The complexity and controversy of fat soluble vitamins absorption
Fat soluble vitamins include D3, Vitamin A, Vitamin E, Vitamin K and a form of vitamin C called Ascorbyl Palmitate. It is common knowledge that fat soluble vitamins absorb better when eaten with a meal that contains fat. The controversy is do these vitamins compete with one another for that fat to be able to be absorbed and does that warrant the need to separate each fat soluble vitamin from one another to do so? We have theories and then we have research. What do we follow and how does it pertain to us an individual’s?
1. D3 is a hormone that is found to be deficient in persons who have one or more autoimmune diseases, as well as people with heart disease and type 2 diabetes.
“It turns out that vitamin D is best absorbed with a low-to-moderate amount of fat, compared to no fat or lots of fat. Specifically, researchers have showed that 11 grams of fat leads to higher absorption than either 35 grams or 0 grams, at 16% higher and 20% higher respectively”
Meal conditions affect the absorption of supplemental vitamin D3 but not the plasma 25-hydroxyvitamin D response to supplementation https://www.ncbi.nlm.nih.gov/pubmed/23427007
“We conclude that absorption was increased when a 50,000 IU dose of vitamin D was taken with a low-fat meal, compared with a high-fat meal and no meal, but that the greater absorption did not result in higher plasma 25(OH)D levels in the low-fat meal group.”
It was found that 11 grams of fat/99 calories were suitable for proper absorption of D3.The question is why wouldn’t the plasma 25(OH) D levels be higher with better absorption? https://www.ncbi.nlm.nih.gov/pmc/ar...
Ingested and cutaneously produced vitamin D is rapidly converted to 25(OH)D, but in serum only a fraction of 25(OH)D is converted to its active metabolite 1,25(OH)2D. Thus, measurement of the total 25(OH)D level is the best test to assess body stores of vitamin D. The total 25(OH)D level allows for the diagnosis and monitoring of vitamin D deficiency, whereas quantification of 25(OH)D2 and 25(OH)D3 fractions may facilitate treatment monitoring. For example, in patients without clinical improvement after D2 or D3 supplementation, lack of increase in the corresponding 25(OH)D2 or 25(OH)D3 and total 25(OH) D levels may indicate inadequate dosing, nonadherence, or malabsorption. Some laboratory assays for vitamin D cannot differentiate between 25(OH)D2 and 25(OH)D3 and will only report a total 25(OH)D level. Some laboratory assays under detect D2 metabolites, which may give the appearance of ineffective D2 supplementation.
2. Vitamin A has also been linked to autoimmune diseases and is suggested to be added to our dietary supplementation in lowering the pro-inflammatory response
Fat-soluble vitamin intestinal absorption: absorption sites in the intestine and interactions for absorption. https://www.ncbi.nlm.nih.gov/pubmed/25442537
“Vitamin A also significantly decreased the uptake of the other FSVs (fat soluble vitamins) but, conversely, its uptake was not impaired by vitamins D and K and even promoted by vitamin E.” This abstract may be confusing but simply put, Vitamin E can enhance the absorption of Vitamin A, while Vitamins A will hamper vitamins D and K ability to absorb. Vitamin D and K should not be taken with Vitamin A.3.
Vitamin E is suggested in low doses (200-400 IUS) and mainly to assist the absorption of selenium and both aid in the metabolism of T3 hormone. Higher doses have been associated with the risk of vitamin K deficiency. Lower doses have been found to enhance the absorption of vitamin A.
Complexity of vitamin E metabolism. https://www.ncbi.nlm.nih.gov/pubmed/26981194
“Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review.”(s)
Interaction with vitamin K metabolism https://www.wjgnet.com/1949-8454/full/v7/i1/14.htm
“The interference of vitamin E with vitamin K metabolism and, as a result, with blood coagulation has been known for decades . As shown by several supplementation studies with vitamin E in rats  or humans  an increased risk of bleeding was noted. The underlying molecular mechanisms are still unclear, but recent research has shed new light on this aspect of vitamin E metabolism. Vitamin E and vitamin K share the same metabolic pathways, as the degradation of both vitamins is initiated with a ω-hydroxylation followed by subsequent β-oxidation of the aliphatic side-chain, thus resulting in urinary and biliary excretion of the respective carboxylic acids or conjugates with shortened side-chains .
