Category Archives: Co-existing problems with thyroid hormonal imbalances

Thyroid, kidneys and autoimmune disease connection

Thyroid affects function of many organs. Thyroid and kidneys have a close relationship. Thyroid hormones, T3 predominantly, but also T4 regulate the renal blood flow and the glomerular filtration rate (GFR). T3 thyroid hormone is important in the production of many kidney regulating molecules such as renin. Sub-optimal thyroid hormonal replacement can affect the health of kidneys negatively. Kidneys can eventually decrease in size in hypothyroidism or increase in size in hyperthyroidism (although prolonged, severe and untreated hyperthyroidism may eventually result in deterioration of kidneys). Thyroid hormone have effects on cardiovascular system and the flow of blood into the kidneys. Hypothyroidism can result in abnormalities in renin release. This can cause constriction of blood vessels and fluid retention. This situation is very bad for the heart. In hypothyroidism, the glomerular filtration rate (GFR) can decrease substantially. Opposite goes for hyperthyroidism. Untreated hyperthyroidism can cause kidney damage or make chronic kidney disease worse.

On the other hand, people with renal diseases can have worsening of their symptoms of hypothyroidism as protein bound thyroid hormones may be lost by ‘leaky’ kidneys. People on thyroid hormonal therapy and renal problems may need to take higher doses of hormones.

However thyroid hormones are not the only thyroid related molecules which can affect the kidneys. Thyroid Stimulating hormone produced by pituitary gland in our brain to stimulate thyroid hormonal production in the thyroid also has effects on kidneys. Thyroglobulin molecule produced in thyroid may also affect kidneys in autoimmune thyroid disease. Therefore, optimal and normal levels of these two molecules are also important.

Thyroid autoimmune disease can also affect kidneys. When I was six years old I was diagnosed with kidney problems and spend three months in a hospital. I was on a strict gluten free diet in a hospital, I had to spend most of my time in bed and had daily injections of antibiotics and some others. I remembered my kidneys feeling ’heavy”, my urine was dark brown, I felt very weak and had nausea. I had cravings for bread and bread rolls and one breakfast I attempted to steal one bread roll from the breakfast table I shared with my hospital friends. Unfortunately, despite hiding it, I was discovered by a nurse and the bread roll was taken from me. Looking back I believe my kidneys problems were directly related to my thyroid autoimmunity problems. Fortunately, I have recovered without farther problems.

Thyroid autoimmune disease may be connected to immune complex glomerulonephritis (inflammation and swelling of the tiny filters called glomeruli in kidneys) which causes the kidneys to stop working properly. Generally people with glomerulonephritis recover completely with medical care. It is very rare for it to cause complication such as renal failure.

 It is interesting that it was found that the kidneys can express thyroid hormone stimulating receptor (TSHR) (4, 8). Perhaps it serves as a boost system/ protective back up system for kidneys when thyroid hormonal level is low and thyroid stimulating hormone levels are high as seen in hypothyroidism. It was found in a study (9) that exogenous thyroid stimulating hormone improves renal function in patients with normal healthy thyroid hormonal levels. Also it was shown in a study that injecting recombinant human TSH improved estimated glomerular filtration rate (eGFR) in kidneys in patients with thyroid replacement therapy, which means their kidney function was improved.

Therefore it is possible that kidneys can be a target of thyroid autoimmunity as TSHR is expressed in thyroid but also in other organs such as kidneys. It is the main molecule to which antibodies are produced in Grave’s disease.

