Alzheimer’s Reversal for Doctors: Thyroid Hormone

Alzheimer’s Reversal for Doctors:
Thyroid Hormone

by Steven Wm. Fowkes

These top-down factors are components of the neuroendocrine system.

Thyroid Hormones

Thyroid hormones are at the top of the list for two good reasons, 1) they play the most direct role in regulating basal metabolic rate, which is the foundational dimension of the body’s energy systems, and 2) traditional medical practice for the last 50 years regarding the standard of care for hypothyroid symptoms are woefully dysfunctional.  The widespread medical belief that TSH tests are a reasonable measure of thyroid-gland function and thyroid-hormone function is just plain wrong.  There is no evidentiary basis behind the belief.

Since any and all deviations from the standard of care are potential disciplinary events as far as state medical boards are concerned, despite any clinical benefit that can be documented, despite any medical rationale that may be advanced, and despite any scientific evidence that the standard of care is erroneous, the approaches presented here may entail regulatory risk.  Please see future posts for a discussion of proactive strategies regarding minimizing such risks.

The primary thyroid hormones are T4 and T3.  Roughly 85% of the hormone secreted by the thyroid gland is T4, with 15% T3.  But since T3 is four times more active at the thyroid-receptor level, the activity ratio of thyroid hormones is 60% T4 and 40% T3.  This is the first reason why refusal to measure T3 is medically unwise.

The T3 secreted by the thyroid gland goes directly to the deep tissues of the body and interacts with thyroid hormone receptors on cell membranes, on nuclear membranes, and on mitochondrial membranes.  These receptors coordinate the activation of protein synthesis in the nucleus and mitochondria which increase energy production systems in the mitochondria.  Mitochondrial DNA produces only 13 proteins; the rest are produced in the cell nucleus and transported to the mitochondria for energy production.

The T4 secreted by the thyroid gland has both direct and indirect paths.  There are two selenium-dependent enzymes called deiodinases  that remove one of the iodines from T4 to make either T3, which potentiates the thyroid signal by a factor of roughly four, or reverse T3 (rT3), which drops the thyroid signal to zero.  This is the second reason why refusal to measure T3 (and rT3) is medically unwise.  Statistically, the best correlation of thyroid tests to metabolic rate is the T3 to rT3 ratio.  This is not rocket science.  This is merely comparing thyroid potentiation to thyroid deactivation.

There are two other factors that directly govern the activity of thyroid hormones in the body , 1) autoimmune processes, in which immune dysregulation attenuates the thyroid signal, and 2) thyroid resistance, in which the signal is sabotaged at the receptor and/or transduction level.  While there are thyroid autoimmune tests, there are no tests for thyroid resistance.  [Whole-body calorimetry is a research-only testing capability.]  Generalized resistance to thyroid hormone (GRTH) is the overtly clinical diagnosis, but many scientists and physicians are convinced that sub-clinical GRTH is both widespread and a serious health hazard.

The only clinical assessment that is practical is a thyroid trial, in which a slowly escalating dose of thyroid is administered over an extended period of time, and the effects are monitored for 1) clinical improvements in wellbeing (memory, orientation, proprioception, body temperature, strength, stamina, coordination, etc.) and 2) symptoms of hyperthyroidism (hypervigilance, insomnia, elevated body temperature, irritability, restlessness, etc.).

There are a couple of aspects of a thyroid trial that are inconvenient within a traditional medical practice.  One is the timing.  Most medical practices involve medical appointments that are a month or two apart, and the TSH feedback loop for thyroid hormone is 2-4 weeks.  Therefore, thyroid dosing has to be incrementally increased on a weekly basis, to stay ahead of the TSH negative-feedback loop.  Therefore, there is a higher training burden for the caretaker to make in loco physician decisions and medical-monitoring tasks, like heart rate, Am and PM body temperature, and blood pressure (if indicated), which are the earliest symptoms of hyperthyroidism.  And then there are cognitive assessment tests involving memory, awareness, sleep quality, mood, attentiveness, coordination, dexterity, proprioception, and desicion making abilities, and the physical counterparts involving strength, stamina, tissue healing, food cravings, obsessive-compulsive tendencies, and on and on.

I suggest that baseline monitoring be the test for caretaker compliance.

Iodine and selenium are needed for making thyroid hormones.  These will be discussed in the blogs on bottom-up factors.

2 thoughts on “Alzheimer’s Reversal for Doctors: Thyroid Hormone”

  1. Steve, do you feel high count lacto and bifido probiotics (30 to 200 billion bacteria per dose) can convert T4 into the more receptor active T3? Datis Kharrazian states in his Hypothyroidism book that good bacteria in the gut can up basal metabolism by as much as 20 % by converting T4 to T3. Brenda Watson has probiotic products as high as 200 billion carried in the Renew Life brand. Any dangers to this high of lacto and bifido bacteria count?

    Cliff Colgan Nutrition Therapy Practitioner

    1. Cliff, I’m inclined to disbelieve that bacteria have an interest in T4, T3 or rT3 except to detoxify it as a general reaction to any “poison.” Thyroid hormones (and sex hormones) are neuroendocrine control systems in multi-cellular life forms. There may be an effect, but that effect could be direct (a detox reaction) or indirect (an alteration of gut ecology, decrease in gut inflammation, or shift in host-symbiote dynamics. It is very difficult to separate a pro-metabolic effect, attributed to thyroid hormone activity, from a decreased anti-metabolic effect, like decreased estrogen dominance or an alteration in heavy-metal excretion.

      The subtleties of thyroid receptor activities and substrate binding are not well understood. I do not know of a test, beyond the empirical-oriented thyroid trial, for measuring thyroid resistance / responsiveness. Not having read Kharrazian’s book yet, I do not know what evidence is offered, if any, for the claim. But I do agree that decreased basal metabolic rate is biologically important to most pathologies and that anything that can correct or counteract the endemic downward drift of basal metabolism in our modern society is worth the time to better understand it.

      The downside dangers of high-count probiotics are low from the perspective of acute negative reactions. Most people taking brobiotics have no negative effects at all. It is basically a benign practice. But there are subtleties of gut ecology about which we know nothing. In normal medical science, each answer to a question generates two or three new questions. With gut ecology, each answer generates dozens of questions. The good news is that polymerase chain-reaction testing is giving us real-time genetic information about microbes that we didn’t know even existed let alone know how to culture. So the “danger” to messing around with gut ecology is that we don’t know what we are doing. Although we know that antibiotics produce catastrophic changes in gut ecology by wiping out entire strains of bugs, we don’t know beans about how the remaining bugs adapt to the loss of their competitors or symbiotes. Genetic drift in microbes is, I guess, millions to trillions of times faster than in our tissues. The reintroduction of a single strain of bug, after the wholesale slaughter of bug species, cannot fix the problem. It may help, but the “count” is fundamentally unrelated to the benefit. It is the implantation that matters, and there is very little evidence that count has much to do with that.

      Probiotic counts are a marketing strategy subject to over-reporting and under-reporting biases. The multiplication of the count by 1) pre-ingestion culturing, or 2) successful implantation, will make the counts trivial or irrelevant, depending. The viability of the bug in the capsule is probably more important than the count, and the ability of the bug to reach its “niche” in the gut after ingestion is more important than anything.

      Once we have developed improved sampling devices that can collect microbial DNA from every part of the gut, not just the terminal end of the colon, we will be able to measure the positive and negative effects of probiotic supplementation and antibiotic use. I predict that DNA-based identification and quantification of gut microbes is going to have a profoundly positive effect on our health and wellbeing. —Steve

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