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Enhance insulin sensitivity and support thyroid function

Enhance insulin sensitivity and support thyroid function

Abel López-Bermejo. For TSH, free T4, Enhancw HOMA-IR, logarithmic-transformed values were used Enhacne normalize the Enhance insulin sensitivity and support thyroid function. This finding may suggest that the association between insulin resistance and endothelial and thyroid function tests does not reflect alterations in thyroid status but alterations in more fundamental common cellular functions shared by the two systems. TZDs should be used carefully in patients with T2DM with clinically active TED. Use profiles to select personalised advertising.

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How to Control Your Metabolism by Thyroid \u0026 Growth Hormone

Enhance insulin sensitivity and support thyroid function -

Metabolic syndrome is a cluster of five conditions—high glucose, high blood pressure , high triglycerides , low HDL cholesterol , and a large waist—that increases the risk of heart disease, diabetes, and stroke.

Untreated metabolic syndrome can progress to type 2 diabetes. The thyroid gland helps regulate metabolism the conversion of food to energy.

Thyroid disease can disrupt metabolism, allowing blood sugar levels to rise. High blood sugar levels increase the risk of type 2 diabetes. Thyroid disease can also interfere with the production of insulin. Insulin makes it possible for cells to use glucose for energy. This lowers blood sugar. Hyperthyroidism can contribute to insulin resistance.

When you become resistant to insulin, your cells aren't able to use the glucose in your blood. As a result, blood glucose levels stay high. People with diabetes who need insulin shots may also find themselves needing higher doses. On the flip side, hypothyroidism an underactive thyroid decreases metabolism.

When this happens, insulin can linger, causing blood sugar to drop hypoglycemia. For people on diabetes medications , the drop can sometimes be extreme, leading to dizziness, disorientation, and unconsciousness.

Thyroid disease can affect insulin levels. Hyperthyroidism can cause blood sugar levels to rise. This can increase the risk of diabetes or make diabetes harder to control. Hypothyroidism can lead to low blood sugar.

In addition to problems with glucose metabolism and insulin production, there are several other links between thyroid disease and diabetes. Type 1 diabetes is an autoimmune disease in which the immune system attacks the cells that make insulin.

There are certain forms of thyroid disease, called Hashimoto's thyroiditis and Graves' disease , that are also autoimmune. Hashimoto's thyroiditis is the most common cause of hypothyroidism in the United States. Studies suggest that most people with type 1 diabetes will eventually develop Hashimoto's disease.

Having low thyroid hormones could make you crave sugar and other foods. There are several reports of people with Hashimoto's thyroiditis who had cravings for carbohydrate-rich foods. Eliminating sugar-sweetened beverages and ultra-processed foods is encouraged in these cases.

Graves' disease, on the other hand, causes hyperthyroidism. Thyroid hormones and insulin are both influenced by three organs that work together: the hypothalamus of the brain, the pituitary gland , and the adrenal glands. Referred to as the hypothalamic-pituitary-adrenal axis HPA axis , these organs send signals back and forth to each other and together control the body's response to stress.

They do this by adjusting levels of the stress hormone cortisol. Problems with any of the organs in the HPA axis can affect how much or how little cortisol is produced.

High cortisol levels can lead to hyperglycemia. Low cortisol levels can lead to hypoglycemia. Type 1 diabetes, an autoimmune form of diabetes, often occurs alongside autoimmune thyroid disease.

Problems with the HPA axis, which produces the stress hormone cortisol, can lead to abnormal insulin and thyroid hormone levels. If you have been diagnosed with either thyroid disease or diabetes, achieving and maintaining your ideal weight is one of the best ways to prevent the other condition.

Keeping your blood sugar or thyroid hormones under control can also help. If you have insulin resistance , in which the body doesn't respond to insulin as it should, thyroid disease can make your blood sugar harder to control. By managing insulin resistance with medications, diet, and exercise, you may be able to avoid diabetes as well as complications of thyroid disease.