When vitamin E increases the expression or activity of enzymes involved in its own degradation, it is possible that vitamin K metabolism is also enhanced under elevated vitamin E status; this may lead to higher rates of vitamin K excretion and in turn to vitamin K deficiency with enhanced bleeding risk
The authors observed a downregulation of the expression of CYP enzymes CYP3A, CYP4F4 and CYP4F1, which was explained by an alternative mode of interference of vitamin E with vitamin K metabolism apart from the induced degradation of vitamin K. The induction of the xenobiotic exporters ABCB1/MDR1 and ABCG2/BCRP1 provided the first hints for an increased excretion of vitamin K metabolites into bile. This concept is supported by the 100-fold increased urinary excretion of α-CEHC in response to the application of α-TOH, whereas urinary excretion of vitamin K metabolites remained unchanged.”Vitamin E has shown to degrade vitamin K and increases it’s elimination in bile. Vitamin E should be taken at entirely different time of that day than Vitamin K.
4. Vitamin K1 (MK-4) and Vitamin K2 (MK-7) has emerged as a super vitamin in the prevention of osteoporosis and lowering cholesterol and reducing calcium /plaque on the arteries.Vitamin K was found to require the most amount of fat for best absorption. In addition, a given dose of vitamin K2 will not be fully absorbed and in most cases only half the dose taken will be assimilated. The good news is that only 32 mcg is actually need to achieve the desired effects for bone and heart protection. If one takes a dose of 100 mcg of K2 and only 50% gets absorbed that would be enough. The amount of fat that would need to be consumed to do this is 35 grams of fat/ 315 calories in one meal.
That is more than most women would eat in one meal. When taking D3 along with your K2 this must be taking into consideration. It is not that D3 competes or interferes in the absorption process of K2, it is that K2 requires a high amount of fat in order to absorb that 50% of the total dose taken. Effect of dietary fat content on oral bioavailability of menatetrenone (K1) in humans. https://www.ncbi.nlm.nih.gov/pubmed/8877895
“The oral bioavailability of lipid-soluble vitamin K was influenced by the fat content of a meal, although the increase in bioavailability seemed to reach a peak when the lipid content of the meal was > 35 g.” Please note K2 (MK-7 breaks down to K1 /MK-4)Since we know that a lower fat meal or lower fat content is suitable for proper absorption of D3, 11 grams/99 calories according to the research, one would need to eat a total fat content of 414 calories to be able to take and absorb both vitamins at the same time. What is also widely research are the synergistic effects of combining the K2 and D3 together for osteoporosis and cardiovascular disease relating to plaque and calcium within the heart and arteries and the absorption of D3 and calcium into the bones.Taking both of these supplements together or closely are very important! Below are significant studies showing the synergistic power of both.
[Efficacy of combined administration of vitamin D3 and vitamin K2 for primary osteoporosis]. https://www.ncbi.nlm.nih.gov/pubmed/15775388
Therapeutic effects of systemic vitamin k2 and vitamin d3 on gingival inflammation and alveolar bone in rats with experimentally induced periodontitis https://www.ncbi.nlm.nih.gov/pubmed/25569194
In vitro vitamin K (2) and 1α, 25-dihydroxyvitamin D (3) combination enhances osteoblasts anabolism of diabetic mice. https://www.ncbi.nlm.nih.gov/pubmed/26452518
Vitamins D3 and K2 may partially counterbalance the detrimental effects of pentosidine in ex vivo human osteoblasts. https://www.ncbi.nlm.nih.gov/pubmed/27655488
Combined treatment of leukemia cells with vitamin K2 and 1alpha, 25-dihydroxyvitamin D3 enhances monocytic differentiation along with becoming resistant to apoptosis by induction of cytoplasmic p21CIP1. https://www.ncbi.nlm.nih.gov/pubmed/16142303
Melatonin-micronutrients Osteopenia Treatment Study (MOTS): a translational study assessing melatonin, strontium (citrate), vitamin D3 and vitamin K2 (MK7) on bone density, bone marker turnover and health related quality of life in postmenopausal osteopenic women following a one-year double-blind RCT and on osteoblast-osteoclast co-cultures. https://www.ncbi.nlm.nih.gov/pubmed/28130552
How do supplement with vitamin K2 and D3 and get the most of the powerful synergistic duo?Let’s look at all the things to consider;· We need 35g of fat to absorb K2· We need 11g of fat to absorb D3· Taken together will not interfere with absorption of one another as long as there is enough fat. 35 grams of fat or 315 calories from fat for K2 and 11 grams of fat or 99 calories of fat for D3. The total of 46 grams of fat/ 414 calories to absorb both at the same time. · It is best to take both D3 and K2 vitamins at different times of the day than vitamin A & E. Vitamin A will compete with D and K . Vitamin E can increase the elimination of Vitamin K (i.e urine and bile) and cause K2 deficiency. Vitamin E ,in a low dose will enhance the absorption of vitamin A. D3 and K2 can be taken together or close together and vitamin A and E ( in low dose) can be taken together or close together. 1) Increasing the ability to absorb fat-soluble vitamins, CoQ10 and Boswellia are emerging as possible vehicles to help this issue. More research needs to be done.
