good questionnaire is more sensitive than any biological factor

[alextsakiris]

Ran across this interesting quote from DMT researcher Dr. Rick Strassman:

"It is well-known in clinical psychopharmacology that a good questionnaire is more sensitive than any biological factor in assessing drug effects. In other words, a well-designed rating scale is better than measurements of blood pressure, heart rate, or hormone levels in distinguishing doses of a drug, or different types of drugs, from each other."

CSP - "DMT: The Spirit Molecule'', by Rick Strassman

[porker]

"psychopharmacology"

I'm not sure at all that you can generalise this to pharmacology in general, if that was what you were suggesting...?

[porker]

It's a very interesting article also... A good find

[fls]

Originally Posted by alextsakiris

Ran across this interesting quote from DMT researcher Dr. Rick Strassman:

"It is well-known in clinical psychopharmacology that a good questionnaire is more sensitive than any biological factor in assessing drug effects. In other words, a well-designed rating scale is better than measurements of blood pressure, heart rate, or hormone levels in distinguishing doses of a drug, or different types of drugs, from each other."

CSP - "DMT: The Spirit Molecule'', by Rick Strassman

I'm not sure why you find this notable. The effect which you are interested in is the hallucinogenic effect (in this case). So a questionnaire which asks about the hallucinogenic effect should be a useful measure - just like when we test a drug for lowering high blood pressure, measuring the blood pressure is a useful measure of the effect. Did you expect something different?

Linda

[Pollux]

Originally Posted by fls

I'm not sure why you find this notable. The effect which you are interested in is the hallucinogenic effect (in this case). So a questionnaire which asks about the hallucinogenic effect should be a useful measure - just like when we test a drug for lowering high blood pressure, measuring the blood pressure is a useful measure of the effect. Did you expect something different?

Linda

Maybe they do as a majority of the Endocrinologists do when they want to assess that the patient are "cured". They take a blood-sample to see that TSH is down. How the patient feel, if they still have any symptoms, or if they improved in their wellbeing, they could care less about.
In fact, they dont GAF.

[fls]

Originally Posted by Pollux

Maybe they do as a majority of the Endocrinologists do when they want to assess that the patient are "cured". They take a blood-sample to see that TSH is down. How the patient feel, if they still have any symptoms, or if they improved in their wellbeing, they could care less about.
In fact, they dont GAF.

Now you are talking about something different. The outcome of interest in that case is the absence of disease, not the sense of well-being. The long term harm from hypothyroidism isn't from subjective perceptions, but from the effects of insufficient thyroid hormone. If 'symptoms' are gone but hypothyroidism is still present, the patient will still suffer from that harm (which is considerably more dire than a less than perfect sense of well-being). If 'symptoms' are present but there is sufficient thyroid hormone, then the 'symptoms' are not due to hypothyroidism.

(ETA: You are right that dissatisfaction in the absence of any disease or condition is of less interest to physicians that preventing death, disability, disease, and pain (discomfort).)

In either case, the subjective perceptions are an insensitive and non-specific marker of what you are really interested in - adequate thyroid hormone. This is different from what was brought up by Dr. Strassman, where what we are really interested in is what we are measuring - the hallucinatory experience.

Linda

[Pollux]

Originally Posted by fls

Now you are talking about something different. The outcome of interest in that case is the absence of disease, not the sense of well-being. The long term harm from hypothyroidism isn't from subjective perceptions, but from the effects of insufficient thyroid hormone. If 'symptoms' are gone but hypothyroidism is still present, the patient will still suffer from that harm (which is considerably more dire than a less than perfect sense of well-being). If 'symptoms' are present but there is sufficient thyroid hormone, then the 'symptoms' are not due to hypothyroidism.

Which are complete bollox. The subjective perceptions are the symptoms.
The long term harm are the symptoms they have to live through.
When they crash-treat hypothyroidism by forcing down the TSH in a month or two with high doses of Levothyroxine on a disease that slowly progressed over years, most people break down. But as long they forced the TSH down to "the right blood-levels" they dont GAF if they still are symptomatic.
Many dont even take tests for T3, T4 or antibodies.