Another molecule to which antibodies are produced in thyroid autoimmunity (more so in Hashimoto’s thyroiditis) is thyroglobulin, a molecule present in thyroid. Increased levels of thyroglobulin, a molecule which is the building block of thyroid hormones, secreted by thyroid into blood, indicate thyroid damage. Higher levels are seen in thyroid autoimmunity or thyroid cancer. Kidneys were also found to express a protein which is very similar to thyroglobulin (4,10). The function of this similar protein in kidneys is stipulated to be on the DNA level in regulating kidney cell growth. The anti-thyroglobulin antibodies found in autoimmune thyroid disease complex with this similar protein and also with thyroid thyroglobulin (secreted from thyroid into blood) to form immune complexes and produce inflammatory processes in the kidneys. Another issue with immune complex glomerulonephritis is that another molecule called megalin (a receptor that binds thyroglobulin in kidneys), Megalin is regulated by thyroid stimulating hormone. Thyroid stimulating hormone binds to TSH receptors (as mentioned previously thyroid stimulating hormone receptor was found to be expressed in kidneys). The immune system has lower tolerance for this molecule in kidneys in thyroid autoimmunity, especially Hashimoto’s thyroiditis.  Megalin is also important for uptake of other molecules by kidneys such as albumin and vitamin D-binding protein. This might be connected to lowered vitamin D level in people with thyroid autoimmunity.

Immune complex glomerulonephritis can occur with Grave’s disease (as it was in my case), especially in children and it is possible that it may be triggered by an infection or gluten/casein sensitivity. However it can also occur in older people as discussed in a study of a 60 year old hyperthyroid woman with long-standing Graves’ disease treated with methimazole (6).

The rates of kidney involvement in people with thyroid autoimmunity can be as high as in 10–30% of cases (2) and it is much higher in the case of Hashimoto’s thyroiditis when compared with Grave’s disease. Around half of people with Hashimoto’s thyroiditis have a moderate increase in the level of urine albumin due to abnormal permeability of kidneys which is associated with renal damage. It might be therefore advisable (as suggested in scientific study (1) for kidney function to be monitored with thyroid autoimmunity, especially for Hashimoto’s thyroiditis patients.

Basically if your thyroid is off, the kidneys will not function optimally and vice versa. The renal blood flow, glomerular filtration rate, electrolytes and kidney structure and size will be affected. Kidney function test: eGFR and serum creatinine levels can be an indicator of thyroid function for people with thyroid problems. Serum creatinine levels are decreased in hyperthyroidism and increased in hypothyroidism. GFR is increased in hyperthyroidism and decreased in hypothyroidism. Kidney stones can be connected to hypothyroidism. It may relate to the altered kidney filtration rates and imbalances between calcium and magnesium with possible magnesium deficiency.

It is important to have normal blood pressure for kidney health which can also be a reflection of a thyroid function. Cranberry juice has a positive effect on kidney health in general.

References:

  1. Domenico Santoro, Carmela Vadalà, Rossella Siligato, Michele Buemi, and Salvatore Benvenga. Autoimmune Thyroiditis and Glomerulopathies. Front Endocrinol (Lausanne). 2017; 8: 119.
  2. Ronco P, Debiec H. Pathophysiological lessons from rare associations of immunological disorders. Pediatr Nephrol (2009) 24(1):3–8.
  3. Yuqian Luo, Yuko Ishido, Naoki Hiroi, Norihisa Ishii, and Koichi Suzuki.The Emerging Roles of Thyroglobulin. Advances in Endocrinology. Volume 2014 (2014), Article ID 189194.URL: https://www.hindawi.com/archive/2014/189194/
  4. Sellitti DF, Akamizu T, Doi SQ, Kim GH, Kariyil JT, Kopchik JJ, Koshiyama H. Renal expression of two ‘thyroid-specific’ genes: thyrotropin receptor and thyroglobulin. Exp Nephrol. 2000 Jul-Oct; 8(4-5):235-43.
  5. Zheng G, Marino’ M, Zhao J, McCluskey RT. Megalin (gp330): a putative endocytic receptor for thyroglobulin (Tg). Endocrinology. 1998 Mar; 139(3):1462-5.
  6. Horvath F Jr, Teague P, Gaffney EF, Mars DR, Fuller TJ. Thyroid antigen associated immune complex glomerulonephritis in Graves’ disease. Am J Med. 1979 Nov; 67(5):901-4.
  7. Michele Marinò, Gang Zheng and Robert T. McCluskey. Megalin (gp330) Is an Endocytic Receptor for Thyroglobulin on Cultured Fisher Rat Thyroid Cells. Journal of Biological Chemistry. URL: http://www.jbc.org/content/274/18/12898.full
  8. Dutton CM, Joba W, Spitzweg C, Heufelder AE, Bahn RS. Thyrotropin receptor expression in adrenal, kidney, and thymus. Thyroid 1997 Dec; 7(6):879-84.
  9. Flore Duranton, Anouchka Lacoste, Patrick Faurous, Emmanuel Deshayes, Jean Ribstein, Antoine Avignon, Georges Mourad and Àngel Argilés. Exogenous thyrotropin improves renal function in euthyroid patients, while serum creatinine levels are increased in hypothyroidism. Clinical Kidney Journal, Volume 6, Issue 5, 1 October 2013, Pages 478–483. URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438406/
  10. Wu H, Suzuki S, Sellitti DF, Doi SQ, Tanigawa K, Aizawa S, Akama T, Kawashima A, Mishima M, Ishii N, Yoshida A, Hisatome I, Koles NL, Katoh R, Suzuki K. Expression of a thyroglobulin (Tg) variant in mouse kidney glomerulus. Biochem Biophys Res Commun. 2009 Nov 13;389(2):269-7.
  11. Gopal Basu and Anjali Mohapatra. Interactions between thyroid disorders and kidney disease. Indian J Endocrinol Metab. 2012 Mar-Apr; 16(2): 204–213.

