A Presentation at the 3rd Annual Conference of the American Academy of Anti-Aging Medicine Las Vegas, December, 1995.

For inclusion in Advances in Anti-Aging Medicine, Volume 2

October, 1996.

 A Nutritional-Metabolic Approach to Memory-Loss: 18 Years' Experience

John V Dommisse, MD, FRCP(C)

Nutritional, Metabolic, and Psychiatric Medicine, LLC

Cambric Corporate Center

1840 E River Rd, Ste 210

Tucson, AZ 85718-5892

Phone 520-577-1940 Fax -1743






Medicine, neurology and psychiatry have apparently 'forgotten' about the nutritional and thyroid/ hormonal deficiency-states that used to be well-known as causes of dementia. Despite thousands of articles in the 'mainline' medical, neurologic and psychiatric literature chronicling these potentially-reversible causes of dementia, they are not heeded by most physicians, presumably at-least-partly because they are not taught nearly-enough about deficiency-states in medical school and residency-training programs.

Part of the problem is that the laboratory-threshold for diagnosing these deficiency-states - at least in the US - is way too high, leaving patients with early manifestations of these deficiencies untreated until the memory-loss caused by the deficiencies is too far-advanced to be reversed, even if it could have been reversed at an earlier stage.

A psychiatrist who diagnosed early or so-called 'subclinical' deficiencies of vitamin-B12 and other B-vitamins, T4 and T3 thyroid hormones, various minerals, and conditions of copper-excess (caused by copper plumbing), by means of the best blood-tests available, found that none of his ongoing elderly patients developed the dreaded so-called 'Alzheimer's dementia', unless they already had it in too-advanced a stage when they first came to his attention, over an 18-year period in private practice.

By detecting 'occult'/ 'subclinical' deficiencies and maintaining optimal blood-levels of these vitamins, minerals and hormones, physicians could potentially help anyone prevent 'Alzheimer's dementia'.

[Key words: Nutritional and hormonal deficiencies; blood-analysis; reversible memory-loss; prevention of 'Alzheimer's dementia'. (90 references).]



What is Nutritional, Metabolic, & Psychiatric Medicine?


Nutritional, metabolic and psychiatric medicine is based on the rather obvious idea (to everyone except, it seems, some MD's!) that nutrition is the basis of medicine, and that metabolism can be harnessed or naturally enhanced in the service of better health for many people.

In diagnosing nutritional or nutrient deficiencies or excesses, and in determining the metabolic status of any particular individual patient, their actual blood-levels of certain essential vitamins, minerals, hormones or amino-acids can be obtained from a clinical laboratory 75,18 . These blood-tests are not usually requested, in the standard medical practice (although they are applied from standard mainstream journal articles), but can be accurately and reliably done, in several reference-labs around the nation, and reported electronically in one's office, immediately after a result or report is obtained. The blood-levels that the author does cost about $300-450 but that is a lot less than many investigatory tests that reveal abnormalities much less often.

[Hair-analysis has also been used but this method has several disadvantages, compared to good blood-analysis 38 : (1) This method can only detect inorganic matter (the minerals and heavy metals) and not any of the other (organic) elements mentioned above (the vitamins, hormones and amino-acids) since they are destroyed beyond recognition by the burning-to-ash process of the hair-analysis method; (2) Even in the case of the minerals and metals, there can be inaccurate results because the test will read also the quantity of minerals and metals deposited on or in the hair by processes other than bodily chemical processes - e.g., from shampoo or other external contamination of the hair by various chemicals, including mineral and metalic chemicals; (3) Blood-analysis is also much more credible to the medical profession as that is the 'normal' way in which body-constituents are measured; and, finally, (4) In addition, blood-analysis tends, by and large, to measure the current status of the person's chemistry, as opposed to what chemicals entered the hair-follicle, at the base of the hair, from the blood, some weeks or months previously.]