Novel HPLC-UV Method for Simultaneous Determination of Fat-soluble Vitamins and Coenzyme Q10 in Medicines and Supplements. https://www.ncbi.nlm.nih.gov/pubmed/28862306
Investigating permeability related hurdles in oral delivery of 11-keto-β-boswellic acid. https://www.ncbi.nlm.nih.gov/pubmed/?term=Boswellia+and+D3
2) Take the K2 supplement with dinner and add an omega 3 fish oil to increase fat intake3) Take the D3 at bedtime or a few hours after dinner with a tablespoon of nut butter. Suggestions on how to take fat soluble vitamins so they do not compete with one another so you may get the most of your supplementation.
1) Take Vitamin A in the morning with breakfast. Vitamin E in a low dose can be taken as well.
2) If you are taking the myo inositol, selenium and low dose E, first thing in the morning on an empty stomach then you do not need to take more E when you take vitamin A at breakfast.
3) Take Vitamin K2 with Lunch or Dinner whichever is your fattiest meal (35 grams of fat), but also try to take the D3 closely after to reap the benefits of its synergistic power. Take the D3 with at least 11g of fat/99 calories, more fat will not help absorb D3 better and do not forget your magnesium with the D3.
4) Consider that Magnesium is best to be taken along with D3, but magnesium can make some sleepy. If this is the case, take your D3 at bedtime along with the magnesium. If you do not want to eat anything at bedtime (11g of fat) consider an Omega 3 fish oil and /or 100mg of CoQ10. Timing solutions;
Malabsorption is the inability of the intestines to absorb nutrients. In IBD, this occurs as a result of bleeding and diarrhea, as a side effect from some of the medications, and as a result of surgery. Malnutrition may occur in ulcerative colitis, but it tends to be less severe than with Crohn's disease.
Irritable Bowel Syndrome (IBS) is a condition that may be marked by abdominal pain, bloating, fullness, indigestion, belching, constipation and/or diarrhea. IBS symptoms can result from malabsorption of fructose. ... A low-fructose diet has been found to improve IBS symptoms in some patients.
Dec 1, 2018
By Raina Kranz-Kaplan
WHAT IS the DIFFERENCE of having a thyroid gland and not having a thyroid gland when it comes to thyroid disease?
Many of you are unaware of how thyroid hormone is produced and dispersed, degraded and used by the body. The misconceptions that not having a gland is worse than having a gland is not a balanced statement. I am going to try to explain this.
1) Those of you without a thyroid gland, you lose any production of T4 and T3 ( intra-thyroidal production of both hormones) Meaning both hormones are made with in the gland ( about 80% is of T4, 20% of T3)
2) For those of you with Hashimoto's hypothyroid depending on the stage of your disease or the damage done to the gland, you may have some production still within the gland, very little production within the gland or none at all. End stage Hashimoto's usually means no thyroid hormone production at all. The gland is dead.
A healthy gland that produces enough intra-thyroidal hormones will then go through the VERY SAME PROCESS of entering other areas of the body in " TOTAL T4/T3 form ( meaning bound to a protein molecule) From there T4 and T3 further degrades and enters the blood stream as it's bio active free form ( Ft3 and Ft4)
Those of us with a gland and those of us with a destroyed gland or a end stage gland, go through the very same processes once we take our T4 medication.
3) All T4 medication is digested and absorbed in the intestines.Then it is dispersed bound to a protein molecule to organs and tissues in the body. From there T4 hormone is degraded to total T3 and rT3 and then eventually degraded further into FT3 and Ft2, Ft1 with in the blood stream.
This process is the same for everyone on T4 medication with or without a gland.
4) Those of us who still have a gland may actually still be producing some intra- thyroidal T4 and T3, but not a whole lot.
WHAT the biggest difference is for those without gland is the 20% of Total T3 that is produced in the gland. Once that is gone, you will no longer produce any thyroid hormone. If someone who does not have a gland any-longer is only T4 hormone, you have LOST that extra oomph that someone with a well functioning gland has, that 20% of T3.
Those of you with a gland, you will lose that extra oomph too, once your gland is end stage and no longer producing any hormones either.
When you have no more function from your gland (surgical or end stage hashimoto's) and you are on T4 only, you will feel under-treated.
This is how T4 hormone travels through body once you take your medicine.