 

 

 

 

Thyroid hormonal imbalance and blood sugar problems

Thyroid Hormone Imbalances and blood sugar problems

Thyroid hormones imbalances, both hyper and hypothyroidism can cause poor blood sugar control, increase the risk of insulin resistance and the risk of developing type 2 diabetes due to effects of thyroid hormones on the production, demand and performance of insulin in the body and common genetic factors. There is plenty of scientific evidence supporting the contribution of thyroid hormonal imbalances to Type 2 Diabetes Mellitus. All hormonal system are intertwined. Autoimmune thyroid conditions also increase the risk of Type 1 Diabetes Mellitus ( autoimmune illness) and vice versa.

Blood sugar needs to be kept at between 3.9 and 5.5 mmol/L (70 to 100 mg/dL). It is regulated by few factors: glucose storage and release from glycogen by the liver, intestinal absorption, glucose uptake in muscles and fat cells and the production of insulin by pancreas. Insulin is a hormone made in pancreas which takes the sugar out of blood when it gets too high.

Thyroid hormone imbalances change expression of certain genes and production of proteins which can affect insulin sensitivity of cells. They also cause changes in plasma fatty acids which also modulate insulin sensitivity.

Insulin resistance happens when the insulin receptors in body cells do not respond properly to insulin and so the sugar from blood cannot be taken inside of cells to produce energy. Insulin resistance can progress and lead to Type 2 Diabetes Mellitus, a conditions where pancreas can no longer produce enough insulin to overcome insulin resistance.

Thyroid hormone is the hormone that starts the energy production inside of the cells and insulin helps to supply the cells with fuel-glucose. The hormonal systems work together so it is clear that imbalance of one will imbalance the other.

Hyperthyroidism

The increase in thyroid hormones signals the body to rapidly increase energy production and stimulates liver through the sympathetic nervous system. That is the main reason for glucose intolerance. The needs for glucose increase to keep up with an increased metabolic rate. Growth hormone somatotropin is released accelerating the production of liver glycogen to glucose. There is also a rapid glucose absorption from the intestine. In Graves’ disease, more proinsulin is secreted from the pancreas. It is however not properly converted to insulin. Insulin is also more rapidly degraded in kidneys. Hyperthyroidism is associated with insulin resistance of liver cells. The liver cells overproduce glucose and are ‘deaf’ to insulin signals. However, the skeletal muscle cells have an increased glucose absorption. The production of energy from glucose is changed towards glycolysis and lactate formation in muscles. It has been shown in Japanese studies that people with Graves’ disease are twice as much of a risk of developing non insulin-dependent diabetes (type II) diabetes when compared to a healthy population (1).

A medication, called thiazolidinedine, used sometimes to increase insulin sensitivity should not be given to people with type 2 diabetes, thyroid autoimmunity and ophthalmopathy as it may worsen the eye condition (7). Also when people with thyrotoxicosis (excessive thyroid hormones) and diabetes are given too much insulin, they at risk of diabetic ketoacidosis, which increases the risk of a cardiac arrest, therefore these two conditions of hyperthyroidism and diabetes need to be controlled properly.

