- Read more from Head Squeeze
- Clinical Significance
- Review Thermoregulatory disorders and illness related to heat and cold stress
- Impaired thermoregulation
- Basal Body Temperature Tracking – Part One – Thyroid
- Basal Body Temperature
- Thyroid Symptoms
- Hypothyroid Symptoms (more common)
- Hyperthyroid Symptoms (less common)
- HOW to take your Basal Body Temperature for tracking.
- How to interpret your readings.
- What to do with your results
- Disclaimer- The content in this post is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this post.
- Body Temperature and Thyroid Problems
- The Basal Temperature Test
- Other Factors that can Make You Cold
- Energy, Heat, and Metabolism
- Fall Season May Trigger Thyroid-Induced Mood Problems
- How to Improve Body Temperature and Thyroid Function
Read more from Head Squeeze
Among the many symptoms of a cold, we often tend to feel hot and red-faced. It’s our body temperature rising a little to fight off the virus.
But why exactly does getting all hot and sweaty help kill a bug? Headsqueeze’s Greg Foot delves into the body’s biology to explain why becoming a little heated quickens your recovery when you’re unwell.
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When a person who cannot sustain his or her core body temperature presents with heat illness, multiple organ support is indicated. It is imperative to be comprehensive in their care and utilize any and every cooling method available to sustain their body. Support must be provided to their respiratory, hepatic, renal, and circulatory systems. Giving fresh frozen plasma and blood platelets as needed is also recommended. Previous animal studies have also shown that administration of thrombomodulin can be helpful because it demonstrates anti-DIC and anti-inflammatory mechanisms.
Malignant hyperthermia is a rare type of event, but one that is life-threatening. It can occur when a susceptible patient is given certain anesthetic agents, notably halogenated ones or ones that are agents that depolarize neuromuscularly. Predisposed patients who are given such anesthetics either have abnormal ryanodine receptors (RYR-1) or have other myopathies such as Duchenne muscular dystrophy, central core disease, neuroleptic malignant syndrome, and King-Denborough syndrome. Ryanodine receptors are located in skeletal muscles, which typically contain calcium channels and sarcoplasmic reticulum; these are what control the release of calcium. However, in malignant hyperthermia, calcium release is not regulated, and this leads to a continued release, which leads to an increased frequency of muscle metabolism. The clinical features first would present as muscle rigidity and an overwhelmingly high heart rate and end-tidal carbon dioxide. The person’s temperature will increasingly elevate, and soon after, muscle tightening and shortening will occur as well as metabolic acidosis.
The rapid treatment of malignant hyperthermia is of the utmost importance to prevent fatality. Once malignant hyperthermia is suspected, dantrolene must be given intravenously. This will prevent that uncontrolled release of calcium as described above. It is also important to rapidly cool the patient, give 100% oxygen, and regulate metabolic acidosis.
Serotonin syndrome and neuroleptic malignant syndrome are other disorders of temperature regulation. They both are due to adverse drug reactions, and they both present with clinical hyperthermia. It is important to distinguish them from one another. Neuroleptic malignant syndrome (NMS) continues over many days and is depicted by slow movements or the complete loss of voluntary movements. Serotonin syndrome is much more rapid, happening over a timespan of hours and presenting with fast movements such as tremor, muscular spasms, and hyperactive reflexes. These two reactions must be managed rapidly to avoid organ failure, especially if the patient’s temperature goes past 40.5 degrees Celsius. There are both physical and pharmaceutical ways to cool the affected patients. Physical methods include providing cool towels, ice packs, cooling blanket systems, and intravenous infusion of fluids. Pharmaceuticals include sedatives and antipyretics such as paracetamol and NSAIDs. (Note that in critically ill patients, it is important to consider individual patient’s renal function and gastric function before administering NSAIDs.)
Hyperthyroidism is another disorder of thermoregulation. In this endocrinological disease, the core temperature is raised in the body because the basal metabolic rate is raised. Essentially, with this disorder, all of the body’s metabolic pathways are accelerated. Heat production is increased as a result, and both oxygen consumption and ATP turnover are increased. The thyroid is overactive and causes a person to feel too warm.
Certain patients who have endured traumatic brain injuries (TBI) or suffered from cardiac arrests may do well with therapeutic hypothermia. In these patients with TBI and post-cardiac arrest, it is very dangerous for them to have an elevation of their core temperatures. High temperatures in these patients are associated with higher mortality rates and slower recovery, especially neurologically. Thus, hypothermia in post-cardiac arrest patients and perinatal hypoxic patients is used to prevent neuronal injury. This is because therapeutic hypothermia (TH) lowers the body’s demand for metabolic oxygen. With this mechanism, neurons can be protected before they are injured.
When TH is recommended, it should proceed very rapidly. Ice packs and intravenous administration of cold fluids are imperative to keep the patient cool. Cooling blanket systems or cooling suits may be utilized as well as cooling helmets and caps. For post-cardiac arrest patients, intranasal cooling using nasal probes also may be utilized.
In contrast, some diseases that can cause decreased heat production, or hypothermia include endocrinological diseases such as diabetes, hypothyroidism, hypoadrenalism, and hypopituitarism. Those who are most at risk for hypothermia are elderly patients, trauma patients, those who are mentally ill, those who are abusing alcohol, drugs, or on other types of medication, and, lastly, those with low socio-economic status. Ordinarily, people who get hypothermia have an underlying issue—either from a disease or surgery.
When a patient with one of these diseases presents with hypothermia, it is imperative to treat the underlying disease to effectively treat the hypothermia. This includes treatments with pharmaceuticals including triiodothyronine and steroids. Other causes of hypothermia from decreased metabolic rates are people who are very malnourished, those who suffer from burns, and also those with hypoglycemia.
