Rejuvagen Center

For those of you struggling with chronic thyroid challenges and are looking for a better understanding of thyroid physiology and what drives hypothyroidism, tune in to this episode of the FUNK’TIONAL NUTRITION PODCAST! Thanks for having me on the podcast Erin!

So this is the stuff I hear every single day. This is the challenge most of you are up against. This person has been overweight for 25 years and diabetic for 14 years. She has had a TSH ONLY tested and been told that she does not have a thyroid problem.... Impossible! But lets dig a bit deeper. Her medical doctor is following the guidelines and running a TSH with reflex to fT4. This means that ONLY TSH is initially run, if it is above or below the lab reference range of 0.45 - 4.5, the lab will automatically run a fT4. In this person's case TSH was normal so fT4 was not run and she was told no thyroid problem. Why do I say it is likely impossible that she doesn't have a thyroid condition? 1. To get glucose into a cell requires optimal levels of T3 inside the cells. If you are insulin resistant or diabetic you have reduced cellular T3. Cellular / Tissue Hypothyroidism. 2. When you have reduced T3 inside your cells, you have reduced mitochondrial numbers, and a reduced amount of energy that can be generated via the mitochondria. Technically, mitochondria in a hypothyroid cell become MORE efficient, but generate less overall energy and therefore can't process as much glucose. Glucose that does make it into the cell, gets pushed back out of the cell to form cholesterol. In a tissue hypothyroid state, that cholesterol can't be converted efficiently into cell membranes, hormones, etc. and instead heads to the liver to become bile and excreted. But, if the liver is in a hypothyroid state, the LDL carrying the cholesterol can't dock to the liver and dump off the cholesterol. Resulting in increased cholesterol and LDL. More lipids are being stored in the white adipose tissue, resulting in increased inflammation (which lowers TSH, and deactivates T4 and T3 in the peripheral tissues, further slowing metabolism. Continued in comments...

Far too many people are being told they are vitamin D deficient and placed on high doses of vitamin D supplementation. How is vitamin D deficiency determined? Depending on the lab range your doctor uses, you may be diagnoses with vitamin D deficiency and placed on vitamin D supplementation if your 25OHD levels are less 35 for sure and often times if your value is less than 50.... So what's my beef? Why do I have to be the contrarian? My issue is that much like other situations one test is run to assess for the state of a condition or deficiency. There are a number of forms of vitamin D. A few include: - Vitamin D - 25 OH vitamin D - 24,25 OH vitamin D - 1,25 OH vitamin D - 1,24,25 OH vitamin D What is measured in a traditional lab setting is just 25 OHD, the storage form of vitamin D. It is not the active form that carries out the actions of vitamin D that every discusses. 1,25OHD is the active form that does all the work. Approximately 75% of your vitamin D is generated in the skin from sun exposure. 25% comes from food. But this is vitamin D. It is NOT 25 OHD. It is NOT 1,25 OHD. Vitamin D must be converted in the body to the storage form 25 OHD and 1,25 OHD. So what's the point, right? If you get tested for low 25 OHD your doctor is going to say you are vitamin D deficient and likely place you on 5000 IU (or more) vitamin D. But, should we ask a few questions before we load someone on vitamin D? How about these: 1. Why is the person deficient in 25OHD? 2. Is it due to reduced sun exposure? 3. Is it due to reduced dietary intake of vitamin D rich foods? 4. Is it due to malabsorption caused a GI problem? 5. Is it due to magnesium deficiency to support the transport of Vitamin D to the liver to convert to 25 OHD? 6. Is it due to magnesium deficiency preventing the converting enzyme 1a Hydroxylase from converting vitamin D to 25 OHD? Continued in comments...

I am often asked this question regarding Vitamin D by my clients. While I am not your doctor and can't advise you on what to do, I will provide some of my thoughts on vitamin D supplementation and why I think we need to be more cautious on vitamin D supplementation. When people are evaluated for vitamin D status, they are often only tested for 25OHD which is the inactive storage form of vitamin D. All the actions attributed to vitamin D are the result of 1,25OHD NOT 25OHD.... The argument in the literature regarding why not to measure 1,25OHD: --- Serum levels of 1,25-dihyroxyvitamin D have little or no relationship to vitamin D stores but rather are regulated primarily by parathyroid hormone levels, which in turn are regulated by calcium and/or vitamin D. ---- Here is my problem with this statement. It assumes that the up regulation of 25 to 1,25OHD only occurs as a result of low calcium and increased PTH. Anyone looking at the literature knows that 1,25 OHD can be upregulated for other reasons including immune and inflammatory conditions. --- If the doctors only goal is to maintain normal 25OHD levels then yes, only 25OHD needs to be measured. --- However, if the doctors goal is to the best think for their patient they need to do more than just constantly fill up vitamin D stores. The doctor should ask: - WHY are the 25OHD levels consistently low? - Is the person not getting sunlight? - Are they not consuming vitamin D rich foods? - Do they have a GI issue that is resulting in reduced fat and fat-soluble vitamins? - Do they have low magnesium that is preventing the liver from converting Vitamin d into 25 OHD? - Do they have liver dysfunction that limits conversion of vitamin D to 25OHD? - Are they over-converting 25OHD to 1,25OHD due to low serum calcium and elevated PTH? - Are they over-converting to 1,25OHD do to some immune or inflammatory condition? - Are they rapidly deactivating 25OHD to it's inactive metabolite 24,25OHD? Continued in comments...