If you have symptom-free hypothyroidism the chances are you will have a crash'n burn awakening when it really breaks out.
Before TSH and Levothyroxine, hypothyroidism was diagnosed on the symptoms and treated with natural thyroid hormones, and had success with that. The natural thyroid hormones includes all the hormones from t1 t2 (that they dont even know how they work in the body) up to T3 and T4.
Levothyroxine is just T4, and by forcing the TSH down its like bypassing a lit oil-lamp in your car and keep on driving, since now the lamp (TSH) isn't lit anymore.
They also know f***-all about intracellular kinetics of thyroid hormones, but they have decided that if TSH is down the patients should just STFU and go home.


Our Holy Miracle of the Infallible TSH Test - YouTube

Thyroid hormone transport is an extremely important topic. It must be clearly understood by any physician who hopes to accurately evaluate an individual’s thyroid status and to appropriately treat thyroid dysfunction. Unfortunately, only a small fraction physicians and endocrinologists understand even the basics of thyroid transport, because what they have learned in medical school and continue to be taught regarding this topic is incorrect. When one understands the physiology involved with thyroid hormone transport, it becomes clear that standard blood tests, including the TSH and T4 levels, cannot be used to accurately determine intracellular and tissue thyroid level in the presence of a wide range of common conditions, including chronic and acute dieting, anxiety, stress, insulin resistance, obesity, diabetes, depression and bipolar disorder, hyperlipidemia (high cholesterol and triglycerides), chronic fatigue syndrome, fibromyalgia, neurodegenerative diseases (Alzheimer’s, Parkinson’s and multiple sclerosis), migraines, cardiomyopathy, and aging.

Serum thyroid levels are, of course, commonly used as an indication of cellular thyroid activity. In order to have biological activity, the T4 and T3 must, however, cross the cellular membrane from the serum into the target cells. It follows that the activity of these transport processes may have an important influence on the regulation of biological activity of the thyroid hormones. For about two and half decades it was assumed that the uptake of thyroid into the cells is by simple diffusion and that the driving force for this diffusion is the concentration of the free hormones in the serum. This “free hormone” or “diffusion hypothesis” was formulated in 1960 and assumes the concentration of free hormones (free T4 and free T3) in the serum determines the rate and extent of uptake into the cell and thus intracellular thyroid hormone concentration.

This hypothesis and mechanism of thyroid uptake into the cell has been shown to be totally incorrect (1-43). It has clearly been shown that the rate-limiting (most important) step in the determination of thyroid activity is the rate of thyroid hormone transport into the cell (5,20,41,44,45) and that this transport has nothing to do with diffusion, but rather it is energy requiring active transport (1-43,45,46,47,48-64,65,66,67). The incorrect “diffusion hypothesis,” however, continues to be taught in medical school and is believed to be true by most physicians and endocrinologists

It is important to note that because this transport of thyroid hormones into the cell is energy dependent, any condition associated with reduced production of the cellular energy (mitochondrial dysfunction) will also be associated with reduced transport of thyroid into the cell, resulting in cellular hypothyroidism despite having standard blood tests in the “normal” range.

The exact cause of the inhibition of the transport of thyroid is unknown, but it is clear that there are a number of substances that are produced by the body in response to dieting and physiologic stress that negatively effect thyroid hormone transport (5,41). This is clearly shown by studies where cell cultures are incubated with the serum from physiologically stressed or dieting individuals; there is shown to be a dramatic reduction of the uptake of T4 by the cells that correlates with the degree of stress.

Additionally, it has been clearly shown that there are different transporters that are specific and necessary for the transport of T4 and T3 into the cell where they have their effect. The transporter for T4 is much more energy dependent (it requires more energy) than the transporter for T3 (see figure 1) (5,40,41,49,52,53,66). Even slight reductions in cellular energy (mitochondrial function) results in dramatic declines in the uptake of T4 while the uptake of T3 is much less affected (5,41,62,67). Thus, the conditions listed above have, in particular, an impaired transport of T4 that results in cellular hypothyroidism. This cellular hypothyroidism is not detected by serum T4 levels because the less T4 transported into the cell and the lower the cellular level of T4, the higher the serum T4 level. The TSH will also not detect such cellular hypothyroidism because the pituitary has completely different transporters that are not energy dependent and increase transport activity, while the rest of body has impaired thyroid transport.