Unfortunately, there is also an increased chance of developing Type 1 Diabetes, which is Insulin Dependent Diabetes Mellitus, an autoimmune condition. People with thyroid dysfunction (not related to autoimmunity) do not have an increased chance of developing Type 1 Diabetes Mellitus which is an autoimmune illness. Type 1 Diabetes Mellitus can co-occur with Graves’ disease as both are autoimmune conditions and they have common genetic components. This is often seen in younger people with Graves’ disease. The chance of having another autoimmune illness with Graves’ disease is about 9-10% and slightly higher for Hashimoto’s thyroiditis (19).

Hypothyroidism

T3 is an extremely potent elixir of life. Hypothyroidism and insulin resistance go together. Lack of T3 (even sub-clinical) may lead to blood sugar problems, insulin resistance and type 2 diabetes. The risk of developing type 2 diabetic is higher in hypothyroidism than hyperthyroidism. Low T3 causes liver and pancreatic function to be poor, lowers the secretion of insulin and stresses those organs. Low T3 also causes impaired glucose metabolism in peripheral tissues. The peripheral muscles become less responsive to insulin. The transport of glucose inside of cells is impaired due to lowered expression of transport genes due to hypothyroidism. Also there is reduced disposal of glucose. Under methylation issues has been postulated as a possible mechanisms, which increase insulin resistance. Another one is the dysregulation of metabolism of leptin, hormone which regulates hunger. Hypothyroid people store less glucose in the liver as glycogen and are more prone to low blood sugar. As a consequence, both adrenaline and cortisol start rising at night.  Adrenaline can peak around 2am and a person can wake up with heart palpitations. Cortisol hormone may be high in early morning, raising fasting blood sugar. I certainly had that happen to me when I was hypothyroid as mentioned in my previous post. I used to get up and have a snack in the middle of the night, which always stopped the heart palpitations.

Thyroid is a major player in the part of brain called hippocampus which is very vulnerable brain region in general as it modulates glucose metabolism and insulin signalling. Damage to hippocampus has been connected to hypothyroidism, memory problems, special navigation problems, dementia and Alzheimer’s disease. It may also be connected to the development of type 2 diabetes.

Metformin is sometimes given to people with insulin resistance to improve their insulin sensitivity, however optimal thyroid hormonal replacement may also be effective in increasing insulin sensitivity in some cases. Metformin may deplete vitamin B12 so it is important to watch your levels. It was noted that the levels of TSH decrease with metformin in people on levothyroxine hormonal treatment which indicates that there is an improvement in hypothyroid state (10, 11) without a change in FT4 levels, thyroid hormones seem to work better with improved insulin sensitivity. This is not surprising as too much insulin is antagonistic to thyroid hormones and blocks thyroid hormonal receptors.

In my personal case, I had blood sugar issues when I was on levothyroxine only hormonal replacement and also when I suffered from thyrotoxicosis. My glucose tolerance test was impaired.

Natural desiccated thyroid and levothyroxine combination had normalised my blood sugar. Natural bio-identical progesterone hormone which I was taking while on levothyroxine only hormonal replacement also helped in improving my blood sugar. Progesterone enhanced my T4 into T3 conversion all by itself and improved my hypothyroid symptoms.

Obviously type 1 diabetics need insulin hormone for survival as the pancreatic beta cells producing insulin are destroyed by an autoimmune reaction.

Ways which may improve insulin sensitivity and lower blood sugar:

Vitamin D helps thyroid autoimmunity and insulin resistance and increases insulin secretion from pancreas (16).

Optimal thyroid hormonal levels, proper control of hyperthyroidism and hypothyroidism is important.

