Lyme Disease and Thyroid Hormone

Borrelia burgdorferi, seen with dark-field microscopy: this is what the germ looks like.
Figure 1: Borrelia Burgdorferi, dark-field microscopy

About Lyme disease: its relationship to Intracellular Hypothyroidism: origin, symptoms, diagnosis, treatment.

An old friend, who is an avid and successful vegetable gardener, is passionate about mushrooms, especially chanterelles (Fig. 2), which abound in the woods of Ontario and are easily found, if you know what to look for.

Chanterelle mushrooms
Figure 2: Chanterelle mushrooms, tasty and expensive

So successful is he in the chanterelle hunt, that he is able to augment his income (a bit!) by selling them to knowledgeable restaurants. 2023 has been a bumper year, for chanterelles and my friend, while keeping himself amply supplied, sold his surplus for more than $1,000.

In July however he found a small red spot, which began just above his elbow and spread around the arm. Soon he became ill and progressively, so weak that he was admitted to a hospital. Eventually, a blood test showed Lyme Disease and he was started on a course of antibiotics. He is now improving, though very slowly.

My friend’s experience led me to a web search on Lyme disease and being me, I began the search by entering “Lyme disease T3” into Google. Lo and behold, the following appeared on my handheld screen: “The inflammatory cytokines that are produced in Lyme disease impact thyroid hormone signalling. This means thyroid stimulating hormone (TSH) may decline. The conversion of T4 to T3 (the active thyroid hormone) can be reduced, leading to fatigue and low energy levels. Additionally, reverse T3 can become elevated. June 2. 2023.”

I almost fell off my chair: that such a perspicacious (if slightly inaccurate) statement would appear as a first response from Google is mind-boggling! It means that someone, somewhere, is beginning to think about peripheral thyroid hormone metabolism and if we are lucky, the medical establishment will finally begin to consider it seriously.

So let’s discuss Lyme disease.

Lyme disease is caused by a germ called Borrelia Burgdorferi (Fig 1), which looks like the syphilis germ, Treponema pallidum, in that it is a “spirochete”. It is long and narrow, for a bacterium (20 – 30 µm long and 0.2 – 0.3 µm wide), “curly and wiggly” and completely colourless – to see it under a microscope, you have to view it on a “dark field”, as shown in the graphic from Wikipedia, in figure 1. Worldwide, there are 15 species of Borrelia, of which 5 cause Lyme Disease.

Borrelia Burgdorferi is passed to humans by the bite of ticks and lice (Fig. 3). Its presence in our blood can be identified in the laboratory by immunity testing (not by looking for it under a microscope).

Adult deer tick (most infections are from bites by juvenile ticks, or lice.
Figure 3: Adult. Deer Tick

Usually, the tick bite is painless and isn’t noticed by the unfortunate recipient until a red spot appears somewhere on the skin, 3 days to a week (or more) after the bite. Classically, the area around the bite looks like a “bull’s-eye” (Fig. 4), with a red spot in the middle, a surrounding circle of normal -looking skin and a red circle of 6 inches or more, outside of that (figure 4). However it isn’t always that obvious: there might be a simple, small red spot such as one would get from any insect bite, or maybe a rash, or an irregular red area. The inflamed area usually lasts between 3 and 5 weeks and other red spots may develop.

Bull's-eye rash from Lyme disease: this is classic, but the the rash may be different: the "bull's-eye" isn't always present.
Figure 4: (2007, .James Gathany). Erythematous rash in the pattern of a “bull’s-eye”,

observed in about 80% of Lyme disease patients.


Symptoms * begin sometime later, usually with headaches and neck stiffness, more rashes, odd aches and pains, fever, fatigue, numb and tingly areas and even “brain fog”. The affected person may become really ill and the problem can last a long time – years, in some cases.

The symptom list below comes partly from the two references, mentioned below:

*In the acute phase, there is some combination of:

  • Headache, fever and fatigue in the acute phase of Lyme infection, with neck stiffness
  • Additional erythema migrans rashes in other locations
  • Muscle pain, Arthritis and joint pain, often affecting the knees and other larger joints
  • Nerve pain, numbness, and tingling in the hands or feet
  • Facial paralysis, with a drooping appearance and/or loss of muscle tone in the face
  • Heart palpitations, irregular heartbeat, dizziness, shortness of breath
  • Brain fog, short-term memory problems and Changes in vision

*In chronic cases, the history may include:

  • Severe headaches
  • Arthritis, with pain and swelling of joints
  • Heart abnormalities
  • Mental disorders, including depression
  • Cognitive and neurological impairment, such as confusion, short-term memory loss, and brain fog
  • Numbness in the extremities


(1) A discussion of Lyme disease itself is not my main purpose here: for greater detail about the illness, please see an excellent “layman’s” dissertation on the subject, by Mary Shomon, at health central, https://www.healthcentral.com/article/lyme-disease-and-your-thyroid .

(2) Lyme disease is like Covid in two ways – the fatigue is similar and its effects can persist for an extraordinarily long time. Lyme disease doesn’t become chronic in every case, but for those who are affected, it represents a major problem. So much so that, like “Long Covid”, there is a name for it. The term is “Post – Treatment Lyme Disease Syndrome,“or “PTLDS” (I’m tempted to call it “Long Lyme”, a nickname which my Trinidadian friends would find amusing, because in Trinidad, “Lyme” means “hang-out, drink rum, and chat”).