Hypothermia, like hyperthermia, affects all of the human body’s systems. When the core temperature drops below 30 degrees Celsius, the heart responds with arrhythmias. The body may be hypovolemic, hypokalemic, and hypomagnesemic as a result of their hypothermia; therefore, it is important to keep the patient hydrated and to manage their electrolyte disturbances.
The reason that patients with traumatic brain injury are likely to have impaired thermoregulation is that the hypothalamus regulates the core body temperature. When this essential body part is injured, the body is unable to control how it regulates the body’s heat. Other problems in the CNS that affect thermoregulation by the same mechanism can include tumors in the CNS, spinal cord injuries, intracranial hemorrhage, and diseases such as Parkinson, Wernicke encephalopathy, and multiple sclerosis.
Patients who are on the extreme spectrums of age (such as infants and elderly persons) are at higher risk for disorders of thermoregulation and exhibit these features more readily when sick. The very young and the very old cannot increase their metabolic rates, and this can provoke them into hypothermia since they do not have the shivering reflux or much muscle mass. Changes that occur as one ages include those affecting vasomotor sweating function, skeletal muscle response, and temperature perception. Elderly persons have lower than normal internal body temperatures and decreased immunity, so when they have an infection, they may not get the normal pyretic response. Instead, they may present with hypothermia caused by a septic infection. In fact, studies have shown that the core temperatures of elderly patients with sepsis within their first 24 hours of presentation are a huge predictor of their mortality. This is the reason that elderly patients who are septic have a higher mortality rate than younger patients who are septic.
Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37 °C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body’s thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of < 35.0 °C, may present with shivering, respiratory depression, cardiac dysrhythmias, impaired mental function, mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. Management includes warming measures, hydration, and cardiovascular support. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Hyperthermia, defined as a core temperature of > 40.5 °C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.
A condition in which exaggerated or abnormal changes in body temperature occur spontaneously or in response to environmental or internal stimuli.
Impaired thermoregulation is a known complication of many of the diagnoses commonly seen among patients in a PM&R practice. It is seen in patients with spinal cord injury, traumatic brain injury, stroke, and other conditions that cause damage to the brainstem. It also can be seen in patients who take certain medications such as anesthetic agents, tranquilizers, antihypertensive drugs, opioids, and sedatives, in addition to alcohol.
Epidemiology including risk factors and primary prevention
The frequency of impaired thermoregulation is not known. This problem is associated with spinal cord injury above level T6 and with severe traumatic brain injury. In spinal cord injury, it occurs more frequently during extremes of ambient temperature. In patients with traumatic brain injury or brainstem stroke, it can occur frequently in the presence of noxious stimuli, although it occurs more frequently spontaneously in the absence of environmental triggers.
In the normal state, powerful mechanisms exist to measure, assess, regulate, and adjust core temperatures. There are sensory, integrator/regulator, and effector components of thermoregulation. The sensory components of the thermoregulatory control system derive from both internal and external sources. There are cutaneous cold and warm receptors located throughout the skin and superficial tissues, which are more concentrated in the fingers, face, and genitalia, and less concentrated proximally. There also are deep body thermal sensors, located in the abdomen and elsewhere. These sensors send impulses with thermal information through projections into the spinal cord, carried predominantly through C-fiber afferents. These fibers, with cell bodies in the dorsal root ganglion, enter the spinal cord and ascend contralaterally in the spinothalamic tracts through the medial lemniscus to the thalamus, which in turn, has fibers that project directly to the somatosensory cortex to enable conscious appreciation of temperature. The ascending fibers also have additional important projections to the hypothalamus to facilitate unconscious autonomic control of temperature. The preoptic hypothalamus receives and interprets the internal and external temperature information, generates the thermal set point, and integrates thermoregulatory responses. Efferents from the hypothalamus control the bodyâ’s response to thermal changes through descending noradrenergic and cholinergic fibers exiting the spinal cord below the C7 level. The strategies which these effectors use to regulate core temperature include changes in vasomotor (causing peripheral vasoconstriction and vasodilatation) and sudomotor (causing sweating) tone, nonshivering and shivering thermogenesis, and piloerection. Conscious awareness of temperature changes, based in the cortex, enables behavioral adaptations to control temperature, including changing location, adjusting environmental temperatures (e.g., via heating or air conditioning), making postural adjustments, or changing clothing. When core body temperature decreases, sympathetic noradrenergic mechanisms normally induce piloerection, shivering, and vasoconstriction to produce body heat and to shunt blood away from the cool surface. Core body temperature is the result of the balance between heat production and heat loss, both of which are adjusted by the central hypothalamic thermoregulatory controller. When core body temperature rises, vasodilatation and sweating normally help the body to lose some of its internal heat. Medical and neurological problems that interfere with the flow of sensory information and/or motor output reduce the ability of the system to assess and mount a response to changes in temperature. Also, direct damage to the hypothalamus controller can result in dysregulation of temperature control.
In spinal cord injury (SCI), the normal connections are lost between the hypothalamus and both its motor and sensory projections. In high SCI, most of the skin is insensate, and so the person may have little or no sensitivity to heat or cold. In addition, the lack of sympathetic outflow on the effector side results in loss of vasoconstriction or vasodilatation, so heat cannot be conserved or lost in response to central temperature changes. In addition, heat production is limited in response to cold stimuli because of the loss of shivering ability resulting from motor deficits. Sweating is ineffective below the level of injury. With high SCI, heat production may increase only slightly over baseline, so central hypothermia in a cold environment is a significant risk for these patients. The amount of impairment of thermoregulation tends to vary according to level and possibly completeness of injury. Practically, the significant risk of hypothermia in cold external environments occurs more commonly in patients with SCI levels above T6 because of the large surface area for which sensation and shivering ability are lost in those patients.