Optimal hormonal replacement for hypothyroidism, consider NDT or levothyroxine/NDT combination to improve blood sugar control

Balancing other hormones

Other:

Vitamin B1 especially (Benfotiamine, fat soluble form of B1 might be beneficial)

Chromium mineral, vanadium, and B vitamins (Brewer’s yeast can provide these)

Magnesium

Vitamin C, clinical study shows that vitamin C can lower blood sugar (9)

Changes to nutrition (sugar limiting, healthy vegetable rich diet, more fibre, less saturated fat and more essential fatty acids (fish oil, flaxseed, and olive oil), not combining protein and sugar in a meal)

Essential fatty acids, coenzyme Q10, alpha lipoic acid, zinc

Exercise (short bursts of intense exercise were shown to reduce insulin resistance)

Limiting stress as cortisol produced during stress, increases blood sugar

Apple cider vinegar

Herbs which may help:

Gymnema sylvestre (good formula is GlucoBalance by Mediherb which also contains vitamins and minerals), small human study (18) showed positive blood sugar lowering effects.

Others: Bitter melon (also available in capsules), garlic, onion, prickly pear, soursop, chaste berry, Rhodiola rosea, guava leaves, fenugreek used in cooking and cinnamon

 

This post is for educational purposes only. Any supplements to lower blood sugar should be taken under doctor’s supervision.

References:

        1. Komiya I, Takasu N, Yamada T, Ohara N, Ootsuka H, Ota M, Fukushima H, Sekikawa A, Tominaga M, Sasaki H. Studies on the association of NIDDM in Japanese patients with hyperthyroid Graves’ disease. Horm Res. 1992; 38(5-6):264-8.
        2. Lombadiari V, Mitrou P, Maratou E, Raptis AE, Tountas N, Raptis SA, Dimitriadis G. Thyroid hormones are positively associated with insulin resistance early in the development of type 2 diabetes. Endocrine. 2011 Feb; 39(1):28-32.
        3. Brenta G. Why Can Insulin Resistance Be a Natural Consequence of Thyroid Dysfunction? Journal of Thyroid Research 2011. URL https://www.hindawi.com/journals/jtr/2011/152850/
        4. Thyroid Autoimmunity in the Context of Type 2 Diabetes Mellitus: Implications for Vitamin D
        5. Valerie Witting, Dominik Bergis, Dilek Sadet and Klaus Badenhoop. Thyroid disease in insulin-treated patients with type 2 diabetes: a retrospective study. Thyroid Res. 2014; 7: 2.
        6. Chaoxun Wang .The Relationship between Type 2 Diabetes Mellitus and Related Thyroid Diseases. Journal of Diabetes Research. Volume 2013. URL: https://www.hindawi.com/journals/jdr/2013/390534/ref/
        7. Menaka R, et Thiazolidinedione precipitated thyroid associated ophthalmopathy. J Assoc Physicians India. 2010 Apr; 58:255-7.
        8. Yeo KF, et. Simultaneous presentation of thyrotoxicosis and diabetic ketoacidosis resulted in sudden cardiac arrest. Endocr J. 2007 Dec; 54(6):991-3.
        9. Dice, J. F. and Daniel, C. W. (1973).The hypoglycemic effect of ascorbic acid in a juvenile-onset diabetic. International Research Communications System, 1:41. URL: https://www.seanet.com/~alexs/ascorbate/197x/dice-jf-ircs-1973-march-p41.htm
        10. Theodora Pappaa and Maria Alevizakia,b. Metformin and Thyroid: An Update. Eur Thyroid J. 2013 Mar; 2(1): 22–28.
        11. Cappelli C, Rotondi M, Pirola I, Agosti B, Gandossi E, Valentini U, De Martino E, Cimino A, Chiovato L, Agabiti-Rosei E, Castellano M (2009) TSH-lowering effect of metformin in type 2 diabetic patients: differences between euthyroid, untreated hypothyroid, and euthyroid on L-T4 therapy patients. Diabetes Care 32(9):1589–1590.
        12. Abdullah Zeid Badbayyan, Yaman Mazen Almerstani, Mohamed Osama Allulu, Awni Mazen Al-lolo, Ghaliah Abdullah Al-haqas, Abdulrahman Ahmed Alnaser. Association between thyroid hormones. Changes and development of Type 2 Diabetes: (Systemic review). International Journal of Healthcare Sciences. 2016 (4):2:966-971.
        13. Coller FA, Huggins CB. Effect of hyperthyroidism upon diabetes mellitus: striking improvement in diabetes mellitus from thyroidectomy. Annals of Surgery. 1927; 86(6):877–884.
        14. Lambadiari V, Mitrou P, Maratou E, et al. Thyroid hormones are positively associated with insulin resistance early in the development of type 2 diabetes. Endocrine. 2011; 39(1):28–32.
        15. Kapadia KB, Bhatt PA, Shah JS. Association between altered thyroid state and insulin resistance. Journal of Pharmacology and Pharmacotherapeutics. 2012; 3:156–160.
        16. Talaei A, Mohamadi M, Adgi Z. The effect of vitamin D on insulin resistance in patients with type 2 diabetes. Diabetol Metab Syndr. 2013; 5:8.
        17. Beltramo E, Berrone E, Tarallo S, Porta M. Effects of thiamine and benfotiamine on intracellular glucose metabolism and relevance in the prevention of diabetic complications. Acta Diabetol. 2008 Sep; 45(3):131-41.
        18. Diabetes in control. URL: http://www.diabetesincontrol.com/effect-of-extended-release-gymnema-sylvestre-leaf-extract-beta-fast-gxr/
        19. Boelaert K, Newby PR, Simmonds MJ, Holder RL, Carr-Smith JD, Heward JM, Manji N, Allahabadia A, Armitage M, Chatterjee KV, Lazarus JH, Pearce SH, Vaidya B, Gough SC, Franklyn JA. Prevalence and relative risk of other autoimmune diseases in subjects with autoimmune thyroid disease. Am J Med. 2010 Feb; 123(2):183.e1-9