Once the blood-report (in the form of a serum, plasma, whole-blood or red-blood-cell level) is obtained from the lab, further analysis may be required as to the desirability of the 'normal' or 'reference' range of the reported substance. e.g., In the case of vitamin-B12, the 'normal range' in the serum at all US labs is based entirely on the condition of pernicious anemia, an extreme degree of vitamin-B12 deficiency; it is not based on the level necessary to prevent many conditions, including about one-half the cases of so-called 'Alzheimer's' dementia 83 . Many journal-articles, in the 'mainline' medical and psychiatric literature, have shown that serum-levels of 550 pg/ml or more are necessary to guarantee that there won't be a deficiency of B12 in the cerebrospinal fluid and the brain 43,52,57,60,84 . Japanese medical and neuropsychiatric journals take this information into account when deciding on their 'normal range' for vitamin-B12, and regard 500-1300 pg/ml as a better range 43,57 than the ones used in the average US lab: 200-1100! [Which range would you prefer your physician to use?]

After the patient's nutritional and metabolic/ hormonal status is thus calculated, all that remains is for the deficient substance to be prescribed, by the best route of administration, in the best amounts, for the best period of time (often indefinitely or permanently). Further blood-tests are then obtained, 6 to 8 weeks later, of the levels that were abnormal at first testing, to make sure that the abnormality has been adequately - but not excessively - corrected. The clinical results in the patients who have undergone this process have been most gratifying, even in cases regarded as chronic, intractable, refractory or treatment-resistant, such as early 'Alzheimer's' dementia 18 , secondary impotence and low sex-drive 2,3,88 , or tardive dyskinesia 20,49 .


Brief Overview:

Optimizing Nutrient and Thyroid/ Hormonal Blood-Levels

Greatly-Enhances Standard Mental and Physical Treatments


There are thousands of articles, in prestigious 'mainstream' medical and psychiatric journals, documenting the enormous benefits of correcting deficient or excessive blood-levels of certain vitamins, minerals and thyroid hormones. The mental benefits include the reversal of early Alzheimer's dementia (see below). The physical conditions that can benefit from this approach, and thus decrease the effects of aging, include: Chronic fatigue and pain syndromes; secondary impotence and declining sex-drive; hypothyroidism; nutritional anemias; high blood-pressure and cholesterol levels; etc..

So the obvious question must be: "Well, why don't most physicians who deal with these conditions utilize this safe and health-giving technique?" The answer must lie in the fact that the vast majority of US medical schools provide extremely limited instruction in nutritional medicine in the curricula for the MD-degree, and for postgraduate training in family practice and the specialties that impact these conditions. Then the more-basic question is: "Why do medical schools not include nutritional medicine in their curricula?" Several articles and books (including the book Racketeering in Medicine by James P Carter, MD, DrPH 12 ) have suggested that this is because the university medical-teaching centers are much too strongly influenced by the pharmaceutical companies, which handsomely sponsor research and teaching about the actions and benefits of drugs in treating disease, but neither they nor any other companies have any motivation or interest in sponsoring research and teaching of the benefits of natural substances: Natural substances cannot be patented, so, even if such benefits were demonstrated, no company would be able to benefit much by an opportunity to market and sell such a product.

Brain- and nerve-cells are dependent on an optimal intake of proteins/ amino-acids, vitamins and minerals, and on optimal blood-levels of both of the thyroid hormones, in the same way as all the other cells in the body do 89 ; their optimal function cannot occur without these substances providing the cell-structure, energy and chemical or enzymatic reactions that are essential for such function. Only brief examples can be given here.