The preoptic area of the anterior hypothalamus, which houses the main thermoregulatory center, can be damaged by trauma, leading to manifestations of thermodysregulation. Other causes of hyperthermia after traumatic brain injury (TBI) include post-traumatic cerebral inflammation and secondary infection. The development of post-traumatic hyperthermia (PTH) can be seen as a secondary effect of TBI that may negatively influence outcome. An increase in body temperature after injury is associated with increased cytokine release, and both hyperthermia itself and the cytokine release can exacerbate neuronal damage, through the mechanisms of increased oxidative stress, glutamate release, increased metabolic expenditure, increasing blood brain barrier permeability, cerebral edema, and raising intracranial pressure.
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Thermodysregulation can occur early or late after spinal cord injury. Although it also can occur at any time after traumatic brain injury or brainstem damage, it tends to be more frequent during the early post-injury period. It is distinctly episodic.
Specific secondary or associated conditions and complications
Uncontrolled fever is a component of the clinical syndrome known as paroxysmal autonomic instability with dystonia (PAID). Also known as central dysautonomia and central storming, this phenomenon results from altered autonomic activity following TBI, resulting in severe hypertension, fever, tachycardia, tachypnea, pupillary dilation, and extensor posturing. It results from injury to the brainstem, but can also occur following brainstem hemorrhage, elevated pressure on the brainstem, and injury to select cortical areas that influence hypothalamic activity can also be a cause. These regions include orbitofrontal, anterior temporal, and insular areas. Subcortical areas that may influence hypothalamic function are the amygdala, the periaqueductal gray matter, nucleus of tractus solitaries, and both the uvula and vermis of the cerebellum. Damage to these areas release control of vegetative function and results in dysregulation of autonomic balance. PAID occurs in up to one-third of patients in coma or vegetative state. It is more common in patients with severe TBI, but also is seen in patients with hydrocephalus and CNS infection. Clinical manifestations are temperature typically greater than 38.5oC, hypertension, heart rate greater than 130 beats per minute, rapid respiratory rate, associated with agitation, diaphoresis, rigidity, or decerebrate postures. It is possible to have electrocardiographic changes, arrhythmias, increased intracranial pressure, hypohydrosis, and cool limbs.
E. Denis Wilson, md, will address thyroid function and Wilson’s Temperature Syndrome at the 2015 Restorative Medicine Conference in Blaine, Washington, October 1 through 4. Dr Wilson was the first practitioner to use sustained-release T3 thyroid hormone. For 20 years, he has treated more than 5000 patients with T3 and trained more than 1000 physicians on how to use T3 to improve the health of patients with low thyroid function and low body temperature who have normal blood tests. He is the author of Evidence-Based Approach to Restoring Thyroid Health.1
Integrative Medicine: A Clinician’s Journal (IMCJ): What originally drew your attention to issues of thyroid and metabolism?
Dr Wilson: A patient came to my office and she brought with her a book and she said that I should read it. It was called Hypothyroidism: The Unsuspected Illness, by Broda Barnes, md.2 In that book, he explains the importance of using body temperature as a guide to evaluate thyroid function. I was intrigued by that and also his suggested treatment of using desiccated thyroid as an empirical treatment to normalize the body temperature. Though I did not look at the book for a few weeks, I eventually read it and decided to try his approach in a few of my patients. To my surprise, some of those people got 100% better.
That was really illuminating to me because, according to my training in medical school, that was not supposed to happen. These people had normal thyroid blood tests and, supposedly, that meant that they could not benefit from thyroid hormone treatment. These people did not get just a little bit better; they got completely better. It did not work for all the patients I tried it with, but it worked in about 60% of cases.
I was looking at the other 40% and wondering how we could help them, too. It could be that they did not have thyroid problems, or maybe the particular treatment I was using was not really addressing their issue. As I was trying to think of ways to increase the yield, I looked at the thyroid hormone pathways and saw that T4 is converted to T3. It turns out that this step is really important. I thought that, perhaps, these patients have a problem with the conversion of T4 to T3. So I started giving some of these treatment failures—these patients who had failed to respond to the pervious treatment—T3 directly. A lot of those treatment failures became treatment successes. That is how it all started.
IMCJ: Previous to that, had you been seeing a lot of thyroid patients?
Dr Wilson: Not really. I was more involved in primary care practice, but when I started seeing these kinds of thyroid results, the reaction I had was, “If this isn’t true, then perhaps nothing they taught me at medical school is true.” The use of the thyroid hormone blood test to direct thyroid therapy is one of the most dogmatically taught principles in medical school. They acted like the blood tests are absolutely conclusive in managing thyroid health. It was really eye opening to me because this closely held dogma—I could see from my own experience—was not true.
Then I thought, “If that is not true, then maybe nothing is true.” That perspective really opens up the possibilities of different things we can try to help people get better. That is when I really started diving in. When the patients do recover, there is hardly anything more dramatic than a hypothyroid patient’s response to thyroid therapy. It can be very pervasive.
One thing that I have come to understand over the years is that the purpose of the thyroid hormone is to go into the nucleus of the cell, form transcriptional complexes, and dictate the speed at which DNA is transcribed. It actually dictates how fast we live. That is really what metabolism is. It is how fast we live, which is controlled by the thyroid. When a person asks me what thyroid can affect, I respond, “Thyroid really only affects those cells that have DNA.” In other words, it affects every cell. When I saw the profound ramifications a normal body temperature can have on people, I started doing that pretty much exclusively.
