Happy Spring! Thank you to all my new subscribers - I really appreciate your interest!

Once again, it has been a busy few months. I attended the Integrative Healthcare Symposium in NYC in February, which was a great opportunity to learn from physicians such as Aviva Romm MD, Jacob Teitelbaum MD, Walter Crinnion ND, and Leo Galland MD. I continue to see patients at Dr Kennedy's family practice in Rochester Hills (moving to downtown Rochester in June now), and have been helping to grow Beaumont Integrative Medicine in Grosse Pointe. It has been wonderful to meet the community on the east side of Detroit and I feel very welcomed. Both of my locations are accepting new patients.

I have several events coming up in the next few months; please scroll down for details. Beginning this Thursday is my Spring Lecture Series in Rochester Hills, followed in April by my Spring Detox Program in Grosse Pointe. I will be giving talks to private groups in Grosse Pointe and writing an article for the Grosse Pointe News. In June, I will be speaking at my first professional medical conference - the Michigan Integrative Medicine Conference - all proceeds support licensure of naturopathic medicine in Michigan.  

On that note, the Michigan Association of Naturopathic Physicians (MANP) has been busy in recent months. We hired a lobbyist and are in the process of resubmitting our bill for licensure of naturopathic medicine in Michigan. Please consider signing up for our mailing list - we will keep you updated on our activities and let you know when we need your support in signing petitions, calling your representative, etc.
 

I am offering a free lecture series at Dr Kennedy's office in Rochester Hills beginning this Thursday. This is a great opportunity for both prospective and current patients to learn more about my approach to health and disease, and how naturopathic medicine can benefit health concerns like digestive and hormonal imbalances. All talks are free and open to the public. 

Beginning next month, I am holding a group detox through Beaumont Integrative Medicine in Grosse Pointe. Please see flyer below for more information. This will be a more intensive detox program than what I have offered in the past, and includes 28 meal replacements. Anti-inflammatory, nutrient-dense eating style is also a major component of the program. We will pre-screen patients beforehand, and guidance will be provided throughout. Call 248-964-9200 with questions or to register. 

The first annual Michigan Integrative Medicine Conference will take place on June 5 and 6 in Novi, MI. This is a continuing medical education conference open to medical professionals. If you or anyone you know is a medical professional in need of CME, or if you would like to exhibit, please see the website for more information. Early Bird registration ends March 31. We have some great speakers lined up! I will be presenting the Women's Health Research Update. 

Last month, the Dietary Guidelines Advisory Committee, a panel of physicians and nutritionists whose recommendations help to shape American food policy, issued a report that eased previous restrictions on dietary fat and cholesterol. It also imposed new limits on the amount of added sugars consumed, among other recommendations. The guidelines have been modified from past reports that recommended Americans reduce their intake of cholesterol and total fat, due to lack of evidence linking these nutrients to health problems such as high cholesterol and heart disease.

Doctors are known for being slow to adopt new clinical practices in response to new information. There are various reasons for this. Resistance to change is not necessarily a bad thing. (Although in sometimes it can be, as was the case with the antiseptic movement in the 19th century.) Research studies often vary widely in their outcomes, and there is a lot of conflicting information out there. While individual studies can be compelling and even practice-changing, it is the body of research and overall trends that are generally used to influence clinical decision-making. That said, new research and ideas are exciting, and I believe that they can be sensibly incorporated into current practice if they are balanced with a healthy degree of caution and skepticism.

Many of my patients are living with chronic health concerns like Hashimoto's thyroiditis, Crohn's disease, or Lyme disease. Physiology often works differently in these people, and I am always learning about ways to improve on my approach to them. I have begun to notice associations between some of these chronic concerns and certain patterns in physiology. Here are some new ideas I have been incorporating into my clinical thought process over the last few months:

A FEW REASONS WHY TSH IS NOT ALWAYS A GOOD INDICATOR OF THYROID HORMONE STATUS IN THE BODY

I have long advocated for the use of comprehensive laboratory evaluation of thyroid function. But sometimes the results are puzzling. This article from the National Academy of Hypothyroidism seems to answer a lot of my questions related to mechanisms that can create a disconnect between thyroid lab results and patient symptoms, particularly in people who have chronic disease. 

Thyroid stimulating hormone (TSH) is commonly measured to screen for thyroid disorders. TSH is released by the pituitary gland at the base of the brain, after which it travels to the thyroid gland to stimulate release of T3 and T4, the thyroid hormones. T3 and T4 are required for proper metabolism in all tissues of the body. Most of the T4 released by the thyroid gland is converted into the more active T3 once it reaches tissues. The pituitary senses T3/T4 levels in the body and adjusts TSH release accordingly. If adequate T3/T4 is sensed, the pituitary assumes that the body has enough thyroid hormone available and it decreases release of TSH; if T3/T4 levels are low, TSH release increases. It is important to note that the pituitary takes up T4 from circulation, converts it into T3 within the pituitary, and this is what the pituitary uses to sense thyroid hormone levels and regulate TSH release.