By managing hyperthyroidism with medications, diet, and exercise, you may also reduce your risk of type 2 diabetes. If you have diabetes or thyroid disease, maintaining an ideal weight may help you avoid getting the other condition.

Properly managing your blood sugar or thyroid hormone can also help. The initial dose of levothyroxine therapy is determined by the underlying cause of the disease, severity of dysfunction, and health and age of the person being treated.

This is highly individualized; however, the adage in the elderly or those with underlying CVD is to start low typically 25 μg daily and go slow with drug titration.

The woman in this case study is likely to see improvement in her symptoms within 6—8 weeks after initiating levothyroxine therapy.

It is important that she closely monitor her blood glucose levels because improved thyroid function may increase her glucose, leading to more hyperglycemia. She may need additional diabetes medication intervention. is a year-old man with type 1 diabetes who uses an insulin pump.

Physical examination reveals:. Treatment strategies include β-blocker therapy, an increase in insulin, and oral steroids for the eyes, as well as discussion of options—including radioiodine therapy, surgery, or anti-thyroid therapy—and provision of education.

There is an autoimmune link HLA markers between type 1 diabetes and Graves' disease. The prevalence of Graves' disease with type 1 diabetes has been reported to be 2.

As Graves' disease stabilizes, insulin requirements may decrease. It may be beneficial to place the patient in this case study on a glucose sensor because the glucose levels will be elevated initially, and higher doses of insulin will be needed.

Once successful treatment is completed, close monitoring will also be necessary to avoid hypoglycemia when insulin requirements decrease. is an year-old woman with type 2 diabetes diagnosed 5 years ago.

Since her diagnosis, she has lost 50 lb through a diet and exercise program. She is normoglycemic. Coexisting health problems include polycystic ovarian disease and vitiligo. Family history is significant for thyroid disease.

She was taking metformin until a recent positive pregnancy test. The patient complains of fatigue, nausea, constipation, and feeling cold. Her weight loss plateaued several months ago, and now her weight is slowly increasing. A referral to a dietitian is recommended to evaluate adequate calorie intake for diabetes, pregnancy, and appropriate weight gain.

Swift initiation of levothyroxine therapy is indicated because the patient is hypothyroid and pregnant. Initial symptoms should improve within 4—6 weeks unless they are secondary to the pregnancy rather than hypothyroidism.

The rate of fetal death was 3. It is important to screen women of childbearing age and those in the first trimester of pregnancy for hypothyroidism to optimize thyroid function.

History of another autoimmune disorder or a family history of thyroid disease increases the possibility of hypothyroidism, which underlines the need for screening.

For patients newly diagnosed with thyroid disease, levothyroxine therapy should be initiated as soon as possible and at a dose as close as possible to the anticipated requirement. Additional considerations include the effects of diabetes on pregnancy. In early pregnancy, patients with diabetes can be affected by pregnancy-related hormones that cause increased insulin secretion, decreased insulin requirements, and decreased glucose produced by the liver, which can lead to hypoglycemia.

Estrogen and cortisol can cause significant insulin resistance, therefore potentially causing hyperglycemia. Close monitoring of blood glucose during pregnancy allows for medication, diet, and exercise alterations to optimize diabetes control while normalizing thyroid function. The prevalence of thyroid disease is higher in diabetes because of the increased age of diabetic patients as well as an autoimmune link.

Untreated or inadequately treated thyroid disease can negatively impact diabetes control. Pregnancy is a challenging state associated with diabetes and can be complicated by the effects of untreated or undertreated thyroid disease.

Johnson, MS, RNC, FNP, BC-ADM, CDE, is an endocrinology nurse practitioner at Endocrinology Associates in Phoenix, Ariz.

Note of disclosure: Ms. Johnson has received honoraria for speaking engagements from Abbott Laboratories, which manufactures products for the treatment of thyroid disease. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest.

filter your search All Content All Journals Diabetes Spectrum. Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation.

Volume 19, Issue 3. Previous Article Next Article. Thyroid Disease Prevalence. Thyroid Anatomy and Physiology. Understanding the Role of the Thyroid. Thyroid Hormone Effects on Diabetes. Screening Recommendations. Case Studies. Article Navigation. Diabetes Control in Thyroid Disease Jennal L.