Is there a link between hypothyroidism and infertility? Absolutely! Ovulatory function requires optimal levels of T3 at the ovaries.... But it is not always as simple as simply putting more thyroid hormone into the blood stream. TSH may normalize, but that does not guarantee optimal T3 at the ovaries. No hormone works in a bubble by itself. It is often a complex web of function or dysfunction that determines health or dysfunction of the tissues. Excessive cell stress can result in tissue hypothyroidism. Tissue hypothyroidism can result in reduced metabolism and more calories being stored in adipose tissue. As adipose tissue increases: - more inflammation is produced - more leptin is produced - less adiponectin is produced and adiponectin signaling is reduced In a state of low stress and optimal thyroid physiology, as leptin rises it stimulates an increase in TSH, thyroid hormones, and increased metabolism. When there is cellular hypothyroidism, T4 and T3 are not impacting impacting the cell to increase cell metabolism. Thyroid hormone is being deactivated. Metabolism slows. Glucose is not getting into cells as easily requiring more insulin. Cells become insulin resistant. More calories are stored in adipose cells / fat cells. More inflammation is released. More leptin is released. Less adiponectin is released and signaling diminishes at the adipose cells to control inflammation. (adiponectin is anti-inflammatory, insulin sensitizing) The hypothalamus starts to become Leptin resistant due to the excessive level of leptin. You stay hungry. You eat more food. You can't burn the calories. You gain weight. You become more hypothyroid. You become infertile. It is a vicious cycle! I know... HOW DO YOU FIX IT? It depends on the INDIVIDUAL and what is driving their cellular hypothyroidism, their elevated leptin. I wish it was so simple everyone could take the same pill, the same supplement, have the same solution. It isn't that simple.

The amount of T4 and T3 in the blood is important but, as research has pointed out, it is only a part of thyroid physiology. The amount of thyroid hormone in the blood is not necessarily a reflection of the thyroid hormone levels in the cells. Normal levels in the blood don't necessarily reflect euthyroid state in all the cells and tissues.... Too often it is assumed that normal blood values of TSH, and fT4 indicate optimal thyroid physiology in all the tissues, yet the scientific literature indicates the opposite. How do we know if "normal" TSH and fT4 indicate optimal thyroid physiology in the cells and tissues? 1. We listen to our patients. Are they struggling with signs and symptoms of hyper or hypothyroidism. 2. We can observe our patients for signs of hyper or hypothyroidism. 3. We can look at a comprehensive thyroid panel which includes more then TSH and fT4 for indicators of cellular hypothyroidism. 4. We can look at inflammatory tests. Inflammation favors both the increase of T4 to T3 and the increase of T4 to rT3 depending on the tissue type. 5. We can look at other lab values for signs of tissue hypothyroidism. Some examples include: markers of insulin resistance, elevated cholesterol, reduced renal function, reduced mitochondrial function just to name a few. #hashimotothyroiditis #functionalmedicinepractitioner #functionalmedicinecoach #hyperthyroid #functionalmedicinedoctor #thyroidectomy #thyroidwarrior #hashimotoswarrior #hyperthyroidism #hashimotosthyroiditis #thyroidhealth #thyroiddisease #thyroidhealing #integrativehealth #thyroidproblems #hormonehealth #hypothyroid #hashimotosdisease #functionalnutrition #autoimmuneprotocol #healthandhappiness #healthyjourney #integrativemedicine #healthandwellbeing #wellnessadvocate #thyroid #hashimotos #hypothyroidism #functionalmedicine #healthandwellness