IMCJ: What are some of the more frequent symptoms that indicate to you that there may be thyroid dysfunction?
Dr Wilson: Certainly fatigue, chronic fatigue, and headaches—migraine headaches. A huge percentage of patients with migraine headaches have low body temperatures and I have seen so many people when they get their temperatures corrected, their migraines sometimes disappear completely. Irritability, fluid retention, anxiety, panic attacks, PMS, hair loss, depression, decreased memory and concentration, low sex drive, unhealthy nails, low ambition and motivation, constipation, easy weight gain for sure, irritable bowel syndrome, dry skin, dry hair, insomnia, and even some things that people wouldn’t normally expect like asthma.
Even asthma and hives and allergies can sometimes respond to normalizing a low body temperature. Carpal tunnel syndrome and conditions caused by fluid retention—so there’s a tremendous number of things. Some of my favorites to treat are definitely migraines, PMS, and panic attacks. Panic attacks and anxiety symptoms are very debilitating and they are very responsive to normalizing one’s temperature. That is what makes this so fun to address. There are not many good solutions out there.
IMCJ: In many of these cases, the tipping point marker is low body temperature?
Dr Wilson: I would say in every case, yes. It is not possible for a person to have symptoms of hypothyroid unless they have a low body temperature. They can have abnormal blood tests and normal temperature and they will still feel fine but the only way you can have those symptoms of hypothyroidism is by having a low temperature.
IMCJ: Is the breadth of the symptomatology directly the result of the dysfunctional thyroid or does the low body temperature itself cause secondary symptomatology?
Dr Wilson: I believe that it is the temperature itself that causes the symptomatology because the correlation is so complete. My favorite theory has to do with the enzymes we talked about, the transcription of DNA in the nucleus, and that when DNA is transcribed, it makes proteins and enzymes and structural elements. Those enzymes are the key of every chemical reaction in the body and the speed at which those reactions take place and the efficacy of those reactions depend on the enzymes. The whole purpose of an enzyme is to help a reaction take place at a reasonable temperature, like body temperature, when it would not take place at that temperature without it.
Without an enzyme, that reaction might not take place at less than 220°F or something like that. With the enzyme, the reaction can take place at a reasonable temperature or a biological temperature. Let’s put it this way: It is known that those enzymes depend on their shape for their activity. The conformation, or the shape of these enzymes, is what brings reacting molecules in close enough proximity to react. If those enzymes are too hot, they are too loose. If they are too cold, they are too tight. If they are just the right temperature, then they are just the right shape. A change in temperature can have a huge impact on the speed of these chemical reactions.
IMCJ: How does being “too tight” affect the shape of an enzyme?
Dr Wilson: An enzyme is a string of amino acids and it coils upon itself because of the electrostatic charges of the atoms forming a shape. That shape generates active sites where one active site can grab one substrate and another active site can grab another substrate and then, when those substrates are grabbed, the enzyme can change its conformation and bring the reactive species into close proximity so that they can react.
All of that depends on temperature, so what I mean by “too tight”—it is like an old-fashioned telephone cord. Sometimes they get tangled like a knot. If you pick the receiver up, the cord untangles and then when you hang it up again, the cord twists up on itself again. That is what I mean by “tight.” If the cord does not tangle up on itself at all, then it is too loose and it does not really work right. If it is too twisted up on itself, then it is too tight and that does not work, either. You want the enzyme to have just the right shape and that depends on temperature.
IMCJ: Why are the conventional methods of treating hypothyroid inefficient for resolving these cases?
Dr Wilson: It is because the conventional approach is to think that thyroid function—or the adequacy of thyroid function—depends on blood tests. Ever since the thyroid-stimulating hormone, or TSH, test was discovered, or even since they discovered that T4 hormone is converted to T3, there was an assumption made.
If you were the one who discovered that T4 is a raw hormone that is converted to T3 and that T3 is actually the active form of thyroid hormone, then at that moment you could make either of 2 conclusions. You could say, “Wow, T4 is converted to T3 and T3 is actually the active hormone. We really shouldn’t focus so much on T4. We should focus more on T3 and the effects of T3 to see if that interaction is adequate—accomplishing what we want it to accomplish.” That is one conclusion. The other conclusion you could make is, “T3 is the active hormone and since the body converts T4 to T3 automatically in the cells of the body, we do not need to worry about that because it happens automatically. The only thing we have to worry about is to ensure that there is adequate T4 production or supply in the blood stream.”
Those are 2 reasonable conclusions with very different outcomes. For the last 50 years, the latter of the 2 conclusions has been in favor. Over the last 10 years, research supports the idea that regulation of the conversion of T4 to T3 happens intracellularly and it can change dramatically under different circumstances. That conversion is not measured by a TSH test. The TSH test is not a reliable indicator of thyroid status because the TSH could be normal and a person could still have hypothyroidism in the cells. There is extensive research in the last 10 years, specially, to substantiate that. The T4 to T3 conversion can change under a variety of disease states. Studies of 25 different diseases show that the effects of T4 to T3 conversion can be impaired or can be affected by these different disease states. In these disease states, then, TSH is not a reliable indicator of thyroid status.
That is a long answer but the short answer is this: You asked me why the conventional approach to thyroid treatment not very effective and I would just say, “Because they are measuring the wrong thing.” Thyroid blood tests do not measure body temperature.