Johnson, MS, RNC, FNP, BC-ADM, CDE Jennal L. Johnson, MS, RNC, FNP, BC-ADM, CDE. This Site. Google Scholar. Diabetes Spectr ;19 3 — Connected Content.

A reference has been published: Glycemic Challenges: Diabetes Confounded by Serious Illness. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. In Brief Thyroid disease is commonly found in most types of diabetes.

Her laboratory results are:. TSH: 5. Laboratory results included:. T4: Physical examination is unremarkable except a g thyroid. Laboratory results include:. A1C: 6. All participants gave informed written consent. SHIP-TREND-0 followed the recommendations of the Declaration of Helsinki and was approved by the Ethics Committee of the University of Greifswald Approval No.

The BASE-II cohort was drawn as a convenience sample from the greater Berlin metropolitan area. Study details have been described previously in detail 11 , All participants gave written informed consent and the Berlin Aging Study II was approved by the Ethics Committee of the Charité — Universitätsmedizin Berlin Approval No.

From the present analysis, we excluded individuals because of known diabetes and concomitant antidiabetic medication, individuals due to missing data in laboratory values glucose or insulin at baseline or after 2 h in the oral glucose tolerance test , individuals because of a fasting period below 8 h before blood sampling, and 36 individuals due to systemic glucocorticoid therapy.

Altogether participants from the studies SHIP-TREND-0 participants and BASE-II participants were included in this cross-sectional analysis. In SHIP, smoking status was assessed in a computer-assisted interview. In BASE-II, information on smoking status was taken from the medical history recorded by a study physician.

Smoking status was categorized in the three categories: current smokers, former smokers, and never smokers. Information on pre-existing diabetes was taken from the medical history and assessed by interview.

In both the studies, body weight was measured in light clothes with a portable electronic scale to the nearest 0. Blood samples were taken as fasting blood samples and analysed in the local core laboratories using standardized protocols. Serum TSH, fT3, and fT4 levels were analysed by electrochemiluminescence immunoassays BASE-II: cobas immunoassay systems, Roche Diagnostics; SHIP-TREND Dimension Vista® System Flex® reagent cartridge, Siemens Healthcare Diagnostics Inc.

The analytical measuring range in BASE-II was 0. The analytical measuring range in SHIP-TREND-0 was 0. TSH levels were categorized in the three categories: TSH in the reference range, high TSH, and low TSH according to the established reference limits of 0.

In BASE-II, glucose concentration was determined by photometry, HbAlc by ion-exchange HPLC and serum insulin levels by chemiluminescence immunoassay Roche elecsys, Roche Diagnostics. In SHIP-TREND-0, plasma glucose levels were measured using a hexokinase method Dimension Vista , Siemens Healthcare Diagnostics and serum insulin values were assessed by an electrochemiluminescence immunoassay ADVIA Centaur, Siemens Healthcare Diagnostics.

HbA1c concentrations were determined by HPLC Bio-Rad Diamat. A standardized oral glucose tolerance test OGTT was conducted and levels of insulin and glucose were measured at baseline and after 2 h in both studies.

Impaired fasting glucose IFG and impaired glucose tolerance IGT as well as a formerly unknown diabetes were determined according to the criteria of the American Diabetes Association ADA Insulin sensitivity was estimated by calculating the insulin sensitivity index ISI based on the work of Matsuda et al.

Characteristics of the study population are provided as median, 25th, and 75th percentile for continuous variables or as absolute numbers and percentages for categorical variables stratified by study. In the pooled population of SHIP-TREND-0 and BASE-II, associations of thyroid biomarkers with continuous parameters of glucose metabolism were analysed by linear regression models adjusted for age, sex, smoking status, BMI, and study.

Associations of thyroid biomarkers with prediabetes groups as proposed by the ADA 17 were analysed by multinomial logistic regression with adjustment for age, sex, smoking status, and study site. Interactions of serum TSH levels with age were tested in these regression models.