1) Intestinal absorption
2) Disbursement to other organs and body tissues
3) Degradation to total T3 and rT3 within the organs and tissues.
4) Further degradation to Ft4, Ft3 and rT3 with in blood stream.
All T3 hormone medication BYPASSES entering the organs or body tissues. All T3 medication is dispersed into the blood stream and has nothing to do with conversion.
T3 medication does not replace the loss of the Total T3 that was once produced in the gland. T3 medication cannot replace total T3 that is converted from T4 hormones. All T3 medication does is increase the Free T3 levels within the blood stream. So, if you are a poor converter of T4 to T3 within the organs and body tissues, you will ultimately have lower Ft3 levels in the blood stream and may be converting more than you should to rT3. The T3 medication only increases the T3 within the blood stream.
Total T3 hormone is very important in this process. Please do not overlook that need for appropriate levels of total T3. BY adding T3 medication, only your Ft3 will be enhanced. T3 medication does not enhance Total T3 levels. Only good conversion of T4 will increase total T3 levels. Good total T3 levels will result in good further conversion to Ft3.
Most of us eventually need the addition of T3 medication and this is usually due to slower, not efficient conversion of T4 hormones. Age, Disease, Alcohol intake, other drugs and environment are all reasons why our T4 to T3 conversion within the body is diminished.
Whether or not you have a thyroid gland, does not change how the body processes T4 hormone and eventually your labs will indicate the need to add T3 medication.
The only real way to replicate what a healthy thyroid gland produces, would be to manufacture a medication that is both T4 and T3 in the right percentages 80/20 and the T3 is in a bound form like T4 medication. This way the T3 would actually go through the normal degradation, enter the body organs and tissues and then further degrade to Ft3.
What supplements help T4 hormone convert better to T3 within the liver?
Written by Raina Kranz- Kaplan C.P.T, A.C.S.M
Thyroid hormone conversion can be very tricky for many thyroid patients. When deciding to assist this process you should consider things that need to be removed from your diet as well as what should be added.
Let’s take a look at the things that may need to be taken into consideration.
1) Alcohol – All alcohol is processed through the liver. Drinking can slow conversion of T4 to T3 and it can increase the amount of T4 converts to reverse T3.
2) Soy, estrogenic supplements or excess estrogen can interfere with T4 hormone conversion to T3.
3) Over- Training can cause depletion of T3 levels for up 48 hours and can cause higher conversion of Rt3
4) Under eating and or eating too little carbohydrate
6) Lack of sleep
7) Other medications (for example: blood pressure, anti-depressants and anti-anxiety medications)
9) Liver disease
Let’s take a look at what we can do to help us convert our thyroid hormones better.
1) Drinking plenty of water with fresh lemon
2) Dandelion tea or supplements
3) Vitamin C
4) Selenium as L-selenomethionine, and selenium-methyl L-selenocysteine.
Selenium will not help reverse the over conversion of T4 to RT3. It would be better to stop taking selenium temporarily until you have a better ratio of T3/rT3. Also selenium should be tested to make sure you are taking the right amount and not too much. Too much selenium can cause hair loss and dry brittle nails. Zinc and Iron are important supplements, but should be tested to make sure you are not taking too much.
5) Zinc as Gluconate
6) NAC (N-Acetyl – cysteine) specifically lowers the cytokine involved with Rt3 levels. Increased IL-6 Promotes inflammation and raises Rt3 levels in the blood. Lowering IL-6 is one of the things this Powerful antioxidant does. (300mg-600mg)
7) Vitamin D3
8) Vitamin B12
All nutrient levels should be tested before starting any supplement. Finding a baseline will determine if you require a little help or not. Re testing levels at least twice a year to make sure you not over doing it.
DISCLAIMER; the information in this article is meant for educational purposes only. Lab test should be run and evaluated by a medical professional. Supplements should be checked against all other medication and conditions. All changes in your treatment needs to be discussed with your physician.
Originally PUBLISHED ON June 12, 2018 Guest Post by Rachel Hill
Hypothyroidism. Hashimoto’s Thyroiditis. Chronic Fatigue Syndrome. Anxiety Disorder. Adrenal Fatigue. Depression. All conditions I currently have or, in the case of depression, have had at previous times in my life (depression comes in and out of my life as it pleases).
People tell me however, not to let these conditions, physical and mental, define me.
But why? They do define part of who I am and what my life has become and I’m OK with that.
Whilst it’s true that there is so much more to me than my health conditions, they are a huge part of my life and who I am. They’ve shaped who I am today. And in fact, they’ve made me a better person; a more well-rounded person. Someone who appreciates life and the small things more so than pre-diagnosis of any of these conditions.