Using the blood test, if 100 people come in with hypothyroid symptoms and these people are treated based on their blood tests, 5% are going to have problems that show up on the blood test. Of those 5% of people with problems identified by the blood test, probably only 50% of those are going to get better with conventional thyroid approach. That is because only 5 people—out of 100 who have low body temperatures that could be effectively managed with treatment—are going to have abnormal blood tests. If you try to get them better by just trying to normalize their blood tests, that is probably only going to work 50% of the time.
So, you are only taking about 2.5 people out of 100 who are going to be effectively managed. On the other hand, if you take those 100 people with hypothyroid symptoms, you will find that every one of them has a low body temperature. If you were to treat their temperature, you are going to get 80% to 90% of those people’s temperature to normal. For these 80% to 90%, their symptoms are going to dramatically improve, if not resolve completely.
IMCJ: So the crux of the matter is that because the conversion of T4 to T3 is dependent upon an enzyme, there are circumstances—including ambient temperature of the body—that will affect the ability of the enzyme to function or its functional efficiency. That is what the “conventional” approach is missing.
Dr Wilson: That is exactly right. If the body worked automatically and always took care of itself, there would be no disease. But there is disease. There are all kinds of diseases. All kinds of things can go wrong with the body and with every aspect of the body. In fact, I am beginning to be of the opinion that anything that happens in the body can go badly. Anything that can go wrong will go wrong in somebody, someplace, at some time, for some reason.
If you look down the chemical pathways of the human body, you will see that there is Addison’s disease and there is Cushing’s and there are different diseases that we label based on how things go in the chemical pathways.
One really easy way to invent a new condition or new disease is to just find some place in a biochemical pathway where dysfunction has not been named yet and just name it. There has got to be somebody that is going to have a problem in that particular part of the pathway eventually. The deiodinase enzyme depends on selenium and zinc is also important. Of course, if you have a selenium deficiency, T4 to T3 conversion goes down. If you increase selenium in those patients, the T3 levels go up. Obviously, the function of that enzyme is variable under different conditions. It is under regulation and it can be downregulated.
This is a really important point. Many of the important pathways to the body are under regulation. That is how we maintain homeostasis and normal functioning of the body. There is something called the ubiquitin proteasome pathway. The way this system works is that key enzymes in different pathways are under regulation. When the body wants to slow down that particular pathway, it downregulates or increases the destruction of that key enzyme. If it wants that pathway to speed up, it will decrease the destruction of that key enzyme so that the pathway can speed up or increase again.
The fascinating thing about deiodinase enzymes is that researchers have looked at the things that increase the downregulation of this enzyme. What things shorten the half-life of this enzyme? T4 or thyroxin is 1 of the things and the other is reverse T3. Of course, conventional doctors and alternative doctors, even doctors who treat low body temperature empirically in the face of normal blood testes, will often use desiccated thyroid hormone. Desiccated thyroid hormone contains T4 and, presumably, they are using thyroid hormone because they are thinking that even though the blood tests are normal, the person is not getting enough thyroid stimulation of the cell. They attempt to help the patient by giving the patient more thyroid hormone in the form of desiccated thyroid hormone. Desiccated thyroid hormone has T4, which can significantly downregulate the converting enzyme. A lot of the patients who are treated with Synthroid, or treated with desiccated thyroid, actually do not improve as much as we hoped they would. Sometimes they actually get worse.
That is because the T4 in desiccated thyroid can downregulate the enzyme. When that enzyme is downregulated, the T4 gets converted to reverse T3 and both T4 and reverse T3 downregulate that enzyme. Here we are hoping to help the person’s thyroid physiology and help them benefit from more thyroid stimulation of the cell—hoping that we are going to improve their T4 to T3 conversion—and we sometimes actually inadvertently suppress their T4 to T3 conversion and suppress their thyroid hormone stimulation. Thereby, we really do not make the progress that we are looking for.
We are giving them this desiccated thyroid and we are not getting their temperatures up. I would encourage doctors, if they are using desiccated thyroid, to have the patient monitor their temperature to make sure it is going up. If temperature is not going up on desiccated thyroid, there may be a good reason for that and it may not work very well for the patient.
IMCJ: Will people who benefit from this therapy end up having to continue it forever? Is this something that has a definite treatment duration or is it more a situation where you have to read it by the individual?
Dr Wilson: It definitely does depend on the individual. Typically, T3 is not taken for life. There are different problems, which I will address in a second, but the conversion impairment problem—improving T4 to T3 conversion—is something that can normally be corrected in a manner of months. Often the duration is 2 to 3 months, maybe 6, maybe 8, but certainly it is reversible to the point that people do not have to keep taking the treatment for life.
I like to separate the thyroid hormone system into 3 different compartments. One is thyroid hormone supply. The second is thyroid hormone conversion and utilization. And the third is thyroid hormone expression. Historically or conventionally, our medical establishment has hoped that they could measure, predict, and manage thyroid hormone expression based exclusively on thyroid hormone supply. We figured that if we just give a person enough thyroid hormone to normalize their TSH, then the thyroid hormone expression will take care of itself and that person will be fine. My opinion is that you cannot measure thyroid hormone expression with a thyroid hormone blood test.
Thyroid hormone supply is measured with a thyroid hormone blood test. The TSH is a great measure of thyroid hormone supply but the body temperature is the best measure, as it is an exact measure of thyroid hormone expression. When I say it is an exact measure, what I mean is that the whole purpose of the thyroid system is to determine how fast our bodies live and how fast they function. That is exactly what a thermometer is. A thermometer is literally a speedometer. The higher the kinetic energy of the molecules in the air, the warmer it is outside.
