assume otherwise is contrary to the principle of “a high index of suspicion” and will lead to under-diagnosis.

Therefore:
1] Reference groups should strictly include only candidates between 20 and 25 years of age.
2]
Since our metabolic systems are interdependent and unpredictably variable in one way or another, an individual should be excluded from estimation of “normal” values unless his/her results are normal for all other available tests.
3]
Thus, eligibility for an estimation of normal should be denied if the BMI is high or low, or if there is any physiological, metabolic, psychological*, sociological* or genetic abnormality.
4]
Similarly, if the psychological balance is imperfect the candidate should be excluded from the reference group, because childhood PTSD, anxiety, depression and other psychological difficulties are associated with biochemical abnormalities which can make a surprising difference to blood test results.
* Regardless of racial origin, the highest and lowest echelons of society should be excluded, since both highest and lowest social groups are subject to significant stress.

DON’T CONFUSE “NATURAL” WITH “NORMAL”

NATURAL NORMAL: Many systems change over time and “gurus” have a tendency to modify “normal” according to age.

Consider the accepted “natural normal” of DHEA (in micro-moles / Litre), from LifeLabs in 2010, shown in this table:

“AGE-ADJUSTED NORMALS”, DHEA

Age Female MaleCOMMENT
Newborn4.5-104.5-10Mother gives her baby quite a lot, and baby makes some, too
01-12 Yr< 5.0< 5.0We don’t make much DHEA when we are kids
13-29 Yr< 11< 11Just before puberty, production spikes *
30-39 Yr<7.3<14Females slow output, 1% per year, starting at age 25
40-49 Yr<6.5<14Males usually continue high production through age 45, then lose 1%/Yr
50-59 Yr<5.4<8.4By age 50, the ladies are in real trouble **
60-69 Yr<3.5<7.9By age 65, the men are in the same boat **
70-79 Yr<2.4<4.7At age 70, we are all over the hill
80-99 Yr?? 0.0?? 0.0At age 80, only the brain makes DHEA ***
CLEARLY, THIS SCHEDULE TELLS US SEVERAL THINGS:

[1] Males produce more DHEA than females.
[2] Women begin to reduce production by age 25 and men, in their 40s.
[3] Production is at infant levels or less by 60 and by 80, is close to zero.
[4] The researcher of the DHEA range didn’t know what the lower limits are.
[5] DHEA is important. No-one with a low DHEA should be a candidate for estimation of “Normal”.
[6] Falling production with age is natural, but not normal in terms of best function.

* Possibly, reduction of Melatonin just before puberty triggers the DHEA spike: this is not yet proven.
** Over 15 years, I observed that both genders begin low-DHEA symptoms when DHEA falls below 5.0 µMol/Litre.
*** The brain makes DHEA for its own use and is the only source of this all-important prohormone in lesser animals.
Only the great apes, including us, make DHEA in the adrenals as well as the brain.

Consider “natural normal” for Thyroid hormone (reported in picoMoles/Litre), as a second example:

(1) In 2005 Leonard Wartofsky and Richard A Dickey wrote, (paraphrased)

  • “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.”

(2) In 2007 Martin I. Surks and Joseph G. Hollowell said (paraphrased) as follows ……

  • 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.” *
  • “Without thyroid disease, in the 80+ year-old group 14.5% had TSH greater than 4.5 mIU/liter.”
  • “Frequency distribution curves of the 80+ year-old group showed higher TSH.
  • The 97.5 centiles for the 20–29 and 80+ year-old groups were 3.56 and 7.49 mIU/litre, respectively.
  • 70% of older patients with TSH > 4.5 mIU/liter were within their age-specific reference 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:

(A) 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 their data from the calculations. ****
(B) 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 to me is that a large percentage of their 80+-year-olds were hypothyroid.
(C) “AGE-SPECIFIC NORMAL”, or “NATURAL NORMAL” makes no sense.
“Normal” should be understood to mean the status of healthy humans aged 20-25, because at 25+ years, we all begin reduction of our hormone output and by that token, anyone over 25 is to be, at the least, suspected of hormone deficiency-related metabolic aberration.
(C) Anxiety – related psychology, childhood PTSD, obesity, anorexia, chronic illness, or an abnormal finding for any test should disqualify the candidate for all estimates of “normal”.
(D) If the real normal for TSH is < 2.6 and not < 4.1, a whole lot of people are suffering from unsuspected, chronic, true hypothyroidism.
(E) Even Wartofsky and Dickey’s calculations are suspect: perhaps the opinion of some modern Metabolic Medicine practitioners is correct: maybe the upper limit of normal for TSH should be <1.6.

* This implies that 10.6% of the 20-29-year-olds were hypothyroid. They should have been excluded from the calculation. **
TSH >2.5 (??: some functional medicine practitioners say > 1.5?) indicates hypothyroidism, so this means that more than 14.5% of the 80+ – year olds in Surks and Hollowell’s study were hypothyroid. Including them in the “normal” group means that 15+% of 80-yr-olds didn’t get treatment which they needed!
***
You should apply fair logic to every paper you read, to exclude errors and prejudices like these from your beliefs.
**** Think about it – if I am right, since thyroid hormone 3 controls the efficiency of every cell and system in the body, 10.6% of the thyroid test study population should have been excluded from the calculation of “normal” TSH.

Maybe the parameters for all our other tests are wrong and perhaps a lot of test reports are invalid !

COMMENTS

  • DHEA goes down over time by 1-2 %/year, gradual loss of production.
    – Many other hormones suffer the same fate, including Melatonin, Progesterone, Allopregnanolone, Testosterone and Thyroid.
  • Several hormones can “crash” simultaneously, causing various symptoms of deficiency depending on which hormones are involved. This can happen with Melatonin and DHEA 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.
  • Thyroid hormone goes down as we age and this deserves special attention because everything else depends on it.
  • Precise assessment of “normal” is impossible if we believe that natural age related hormonal change is normal.
  • To give medical investigators their due, a concerted effort is always made to include only fit individuals in the group evaluated. However unknown or ignored factors can lead to a “curve ball” situation, causing an incorrect, or unreliable, “normal” range.
  • Since Intracellular Hypothyroidism is the true cause of hypothyroid symptoms and signs TSH is irrelevant to the diagnosis of Intracellular Hypothyroidism, the above discussion is purely with respect to “normal” and has no bearing on the management of Hypothyroidism per se.

SUMMARY

Aberrations of hormonal production are pervasive and the interdependence of hormonal systems is delicate.
Subjects selected for “reference range’ in the assessment of normal should be between age 20 and 25 years.
CANDIDATES’ PRESENT AND PAST HISTORY, PHYSICAL FINDINGS, SOCIOLOGY AND PSYCHOLOGY SHOULD BE “HEALTHY”.
ALL THEIR OTHER TEST RESULTS SHOULD BE 100% NORMAL.

REFERENCES


(1) 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 .https://pubmed.ncbi.nlm.nih.gov/16148345/

(2) 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, https://doi.org/10.1210/jc.2007-1499 01 Dec. 2007.
https://academic.oup.com/jcem/article/92/12/4575/2596923?login=true


ALSO SEE THE BLOG, “WHAT OUR MEDICAL SYSTEM IGNORES”: SHOULD THYROID HORMONE TESTS BE REVIEWED?
R

New Finasteride Lawsuit: Renewed Attention to Psychiatric, ED Adverse Event Reports

Medscape Medical News

Alicia Ault, September 23, 2021 https://www.medscape.com/viewarticle/959296?spon=15&uac=235227EV&impID=3672148&sso=true&faf=1&src=WNL_mdpls_210928_mscpedit_urol

University of the West Indies ranks in the top 1.5% world wide !!!

UNiVERSITY OF THE WEST INDIES COAT OF ARMS

A classmate just sent me this letter from our Vice-Chancellor:

“It is with humility and a profound sense of pride and gratitude that I am able to share with you the very good news that our university has finally reached the top. This is the finding of the Times Higher Education (THE) World University Rankings.