Treatment

Levothyroxine (T4)-only replacement with products such as Synthroid and Levoxyl are the most widely accepted forms of thyroid replacement. This is based on a widely held assumption that the body will convert what it needs to the biologically active form T3. Based on this assumption, most physicians and endocrinologists believe that the normalization of TSH with a T4 preparation demonstrates adequate tissue levels of thyroid. This assumption, however, had never been directly tested until two studies were published (119,120). The first study investigated whether or not giving T4 only preparations will provide adequate T3 levels in varying tissues. Plasma TSH, T4 and T3 levels and 10 different tissue levels of T4 and T3 were measured after the infusion of 12-13 days of thyroxine.

This study demonstrated that the normalization of plasma TSH and T4 levels with T4-only preparations provide adequate tissue T3 levels to only a few tissues, including the pituitary (hence the normal TSH), but almost every other tissue will be deficient. This study demonstrated that it is impossible to achieve normal tissue levels of T3 by giving T4 only preparations unless supra-physiological levels of T4 are given. The authors conclude: “It is evident that neither plasma T4 nor plasma T3 alone permit the prediction of the degree of change in T4 and T3 concentrations in tissues…the current replacement therapy of hypothyroidism [giving T4] should no longer be considered adequate…(119).”

The second study compared the plasma TSH, T4 and T3 levels and 13 different tissue levels of T4 and T3 when T4 or T4/T3 preparations were utilized (120). This study found that a combination of T4/T3 is required to normalize tissue levels of T3. The study found that the pituitary was able to maintain normal levels of T3 despite the rest of the body being hypothyroid on T4 only preparations. Under normal conditions it was shown that the pituitary will have 7 to 60 times the concentration of T3 of other tissues of the body; and when thyroid levels drop, the pituitary was shown to have 40 to 650 times the concentration of T3 of other tissues. Thus, the pituitary is unique in its ability to concentrate T3 in the presence of diminished thyroid levels that are not present in other tissues. Consequently, the pituitary levels of T3 and the subsequent level of TSH are poor measures of tissue hypothyroidism, as almost the entire body can be severely hypothyroid despite having a normal TSH level (120).

These studies add to the large amount of medical literature demonstrating that pituitary thyroid levels are not indicative of other tissues in the body and showing why the TSH level is a poor indicator of a proper thyroid dose. These studies also demonstrate that it is impossible to achieve normal tissue thyroid levels with T4 preparations such as Synthroid and Levoxyl. It is no surprise that the majority of patients on T4 preparations will continue to suffer from symptoms of hypothyroidism despite being told their levels are “normal.” Patients on T4 only preparations should seek out a physician who is well-versed in the medical literature and understands the physiologic limitations and inadequacy of commonly used thyroid preparations.

Thyroid Hormone Transport | National Academy of Hypothyroidism

[fls]

Originally Posted by Pollux

The long term harm are the symptoms they have to live through.

To each her/his own, I suppose. I'm not going to argue with you over whether a sense of tiredness is of more interest than death from heart failure.

The rest of your 'information' is off-topic for this thread.

Linda

[Pollux]

Originally Posted by fls

To each her/his own, I suppose. I'm not going to argue with you over whether a sense of tiredness is more concerning than death from heart failure.

The rest of your 'information' is off-topic for this thread.

Linda

Well, if you think "a sense of tiredness" is all that go along with hypothyroidism I can understand your reluctance to discuss it, with so little knowledge on the subject.

[Arouet]

Originally Posted by Pollux

Well, if you think "a sense of tiredness" is all that go along with hypothyroidism I can understand your reluctance to discuss it, with so little knowledge on the subject.

I think she was saying that there is risk of heart failure, even in the absence of the patient having symptoms.