As a thermometer actually measures the speed of the molecules in the air, it also measures the speed of the molecules in our bodies. When you measure temperature, you are actually measuring how fast the chemical reactions are taking place in the body. If a person has a normal TSH— they have a normal supply—and they have a low temperature, which is low expression, to me, that logically suggests that they have a problem with thyroid hormone conversion and utilization. If a person has hypothyroidism, has had a thyroidectomy, and has a thyroid hormone supply problem, then, yes, they are going to need thyroid medicine the rest of their life. Without a thyroid gland, they are going to need thyroid hormone to produce supply.
Even people who have decent supply might still have a conversion problem. They might still have a low temperature even though they have a normal TSH or even a low TSH. They could actually be hyperthyroid and still have symptoms of hypothyroidism because their temperature is too low. That is because they have a conversion problem. Anyway, to answer your question, the conversion problem is the one that is reversible.
For conversion, you can take them off their Synthroid and you could take them off their desiccated and you can give them some herbs and nutrients to support the conversion of T4 to T3 and you can give them T3 directly if they need that. So, there are some things you can do to support thyroid hormone conversion. If you are successful, in that you are going to be able to get their temperature up to normal, lots of times you can wean them off the T3 and, perhaps, put them back on the Synthroid or desiccated thyroid hormone. At that point, they may be able to maintain a normal temperature. With that medicine, they may be able to maintain a normal temperature indefinitely—or maybe in 5 years, or maybe in 10 years they have another relapse and need another tune-up.
IMCJ: By getting the body temperature up, a patient then is hopefully creating this enzyme in the right geometry to sustain it on their own?
Dr Wilson: Yes. It is just speculation why people tend to get better and seem to stay better. My feeling is that there are a couple of ways to address this thyroid hormone conversion problem. One is with herbs and nutrition. If you properly support the enzyme and the body, then perhaps the enzyme will start functioning better and the conversion improves and the temperature goes up. Even without weaning off Synthroid or without weaning off Armour, sometimes lifestyle, nutritional, and herbal support is enough to improve conversion to the point that they are able to have a normal temperature and to feel well. That is sometimes a good solution and, apparently, you have just supported the converting enzyme. On the other hand, some people are going to need to have their thyroid hormone pathways cleared out. Sometimes, people do not get better until you wean them off the Synthroid and wean them off the desiccated thyroid and replace them for a time with T3 by itself—T3 alone. When you give somebody T3 alone, their TSH goes down and their T4 goes down and their reverse T3 goes down. We have already talked about how strongly T4 and reverse T3 will downregulate the converting enzyme.
These can decrease the half-life of the converting enzyme from 40 minutes down to 20 minutes or, in other words 50%, so it can be dramatic. What if, by reducing the T4 and the reverse T3, that that downregulation was relieved and reduced to the point that the deiodinase enzyme could upregulate? Enough to increase to the point that it could restore better T4 to T3 conversion? Some research suggests that there might be a genetic coding problem of the deiodinase enzyme in some people, but I think that, even with normal coding of the deiodinase enzyme, the deiodinase enzyme can get bogged down under periods of stress. And under periods of stress, the conversion of T4 to T3 goes down. That is well known—for decades. When that happens, the reverse T3 goes up. Again, the T4 and reverse T3 can further suppress the deiodinase enzyme, so I feel that this situation can set up a persistent impairment or suppression of the deiodinase enzyme to the point that a person is going to have a hard time maintaining a normal temperature.
IMCJ: Then is there any direct evidence at this point that the stress hormone, cortisol, interferes with the process directly?
Dr Wilson: Yes. Cortisol has been shown to directly inhibit the conversion of T4 to T3 for sure. One other thing: I do want to make it clear that I do not mean reverse T3 on a blood test. I am not saying that measuring reverse T3 in a blood test is going to be useful at all, because I haven’t found it to be. I have not found it to be predictive or reliable. Some people with lower reverse T3 levels still have low body temperatures. You can have a person with low TSH, which makes them look like they are hyperthyroid, and then they have a high total T3, which makes them look like—if anything—they are making plenty or too much T3, and they could have a low reverse T3, which makes them look like if anybody is converting T4 to T3 very well, it is this person.
They could still have low temperature regardless of anything that the blood tests say. I still think that they could have impaired conversion at the level of the cell that is invisible on the blood test. The blood tests do not measure what is happening inside the cell. They only measure what is floating around in the blood stream.
IMCJ: To wrap things up, when you speak at the Restorative Medicine Conference in October, what more are people going to learn at your presentation?
Dr Wilson: I will talk about the specifics of the nutritional and herbal support. I will talk about the specifics of T3 therapy and how to monitor and manage patients. Basically, they will learn how to normalize somebody’s body temperature in a way that will help patients recover from their symptoms and hopefully remain improved even after their symptoms have been discontinued.
For more information about the 2015 Restorative Medicine Conference, please visit http://www.restorativemedicine.org/.
Basal Body Temperature Tracking – Part One – Thyroid
Tracking basal body temperature can be a useful tool that can help you to uncover hypothyroid and even hyperthyroid patterns, just by taking your temperature at the same time every morning for five consecutive days.
Heads Up Health makes it easy to track, trend and compare your basal body temperature readings alongside all your other health metrics. Start your free 30-day trial using the button below. Or, read on to learn more about basal body temperature and how to track it.
Basal Body Temperature
When tracking basal body temperature, we want to track your resting temperature which is a reflection of your metabolic activity with minimal influence from outside factors like digestion, exercise, stress, etc. After you’ve been asleep for several hours, the body has ideally settled into its resting metabolic pattern, so we have a way to compare your temperature with as little interference as possible.