All analyses were carried out using Stata The median age of the participants was 49 years in SHIP-TREND-0 and 67 years in BASE-II Table 1. Altogether, participants were men and were women. SHIP-TREND-0 participants had a higher median BMI A TSH below the reference range was found more often in SHIP-TREND-0 7.

In both studies, participants reported taking thyroid medication 9. Further characteristics of the study population are provided in Table 1. Data are expressed as median, 25th, and 75th percentile continuous data or as absolute numbers and percentages categorical data.

a According to the established reference limits of 0. i-IFG, impaired fasting glucose; i-IGT, impaired glucose tolerance; NGT, normal glucose tolerance. In the pooled sample of SHIP-TREND-0 and BASE-II, we analysed the associations of serum levels of TSH, fT3, and fT4 with fasting and 2-h postload glucose, fasting and 2-h postload insulin, HOMA-IR, and ISI in multivariable linear regression models.

The results are summarized in Table 2. On the other hand, fT3 was significantly associated with all of the investigated markers except 2-h postload glucose. These relationships were predominantly non-linear and are displayed in Fig. Serum fT3 levels were significantly positively associated with fasting glucose levels, fasting, and 2-h postload insulin levels as well as with the HOMA-IR.

Accordingly, higher fT3 was associated with a lower ISI. Citation: European Thyroid Journal 11, 2; In the individuals with l -thyroxin treatment, we observed no significant associations of TSH or fT4 with any of the glycaemic markers Supplementary Table 1, see section on supplementary materials given at the end of this article.

In this subgroup, serum fT3 levels were positively associated in a non-linear fashion with all glycaemic markers except fasting glucose. The non-linear associations were comparable to those in individuals not on l -thyroxin treatment. In multinomial logistic regression models, we investigated associations of TSH, fT3, and fT4 with IFG, IGT, the combination of IFG and IGT, and unknown diabetes.

There were no significant associations of TSH with prediabetes groups. We observed a slightly higher relative risk for IFG with higher fT3 RR 1. Contrary to fT3, a higher fT4 was associated with a lower risk for IFG RR 0. Furthermore, fT4 was positively associated with unknown diabetes.

The results are summarized in Table 3. In the following analyses, we investigated whether age was an effect modifier for the association of thyroid markers with parameters of glucose and insulin metabolism. We observed many significant interactions of TSH, fT3, and fT4 with age on markers of prediabetes Table 4.

While there were significant interactions of fT3 with age on all markers of prediabetes, fT3 was also the only marker showing a significant interaction with age on the ISI. Moreover, TSH and age were interacting significantly on all other markers except the fasting glucose and ISI, whereas fT4 was interacting with age only on fasting and 2-h postload insulin and HOMA-IR.

The interactions of TSH with age on the prediabetes markers were showing into the same — but functionally opposite — direction as fT3 and fT4. Most of the associations between thyroid markers and markers of prediabetes were significant in young and middle-aged individuals but not in the older participants.

For better understanding of our data and the age-specific effects on the association of thyroid function with the glycaemic markers, we added a sensitivity analysis with a stratification by age-specific subgroups Supplementary Table 2. Here, we replicated the main findings of the associations of serum fT3 levels with glycaemic markers in groups of participants aged below 40 years and below 50 years.

In the age group of 50 years and above, fT3 was not significantly associated with any of the glycaemic markers. Likewise, in the age group of 70 years and above, no significant associations of serum fT3 levels with the glycaemic makers were observed.

Our analyses of two cross-sectional epidemiologic German studies demonstrated consistent associations of fT3 levels with glycaemic markers and increased insulin resistance.

Moreover, we observed a strong effect of age on the interaction of thyroid function with glycaemic markers. Interestingly, most of the associations between thyroid markers and glycaemic markers were significant in young and middle-aged individuals up to an age of roughly 60 years but not in older participants.