 

 

 

 

 

Thyroid problems and blood pressure connection

Thyroid problems and blood pressure connection

Blood pressure can be affected by many factors. Thyroid hormone imbalances affect blood pressure greatly. In my previous post, I had talked about body temperature being indicative of thyroid dysfunction. Blood pressure is also a strong indicator of thyroid function for people with thyroid hormonal imbalances. It is important to observe body signals as they are number one indicators that something is not right with thyroid hormones for people with thyroid issues.

I remember one day driving to my doctor for a check- up visit in heavy traffic while munching on chocolate coated coffee beans. I was almost late and when I saw my doctor, I was a bit flustered. I had a busy, stressful day. During a consultation with my doctor, she measured my blood pressure and it was through the roof. I do not know about you but I always get a bit nervous when my doctor is about to measure my blood pressure despite trying to stay calm and breathing deeply. Just feeling stressed, uncomfortable can raise blood pressure by itself. Blood pressure often fluctuates throughout the day. However it is not the temporary spikes of blood pressure we have to worry about but the sustained, chronic high blood pressure. Some people are not aware of their raised blood pressure. Blood pressure problems may be silent. For me, headaches, general tension, pins and needles in my arms and whooshing sound in my ears in the evening points to a possible blood pressure problem and possible hormonal imbalance. During my consultation that day, I had found out that my TSH value was 0.22, too low for me. I operate best at value of 1.7 so the dose of my hormonal replacement was slightly reduced and blood pressure came down. I also stopped drinking coffee and went to have decaffeinated variety and no more chocolate coated coffee beans!

I will explain how thyroid hormones affect blood pressure. When your doctor measures your blood pressure with a blood pressure monitor (sphygmomanometer), she or he inflates a cuff on your arm to collapse and then release the brachial artery under the cuff. A doctor usually uses a manual sphygmomanometer and listens to your brachial artery through a stethoscope. However there are digital blood pressure monitors available as well. When the pressure is released slowly from the cuff, the doctor listens to a first whooshing sound in your artery. This sound represents your systolic reading, it is when the blood starts flowing again in the artery, forced through by a heartbeat. Then as the cuff falls farther, the sound stops and the reading of diastolic blood pressure is taken at that moment. That reading represents the blood pressure in your artery between the heart beats, at the resting phase of the cardiac cycle. Therefore, blood pressure represents the force of blood against the arterial wall. The systolic pressure shows the power of the heart contraction and the force of blood being pumped in the artery. The second diastolic pressure represents the dilation and flexibility of the arteries.