Most everyone knows someone with a thyroid condition. Maybe you even suspect that you have a thyroid condition, but haven’t made an appointment with your doctor yet or your labs have all come back normal. If you suspect that you may have a thyroid condition, these are some of the symptoms that you may be experiencing.
Hypothyroid Symptoms (more common)
- low body temperature-feeling cold in a warm room, or having cold hands and feet consistently.
- apathy or depression
- lack of motivation
- inability to lose weight or weight gain
- frequent colds
- swelling in ankles
- lack of libido
- hair loss
- insomnia and more.
Hyperthyroid Symptoms (less common)
- increased heart rate
- frequent and loose bowel movements
- unintended weight loss and more.
Hypothyroidism is so prevalent that its become a thing we just expect to have happen to us at some point, and we often accept that these symptoms are just a consequence of getting older. Symptoms are messengers from our body, alerting us to a system that is out of balance. The thyroid influences almost every cell in the body, so when it’s not supported, the symptoms can present in other areas of our bodies. Using the basal body temperature readings developed by Dr. Barnes can help you to hone in on a potential thyroid condition and allow you to seek the help you need to support your thyroid.
The basal body temperature test can be used whether or not you’ve had a thyroid test recently. Thyroid hormones are made in the thyroid, but most of the active (energy) thyroid hormone T3 is converted from the inactive (storage) T4 form in other parts of the body, which means that thyroid function is about more than just the TSH hormone levels in the blood. Other sites of conversion include the gut (20%), liver (40%) and peripheral tissues (20%). A compromise in the liver or gut can cause a decrease in the conversion of the inactive thyroid hormones to the active thyroid hormones. Another factor to consider is vitamin and mineral deficiencies as the thyroid uses iodine, selenium, zinc, magnesium, the amino acid Tyrosine, as well as vitamins A, C, D, B2, B3, B12 and healthy fats to function optimally.
Because your gut health is a major site of thyroid conversion, Tracking your Bristol Stool Chart can be another piece to the puzzle when trying to figure out a thyroid pattern. Thyroid dysfunction can alter bowel movement patterns as well, which can clue us in to the possibility of a thyroid issue.
The body can compensate for quite a while on reduced resources before the blood will show a significant change to be diagnosed with a thyroid disorder. Tracking your basal body temperature for 5 days can give you a better understanding of a trend for either hypo or hyper thyroid patterns, so you can further explore paces where the breakdown may be happening. Hypothyroid is much more common than hyperthyroid, but either can occur. For more info on what labs are important to ask for when you talk to your doc, check out Amy Berger’s article on Thyroid testing here. Though she talks about it in the context of a low carb diet, the testing info will apply to anyone who thinks they may need a thyroid panel worked up.
HOW to take your Basal Body Temperature for tracking.
Prepare the night before you want to start tracking you basal body temperature. You’ll need a thermometer (glass is preferred as it’s more accurate than digital for this purpose-avoid mercury and opt for a Geratherm glass thermometer which you can find here), your phone/device for timing and documenting your results.
*Note – if you sleep with a heated blanket, or multiple heavy blankets, you’ll want to remove them for the nights that you’ll be collecting your data, to get an accurate reflection of your body temp.
- Shake down your thermometer so that it’s ready for morning. Place all supplies by the bed where you can reach them with minimal effort in the morning.
- When you awaken, you will take your thermometer and place it in your armpit for minimum of 5 min (glass will need at least 4 min for accuracy), first thing in the morning. Try to move minimally so as to not rev up your body temp. After 5-10 min, record your temperature and go about your day as normal.
- Repeat this process for 5 consecutive days.
- Ladies, you will want to avoid starting or collecting data on day 19-22 of your menstrual cycle as there are fluctuations due to other hormones as well as related to ovulation, which we will talk about in a subsequent basal temperature tracking article.
How to interpret your readings.
Dr. Barnes found that a normal resting body temp should be between 97.8-98.2 degrees Fahrenheit. If it is consistently lower, then there is a trend toward a hypothyroid (decreased function) pattern. If consistently above 98.2, then this indicates a trend for more of a hyperthyroid (increased function) presentation. If results are mixed, both high and low, this is often more indicative of a primary adrenal stress pattern, as the adrenals and thyroid are closely linked, which would allow for the variation in body temperature.
What to do with your results
If you find that your temperatures indicate the possibility of thyroid or adrenal stress, take your readings in your Heads Up Health app to your functional health doctor/provider so you can further investigate where the breakdown could be and support for healing.
Body Temperature and Thyroid Problems
Too hot? Too cold? How do you know if this indicates poor thyroid function or something else? When your thyroid hormone is working properly inside cells you will make 65 percent energy and 35 percent heat as you burn calories for fuel. Thyroid hormone governs your basal metabolic rate, orchestrating the idling speed at which all cells make energy and thus heat. A classic symptom of poor thyroid function is being too cold.
Conversely, a classic symptom of hyperthyroidism is being too hot (making too much heat). However, many people with low thyroid are too hot — a seeming paradox that I will explain shortly. Generally, you know all too well if you fit into the too cold category. You always want the thermostat set higher than everyone else or you wear an extra layer of clothes. You go to bed with socks on your feet or want extra layers of blankets. When this type of coldness matches up with the symptoms of thyroid-related fatigue, you fall into the classic pattern of sluggish thyroid.