I think this is the most important concept I explain to my clients. And I think it is empowering to the client to realize their thyroid physiology is often not broken, it is adapting to protect them from excessive cell stress. When you realize that cells in danger deactivate thyroid hormone as part of a protective response to slow down metabolism, reduce glucose and other fuel transport into cells, increase inflammation, and defensive chemicals, you can start to understand wh...y you don't healed by more thyroid medication. You can start to understand why switching thyroid medications, types of medications, and doses only provide temporary improvement, if that. Before you ask me how do I recommend fixing your hypothyroidism, or make a comment like "but how do I fix it", realize that the solution improving your hypothyroid state is different then someone else's. For decades we've been told that fixing TSH fixes hypothyroidism, but it often doesn't. Thyroid hormone replacement therapy (THRT) does not "fix" hypothyroidism. THRT just puts more thyroid hormone into the body. If you have no cell danger response and homeostatic (no excessive cell stress) thyroid hormone regulation, thyroid hormone from THRT will reach the cells and tissues and be used to increase cell metabolism, growth, and energy production. If you have a cell danger response and allostatic thyroid hormone regulation, thyroid hormone from THRT will lower TSH, but will be deactivated by cells in a danger response away from the hypothalamus. You will continue to have hypothyroid symptoms despite a normal or low TSH. The lower you drive TSH, the more hyperactive the brain becomes and the more hypothyroid the body becomes. THRT will not eliminate what is causing the cell stress. It will not eliminate the danger response. It will not change thyroid allostatic regulation to homeostatic regulation. Continued in comments ...

Dr Eric and Dr Erica answer more of your questions regarding hypothyroidism. If you have questions about hypothyroidism or any aspect of your health, submit the questions to the podcast to [email protected]. In today's episode the doctors answer listener questions including: Why does blood glucose rise when I do Intermittent fasting?... Why is fasting blood glucose high if insulin is low? Are T4 / T3 combo medications bad? Why does Ketogenic diet make me feel worse? It seems like I have to keep increasing T3 medication just like I had to do with T4 medication, WHY? More ... All Thyroid Answers Podcast episodes are available on Youtube, Apple podcast, Spotify or wherever you get your podcasts. Have questions you need answers to? Send questions to office at www.rejuvagencenter.com. #hashimotothyroiditis #functionalmedicinedoctor #thyroidawareness #functionalhealth #autoimmunity #thyroidectomy #thyroidwarrior #hashimotoswarrior #autoimmunediet #hashimotosthyroiditis #thyroidhealth #thyroiddisease #immunology #healthawareness #thyroidhealing #thyroidproblems #antiinflammatorydiet #hypothyroid #hashimotosdisease #autoimmuneprotocol #eathealthyfood #journeytohealth #healthyjourney #digestivehealth #thyroid #healthyself #hashimotos #hypothyroidism #autoimmune #autoimmunedisease

... thyroid physiology works / regulates differently in states of homeostasis (low stress - sufficient energy to run body needs) vs allostasis (high stress - insufficient energy to run body needs). When your body is perceiving excessive stress or danger the body shifts the focus from growth and anabolic metabolism to cell defense and catabolism. We see upregulation of systems/pathways like the AMPK. The goal is to reduce energy expenditure (slow non-essential metabolism neede...d for immediate survival) while increasing energy production. Thyroid hormone is used to help regulate cellular metabolism. The net reduction of thyroid hormone within cells and tissues and the net reduction of thyroid hormone by the thyroid gland helps to support the shift in cell metabolism. Said differently, your hypothyroid symptoms are the result of normal homeostatic thyroid regulation being turned down, so that cell energy is shifted toward cell defense. Your thyroid physiology isn't broken, it is adapting to danger signals. When the danger response is persistent and prolonged thyroid gland damage occurs as part of the defensive response to reduce anabolic metabolism. Unfortunately you don't feel well. You have symptoms. You have upregulation of inflammation. You don't have the energy to exercise. You don't have cellular energy being put toward optimal hair growth, skin health, hormone regulation, and GI physiology. As a result, these systems start to malfunction and develop symptoms and dysfunction. We rush in to make / force these systems work without realizing that these things are all the result of cells, tissues, and bodies in a state of chronic excessive stress response. We don't realize that these systems are turned down ON PURPOSE. This is why when you add more thyroid hormone in the form of medication it does not eliminate your symptoms and often makes some of the systems worse. Continued in comments ...

Sometimes I have so many emails I just want to delete them all and start the day with a fresh slate. I However sometimes there is gold in some of the emails. This morning was one of those days. I opened an email from my brother. Usually his emails contain snippets from something political, world politics or something military oriented.... My brother is one of the best people I know. He has spent over 30 years in the military serving our country. He is not only my brother but one of my closest friends. He is my hero. In his email he shared this simple message. If you started your day reading this and than lived these concepts throughout the day your life, health, and relationships (including with yourself), would all have a significant opportunity to be better than they are right now. None of us are perfect. We all lose our way at times. We all get diverted from the original path. But if you repeated these concepts to yourself at the start of the day and the asked yourself at the end of the day, was this how I lived today. It would be really difficult to not see an improvement in every aspect of your life. Despite all the challenges we face right now, things could be worse. Realize that for most people with the ability to have an IG account, they have it so much better than many others. The way we improve our lives, or communities, our stat, our country and our world is not by telling other people how to talk, how to think, how to behave. We don't improve ourselves or others by shaming, canceling, or trying to force our opinion onto others. We don't fix hatred, by spewing more. We don't fix disruptive behavior with more disruptive behavior. We don't improve communication by preventing free speech. We don't bring people together, by telling them how awful they are. Continued in comments ...