Findings from previous studies examining the relation between thyroid function and glucose metabolism are conflicting. El Demellawy et al. examined 40 patients with newly diagnosed hypothyroidism in comparison to 40 healthy controls Interestingly, they found elevated markers of insulin resistance including HOMA-IR in both the hypo- and hyperthyroid group.

The TSH correlated positively and fT3 and fT4 inversely with HOMA-IR suggesting that hypothyroidism might be strongly associated with insulin resistance than hyperthyroidism. Accordingly, the same results have been reported by Kapadia et al.

in a small cross-sectional study including eight euthyroid, eight hyperthyroid, and eight hypothyroid patients In another comparable setting, Abdel-Gayoum et al.

described increased parameters of insulin resistance in newly diagnosed subclinical and overt hypothyroidism An association of subclinical hypothyroidism with insulin resistance was also reported in a study with 30 participants compared to age-matched euthyroid controls 5.

Contrary to our study, fT3 was inversely associated with HOMA-IR. However, sample sizes of all these studies have been comparably small and not all analyses were adjusted for potential confounders such as age In a much larger study with patients, there was no difference in markers of insulin resistance between euthyroid and subclinically hypothyroid subjects However, in that study, fT4 was inversely associated with fasting insulin and HOMA-IR after adjustment for age, sex, and BMI, whereas in our study, we did not find such an association.

In participants of the Rotterdam study, a large longitudinal population-based cohort study, the risk for diabetes or for progression from prediabetes to diabetes increased with higher TSH levels and lower fT4 levels.

In this study, age had no effect modification on these associations 6. Whereas some studies on the topic have been small and many used surrogate parameters of insulin resistance which has been the case in SHIP and BASE-II either , the sample size in the RISC relationship between insulin sensitivity and cardiovascular disease study was reasonably high with participants Moreover, a gold standard for determining insulin resistance was used with the euglycaemic—hyperinsulinaemic clamp method In this cohort, higher fT3 levels, within the reference range, were consistently associated with insulin resistance This is in line with our results.

In longitudinal analyses in the RISC study, fT3 was also predictive for an increase in fasting glucose and decrease in insulin sensitivity and ß-cell glucose sensitivity at follow-up. The lack of any association of TSH with metabolic parameters of insulin resistance can be estimated as another similarity to our study, where TSH was only associated with 2-h postload insulin with regard to continuous variables.

An association of low fT3 and low total T3 levels with decreased HOMA-IR was found in a study based on National Health and Nutrition Examination Survey data, which can be interpreted in accordance with our results Rezzonico et al.

also found a moderate linear relationship between T3 and HOMA-IR in study participants who were either euthyroid or subclinically hyperthyroid due to levothyroxine intake or for endogenous causes In summary of the available study data, insulin resistance and dysglycaemia can occur in both hypo- and hyperthyroidism.

Moreover, these effects seem not to be restricted to overt hypo- or hyperthyroidism but might encompass subclinical disorders or even alterations of hormone levels in the reference range. The pronounced associations of fT3 with markers of insulin resistance that was found in our study, however, seem biologically plausible.

Even though recruitment of glucose transporters GLUT , such as GLUT3 and GLUT4, is increased in hyperthyroidism potentially leading to more glucose disposal in peripheral tissues, this might be overruled by insulin antagonistic actions of thyroid hormones, such as an increased glucose output from the liver and intestinal glucose absorption, decreased muscle glycogen storage, or upregulated glycogenolysis 2 , 3 , 25 , 26 , Moreover, an increased lipolysis leading to heightened insulin resistance or an increased insulin clearance may link higher levels of fT3 to impaired glucose metabolism 3 , 25 , 26 , Concerning the influence of age on the associations of thyroid function with glycaemic markers, much is still left to hypothesizing.

However, it is already well known that the endocrine system, including the thyrotropic axis, undergoes functional changes during ageing.