The truth is, if you have a long term health condition, it will most likely play a part in defining who you are. If it has such an impact on your life that it prevents you from having a ‘normal’ life, then it is part of your existence right now and often defines what you’re able to do. And that’s OK. The conditions I live with have meant I now work part-time, can’t exercise as much as I used to (I used to be incredibly active) and can’t be as sociable as I once was.
I don’t want to be defined solely by my health conditions but at the same time, they are what’s made me who I am.
Going through the many years of not knowing what was wrong with me, in terms of physical symptoms piling up, until I was eventually diagnosed with autoimmune thyroid disease, and also the anxiety I’ve experienced my whole life, without knowing that that’s what it was. Going through the pre-diagnosis, the diagnosis and now the ‘trying-to-cope-with-it-and-manage-the-conditions’ stages, I have become an advocate for my own health; I’ve become stronger in various ways.
I have learnt to stand up for myself. I am stronger in taking more control over my health and the pursuit of making peace with what life has handed me. And peace with myself. This has also made me more confident, independent and self assured. I’m very different to the person I was five years ago.
The conditions I have have helped me to realise that I am not Superwoman and that I needed to scale back on my commitments and expectations. Leading up to diagnosis of my physical health conditions, I was running myself in to the ground thinking that I should be working towards being supremely fit, having the ‘dream job’, a perfect house and very busy social life. When you develop health conditions that quite physically limit how much you can do, you have to take a step back and reevaluate. Reevaluate what is important and what you can do.
Compared to who I was five years ago, I am wiser, more mature, more independent, have my own voice and the strength to do more than I ever thought possible. And I don’t mean physically. I don’t mean run marathons or work a seventy-hour-a-week job. I do more for me and others in the same kind of situation; I speak up. I do more of what my body and mind needs and requires from me in terms of consciously looking after myself better but I’m also a voice for other thyroid patients, through my advocacy work.
My health conditions, and I call them my health conditions because they have formed such a huge part of who I am and what I get fulfillment out of doing, have led on to amazing opportunities. Helping others with thyroid disease, providing a voice for them and advocating for better diagnosis and treatment is a huge part of the person I am today. It’s what drives me and keeps me going on rough days. Of course, there is still so much more to me than these health conditions – I love vintage and retro fashion, I’m a total foodie, enjoy craft projects and musicals – but the truth is, my health conditions have given me more purpose. I know now that I was put on this Earth to weather the storms and come out stronger, telling others that they can do the same and that the support is out there. As it’s changed my life and who I am so much, I am defined by it.
But there is this idea in society that everyone should be aiming for ‘happiness’. That ‘being happy’ is the ultimate goal in life. Yet, if I was to become ‘happy’, for example in the sense that being 100% healthy would equal being happy, I’d lose myself. I’d lose who I was. I’d lose what makes me, me.
What is often missed is that it’s OK to not be happy. When we question that the end goal, the ultimate aim in life, is to be ‘happy’, we ask ‘what is happiness anyway?’ It’s not a destination, it’s an emotion. Emotions come and go all the time, in fact, throughout one day alone we go through numerous emotions. How unattainable a goal it is to reach that place that can’t be sustained forever? An emotion, a feeling, where we inevitably won’t stay?
Life dishes out its trials and tribulations. It gives us challenges, difficult times and of course the best of times. And this is life. In many cultures, to be ‘happy’ means to find your soulmate, get married, have a family, buy a beautiful house, have lots of money in the bank and a dream career. But this is so unattainable, even more so for those of us with health conditions. Mental and physical health conditions.
What is with this pressure to find your ‘soulmate’? ‘The One’? Why can’t you be content with whoever you enjoy spending time with? Why must people feel pressured to follow social convention at all? For many of us with mental and physical health conditions, ‘the dream career’ isn’t an option we have. Many can’t work or those who do are limited in what kind of job they can do or how many hours of work. Why must a job exist solely to get you to a ‘dream career’? Why do we need this to be ‘happy’? There is so much more to life than a job, focus on money and pleasing society.
I just want to feel at peace. And in that I mean accepting that I’ll feel sad some days, angry or frustrated others and, on the rare days, just happy. Because peace is accepting all of this. Peace is accepting that life is life and there is no one emotion or ‘state of happiness’ that will suddenly all fall in to place when we tick things off a checklist set by society. Many of which don’t live with conditions that can limit or affect what they’re able to do daily.
Just making peace with the fact that we’re human and we come in a whole range of emotions is absolutely fine. We’re allowed tricky days, days where we barely make it through, and we’re allowed fantastic days. Those days that are the happiest of our lives.