Has this happened to you? Do you need to take an antihistamine to get to sleep at night? The likely culprit here is too much or too little thyroid hormone getting to the hypothalamus resulting in mast cells degranulation, and excess histamine in the hypothalamus (brain). Histamine stimulates you to be alert and awake. In this situation, there is too much histamine circulating at night, causing the insomnia. ... This person stated that the only thing that seemed to work to help her get to sleep was a H1 blocking antihistamine. This was the clue that let us know it was excess histamine. The next thing to consider was if the histamine was caused by too much thyroid hormone or too little. When we reviewed the rest of her bloodwork and story we could see that she did not have the symptoms to the same degree with T4 medication. Symptoms got significantly worse with switch to T4/T3 medication. A review of her thyroid panel, comprehensive metabolic panel, diet, health history and symptoms provided the rest of the picture. The person demonstrated multiple lab indicators of GI malabsorption. She was on a high dose of T4/T3 medication and yet her T4 and T3 levels in the blood were functionally low. She was clearly not absorbing her thyroid medication efficiently. With less thyroid medication being absorbed, there was less thyroid hormone getting to the hypothalamus. Mast cells in her hypothalamus were degranulating, releasing T3 to support the hypothalamus, but with the T3 came a bunch of histamine which was causing insomnia. So why did the insomnia get worse with switch to T4/T3 medication? Continued in comments ...

I take about 8 discovery calls per week to answer questions for people regarding thyroid physiology. One of the biggest things that I try to help them understand the difference between the allopathic medicine approach to thyroid care and what I believe should be the functional medicine approach to thyroid care. In allopathic medicine your primary care or endocrinologist IS focused on manipulating your lab values. It is thought that if lab values can be manipulated into range,... the patient has been "fixed". In reality, the lab value has been "fixed" but the patient has only been "managed". The underlying cause is likely still present and the patient will need to be managed for the rest of their life with medications to keep their "LAB VALUE" fixed. They may feel better, but the are likely not healthy or well. In my opinion a good functional medicine practitioner understands that lab values are a sign of a problem or adaptation and NOT the problem. My job is to help find the cause or causes of WHY your lab values are out of range. My job is to help you fix YOU so that the lab values change. I've had 3 calls this week where the person calling said their functional or integrative doctor had tried lots of different types of thyroid medications, and supplement to try and "fix" their low T3 and high rT3 but nothing was really helping improve how they felt. They wanted to know why, and what I might do differently. This is when I usually explain that what their previous doctors were doing was not functional medicine. Their doctors were still practicing allopathic medicine concepts. Their doctors were still trying to manipulate lab values, they were just using different medication and supplements. What I do different ... CONTINUED IN COMMENTS

Seems like a straightforward question. The answer is anything but straightforward. The answer might depend on whether you are the patient or the clinician. The answer is influenced by how you define hypothyroidism, how you diagnose hypothyroidism, or how you address hypothyroidism. Hypothyroid symptoms are caused when there is insufficient T3 reaching the receptors inside your cells and tissues.... The next question might be, does insufficient cellular T3 ONLY occur when the thyroid gland has lost 90% of its output and you are diagnosed with primary hypothyroidism or is it possible that cells and tissues could have insufficient T3, despite a normal TSH and T4? Or is it possible that you could have insufficient T3 reaching cells and tissues when the thyroid gland has only lost 10, 30, 50, or 80% of its output? Is it possible to have low T3 in some cells and tissues despite no loss of function of your thyroid gland? The answers are as follows. Cells and tissues can have insufficient T3 despite a normal TSH, normal thyroid gland output, or normal levels of T4 or T3 in the blood. So if this is the case, when does hypothyroidism start? In medicine it seems that hypothyroidism "starts" when the damage to the thyroid gland becomes so bad that 90% of gland output is lost, TSH is above lab range and T4 is below lab range. Hypothyroidism essentially starts when the thyroid gland becomes significantly damaged, and medication is often required. But, your hypothyroid condition didn't start when the thyroid gland finally gave out. Something caused the gland to start becoming damaged. It was a process. The issues that initiate Hypothyroidism often "start" months or decades before obvious signs or symptoms. Cellular hypothyroidism and immune infiltration of the thyroid gland often starts long before labs go out of range, long before a primary hypothyroid diagnosis. So when does hypothyroidism start? Continued in comments ...