The 2022 ranking results, officially released on September 2, show that The UWI soared above prior years’ results. This excellent outcome is achieved despite the budgetary challenges associated with the growing fiscal problems of our contributing governments, the financial difficulties of our private sector, and the aggravation caused by the impact of the COVID-19 pandemic.

The ranking result shows that The UWI, from a global field of some 30,000 universities and top class research institutes, now ranks in the top 1.5% of the world’s best. This is an historic achievement and worthy of celebration. We have every reason to join with our global colleagues in marking this Caribbean journey to the top of the university world.

We must celebrate the visionary leadership and contribution of earlier colleagues on whose strong and dependable shoulders we stand today. I offer unlimited respect to you—the inspirational, irrepressible UWI community. We thank our governments especially, who have empowered their UWI through the good and bad times. Thanks to them, we are an excellent global university rooted in the Caribbean.

Despite COVID-19 and related challenges and disasters, the university’s management did not flinch nor did we retreat from our commitment to lead this university through whatever turbulence surrounded us. With your solidarity, we stood up to face the headwinds emanating from multiple quarters; we represented the culture of resilience embedded in our history, and we summoned our collective energy to propel us to this coveted place.

Congratulations UWI! We are at 1.5 and we are very much alive! Let us be even more focused and resolute as we enter this new academic year.

I take this opportunity to give thanks for the grace we have experienced while offering condolences and solidarity with each and every one of you who suffered loss and is experiencing illness.

This year we have declared to be the onset of the ‘Revenue Revolution’ in which we convert our top ranking global reputation into sustainable revenue. This is our core project for the foreseeable future. We will achieve this target. Yes we will.

Blessings!

Professor Sir Hilary Beckles: Vice-Chancellor

Hormone therapy does not cause dementia

https://medicalxpress.com/news/2021-09-menopausal-hormone-therapy-linked-dementia.html

I am publishing this link because the headline sounds interesting and will pique your interest, but in fact the article as written is only in regard to “Menopausal hormone therapy” and nothing to do with the multi-hormonal support provided by Bioidentical HRT as you and I know it.

With a headline reading “Menopausal hormone therapy not linked to increased risk of developing dementia”, the British Medical Journal avers that treatment with “estrogen and progestagen” does not cause dementia. However since it goes on to explain their view that “The primary indication for hormone therapy continues to be the treatment of vasomotor symptoms, and the current study should provide reassurance for women and their providers when treatment is prescribed for that reason”, ** it is evident that the body of the article has no bearing on detailed hormone balancing programs, in which all deficient systems are supported.

It is clear that the writer is not familiar with the reasons for HRT, that “Menopausal hormone therapy” is quite different from Bioidentical HRT and that the other ruminations in the article, particularly with respect to Alzheimer’s disease, are not robust. So while the conclusions drawn may be correct for a patient population receiving “Menopausal hormone therapy”, said conclusions should not be applied to persons treated correctly in a full, complete and closely supervised BIHRT program.

** Vasomotor symptoms do provide a trigger which indicates that the time has come to examine the hormonal balance and initiate BIHRT. However the object of BIHRT, as you will agree, is not just to stop the symptoms, but to prevent the complications, of menopause: the list includes osteoporosis with “fragility fractures”, weight gain (therefore diabetes, hypertension, etc.), psychological disturbance including anxiety, irritablilty and depression, hair loss, skin changes, insomnia, functional hypothyroidism and and the rest of the downside of menopause. The vasomotor symptoms do go away with treatment, which is the patient’s primary concern, but ** the HRT professional does not treat complaints. A BIHRT Rx is written to ensure health, preserve life and maintain lifestyle. It is not solely “treatment” for the symptoms of menopause.

WHAT YOU CAN DO TO PREVENT ALZHEIMER’S DISEASE

Don’t wait until you develop Alzheimer’s disease – prevent it!