With Long Lyme in mind, I searched Google: I browsed many websites for information on, and an intelligible explanation of, chronic Lyme disease. Eventually, I found an article by Laurence Geebelen et al., entitled “Non-specific symptoms and post-treatment Lyme disease syndrome in patients with Lyme Borreliosis: a prospective cohort study in Belgium (2016–2020)”, published in BMC Infectious Diseases volume 22, article number 756 (https://doi.org/10.1186/s12879-022-07686-8). I would recommend this article, for details of the type, frequency and severity of symptoms, associated with “Long Lyme”.

Geebelen et al. reported on a detailed study of patients with “Long Lyme” in Belgium. To quote the article, “Patients with Lyme borreliosis may report persisting non-specific symptoms, such as fatigue, widespread musculoskeletal pain or cognitive difficulties, resulting in substantial reduction in previous levels of occupational, educational, social, or personal activities. When present for more than 6 months, causing a reduction in daily activities, it is referred to as Post-Treatment Lyme Disease Syndrome (PTLDS).”

Geebelen et al also linked Long Lyme with chronic fatigue syndrome (see CBHRT.ca).

PTLDS may continue for years.

Association of Long Lyme with decreased functionality of Thyroid Hormones

The symptoms of Long Lyme are at least similar to, if not identical with, those of Intracellular Hypothyroidism, which is responsible for the symptoms in Chronic Fatigue Syndrome, Long Covid and Fibromyalgia and which accompanies and complicates virtually all severe illness. As such, it seems highly likely that some of the symptomatology of PTLDS may be due to Intracellular Hypothyroidism (IH: a.k.a. Low T3 Syndrome, Euthyroid Sick Syndrome, Nonthyroidal Illness, etc.), especially since IH accompanies virtually all severe, stressful diseases.

If this is so, diagnosing and treating coexisting IH would go a long way toward ameliorating the symptoms of Lyme disease.

Treatments for PTLDS

PTLDS is difficult, or impossible, to cure. As is the case when doctors do not know the reason for a patient’s symptoms, many methods of reducing discomfort have been tried, among them Dr. Daniel J Cameron’s recommendation of LDN (low dose Naltrexone), Dr. Kent Holtorf’s suggestion of Antabuse and Dr. K Passero’s course of Probiotics and Colostrum for the immune system and the gut, Alpha Lipoic Acid for nerve support and nerve pain, Cat’s Claw for joint pain and inflammation and Turmeric for inflammation.

To these, I would add (1) Progesterone and PEA, to increase brain-based Allopregnanolone (for painkilling, better sleep and stress reduction), (2) DHEA, to raise Testosterone in women (and Oestrogen in men), to improve both Thyroid hormone function and general cellular metabolism,
(3) Slow-release Triiodothyronine, to counteract the effects of IH, if suppression of the T3/rT3 ratio is demonstrated (based on a full thyroid profile, including TSH, FT4, FT3 and rT3).

Doctors should add a full “thyroid profile” to the list of investigations for Lyme disease, to find out whether Intracellular Hypothyroidism is part of the reason for the patient’s symptoms.

At the time of diagnosis, the “workup” (investigation) for everyone who develops Lyme disease should include TSH, FT4, FT3 and reverse T3, so that Intracellular Hypothyroidism, if present, can be definitively diagnosed based on the T3/rT3 ratio. If and when the ratio is found to be positive (less than 20.0), the patient should be treated with oral, slow-release triiodothyronine, sufficient to raise the serum FT3 to between 4.5 and 6.1 pmol/litre. If the ratio is negative (more than 20.0) for IH, the study should be repeated following antibiotic treatment for Lyme disease, because the stress of chronic disease is a cause of IH.

Treating IH with slow-release triiodothyronine will reduce, or eliminate, IH symptoms and the adverse effect of Lyme disease on the patient’s quality of life will be minimised.


Here, links are provided, in view of a reference list: I am Indebted to the authors of the articles mentioned, for the list of symptoms and the general information on which this blog post is based.

I am a Toronto-trained Urologist. I practiced in downtown Toronto, from 1977 to 1997, when I went to Saudi Arabia as chief of Urology at the Armed Forces (teaching) hospital in Tabuk. Returning to Toronto in Y2000, I switched to family practice. In 2007, began to prescribe Hormone Restoration Therapy and in 2012, I became a member of the American Academy of Antiaging Medicine [A4M]. I successfully wrote the A4M's written examination in December, 2013 and In May, 2016 I passed the oral examination, for accreditation as a BHRT consultant. In 2014 I began BHRT practice in Collingwood, Ontario and in January, 2017, joined the Stone Tree Naturopathic Clinic. Now I am 82 and have retired, but it seems wasteful to jettison my learning and experience: the medical establishment knows nothing of BHRT / Functonal medicine and I feel obliged to offer my knowledge in the interest of those who are willing to think outside the box. MY QUALIFICATIONS: MB, BS, (from UWI), 1964. LMCC 1969. FRCSC (Urology), 1974. ECFMG 1984. Florida license 1998 [inactive], ABAARM Certification [A4M], 2016. I am a Member of CSAMM [the Canadian Society for Aging and Metabolic Medicine], the OMA&CMA, SUSO, CUA, RCP&S/C. PRACTICE TO DATE: Consultation in Functional Medicine, including assessment of Chronic Fatigue Syndrome, Fibromyalgia, Andropause, Menopause, Teenage and Postpartum Depression/Panic Attacks, Thyroid Hormone malfunction, Infertility, Sexual Dysfunction and “the Undiagnosable”. ALL ARE WELCOME to read, comment or question!

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