(1) It has now been recognized, at least since the 70's, that the brain's neurotransmitters (chemical 'messengers' called serotonin, dopamine, noradrenaline, acetylcholine, GABA, endorphins, etc.) are crucial in several conditions, including memory-functions 31 . These neurotransmitters are formed from amino-acids, catalysed by other food-substances in our diets: numerous vitamins, minerals, thyroid and other hormones 89 . So, when dealing with these disturbances in brain-function, it seems appropriate to have the blood-levels of these crucial substances tested at a reputable clinical laboratory, and to optimally-correct any deficiencies and imbalances that are thus revealed. When it is discovered how often, in these conditions, these blood-levels are deficient or out of balance with each other, it becomes even more puzzling as to, not only why these levels are not obtained much more frequently, but why such measurements are actually even excluded from most of the 'practice-guidelines' and protocols on which modern health-insurance companies base their payment-or-denial decisions with regard to reimbursement for various medical and psychiatric services and practices. This is a strong disincentive for physicians to order these tests, unless they are independent of any managed-care companies.

(2) Another example is in the matter of vitamin-B12 deficiency and brain-energy, mood, memory, oversuspiciousness (paranoid thinking) and emotional/ behavioral control. There are literally hundreds of articles documenting, not only that clear and severe blood-deficiencies of this crucial brain-vitamin can cause potentially-reversible dementia and depression-with-pseudodementia 13,36, 67,73,87 , but also that so-called 'low-normal' blood-levels can cause these conditions 4,11,32,43,47,52,57, 60,79,83,84 . This fact begs the question: "Then why are these levels considered low-normal?" (Because psychiatric conditions are not real conditions but 'only in the mind'?). Therefore the people who rapidly develop severe deficiencies of this vitamin are the lucky ones because their deficiency will be detected by standard blood-testing. The ones who develop it slowly will gradually slide into dementia, they will be called "Alzheimer's" cases - and by that time the condition will be irreversible!

(3) A final example, which highlights the disadvantages of some of the frugal cost-cutting that is occurring in modern US medicine, has to do with the blood-tests that are done to detect underactive thyroid hormone function in the blood, very important for maintaining memory and other cognitive functions, among its numerous other requirements in physical and mental function. Both thyroxine (T4) and triiodothyronine/ liothyronine (T3) are secreted by the thyroid gland 9 . They are manufactured in the gland from the amino-acid L-Tyrosine and varying combinations of iodine atoms. T4 is further, normally, converted to T3, in the liver, brain and various other 'peripheral' areas in the body. T3 is 9 times more active than T4; in fact, T4 is sometimes regarded only as a pre- or pro-hormone. When the blood-levels of these 2 hormones are deficient, the pituitary gland, which sits in the middle of the skull, is supposed to secrete greater amounts than normal of Thyroptropin, the Thyroid-Stimulating Hormone (TSH). TSH can be measured by 3 different tests, of varying sensitivity and corresponding cost. TSH, in turn, is controlled by the Thyrotropin-Releasing Hormone (TRH), which is secreted by the hypothalamus. The hypothalamus, in turn, is controlled to some extent by the cerebrum and the limbic system (the thinking and emotional parts of the brain, respectively) and by general bodily health. For example, depression and acute cardiac or pulmonary illness are thought to diminish TRH-secretion, which then has the effect of reducing the circulating blood-levels of both TSH and the 2 thyroid hormones, T4 and T3, but especially of T3 (partly because TSH is also involved in the T4-to-T3 conversion process, by activating 5'deiodinase, the enzyme catalyzing it). In the case of the acute illnesses, this is thought to have a life-protective function, by temporarily reducing the body's metabolism; but in depression and numerous chronic diseases, like chronic fatigue syndrome, and in low-caloric dieting (semi-starvation), which cause the same low-metabolism effect, this mechanism is actually counter-productive. It is logical in such cases to supplement with T3 (Cytomel, Armour Thyroid) as well as T4 (Levoxyl, Synthroid) 23,24,34 .