On June 7th, 2021, the American Food and Drug Administration (FDA) “conditionally” approved Aducanumab (Aduhelm), an amyloid beta-directed monoclonal antibody which treats Alzheimer’s disease by removing BetaAmyloid from the brain.
Aducanumab is the first new Alzheimer’s drug since 2003, and the first potentially disease-modifying agent.
Aducanumab treatment costs US $65,000 per year.

The approval is surprising, because:
(1) Of (only) two trials, one showed no benefit from the drug.
(2) One third of drug recipients developed brain swelling and other side effects.
(3) Only 9% of patients’ Alzheimer’s improved.
(4) The drug does not produce a cure, because it only removes Amyloid present in the brain – it does not prevent the accumulation of more amyloid.
(5) Several previous Amyloid-removing drugs had no beneficial effect on Alzheimers patients.

SO MAYBE THE BEST SUGGESTION IS, LOOK AFTER YOURSELF.
Don’t wait for a diagnosis of Alzheimer’s disease, because by the time it’s diagnosed, half of your brain power is gone and cannot be rebuilt.
Instead, rdo your best to prevent Alzheimer’s by attention to and maintenance of your Hormone, Mineral and Vitamin balance.

The point here is that while we do not have scientific proof that optimal hormone balance can prevent Alzheimer’s, balancing does no harm, provides many other benefits and should be done anyway.

YOU CAN DO A LOT TO PREVENT ALZHEIMER’S DISEASE

In managing aging generally and to prevent Alzheimer’s in particular, try to ensure that the hormonal milieu in which your body functions is optimal for cell maintenance and efficiency.
If your hormones are unbalanced, the nutrients you take will not work as well.
So:
(1) Balance your neurosteroid hormones, DHEA, Testosterone, Oestradiol and Progesterone, to provide a “level base” for all your cells AND to support your brain’s supply of Allopregnanolone, for its nightly cleanup.
(2) Balance the thyroid hormones, to guarantee a good supply of T3 hormone, which is necessary for the efficient function of every cell.
(3) AVOID foods containing High Fructose Corn Syrup; see “Drop Acid“, by Dr David Perlmutter and take his advice regarding diet as far as you can.
(4) But ! Don’t expect your diet to supply your body with the vitamins, amino acids and minerals which it needs to run itself as it should.
(5) Check my recommendations, below and read the book which they are based on, ‘the end of Alzheimer’s“, by Dr. Dale Bredesen, .

REGARDING DIETARY SUPPLEMENTS
The list is from “The end of Alzheimer’s”, by Bredesen, modified by me.
Items marked with * are important: those marked ** are advised for everyone.

ESSENTIAL VITAMINS, AMINO ACIDS AND MINERALS:
Acetyl L-Carnitine**, 500 mg …….. works with CoQ10, maintains mitochondria, heart, muscles, brain and nerves.
Chromium Picolinate*, 25 µg ……… if your diet includes cruciferous vegetables, you probably don’t need chromium.
Citicholine*, 250 mg twice daily ….. Helps the brain, assists the adrenals. Do not take if you have PCOS or diabetes.
Co Q10**, or Ubiquinol, 200 mg …. Supports mitochondria. Destroyed by statins. If you are taking statins, you must take Co Q10.
Magnesium Threonate **, 200–400 mg, the best Magnesium salt, for brain care and all muscle, including heart and bowel, not just skeletal, muscles. Melatonin**, 1–10 mg, available as drops, tablets. Sublingual is probably best.. ..Melatonin, our second best antioxidant, has recently been attacked: look it up !
Methyl Tetrahydrofolate (MTHF, Vit. B9, not “Folic acid”)** 1–5 mg. Start w.1mg.
NAC (N-acetylcysteine), 600–1800 mg**. It boosts glutathione, the most important antioxidant. Nicotinamide riboside (Vit. B3)**, 100 mg ….. Anti-inflammatory. It helps heart and kidneys. Omega-3*, 1 g ….. A healthy diet includes sufficient omega-3, but for “brain building”, take 2 g.
Pyrroloquinoline quinone, (“PQQ”) 20 mg** supports mitochondria & cognition.
Resveratrol**, 100 mg: Resveratrol has been credited with life extension. Drinking red wine does not provide sufficient resveratrol.
Selenium, 200 – 400 µg, (2 Brazil nuts) for thyroid function and to prevent autoimmune disease.
Trimethyl glycine (betaine)*, 500 mg, 2x/day, produces SAMe. Anti-inflammatory, anti-homocysteine.
Zinc**, 40 mg: do not add copper, unless instructed to do so by your Healthcare provider.