I just read a blog from a doctor that provided recommendations for reversing insulin resistance if you have hypothyroidism. The guidance provided in my opinion is flawed and I will cover why in this post. Recommendation 1: Measure TT3 and fT3 levels. If they are low, T3 medication should be provided. Lets think about this. You are hypothyroid. You are taking T4 replacement therapy and T3 / fT3 levels are still low. This means that tissues are likely favoring the deactivation... of T4 to rT3 vs the conversion to T3. If the tissues are favoring deactivation of thyroid hormone, what happens when you add T3 medication? True more T3 will likely get into cells, but the same deactivation process will be deactivating T3 as well. So, after a short honeymoon period, this stops working. But, your anxiousness, brain fog, and insomnia will increase. Recommendation 2: Low carbohydrate diet This I would agree with to some degree. Lowering your carbohydrate intake will reduce the need for insulin to be produced. However, if you have a cell danger response and cellular hypothyroidism, your cells and tissues are actively trying to reduce glucose coming into your cells. They are insulin resistant on purpose, not because of too much carbohydrates. So lowering excess carbohydrates is good in my book, but doing that on its own won't fix insulin resistance if CDR and cellular hypothyroidism are present. Rec 3: High Intensity Interval Training Look I love HIIT. But for someone with CDR, CHT, reduced mitochondrial function, poor energy production, and poor recovery this will backfire. When you have a CDR, your tissues are in defense mode not muscle building mode. Rec 4: Intermittent Fasting / Time Restricted Eating This I fully agree with. No arguments at all. I think this needs to be done under guidance as a person with CDR and CHT is may struggle with the transition. Continued in comments ...

Have you noticed this as well? Seems odd, right? If your doctor is increasing the dose of T4 medication, shouldn't T3 levels rise?... It depends. It depends your cells and tissues are in a state of excessive cell stress / cell danger response. If your cells and tissues are in a low stress homeostatic state, than yes we might assume that if your thyroid gland is not making sufficient thyroid hormone, and there is not an active cell danger response, T4 should convert to T3 efficiently. However, thyroid physiology behaves a bit differently when your cells are in a "danger" response. When cells perceive excessive stress or danger hypothyroidism is INDUCED in the cells as a protective mechanism. Chronic persistent CDR can result in damage to the thyroid gland and primary hypothyroidism. We often look at the loss of function of the thyroid gland, as dysfunction of the immune system instead of what it likely really is, part of the protective mechanism to reduce metabolism under times of excessive cell stress. Instead of realizing thyroid physiology isn't broken, but adapting, we start loading the body with thyroid hormone to replace what the gland is not making. If your physiology is no longer in CDR, this should help improve hypothyroid signs and symptoms, improve TSH and raise BOTH T4 and T3. However, if your body is in an active CDR, you may see a temporary improvement of signs and symptoms that quickly plateaus. TSH and fT4 levels may normalize. But if someone is testing T3 and fT3 levels what we often see is they do not normalize, especially from an optimal level perspective. You continue to complain of chronic hypothyroid symptoms, your doctor increases T4 med, and T3 gets worse along with symptoms. Well, you may actually start to see some hyperthyroid symptoms as well as TSH drops below 0.50. Why does this happen? Continued in comments ...

Not a day goes by that I don't have this conversation with someone that schedules a discovery call or initial consultation. I get it. You are struggling. Want answers and a solution. Unfortunately there are very few people that see their thyroid physiology and chronic hypothyroid symptoms improve with an individual supplement or two. I do not have a secret supplement concoction that fixes your thyroid, fixes why you have conversion issues, or magically gets T3 to bind to re...ceptors. I know people post this stuff, but it just isn't true. The reality is most people struggling with chronic hypothyroidism, chronic hypothyroid symptoms, struggling to find the right type of medication and dose, or have tried all the "thyroid" formulas will never get better. You might feel a bit better as you try something new (the honeymoon period), but it typically doesn't last. Why? Because all those things are addressing the effect, not the cause. Let me give you a typical scenario. Patient says last year she started gaining weight. She had some other symptoms as well and a friend said maybe she should be checked for hypothyroidism. First time she was tested, TSH was normal. Dr said not a thyroid problem and recommended stress management, reduced food intake, eating frequent small meals, and increase her exercise from 4x/week to daily. Three months later she returns for new labs and check-up. She is frustrated as she has put on 10 pounds in last 3 months despite following advice. New panel shows she is now hypothyroid. Dr prescribes T4 medication. Over the next 9 months she continues to struggle with chronic hypothyroid and hyperthyroid symptoms. She sees a couple endocrinologists, tries multiple forms of T4 and T4/T3 medication. She is beyond frustrated at this point. Continued in comments ...