Psychiatrists seem to be the main physicians paying any attention to the latter half of this equation, partly because they are the ones left to deal with the consequences of the 'incurable' depressions, chronic fatigue and other conditions resulting from this non-thyroidal state (meaning that it does not originate in the thyroid gland - not that it does not depress thyroid hormone levels, especially T3). Since it is not caused by an abnormality within the thyroid gland itself, thyroidologists, endocrinologists and internists tend to wash their hands of responsibility for it, and psychiatrists are forced to come up with rationales like 'enhancing antidepressant medication's efficacy' to justify the prescribing of thyroid hormones 15,16,45,46 .

One more fact should be stated: In measuring the blood-levels of T4 and T3, one has 2 choices; one can measure the total T4 and T3 levels (including that large percentage of them which is attached/ bound to serum proteins), or one can measure the free or unbound fractions only, which are the only portion of these hormones that are functionally active as thyroid hormones. There is also a measure of T3 function that is even cruder than the total T3 level and that is the so-called T3 resin-uptake test. The total and uptake tests are relatively quite a lot cheaper than the free- or unbound-level tests.

Given all these facts, together with the fact that all the above mental and physical conditions can be caused, aggravated or rendered incurable by deficiencies or imbalances in the thyroid-pituitary-hypothalamic axis, which facts I don't believe are in dispute in any thyroidology, endocrinology or internal-medical circles, it is hard to believe - but nevertheless true - that often the only test done to screen for thyroid dysfunction is the total T4 test! Sometimes a T3-uptake test will also be done; and sometimes a TSH level (of varying degrees of sensitivity) will be done, with or without the benefit (such as it is) of the total T4 and T3 uptake tests as well. Very-occasionally, a free-T4 and total T3 level will be done but usually not as an initial screening test but only after initial tests have given a suspicion of thyroid malfunction. However, the free T3 level, the only accurate measure of the much-more-active of the 2 thyroid hormones, is hardly ever done, and then only at an advanced stage of investigations for a serious thyroid condition. And it is hardly ever done in monitoring thyroid treatment, even in the rare cases where T3-containing preparations are used! No wonder physicians have become afraid of T3-containing thyroid hormone treatments: The T3-level could go dangerously high, e.g. in a person who converts T4 perfectly-adequately to T3, even killing him. I believe this factor (inappropriate non-measurment of the T3 hormone), and not any possible 'instability' of Euthroid, Armour Thyroid and other T4/T3-combination preparations, is the real underlying reason why these T3-containing preparations have been removed from the market at various times.

The rationale for all this 'penny-wise, pound-foolish' thyroid-medical cost-cutting is that the few tens of dollars more that it would cost to do all 3 crucial tests, right from the start of any screening for thyroid hormone imbalances, is not warranted. Given that these accurate and sensitive tests are normally only done after the initial inaccurate tests have shown a deficiency, excess or imbalance, numerous patients, who have developed one or more of the above serious conditions, which are only completely-reversible in the relatively-early phases of thyroid-imbalance, are diagnosed only some years later!

Let us now examine in more detail the dementing effects of the nutrient and hormone deficiencies and imbalances mentioned above.



The Nutrient and Thyroid/ Hormonal Deficiencies and Imbalances

that are Known to Cause Dementia




1. Cobalamin (Vitamin-B12)

Traditionally, vitamin-B12 deficiency has been thought of almost entirely in terms of a severe form of macrocytic anemia, namely pernicious anemia (PA). However, in the past 90 years or so, there have been an increasing number of papers, in the mainstream, reputable medical, neurological, and psychiatric literature, showing that B12 deficiency can occur in the nervous system (brain, spinal cord and peripheral nerves) without any anemia, macrocytosis or other hematological signs 11,25,27,32, 50,52,53,57,60,79 . The main effects of the deficiency on the nervous system include dementia 90 .

In the past 11 years, papers have appeared showing that sometimes the cerebral effects can occur without the spinal and peripheral neurological effects either 27,47,76,83,84. Some of these papers have also shown that the cerebral effects can occur with a so-called 'normal' serum B12 level 11,47,52 with the CSF-B12 level being suppressed below its normal range 33,57,60,84 . The highest serum levels that have been associated with deficient CSF levels and psychiatric syndromes have included those up to 550 pg/ml 84.

