Thyroid: Therapy, Confusion and Fraud (1)

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Events in the tissues

Besides the effects of commercial deception, confusion about thyroid has

resulted from some biological clichés. The idea of a " barrier

membrane " around cells is an assumption that has affected most people

studying cell physiology, and its effects can be seen in nearly all of the

thousands of publications on the functions of thyroid hormones. According to

this idea, people have described a cell as resembling a droplet of a watery

solution, enclosed in an oily bag which separates the internal solution from

the external watery solution. The cliché is sustained only by neglecting the

fact that proteins have a great affinity for fats, and fats for proteins; even

soluble proteins, such as serum albumin, often have interiors that are

extremely fat-loving. Since the structural proteins that make up the framework

of a cell aren't " dissolved in water " (they used to be called

" the insoluble proteins " ), the lipophilic phase isn't limited to an

ultramicroscopically thin surface, but actually constitutes the bulk of the

cell.

Molecular geneticists like to trace their science from a 1944 experiment that

was done by Avery., et al. Avery's group knew about an earlier experiment, that

had demonstrated that when dead bacteria were added to living bacteria, the

traits of the dead bacteria appeared in the living bacteria. Avery's group

extracted DNA from the dead bacteria, and showed that adding it to living

bacteria transferred the traits of the dead organisms to the living.

In the 1930s and 1940s, the movement of huge molecules such as proteins and

nucleic acids into cells and out of cells wasn't a big deal; people observed it

happening, and wrote about it. But in the 1940s the idea of the barrier

membrane began gaining strength, and by the 1960s nothing was able to get into

cells without authorization. At present, I doubt that any molecular geneticist

would dream of doing a gene transplant without a " vector " to carry it

across the membrane barrier.

Since big molecules are supposed to be excluded from cells, it's only the

" free hormone " which can find its specific port of entry into the

cell, where another cliché says it must travel into the nucleus, to react with

a specific site to activate the specific genes through which its effects will

be expressed.

I don't know of any hormone that acts that way. Thyroid, progesterone, and

estrogen have many immediate effects that change the cell's functions long

before genes could be activated.

Transthyretin, carrying the thyroid hormone, enters the cell's mitochondria and

nucleus (Azimova, et al., 1984, 1985). In the nucleus, it immediately causes

generalized changes in the structure of chromosomes, as if preparing the cell

for major adaptive changes. Respiratory activation is immediate in the

mitochondria, but as respiration is stimulated, everything in the cell

responds, including the genes that support respiratory metabolism. When the

membrane people have to talk about the entry of large molecules into cells,

they use terms such as " endocytosis " and " translocases, "

that incorporate the assumption of the barrier. But people who actually investigate

the problem generally find that " diffusion, " " codiffusion, "

and absorption describe the situation adequately (e.g., B.A. Luxon, 1997;

McLeese and Eales, 1996). " Active transport " and " membrane

pumps " are ideas that seem necessary to people who haven't studied the

complex forces that operate at phase boundaries, such as the boundary between a

cell and its environment.

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