Have you been told you are insulin resistant, have fatty liver, have prediabetes, or have type 2 diabetes? Do you struggle with belly fat you just can't lose? Have you been told to eat less food, eat less carbs, or exercise harder to loose your belly fat? Have you been prescribed medications like metformin?... Have you been told the solution is a bunch of supplements that help glucose get into the tissues? Have you been told that it is because of hypothyroidism and you were given T4 therapy? When that didn't work were you told it was because you don't convert T4 to T3 well so taking a T4/T3 medication would work? When that didn't work were you told you needed a T3 only medication, a glandular, or special nutrients to "optimize the thyroid"? AND NONE OF IT WORKED! I hear these things from my new clients all the time. They are led to believe their body is breaking down. They are told that their body is not working well to process glucose because something is "broken". When we continue to spread this dogma, it puts the person in the situation in a bad position. It puts them in a situation where they feel their own body is failing them. That they must now work against their own dysfunctional body. But, if we step back and really take a deeper look at what is going on, the body is NOT letting you down. It is NOT working against you. You are not having a insulin resistance and storing body fat because your body is broken, but because it is actually working. When you put more carbohydrates into a body that is struggling with excessive chronic stress, insulin resistance and storage of body fat is your body's protective adaptation to protect itself from perceived danger. Trying to "fix" insulin resistance by trying to force the cells to take on more glucose they don't want is nuts. Medications that try to increase insulin to overwhelm the resistance of the tissues is not the solution either. Continued in comments ....

I was asked this question yesterday. You too may be asking this question. For many people who struggle with chronic hypothyroid symptoms this is there question. This is there frustration. So, what is the answer? I used the following analogy for the client. Hopefully it helps some of you.... If your car was not running properly and you took it to a mechanic and they quickly looked at just the gas gauge and saw it was near empty and said the reason the car wasn't running well was because there wasn't enough gas in the car, you might accept that as the reason. Just like when your doctor says your TSH is high, you need more thyroid hormone. The mechanic fills the tank with the lowest grade gas (Levothyroxine) and sends you on your merry way. The car still does not run well, but the mechanic tells you it will just take time for the car to normalize. The next day the car is still not running well, so you take it to another mechanic. He looks at the gas gauge only and says the gas tank is not quite full, maybe more gas (stronger dose of Levothyroxine) will make it run better. He overflows the tank just to make sure the tank is full. Continued in comments ...

I've had a number of patients over the years tell me that they had Graves Disease, where treated for it and then developed Hypothyroidism. For many of my patients they report having this experience not long after a pregnancy. I often try to clarify if they were diagnosed with hyperthyroidism as a result of postpartum thyroiditis or actually diagnosed with Graves Disease. Most aren't sure. You may not be sure either so a good topic for a post. ... Their previous labwork should tell the story. But the most likely diagnosis is postpartum thyroiditis manifesting as hyperthyroidism. Why would I say that? Because postpartum thyroiditis (PPT) is 20x more common than Graves. For many who develop PPT, they initially have a hyperthyroid phase starting about 2 months postpartum. Below are the clues that differentiate PPT Hyperthyroidism from Graves Disease. PPT Hyperthyroidism: - Prevalence: 6% of pregnancies - Timing of onset: between 2-6 months postpartum (PP) - History: No previous history of Graves, possible previous history of PPT, family history of PPT, or other autoimmune disorders - Severity of symptoms: mild - moderate - Duration: resolves in 4-8 weeks or develops into hypothyroidism - Thyroid enlargement: none or small diffuse goiter with no bruit - Exothalmosis: none - TSH Receptor Antibodies: possibly (about 25% of cases) - Nuclear Imaging: No uptake Graves Disease: - Prevalence: 0.2% of pregnancies - Timing of onset: between 4-12 months postpartum (PP) - History: Previous history of Hyperthyroidism - Severity of symptoms: severe - Duration: Continues until treatment - Thyroid enlargement: small to large diffuse goiter may have bruit - Exothalmosis: 10 - 25% of cases - TSH Receptor Antibodies: Very likely (about 90% of cases) - Nuclear Imaging: Positive uptake Hope this helps your understanding!