But reaching happiness isn’t a destination or goal. You can’t keep it. It’s isn’t a possession.
And being defined by my health conditions is fine by me. I own them. They don’t own me.
This post was originally written for The Mighty.
You can click on the hyperlinks in the above post to learn more and see references to information given.
You can find Rachel @ TheInvisibleHypothyroidism.com
Guest post written by Raina Kranz-Kaplan A.C.S.M, CPT.
First posted SUNDAY, NOVEMBER 26, 2017
Impaired exercise tolerance with suppressive thyroid hormone treatment, to sub-clinical hyperthyroid
Let’s begin with the understanding that this article is being written to help explain what occurs to the body under certain alterations in metabolism, due to thyroidectomy and or RAI. The studies used involved patients with differentiated thyroid cancer and those who may still have their thyroid glands and are sub –clinical hyperthyroid. The state in which we are discussing, is Sub- Clinical Hyperthyroid states and its effects on muscle strength, endurance and cardiovascular endurance and recovery.
Sub-clinical hyperthyroid is clinically described as a Thyroid stimulation hormone (TSH) below the general reference of (0.20-0.30) with Ft4 and Ft3 levels within range. Many patients who have had their thyroid gland surgically removed and gone through RAI treatment for thyroid cancer, are then treated with suppressive therapy to ensure no regrowth of tissue. There are pros and cons to this treatment and latest findings are changing as to whether suppressive treatment to Sub clinical hyperthyroid or complete suppression is needed in all cases of thyroid cancer. This is not the topic of discussion – I just wanted to address the subject briefly as some of you will be having their dose adjusted to accommodate any reclassification of your diagnosis. Please discuss this with your Doctors.
The purpose of this article is to shed light on the fatigue and lack of energy many thyroid cancer survivor’s experience once finishing their initial treatment. We will not be discussing and side effects of RAI and only addressing the physical, emotional and quality of life aspects when it comes to achieving healthier life.
Let’s talk Optimal Thyroid levels vs Sub clinical hyperthyroid levels.
Optimal thyroid levels are subjective and individual. Each person requires a different level of hormones to feel their best and what it takes to get there is also unique to each patient. That being said, Sub clinical hyperthyroid is not considered optimal thyroid levels. People who present with Sub clinical hyperthyroid levels are watched carefully, tested for Graves’ disease, may have higher blood pressure and resting heart rates. Whereas optimal thyroid levels, are more conducive with a higher perception of quality of life, less physical and less cardiovascular limitation’s.
Exercise and physical response
Training effect/ increased Vo2 (oxygen consumption): is described as a positive correlation to the amount of oxygen one can assimilate and use for muscle contraction at a given intensity. The training effect is relative to an increased amount of work one can perform due to the increased amount of oxygen.
People who have levels considered to be Sub-clinical hyperthyroid either due to suppressive therapy or due to graves’ disease or another thyroid disease experience impaired functional response to exercise – marked by lower values of oxygen consumption and exercise duration. They also experience early onset aerobic threshold (tiring more easily and sooner) and have slower recovery heart rates and blood pressures.
This will make it very difficult for those with Sub clinical hyperthyroid to make progress with exercise and limit their abilities to function at levels that require higher intensities and longer durations. Strength is impaired as well. Sub clinical hyperthyroid levels create lower muscle function and functional capacity of the shoulder and quadriceps and a higher degree of fatigue overall.
The subjects tested for physical impairment ranged from overt hyperthyroidism, subclinical hyperthyroid due to Graves’ disease, toxic goiter and suppressive thyroid hormone treatment due to differentiated thyroid cancer. The studies consistently showed the correlation was due to actual thyroid levels rather than a particular cause or variation of thyroid disease. The same correlation could be made with those who were diagnosed with overt hypothyroidism, still have their thyroid gland, but are over medicated on thyroid hormone replacement. The Sub-clinical hyperthyroid level is the reason for the overall fatigue and low perception of quality of life.
Physical intensity, duration and frequency and its effects on thyroid disease.
It is time to think outside the box and lets delve into what occurs under different scenarios and exercise with various thyroid levels.
Euthyroid describes “normal thyroid levels” if we are speaking of the apparently healthy void of thyroid disease, these levels can be anywhere within the normal reference range. For example; TSH (0.40-4.50). Those with hypothyroid disease due to hashimoto’s or for some reason other than thyroid cancer have had their thyroid removed (not being suppressed to subclinical hyperthyroid) use the term “ optimal’ when trying to achieve a state of well-being. Generally speaking, the aim is to get the TSH closer to 1.0 and somewhere between (0.50-1.5). These levels has not only been shown to be beneficial for hypothyroid patients – they are also beneficial for overall health.