Since it is impractical and excessively-invasive to do CSF levels on most patients, the author decided to forgo CSF-level determinations as a routine investigation and to simply cover all chances of this deficiency by treating all the serum levels that have been associated with CSF deficiencies and psychiatric syndromes 22 . In order to 'play it safe', he has adopted 600 pg/ml as the lower limit of normal for his patients (even this level is insufficient in alcoholics and others with liver-damage, in which the B12 molecule cannot be adequately methylated to make it biologically active, esp. for its brain functions 83 ), and he starts them off with one intramuscular injection of 1mg (1000mcg) of vitamin-B12 for every 50 pg/ml that their level is below 600 pg/ml, given every 2-7 days. Then he maintains their level between 1000 and 3000 pg/ml with the high-dose oral (Swedish) method of treatment 5,6,42,51 for the rest of their lives. The only patients who cannot build up ideal serum levels on this treatment are those with Crohn's Disease (regional ileitis) or those who have had a resection of the terminal 12 inches of the ileum, the only area where B12 is absorbed 17 .

Smith had already warned, more than 35 years ago, that the dosages for the treatment of the neuropsychiatric manifestations of this deficiency had to be maintained at higher levels than the treatment for the hematological manifestations did 73 . And Whitehead and Chohan showed that the higher-intensity treatment had to be maintained for longer periods of time as well 87 . Since there does not appear to be any upper limit of non-toxicity 59 , there is no 'down side' to this practice, except the (low) economic cost, which almost all recipients agree is worth it.

The psychiatric conditions that are now accepted as resulting from this deficiency include about one-third of cases of dementia 13,32,47,52,76,84 . 'Atypical' B12 deficiency, a condition that is not clearly due to a lack of intrinsic factor 11,25 and which appears to affect humans neurologically and psychiatrically rather than hematologically 52 , is being reported more and more frequently in the past 10 years or so 21,22 . It poses a much greater danger to humans nowadays than does pernicious anemia, which is usually well diagnosed and treated.

Another tradition of B12 diagnosis, the standard Schilling's test, has fallen into disrepute in knowledgeable circles as it only measures free-B12 absorption, not protein-bound B12, which is the naturally-occurring form of the vitamin in the diet 11,25 .

Other tests for B12 deficiency have been proposed in the past 10 years or so, such as the serum and urinary methylmalonic acid test, the serum homocysteine, the deoxy-uridine suppression test, etc., but they are not specific for B12 and are not sensitive enough to always pick up atypical or brain B12 deficiency, so the author sticks to the sensitive interpretation of the serum level (not accepting any level under 600 pg/ml as normal, and no level under 1000 pg/ml as optimal). The transcobalamin-II saturation with B12 (holotranscobalamin) test appears to be promising, as it could detect one of the causes of deficient CSF B12 when serum B12 is normal, but it is not freely available or affordable, as far as I have been able to ascertain.


2. Folic Acid

Folic acid is required in certain vital enzyme-reactions that occur in the brain, in the formation of the neurotransmitters 7,8,56 . Although folic acid and vitamin-B12 are well-known as a collaborative team in the prevention of megaloblastic anemia 19 , folic acid's role in the prevention of neuropathy, spinal cord damage and cerebral effects such as dementia, is less well known. Until fairly recently it was felt that all the neuropsychiatric effects of whatever caused megaloblastic anemia were due to the B12-deficiency component of that syndrome. That is now known not to be the case and that folic acid has certain unique functions in the central nervous system. Senile dementia of the Alheimer type (SDAT) is also sometimes caused by folic acid deficiency 26,48,72,74,78 and I have seen 2 such cases in my practice. The response to the treatment in this case is much slower, because of the chronic nature of the changes which have caused the dementia.