VITAMINS:
Some combination of the following (most of these are present in a normal diet, so if you are healthy and eat well, there is no need to adhere closely to the dosages noted below).

Vitamin B complex: take a VBCo pill once or twice daily. Vitamin B preparations, made by many different manufacturers, are more or less equal: pick one based on how closely its ingredients match the list below:
Vitamin B1* (Thiamine), 50 mg……
Vitamin B2*(Riboflavin ):…… from food: supplementation not usually necessary.
Vitamin B5 (Pantothenic acid)* 100 mg ; from food – supplementation not usually necessary.
Vitamin B6*: P5P (Pyridoxal 5 Phosphate), 2 mg ……. too much B6 is toxic.
Vitamin B9, MethylTetraHydroFolate, MTHF: essential brain antioxidant.
Vitamin B12: Normal blood level =138-652. Optimal = >650…….Rx methylcobalamin, or Adenosyl Cobalamin 1 mg. Most of us don’t need it.
Vitamin C**, 2–3 g (Linus Pauling used to recommend 9 g per day).
Vitamin D3**, 3000+ iu: ask for a test – take enough to produce a blood level of 100-200 nmol/L.
Vitamin E, Max. 800 units: too much Vit. E slows blood clotting.
Vitamin K2**, 100 mg: from “leafy greens”. It works against blood thinners.

BOTANICALS (discuss with your Naturopath, Herbalist or health food person): Curcumin, 500 mg daily. Ashwaghanda, 500 mg twice daily (calming, reduces amyloid). Bacopa Monieri, 250 mg, twice daily (improves cholinergic neurotransmitter systems).
Gotu kola, 500 mg twice daily (improves alertness).
Lion’s mane, 500 mg (increases nerve growth factor).
Rhodiola, 200 mg (antianxiety).
Shankhpushpi (“skullcap”), 2 caps (enhances branching of neurons).
Guggul, 300 mg with meals (absorbs toxins in the bowel).
Black cumin:? Dosage (antiallergic, immune booster, antioxidant, ? Bactericidal for H. pylori).

THIS LIST IS HUGE.
Maybe you only need a small selection.
Discuss it with a Functional Medicine MD, Naturopath or Herbalist.
Ask your pharmacist or health food store for products with combinations of nutrients.

ADDENDUM, regarding MTHF:
MethylTetraHydroFolate, MTHF, is too complicated for me to attempt to explain in detail, so let’s put it this way:
Basically MTHF, or Vitamin B9, is present in many foods, so only a few people need to take it.
Working with Vitamin B12, it is essential for making several very important amino acids and proteins, but particularly, MTHF is used to make Methionine, which is very important in our metabolism and which is destroyed by inflammation and oxidation.
As Methionine is used up it is converted to Homocysteine, so we can see who needs MTHF by testing the blood for Homocysteine.
If Homocysteine is high, we know that the person needs extra MTHF, to recycle their homocysteine back to methionine (using an enzyme called methionine synthase ). ***

We can’t live without MTHF, but a small percentage of us are genetically unable to process large amounts: my suggestion is that we should routinely take 1mg daily and increase our dose if a Homocysteine test shows that we need more.

*** From Wikipedia:
“Levomefolic acid is generated by methylenetetrahydrofolate reductase (MTHFR) from 5,10-methylenetetrahydrofolate (MTHF) and used to recycle homocysteine back to methionine by methionine synthase (MS)”

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