Have you heard this term? Did you develop hypothyroidism not long after a pregnancy? Postpartum thyroiditis (PPT) is an immune / inflammatory condition that develops in women within one year after a pregnancy. ... To be diagnosed with PPT you would not have had an overt thyroid disorder prior to pregnancy, meaning hypothyroidism or hyperthyroidism. PPT usually becomes evident sometime after 6 weeks postpartum. PPT can take 3 primary forms: 1. Hyperthyroid physiology 2. Hypothyroid physiology 3. Hyperthyroid phase followed by a hypothyroid phase About 25-30% (some estimates are as high as 50%) of those who develop PPT go on to develop full blown primary hypothyroidism within 5 - 10 years. What puts you at greater risk of developing PPT? 1. Pre-existing cellular / tissue hypothyroidism 2. Pre-existing thyroid antibodies 4. Pre-existing autoimmune disorders 5. Family history of hypothyroidism, hashimoto's, or postpartum thyroiditis 6. Previous episodes of PPT What can you do to reduce risk of developing PPT? 1. Have a comprehensive metabolic panel and FULL thyroid panel run prior to or at the onset of pregnancy. Your OB-GYN will likely not run either due to insurance and medical guidelines. 2. Improve diet, sleep, respiration, lifestyle, emotional stressors to best ability prior to pregnancy, through pregnancy, and after pregnancy. 3. If you have TPO antibodies prior to pregnancy but not hypothyroidism be sure to work on step 2 and make sure you are consistently taking a quality prenatal multi with iodine and selenium. 4. Do not overload either selenium or iodine. Follow you functional medicine's recommendation for dose. 5. If thyroid antibodies are positive going into pregnancy or during first trimester, have them monitored along with rest of thyroid panel each trimester and postpartum to be alert for problems. Continued in comments ....

Another day another post about thyroid physiology and lab testing. Do you ever get confused about which thyroid tests should be run? Do you ever find it frustrating....... - your medical doctor or endocrinologist says only TSH and fT4 should be run - someone else says TSH, fT4, fT3, and thyroid antibodies - someone else says that all thyroid tests matter (TSH, T4, T3, fT4, fT3, T3U, rT3, TPO ab, Tg ab) - someone else (like me) says that not only do all tests matter, you can't just look at the thyroid panel. You have to look at the thyroid panel in context with other lab values, your signs and symptoms, your medications, your supplements, and your health history Does this irritate you and leave you confused? Why are there so many opinions and who is right? Everyone is looking at thyroid physiology from a different perspective or bias. Each person recommends and orders the thyroid tests that support their bias, diagnosis model, and treatment model. Your endocrinologist only thinks TSH and fT4 are only needed because they are following medical guidelines. From their perspective hypothyroidism that they can diagnose and treat starts when the gland can no longer make enough thyroid hormone (> 90% destruction of gland), TSH rises and fT4 falls out of lab range. The treatment for primary hypothyroidism is to provide enough T4 replacement to bring TSH back into lab range. NONE of the other thyroid tests are needed in this model to diagnose or treat so all other tests are not necessary. Someone who is say, more integrative or dips their toes in functional medicine and treats hypothyroid patients with mixed thyroid replacement (armour, NP thyroid, compounds) will find that adding free T3 is important. They want to see if they not only improved TSH but fT3 and fT4 as well. They may want to measure thyroid antibodies to confirm hashimoto's, but also because they may be trying to provide treatment to lower thyroid antibodies. Continued in comments ...

Check out the most recent episode of Thyroid Answers Podcast. In this episode we talk with Dr Leah Austin on the challenges hypothyroid patients have in the allopathic model. Dr Austin is an integrative medical doctor who blends both conventional and functional medicine to help her patients. Dr Austin understands the frustration people experience who have chronic hypothyroid symptoms, despite conventional medical treatment for hypothyroidism.... Many people who have chronic hypothyroid symptoms despite conventional medical care for hypothyroidism start to investigate functional medicine concepts and therapies. They become frustrated that their medical doctors won't run more comprehensive thyroid panels, won't prescribe anything other then T4 medication, and focus more on normalizing TSH then what their patient is telling them about how they feel. Dr Austin provides some clarity on what the medical doctors training is and what the guidelines are for testing and treating. The doctors discuss how medical doctors are following their training and guidelines. The discussion continues regarding how there is often a mismatch between what a hypothyroid patient wants and what conventional medicine is able to provide. We finish the discussion with what expectations should be of medical assessment and treatment of hypothyroidism. We discuss the strength of functional medicine and why it has such an important place in helping people with hypothyroidism. #cellularhypothyroidism #thyroid #thyroidproblems #thyroidhealing #thyroidweightloss #thyroiddiet #thyroiditis #thyroidhealth #thyroidsupport #hypothyroidism #hypothyroidismweightloss #hypothyroid #thyroiddebacle #thyroiddebaclebook #hashimotosdisease #hashimotosthyroiditis #hashimotosweightloss #hashimotos #hashimotoshealing #functionalmedicine #rejuvagen #chronicillness #rejuvagencenter