While measuring TSH can certainly catch many cases of thyroid dysfunction, this screening test is not perfect. (No test is perfect, as much as we would like to believe that they are.) It is not uncommon for me to see someone who is medicated for hypothyroidism display a low TSH on lab results (which would suggest high thyroid function), yet struggle with symptoms of low thyroid function - such as fatigue, weight gain, constipation, dry skin, hair loss, and depression. What is going on here? Indeed, addressing the whole person is very important - in order to promote healthy thyroid function, we must also support the hypothalamus, adrenal glands, optimize digestive function, and address psychosocial aspects, just to name a few. But this disconnect between patient symptoms and lab results also seems to relate to how the TSH is regulated.

The key point is that TSH is regulated by T3 levels WITHIN the pituitary, which may not be indicative of T3 levels throughout the body. The reason for this has to do with how T4 is converted into T3. In the pituitary, the enzyme Type II Deiodinase makes the conversion. Throughout the rest of the body, the enzyme Type I Deiodinase makes the conversion. Type II Deiodinase is much more efficient at converting T4 to T3, so pituitary T3 levels may always be slightly higher than those in the rest of the body.  Furthermore, in some people, Type I Deiodinase may be inhibited, which could cause T3 to be adequate within the pituitary (leading to less TSH release), while T3 levels are actually low throughout the rest of the body. This scenario could cause the clinical picture I described above, in which the person feels hypothyroid, but the TSH is actually low (T3 may be low in this case as well).

What are some of the co-existing conditions that could contribute to this disconnect between T3 levels in the pituitary and the rest of the body? This article mentions physiologic and emotional stress; depression; dieting; weight gain and leptin resistance; insulin resistance, obesity and diabetes; inflammation from autoimmune disease or systemic illness; chronic fatigue syndrome and fibromyalgia; chronic pain; and exposure to toxins and plastics. In addition, Type I Deiodinase activity is also lower in females, making women more prone to tissue hypothyroidism despite having normal TSH levels.

This correlates with what I see in practice, and is part of the reason why I recommend measuring not only TSH, but also free T3 and free T4, and always correlating lab results with symptoms. (Reverse T3 and thyroid antibodies can also be important to measure and would be the topic of another discussion.)

For some time now I have suspected that at least for some people, Vitamin D status may be more of a marker of health, rather than simply a nutrient that needs to be supplemented. It is not uncommon to see Vitamin D deficiency in people who supplement adequately. Some of these people may have a true deficiency, perhaps due to lack of sun exposure, living at a high latitude, or poor absorption. Deficiency may be secondary to issues like chronic kidney disease. Other people may have a functional deficiency, perhaps due to genetic variations in the Vitamin D binding protein (1, 2, 3) and/or Vitamin D receptor (1, 2, 3). For others (and these are usually people with autoimmune and inflammatory syndromes, or chronic infections like Lyme disease), I suspect that low Vitamin D may be a consequence of immune or inflammatory-related processes in the body. There is evidence to support this hypothesis (1, 2; and it is important to keep in mind that it is still only a hypothesis, and somewhat controversial).

But first a bit of physiology: Vitamin D has two forms in the body - 25 hydroxy and 1,25 hydroxy. Vitamin D obtained from sunlight, food, and supplements is first converted into 25 hydroxy Vitamin D in the liver, and then to 1,25 hydroxy Vitamin D in the kidney. (25 hydroxy is the major circulating form and what is commonly measured in blood tests, due to its greater stability.) 1,25 is considered to be the "active" form that can bind to the Vitamin D Receptor (VDR) within cells and activate DNA transcription. 

An important aspect of VDR binding is the ability of 1,25 hydroxy Vitamin D to stimulate production of infection-fighting compounds (1, 2, 3). Some researchers have hypothesized that, in an effort to fight infection, the body up-regulates its production of 1,25 hydroxy Vitamin D. If the infection is temporary, the body recovers and Vitamin D levels come back into balance. But if the infection persists (such as with chronic Lyme disease or Epstein-Barr Virus, for example), 1,25 hydroxy Vitamin D could be chronically elevated. This could cause the 25 hydroxy Vitamin D precursor to be used up, resulting in low serum 25 hydroxy Vitamin D levels. Furthermore, they hypothesize that chronically elevated 1,25 hydroxy Vitamin D leads to chronic inflammation throughout the body. This could explain why low 25 Hydroxy Vitamin D is associated with chronic health concerns like heart disease, diabetes, allergy, autoimmune disease, infections, depression, and cancer.   

What will I do with this information? I will not necessarily recommend that people stop supplementing with Vitamin D if 25 hydroxy is found to be low. But it may help me understand why certain people might have chronic Vitamin D deficiency. It also reinforces the importance of treating the underlying pathology with each person - for instance, addressing an autoimmune process or a chronic infection. I have started measuring 1,25 hydroxy more regularly when indicated by history. If 1,25 hydroxy is elevated, while 25 hydroxy is low, I think about identifying sources of infection or inflammation in that individual. Ultimately, this hypothesis of inflammation-induced Vitamin D deficiency is just another piece of the puzzle and needs to be considered among all other contributing factors for each person.