3, and 4. Thiamine (Vitamin-B1), and Niacin/ Nicotinic Acid (Vitamin-B3)

Since even 'junk-food' cereals are now supplemented with these 2 vitamins, at least, deficiencies of them are restricted to the most severe alcoholics 41 , and individuals on very restricted nutrition, for whatever reason 70 . The acute organic-psychotic manifestation of B1 (thiamin) deficiency is known as Wernicke's encephalopathy, and the chronic one Korsakov's (organic) psychosis. Therefore, it is recommended that chronic alcoholics be given supplements of these vitamins, especially B1; and fortification of alcoholic beverages has also been advocated.

Niacin (B3) deficiency classically causes pellagra, a serious and often-fatal disease which affects the skin and gastrointestinal tract as well as the brain (dementia, psychosis and depression). Since tryptophan is the precursor of this vitamin, areas where poor people subsist heavily on corn, which is totally lacking in this essential amino-acid, used to be very susceptible to the psychosis from this condition. Prior to the discovery of the cause of this psychosis, half the psychiatric hospital beds in the South were said to be filled with the victims of pellagra. Nowadays, pellagra tends to occur only in severe alcoholics on a very poor diet.


5. alpha-Tocopherol (Vitamin E)

All I had wanted to say about this vitamin, which has even become a craze in mainline medicine because of its lipolytic and vascular effects, was that it would obviously help to prevent those aspects of ageing and memory-loss that are caused by arteriosclerosis. Then I came across a brand-new paper suggesting also a direct role for vitamin E in preventing aging 65 .





1. Iron

Pollitt and Leibel 63 co-edited a monograph on brain biochemistry and behavior in iron-deficiency. They showed its negative effect in dopamine-receptor dysfunction, catecholamine metabolism and other brain-functions - even without anemia being present. Three years later, Pollitt and others 64 reported, in a letter published in The Lancet, on the findings of a United Nations nutrition group at a major nutrition conference held in Bali in 1984, that body iron status among school-age children correlated positively with educational achievement and problem-solving ability. There is no reason to believe that older people, esp. the very old, would be any less affected by iron deficiency, and good reason to believe they would be affected more, although this condition is not common in older people, except after acute or chronic blood-loss or cancer.

A 1986 editorial in the British Medical Journal entitled 'Happiness is: iron' 1 said that there is now substantial evidence that iron deficiency, due to a specific effect of the deficiency itself on the brain-chemistry and not due to the non-specific effect on the brain of the decreased oxygen-carrying capacity of the blood, has an adverse effect on brain function. It pointed to several studies that showed that in rats iron deficiency causes abnormal serotonin metabolism and learning; and that in children it causes lack of responsiveness to the environment, poor recall (author's accentuation) and performance, and increased unhappiness, tension and fearfulness.


2, and 3. Zinc and Copper

Excess copper has been known to cause brain injury, including dementia, according to Sandstead 71 and Nolan 61 . Hypercupremia can be treated with zinc, which has a competitive relationship with copper, forcing its level down 62 . And, since the excess is usually caused by copper plumbing 71,62 , getting patients to use only distilled or copper-filtered water for their cooking and their drinking of water and beverages usually takes care of this problem. Hansen et al have documented the depression and neurological dysfunctions associated with copper and zinc deficiencies, including dementia 40 ; and Burnet 10 , Constantinidis 14 , Hambidge 39 and VanTiggelen 83 have all, independently, shown evidence of a role for zinc deficiency in the pathogenesis of Alzheimer's dementia. So why are these blood-levels hardly ever obtained in the investigation for reversible causes of dementia? Especially in alcoholics 83 and patients on diuretic therapy 68 , in whom this deficiency occurs quite often.