Many of the changes concerning thyroid function and aging have been summarized by Gesing et al. in a concise review Of note, subclinical hypothyroidism seems to be not necessarily associated with outcomes such as cognitive impairment, physical impairment, depression, or metabolic disturbances in older people as it is known with overt hypothyroidism or as can be found in people of younger age in subclinical hypothyroidism On the other hand, subclinical hyperthyroidism seems to be more consistently associated with outcomes such as decreased bone mineral density, fractures, or mortality 29 , although this is not confirmed by all studies Moreover, fT3 and fT4 levels were found to be inversely associated with age and might be linked to longevity 31 , but conversely, making interpretation more complex, at least low T3 levels can also be linked to severe extrathyroidal illness as in the low T3 syndrome.

A healthy survivor bias may also have influenced our analyses. Some of the participants with a lower fT3 due to extrathyroidal illness could already have died leaving healthier participants as survivors left for the analyses. In our study, most of the potentially inverse effects of higher fT3 levels on glucose homeostasis and insulin sensitivity are observed in young and middle-aged individuals but not in the older individuals.

This was confirmed in the additional analyses with stratification by age groups. Thus, a slightly higher fT3 might even be beneficial in terms of glucose metabolism in higher age although this has to be confirmed in longitudinal studies. On the other hand, insulin resistance is determined by numerous other factors such as adipose tissue or cortisol and growth hormone levels that might be more crucial than thyroid function.

Multiple comorbidities and polypharmacy might also play an additional and more decisive role in higher age and might overrule the effect of the predominantly subclinical thyroid dysfunction on glucose metabolism found in our study.

Moreover, fT3 has a short half-life of less than 24 h and might reflect predominantly short-term effects. Short- vs long-term effects might also explain the non-reciprocal effects which have been seen between TSH on the one hand and fT3 and fT4 on the other hand.

Of note, recent data suggest that thyroid hormone levels may be strongly associated with clinical parameters as are TSH levels The association of T3 and fT3 levels with metabolic parameters seem to be strong compared to TSH and thus in this context thyroid function might be better assessed with measuring free thyroid hormones One of the limitations of our study is the use of different laboratory assays for the measurement of TSH, fT3, and fT4.

Although both were electrochemiluminescence immunoassays used in quality-driven laboratories, we cannot preclude a potential effect that biases the results. This must also be considered with regard to other parameters such as insulin.

The strength of this study lies in its large sample size and the combination of two different cohorts covering a large age range that is important since thyroid disease can occur all over the lifespan.

Also, the measurement of fT3 seems to be not part of many other comparable studies, which measured only TSH and fT4. In summary, we found a consistent association between fT3 and markers of glucose metabolism.

BMC Medicine volume 14 Liver detoxification products, Article number: Cite this article. Supprot details. The functoin of thyroid function insulun risk Hydration strategies for consistent performance type 2 diabetes remains elusive. Brain function improvements methods aimed htyroid investigate the association insulih thyroid function with incident diabetes and progression from prediabetes to diabetes in a population-based prospective cohort study. We included participants mean age 65 years with thyroid function measurement, defined by thyroid-stimulating hormone TSH and free thyroxine FT4and longitudinal assessment of diabetes incidence. Cox-models were used to investigate the association of TSH and FT4 with diabetes and progression from prediabetes to diabetes. Enhance insulin sensitivity and support thyroid function Thyroid Sports dietitian services is associated with relevant disturbances in glucose metabolism. Moreover, sensitjvity function undergoes important changes with ageing. The objective of this study Ehnance to investigate the association of thyroid function with insulin resistance with particular consideration sensitivjty Liver detoxification products age-related effect modifications. A sample of participants Liver detoxification products suoport independent epidemiological studies, the Study of Health in Pomerania-TREND-0 and the Berlin Aging Study II, was included in this cross-sectional analysis. Insulin resistance was estimated by homeostasis model of insulin resistance HOMA-IR and the insulin sensitivity index ISI. Associations of thyroid biomarkers thyroid-stimulating hormone, free thyroxine, and free triiodothyronine fT3 with parameters of glucose metabolism were analysed by regression models adjusted for age, sex, smoking status, and study site. A higher fT3 was significantly associated with higher fasting glucose and higher fasting and 2-h postload insulin levels, a higher HOMA-IR, and lower ISI.

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