Normal blood pressure is around 120 (systolic) and 80 (diastolic), 120/80.

High blood pressure is 140/90 or above.

The operating centre for blood pressure is present in the brain stem where signals from the body are processed. Blood pressure system is regulated by renin- angiotensin- aldosterone system and by sympathetic nerves and hormones adrenaline and noradrenaline.

While, there are many factors which can influence blood pressure, I will concentrate on thyroid dysfunction specifically in this post. Both the sympathetic and hormonal systems are deregulated in thyroid dysfunction. It has been suggested in scientific literature that there is a disconnection in the renin-angiotensin-aldosterone system in both hyperthyroidism and hypothyroidism as the functioning of kidneys is affected. Thyroid and renal function are interrelated.

 

Hyperthyroidism

People with Graves; disease have an increased rate and depth of respiration as well as higher blood pressure and a rapid heartbeat. There may be over 100 heart beats per minute. The systolic blood pressure is usually considerably higher than 120 and more raised than diastolic. Normal blood pressure is around 120 (systolic) and 80 (diastolic). In hyperthyroidism the reading for blood pressure is generally (≥140/<90 mm Hg). It is called systolic hypertension. It is also called secondary hypertension as thyroid hormones are the underlying cause of the high blood pressure. The pulse pressure is the difference between the systolic and diastolic pressure. The normal resting pulse pressure is therefore around 30-40 mmHg. People with GD have widen resting pulse pressure.

Too much thyroid hormones in blood increases metabolic rate. The heart and cardiovascular need to adjust. The excess of thyroid hormones increases the use of oxygen in the body. The sympathetic nervous system (SNS) is dominant in Graves’ disease, activated by excessive thyroid hormones. It is a system which is normally responsible for a ‘fight of flight’ body response to a dangerous and stressful situation and it releases catecholamines- epinephrine and norepinephrine from adrenal glands to accelerate the heart rate and increase blood pressure. The effects of hyperthyroidism include increased cardiac output, contractility, tachycardia, widened pulse pressure and dilation of peripheral blood vessels. Heart often goes into a ‘marathon run’. Heart related problems, such as palpitations (strong and fast beating of the heart) is a common symptom of Graves’ disease. This can also cause irregular heartbeat sometimes. Atrial fibrillation (type of a heart arrhythmia) can be seen.

Thyroid hormones increase other hormones such as aldosterone (from adrenals) and renin (from kidneys) secretion. This also increases blood volume and blood pressure by causing water to be reabsorbed along with sodium while more potassium is excreted in urine. Thyroid hormones and kidneys stimulate the development of red blood cells which also increases blood volume. Kidneys increase in mass with hyperthyroidism. Long term hypertension may lead to heart disease as it strains the heart. 

Hypothyroidism

Generally, hypothyroidism can in time significantly increase diastolic pressure, raising it above 90 mm Hg. It is often called hypothyroid hypertension. This is due to the fact that over time, continuous hypothyroidism causes changes to blood vessels, they become ‘stiff’ and constricted. The systolic blood pressure reading may also become elevated. However, there is a narrow pulse pressure.

Hypothyroidism is very stressful for the body. The body has to increase blood pressure to fight the slow metabolic rate and consequences of negative effects of low thyroid levels. It tries to do it with other hormones and molecules. The sympathetic and adrenal system is activated. The levels of adrenal norepinephrine were found to be elevated in hypothyroidism. Adrenal aldosterone hormone imbalance is connected to hypothyroidism and its increased levels may result in a constriction of blood vessels and elevated diastolic (bottom number) blood pressure. Cortisol hormone levels spike at times, especially in the morning in order to raise blood pressure and to increase the heart rate. Aldosterone hormone can spike about 2am. I had found myself  awake at 2am with heart palpitation when I was on a levothyroxine hormonal replacement only. I discovered that if I had something to eat in the middle of the night, my palpitations would stop. Aldosterone hormone increases blood pressure to deliver more glucose to body tissues when levels get too low due to hypothyroidism. At the same time the kidneys function is slower and they can get smaller in size. It was found that plasma renin (produced in kidneys) and angiotensin levels were lowered with hypothyroidism. Water clearance is reduced. Hypothyroidism is a low-renin hypertensive state, which means that levels of sodium in body decrease causing fluid retention. Low thyroid hormonal levels result in the inflammation and plasticity loss of blood vessels. Arterial stiffness is an important determinant of arteriosclerosis, which increases the risk for heart attack and strokes. Thyroid hormones promote the synthesis and action of vasodilators which acts directly on muscles in our arteries. However with low levels, the vessels become less flexible. The synthesis of nitric oxide (a powerful chemical, which dilates blood vessels) from L-arginine is stimulated by T3. Imagine your heart trying to pump blood through blood vessels in the body, which cannot effectively dilate and a resulting stress and damage to the cardiovascular system.