4. Electrolytes (Sodium, Potassium, Calcium, Magnesium and Phosphate)

In an excellent review of this area of nutritional medicine, Webb and Gehi 85 document the organic mental disorders that can be caused by low serum sodium, potassium and magnesium, and by high serum calcium levels; and the organic mental disorder caused by high serum sodium and by low serum calcium and phosphate levels. These abnormalities can result from excessive or deficient water-intake, vomiting, diarrhea, malabsorption, diuretic-use, alcoholism, diabetes and other metabolic and other medical causes. These effects are usually dramatically reversed by appropriate correction of the imbalance, preferably intravenously in acute and severe cases, orally in chronic and less severe cases.

John Taylor described a case of a 74-year-old woman who was confused, depressed and suspicious due to a relatively minor degree of hyponatremia, who improved rapidly when the electrolyte-imbalance was corrected 80 . And Traviesa suggests that magnesium deficiency may be the cause of thiamine (vitamin-B1) refractoriness in Wernicke-Korsakoff encephalopathy 41 , a cause of dementia, even in non-alcoholics 70 .


5. Aluminum

A book suggesting that the association of high levels of aluminum in the autopsied brains of Alzheimer's disease victims indicates a causative relationship has recently been published 86 , also advising people to eliminate aluminum from their kitchens and beverage and food containers. Weiner cites a British study showing that people in areas with aluminum-richer water were 50% more likely to develop Alzheimer's dementia. However, current scientific consensus is that the higher aluminum levels are a result of the Alzheimer's pathological process rather than the cause, much like calcium is deposited in old tuberculous lesions.








Several papers in the past 10 years or so have pointed to a deficit of T3 thyroid hormone in depressed patients, T4-treated patients, and patients on semi-starvation diets, and to a greater effect of T3 (or a T4/T3 combination), as opposed to T4-only, in relieving both depression and hypothyroidism 15,16,34,45,46 .

The successful T3-augmentation of T4-replaced antidepressant-resistant patients has surprised many authors because they still labored under the belief that T4-replaced hypothyroid patients are always adequately treated.

All the latest authoritative texts on the thyroid gland and the treatment of its underactivity 9,35,44,82 point to the great importance of T3 thyroid hormone, and to its 9-times-greater activity, compared to the T4 hormone, which they consider virtually merely a pro-hormone or pre-hormone. But then, when it comes to treatment, they all recommend the sole use of T4 in almost all cases! There are some (both theoretical and practical) reasons for this, at least in the past, but I suggest that, nowadays, with the ready availabilty of the very accurate free-T3 bloodlevel, these arguments no longer hold water. They mainly center around the greater stability of the thyroxine (T4), in comparison to triiodothyronine (T3), which has wider diurnal and post-dose fluctuations. Twice-daily and after-meal dosing of all preparations containing T3 goes a long way toward removing this objection, and the regular measurement of the free-T3 level takes care of most of the remaining objections 23,24 .

It is assumed that, except in the 'euthyroid sick syndrome' and certain special situations, such as lithium therapy 77 , T4 converts peripherally to T3 in fairly standard amounts and at fairly standard rates. It only takes the consistent measuring of both free-T3 and free-T4 bloodlevels, in all one's hypothyroid patients, every time, to very rapidly dispell this myth 23 . If one believes that, except in severe acute illness, both the T3 and T4 hormones need to be in their mid- to high-normal ranges, one soon discovers that, while a certain minority percentage of hypothyroid patients do convert enough T4 to T3 at a sufficient rate for T4 treatment to be adequate as a source of T3, a substantial majority of such patients require some combination of both exogenous T3 and T4.

The other big double-myth is that (a) an elevated ultrasensitive-TSH level is always required before a diagnosis of hypothyroidism can be made; and that (b) its nearly-complete suppression always means that excessive treatment is in place. There seem to be subtle failures of TSH response to low thyroid hormone levels that cannot be explained purely by the usual forms of hypopituitarism (with secondary hypothyroidism), or by the euthyroid sick syndrome. Whether we are dealing here with tertiary (hypothalamic) hypothyroidism or with a TSH-specific hypopituitarism or whatever, I suggest that more reliance be placed on the absolute free-T3 and free-T4 levels in both diagnosing and monitoring hypothyroidism.