Person’s diagnosed with hypothyroidism also experience a form of exercise intolerance mostly due to having low thyroid function. This interprets in a slower metabolism. Lower resting heart rate, lower body temperature’s, lower blood pressures and low energy levels. Dysfunction at the cellular level resulting in decreased mitochondria and faster fatigue rates during exercise. Many hypothyroid patients do not sweat during exertion. Exercise protocols for hypothyroid patients even medicated to optimal levels need to modify intensity, duration and frequency so that they do not over expend thyroid hormone.
As you can see, both sub clinical hyperthyroid and hypothyroid patients will have some degree of physical impairment due to “non- optimal” thyroid levels. You can actually remove the thyroid gland and see that depending what level a patient is medicated to will result in either a correction in metabolism or an impairment.
Physical activity on thyroid hormone
What occurs to thyroid hormone during exercise is pertinent to how those with thyroid disease may need alter training to increase training effects and benefits. I want to keep this section very simple so, lets focus on intensity of exercise first.
1) Lower intensity aerobic activity 50% -60% of maximal attainable heart rate
2) Moderate intensity aerobic activity 61%-75% of maximal attainable heart rate
3) High intensity aerobic activity 76% -85% of maximal attainable heart rate.
You can apply the above to intensities for circuit training, HITT training, boot camp, weight training. Any of these can be modified for any level, by monitoring heart rate, increasing rest intervals, using lighter or heavier weight and modifying exercises.
Triiodothyronine (bio-active thyroid hormone) also known as T3, is the hormone used for energy and is the gas pedal of thyroid economy. When this level drops generally so does functional output. This is the hormone we need to exercise. The one fact we all need to know is this for all individuals healthy and those with thyroid disease “on thyroid hormone replacement” it does not matter.. Training at a threshold higher than 70% will cause a drop in both total and free T3 levels. The difference is healthy individuals have the ability to actually produce more thyroid hormone as needed and we do not. We are completely dependent upon a given dose and how we use that amount of thyroid hormone needs to be taken into account when we exercise and in our daily lives.
The suggestion for those who are medicated to “Optimal” ranges is to not exert energy over 70% of ones given max heart rate. This is preserve Total T3 and free T3 levels and allow for the body to recover in 12 -24 hours vs 24 hours or more. The next thing to take into account is duration. The amount of time one should exercise with thyroid disease without over-using precious T3 hormone. The studies show that 40 minute – 60 minutes is the allotted time. Frequency the amount days one with thyroid disease should train is between 4-6 days a week.
I am going to break this down.
Novice individual’s 3 days a week 20 minutes /50-60% of max heart rate / for 6 weeks before increasing intensity, duration or frequency
4-5 days a week at 45 minutes – 60 minutes/ 70% of max heart rate
5-6 days a week at 40 minutes /70% of max heart rate
These parameters have shown to reverse mitochondria deficit and increase quality of life.
(Sources) For Hypothyroid
How does this apply to sub- clinical hyperthyroid patients or those being suppressed to sub-clinical hyperthyroid due thyroid cancer? We are dealing with a totally different set of circumstances. The muscle weakness and fatigue is purposely being imposed and for good reason so we have to take that into account. There is several studies that show that exercise for those that fit into this category can benefit immensely and the benefits can be seen and felt after 3 months of consistent movement.
Being slightly over medicated (sub clinical hyperthyroid) you would assume that having more thyroid hormone available would result in more energy than your hypothyroid counterparts it does not .As I mentioned before this state in of itself is causing the impaired physical function.
Sub clinical hyperthyroid and hyperthyroid states cause specific impairment that differs immensely from the impairment that occurs with hypothyroid states. Hyperthyroid status increases RESTING heart rate, RESTING oxygen uptake, exercise heart rate and cardiac output. However maximal oxygen uptake during exercise is decreased despite increased heart rate and increased cardiac output. Fatigue sets in faster due to a 25% increase in lactic acid with in the muscles and maximal oxygen reduction. These effects are associated with a 21-37% decline of the oxidative and glycolytic enzymes in skeletal muscle, specifically a 15% decline in the type IIA muscle fiber. This is due to the accelerated protein catabolism due to the sub clinical hyperthyroid state. The excess amount of thyroid hormone actually leads to a reduction glycogen within muscle tissues.
What does this mean for those being medicated to a subclinical hyperthyroid state?
What are Type IIA muscle fibers?