The Basal Temperature Test
In many cases of poor thyroid function a cold feeling is not quite so obvious. Dr. Broda Barnes pioneered the use of the basal temperature test to help identify sluggish thyroid function. To do this, place a thermometer (not digital) under your arm for 10 minutes before getting out of bed. This should be done 10 days in a row, averaging the daily reading. Menstruating women should start the 10 day test when their menstrual cycle begins, as basal temperature naturally rises 2 degrees at ovulation. If your waking temperature averages from 97.8 to 98.2 degrees it is normal. Less than 97.8 reflects sluggish thyroid function.
Other Factors that can Make You Cold
Note that other factors besides thyroid that can make a person run too cold. Common ones include: A) Protein malnutrition results in a loss of muscle. Individuals with borderline thyroid should eat at least half their ideal weight in grams of protein per day (avoid excessive intake of soy protein). B) A lack of nutrients to produce cellular energy (coenzyme B vitamins, malic acid, Q10, magnesium). C) A lack of nutrients to implement cellular DNA thyroid instructions (iron or zinc). D) Excessive stress, which pools blood around central organs and makes hands and feet cold. Anti-inflammatory nutrients are required to fix this, along with stress management. Fish oil and squalene are very helpful. E) A viral infection, even a subclinical viral infection. Viruses hijack cellular energy production, shutting down energy and heat production, and making excess lactic acid. This leaves one feeling cold and achy from the lactic acid. This is why you get the chills from the flu.
Many viruses, like Epstein-Barr or cytomegalovirus, can operate on a low grade basis – enough to make a person cold, tired, and achy. Such individuals often wake up with a sore throat in the morning. These coldness issues can masquerade as thyroid problems, and in some cases may in fact be the primary cause of the low thyroid symptoms.
The proof of the source of the problem is in the solution. Whatever helps get energy on and temperature up is what is needed. Sometimes this means thyroid support nutrition. Sometimes it means addressing any issue in the common factors, A-E, listed above. And many times it is some combination of approaches, including thyroid support.
Energy, Heat, and Metabolism
Rather than being too cold, many individuals with sluggish thyroid symptoms may even be hot. Remember, normal cell energy production is 65 percent energy and 35 percent heat. In classic low thyroid both numbers drop. However, if thyroid hormone is still signaling cells to go, but cells lack nutrients to properly make energy, then a person may make 50 percent energy and 50 percent heat. If the problem worsens a person could make 35 percent energy and 65 percent heat. Such a problem will present itself as low thyroid, but it is really a deficiency in energy-producing nutrients like coenzyme B vitamins, malic acid, Q10, magnesium, and antioxidants.*
A common reason for low thyroid symptoms with excess heat occurs in the overweight individual. In this case the body is trying to dispose of surplus fat calories by converting them to 100 percent heat. Even though cells are not making adequate energy or heat for proper metabolic purposes, the heat is coming from the desperate attempt of the body to get rid of fat so it doesn’t clog organs, cells, and arteries.
Eating according to the Leptin Diet helps solve this problem. Those with thyroid problems often have trouble with temperature extremes, especially hot and cold days. Hot humid days are stressful; frigid winter days are stressful. The body’s heat regulating system simply struggles to keep up with environmental demands, especially when they are more extreme. The ability to heat up during exercise and cool down following exercise is a test of the thyroid system and a vital necessity for staying physically fit. Easily overheating from exercise, especially in warmer weather, is a sign of weakness in the thyroid system as is becoming too weak or dizzy during moderate exercise. Aging is generally associated with deteriorating thyroid function and troubles regulating body temperature.
Fall Season May Trigger Thyroid-Induced Mood Problems
It could be a beautiful Indian summer fall day, but if you have a sluggish thyroid your mood may already be taking a beating. Fall and spring are often difficult times if you have a struggling thyroid gland. Large fluctuations in temperature pose a unique stress to the thyroid system. Thyroid hormone adjusts itself once every seven days (the half life of the hormone). While the liver has some ability to slightly modulate the rate at which T4 is converted to T3 on a daily basis, the basic production of thyroid hormone changes more slowly. When daytime high temperatures vary 25 – 40 degrees over a period of a few days, the thyroid system really struggles to keep up.
The Northern states have a tough time in the fall from the thyroid’s point of view. The first and most obvious symptom is just feeling jolted by the weather changes. Other symptoms include feeling more sluggish, more tired, and your mood may start to suffer. The desire for sweet tasting food increases and you may put on a few pounds. If you have a borderline thyroid status entering the fall season, it is not uncommon to find yourself in a mental funk, even feeling depressed.
Extra nutrient support for the thyroid is vital during this time. Heading into the holidays with a sweet tooth raving and an unstable mood is setting the stage for bottoming out in the winter months. Understanding your body’s heating and cooling system is central to effectively managing thyroid health.
How to Improve Body Temperature and Thyroid Function
Several basic nutritional inadequacies stress thyroid function. These are the very first things anyone concerned with thyroid health should supplement. Core nutrients needed for healthy thyroid function include selenium, l-tyrosine, manganese, iodine, B12, and zinc.
Iodine is absolutely necessary for thyroid hormone formation. I recommend a water-soluble and extremely biologically active form of iodine called Iosol Iodine. It is one of the best supplements to help warm body temperature. Unlike potassium iodide, which can clog the thyroid gland due to its poor solubility, Iosol Iodine readily washes away if it is not needed. It is hands down the best iodine on the market today.
Optimal nutrition can improve the formation of thyroid hormone in the thyroid gland, enhance the conversion of basic thyroid hormone T4 to the biologically active T3, and enhance the nutritional ability of cells to utilize thyroid hormone. This helps you to have better body temperature, energy, mood, and metabolism.