And the T4 (or total T4), T3-uptake, FTI, 'T7', total T3, and T3-by-RIA tests should be abandoned because they are too unreliable as gauges of thyroid function 9,35,44,82 . I have observed hundreds of patients whose thyroid status was previously regarded as normal, based on these tests (and sometimes even with a normal TSH level), who are very grateful for the treatment they started receiving when the free-T3, free-T4 and ultrasensitive TSH levels were done exclusively, then sensitively interpreted and responded to.

Using this approach, one does not need to resort to the use of tricks like T3- or T4-augmentation of antidepressants, or argue about which is the better of the two 46 . One merely needs to test sensitively for the presence or absence of grade-1, -2 or -3 28,37 , primary, secondary or tertiary hypothyroidism 9 and treat it if it exists, whether the patient is depressed or whether the patient has other effects of hypothyroidism, like chronic fatigue, memory-loss, constipation, very dry skin, hair-loss, impotence 3,88 , unexplained weight-gain, dementia, paranoid psychosis 54,66 , or whatever - always ensuring that a 'balance' of free-T4 and -T3 is achieved, when possible (ie, when there is no acute 'euthyroid sick' situation) 23 .





One of the latest ways of postponing 'old age', and menopause/ andropause and its attendant memory-loss problems, is the use of dehydroepiandrosterone (DHEA) 30,55,58 and pregnenolone 29,69 , mostly in the 'alternative' medical community. Pregnenolone is formed from cholesterol and forms DHEA, which, in turn, forms estrogen and testosterone; and pregnenolone also forms progesterone, aldosterone, corticosterone and cortisone. It would appear that the prescription of these precursor-hormones is more beneficial and causes less side-effects and toxicity than prescribing the end-hormones singly.





The reference papers show that, by correcting individual deficiencies/ excesses/ imbalances of various nutrients and hormones, early dementia can be reversed or at least prevented from getting worse. This effect is magnified many times when all the deficiencies/ excesses/ imbalances in any one individual patient are corrected optimally, creating the potential ability, already today, of reversing early dementia and preventing dementia in almost any patient! This is already the anecdotal experience of at least one medical practitioner. It remains for others to replicate his experience and for definitive research to prove this hypothesis.






In our society's rush to cut costs in the spiraling health-care economy, let us be sure that what is cut out is only the 'fat', such as unnecessary surgeries, hospitalizations, MRI's, CAT scans, expensive and habit-forming and potentially-toxic medications, etc.; but let us not take ill-considered short-cuts in assessing such basic and powerful medical aspects as the actual nutritional and natural-hormonal status of our patients.





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3. Baskin HJ. Endocrinologic evaluation of impotence. South Med J 82, 4: 446-9, 1989.

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7. Botez MI, Fontaine F, Botez B, et al.. Folate-responsive neurological and mental disorders: Report of 16 cases. Eur Neurol 16: 230-46, 1977.

8. Botez MI, Reynolds EH (eds). Folic Acid in Neurology, Psychiatry and Internal Medicine. NewYork: Raven Press, 1979.

9 . Braverman LE, Utiger RD, Eds. Werner & Ingbar's "The Thyroid: A Fundamental and Clinical Text", 6th Ed. Philadelphia: JB Lippincott, 1991.

10. Burnet FM. A possible role of zinc in the pathology of dementia. Lancet i, 8213 (Jan 24): 186-8, 1981.

11. Carmel R, Sinow RM, Karnaze DS. Atypical cobalamin deficiency (due to proteinbound-cobalamin malabsorption). J Lab Clin Med 109, 4(April): 454- 63, 1987.

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