Muscle fibers break down into two categories
1) Slow twitch (low force/low power/low speed /high endurance)
Exercise training that would utilize these muscle fibers are low intensity and long duration exercises, like walking. Hypothyroid patients benefit from this type of training
2) Fast twitch muscle fibers breakdown a little more into two sub categories. (Type IIA and Type IIB)
Type IIB (high force/high power/high speed/ low endurance) this type of training is typically sprinting. The Type IIA muscle fibers have the most impairment with sub clinical hyperthyroid and hyperthyroid states and the level of intensity falls somewhere in between slow twitch muscle fiber training and fast twitch Type IIB muscle fiber training.
Type IIA, known as fast oxidative are used during sustained power activities and are usually more resistant to fatigue then the Type IIB muscle fibers. In sub clinical hyperthyroid and hyperthyroid states, the Type IIA muscle fibers give out sooner than they should. This results in loss of lean muscle and weakness.
1) Slow twitch muscle fibers work in lower intensity – longer duration training (i.e walking)
2) Fast twitch muscle fibers Type IIA work in moderate intensity – sustained power activities (i.e interval weight training)
3) Fast twitch muscle fibers Type IIB work in high intensity – short duration /high intensity bursts of power at maximal or near maximal effort.( i.e Cross-fit, HITT, Bootcamp)
Patients being medicated to subclinical hyperthyroid and hyperthyroid states would benefit from sustained moderate intensity resistance training. The studies suggest starting with twice a week 20-30 minutes in duration. Using a sustained/steady method movement with little rest in between sets. One way of doing this is choosing 1 exercise for each of the larger muscle groups in the body and performing a set of 12 repetitions for each body part with little rest in between.
Example; Chest, Back, Legs.
Chest press > Lat pull down > kettle bell swing w/ squat. These can be repeated after a short rest, stretching in between or an active rest of 2 minutes at moderate intensity on a piece of cardio equipment or by stepping up and down on a step 4-6 inches.
Generally repeated for a total of 2- 3 cycles.
This can be modified to just doing the resistance exercise and stretching in-between sets and progress gradually to heavier weights, longer workouts and more times per week.
The premise is subclinical hyperthyroid and hyperthyroid patients will not benefit from lower intensity and longer duration training nor will they benefit from higher intensity/power /shorter training programs.
Heart rate was not defined in the findings, so I will suggest a parameter that is more in line of what would be used for those who are on medication to control heart rate and or blood pressure (beta-blockers and other medications like them) It is called “ Perceived Exertion “. Typically you go by how you feel and there is a chart you can use to determine at what level you are working at and what is right for you. Below is a link to the Borg scale of perceived exertion.
Keep in mind less is more and the more consistent you are with your exercise the more you can do over time.
(Sources) For subclinical hyperthyroid and hyperthyroid.
[Resistance training improves muscle function and body composition in patients with hyperthyroidism.]
To evaluate the effect of resistance training on skeletal muscle performance and body composition in patients with medically treated hyperthyroidism.
Nonrandomized controlled trial.
Large public tertiary hospital.
Sixteen sedentary patients with recent clinical diagnosis and laboratory confirmation of hyperthyroidism (7 men, 9 women; age, 38+/-11 y; weight, 58.4+/-2.6 kg; height, 1.6+/-0.3m) were assigned to the control group (medical therapy; n=9) or training group (medical therapy associated with resistance training; n=7). An age- and sex-matched healthy group served as controls (3 men, 5 women; age, 40+/-3 y; weight, 68.4+/-4.3 kg; height, 1.6+/-0.3m).
Resistance training twice a week for 16 weeks.
MAIN OUTCOME MEASURES:
Peak muscular strength (by dynamometry and 1 repetition maximum method) and endurance (30% of peak force) for 7 movements and anthropometric measurements.
The hyperthyroid patients as a group had lower baseline overall strength values when compared with healthy subjects (200.3+/-16.0 kg vs 274.9+/-21.8 kg, respectively; P=.006). Overall absolute increases in strength (49 kg vs 91 kg, P<.05) and endurance (78.5x10(2)kg/s vs 176.9x10(2)kg/s, P<.05) were higher in the training group compared with the control group. Body weight increased in both groups, but the sum of muscular circumference increased only in the training group (training group, 92.6+/-3.3 cm vs 97.1+/-3.8 cm; control group, 94.6+/-2.2 cm vs 94.4+/-2.1cm; P<.05), with no change in the sum of skinfolds.
Resistance training accelerates the recovery of skeletal muscle function and promotes weight gain based on muscle mass improvement in patients with medically treated hyperthyroidism.
About Raina: Thyroid Advocate contributor at Thyroid Nation, Owner/Personal Trainer at Conscious Fitness of Hollywood Florida