Everyday there is a new post by someone stating something like, "EBV is the cause of hypothyroidism" or "gluten is the cause of hypothyroidism" or " iodine deficiency or excess is the cause of hypothyroidism. This can cause the person on the hypothyroid spectrum to be on extremely focused on eradicating the "one cause". Once they eradicate the one cause, they may sense a little improvement but eventually become frustrated because they are still symptomatic. The removal of t...he "one cause", didn't remove their chronic hypothyroid symptoms, and so they are off in search of the next "one cause". The point of this post isn't that EBV, iodine, gluten, or any other "one thing" couldn't be the "one cause" for someone's hypothyroidism. Instead the point is that for most people I see there isn't just "one thing" that is contributing to or causing their hypothyroidism. For most of the people I meet, their hypothyroidism developed slowly and steadily over time. When we go back and look at their health history and timeline, it becomes clear that their was an accumulation of stressors "causes" that eventually led to the excessive cell stress that triggers hypothyroidism. Many times people (nor their doctors) are aware that their antibiotic use early in life, caused an imbalance of gut bacteria that decades later contributed to developing hypothyroidism. Or that the birth control they took was slowly reducing the amount of iodine coming into their body or their thyroid gland. They don't realize the years of disturbed sleep patterns triggers a low grade stress response that eventually impacts their thyroid physiology. They may not realize that breathing through their mouth at night causing cell hypoxia, that initiates tissue hypothyroidism. For most people their is no "one thing". Instead what is causing their hypothyroidism is the "load" of chronic persistent stressors on our cells and tissues. I know, how do you "fix" your hypothyroidism? Continued in comments ...

I get this question all the time on discovery calls from people who have been diagnosed with hypothyroidism and continue to struggle with hypothyroid symptoms. They are usually frustrated because they have usually seen at least one endocrinologist, and integrative medical medical doctor and usually one or two functional medicine doctors. They get T4 therapy (synthroid or levothyroxine) from the medical endocrinologist, and that may improve TSH but not their symptoms.... They go to an integrative doctor who may prescribe Tirosint because it is a gluten free version of Levothyroxine. Again, TSH improves, but hypothyroid signs and symptoms persist. Their integrative doctor then gets creative trying combinations of T4/T3 combinations like NP Thyroid, Nature-Throid, Armour, or compounded blends of T4 and T3. They may try T4 and T3 as separate medications. And sometimes T3 on its own. But the story doesn't change, blood levels of TSH, T4 and T3 might improve but signs and symptoms persist. In desperation they reach out to functional medicine practitioner who suggests glandular thyroid products plus a bunch of supplements to provide the precursors to make more thyroid hormone and to support conversion of T4 to T3. Things like Tyrosine, Selenium, Iodine, Glutathione, and Magnesium. While all these strategies have the ability to work for some people, they people calling me have usually failed with all these strategies and they are wondering what is left. They want to know what is the right cocktail of T4, T3, or supplements that will make them feel better. If this is you. You have been through the same steps, what you need to consider is that maybe you are trying to solve the wrong problem! What? Continued in comments ...

I was asked over the weekend why I am so worked up about thyroid physiology and why I think we need to change the way we look at and address thyroid physiology. This quote says it all. If this statement doesn't make you start to question the importance and significance of thyroid physiology, I don't know what will.... We have a crisis on our hands. The statistics are down right frightening. For those of you who think the solution is just provide more thyroid hormone and that will fix the problem, it won't. We need to consider that "adapted" thyroid physiology that results in tissue hypothyroidism is not "the" problem. More thyroid hormone into a system that is trying to slow metabolism on purpose will make TSH improve but doesn't necessarily "fix" tissue levels of thyroid hormone. We need a shift in the paradigm. We need to understand that hypothyroidism occurs in the tissues often times despite normal thyroid gland function, normal TSH, and thyroid hormone medications. How do we help the autistic community. We do a better job of preparing parents for a healthy pregnancy. We do a better job of helping parents know they are in a state of chronic cell stress and adapted physiology. We do a better job of reducing the excessive stress that "causes" adapted thyroid physiology and tissue hypothyroidism. We argue what is the thing that causes ASD. It is likely not the thing, but the stress load we put on our children and young adults that drives the chronic cell stress response. It is emotional stress, trauma, toxins and chemicals, crappy processed foods, antibiotics, detergents, etc. The "load" results in people who unknowingly head into pregnancy with tissues and systems not optimized for pregnancy. We need to help the kids, the parents, and families once Autism is identified, but we need to reduce the risk of development in the first place by better identifying those with excessive cell stress and tissue hypothyroidism.