My own experience

The levothyroxine hormonal replacement after my thyroid surgery has raised my T4 levels high over time (in the top of the T4 reference range) while my T3 hormonal levels were low borderline. I suffered from T4 thyrotoxicosis and T3 deficiency. I had developed severe high blood pressure, felt stressed, had needle and pins in my arms and suffered from severe migraines. I went to see a doctor who prescribed a beta blocker -propranolol for my blood pressure problems. I started taking the medication but after few weeks I developed severe muscle spasms, horrible pains in my jaw and terrible muscular pain coupled with some degree of depression. I went to a doctor again and I got prescribed strong antibiotics because he believed my inability to open my mouth and the pain in my jaw and ears indicated some severe throat infection. I came home, while drinking water through a straw and shaking, I had a light bulb moment and realized that propranolol stopped the conversion of T4 (levothyroxine) to T3 (active hormone) in my body. The blood pressure medication had severely depleted my T3 levels which were low to start with. I did not have throat infection or some other terrible illness, I had a severe T3 deficiency. The balance between T4 and T3 is vital. It seemed that in my case, the high T4/low T3 levels caused my high blood pressure. Both, my systolic and diastolic readings were increased but my diastolic blood pressure was significantly raised.

My experience has lead me on a journey of discovery. I had learned that balancing my hormones is important for lowering my blood pressure. I added Natural Desiccated Thyroid (NDT) to my levothyroxine treatment, which ended my blood pressure problems at the time.

Since then, I had invested in blood pressure monitor and check my blood pressure occasionally. It is important to make sure the thyroid hormonal replacement is optimal as any imbalance will eventually show in blood pressure changes. Also, levothyroxine only treatment created a state of oestrogen dominance in my body, which farther decreased T4 into T3 conversion. Natural progesterone cream also helped to get my blood pressure to completely normal levels. More on that in later posts.

References:

  1. Danzi S, Klein I. Thyroid hormone and blood pressure regulation. Curr Hypertens Rep. 2003 Dec; 5(6):513-20.
  2. Fommei E, Iervasi G. The role of thyroid hormone in blood pressure homeostasis: evidence from short-term hypothyroidism in humans. J Clin Endocrinol Metab. 2002 May; 87(5):1996-2000.
  3. Marcisz C, Kucharz EJ, Marcisz-Orzel M, Poręba R, Orzel A, Sioma-Markowska U. Changes of poststimulatory plasma renin activity in women with hyperthyroidism or hypothyroidism in relation to therapy. Neuro Endocrinol Lett. 2011; 32(3):301-7.
  4. Julia H. Hauger-Klevene, Harold Brown, Jose Zavaleta. Plasma Renin Activity in Hyper- and Hypothyroidism: Effect of Adrenergic Blocking Agents. J Clin Endocrinol Metab (1972) 34 (4): 625-629.
  5. Ogihara T, Yamamoto T, Miyai K, Kumahara Y. Plasma renin activity and aldosterone concentration of patients with hyperthyroidism and hypothyroidism. Endocrinol Jpn. 1973 Oct; 20(5):433-7.
  6. Hypothyroidism and Hypertension. Stella Stabouli; Sofia Papakatsika; Vasilios Kotsis URL: http://www.medscape.com/viewarticle/733788_3