Thyroid-stimulating hormone

Case report links artificial sweeteners, Hashimoto’s thyroiditis.

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Recent literature suggest sugar-sweetened beverages increase the likelihood of incident obesity and diabetes. However, data from a case report presented here suggest that patients who consume a large amount of artificial sweeteners, such as Splenda, are also more likely to develop Hashimoto’s thyroiditis.

“We know that in the 20th and 21st century there is an increasing consumption of sugar substitutes. If you look at the literature in animal studies, it suggests it may cause obesity and some tumors. I found that this sugar substitute increases insulin levels in consumers and high insulin levels may be associated with obesity,” Issac Sachmechi, MD, FACE, FACP, clinical associate professor of medicine at Icahn School of Medicine at Mount Sinai; and chief of endocrinology at Queens Hospital Center, said during a press conference.

According to abstract data, Sachmechi treated a woman aged 52 years with a history of high intake of artificial sweeteners and a diagnosis of Hashimoto’s hypothyroidism in 2008. The patient’s TSH measured 12.2 mIU/L, free T4was 0.5 ng/dL and antithyroid peroxidase antibodies (TPOAb) were 196 IU/mL.

Sachmechi treated the patient with levothyroxine 0.75 mg per day and normalized her TSH (between 1.23 mIU/L and 2.16 mIU/L) over 3 years of treatment. Subsequently, the patient stopped ingesting the sweeteners in February 2012 due to weight gain.

This resulted in a TSH level of 0.005 mIU/L, where it remained low despite a decrease of levothyroxine dose to 0.05 mg per day. Furthermore, a complete discontinuation of the drug was followed with normal TSH and anti-TPOAb <20 IU/mL, TSI of 113% and TBII <6%.

Sachmechi reported that the patient continued to be clinically euthyroid without further treatment during subsequent follow-up visits.

“We know there is an increased prevalence of Hashimoto’s hypothyroidism and differentiated thyroid cancer without currently known etiologies. “It is possible that the artificial sweetness may have a roll in this,” Sachmechi said.

“We plan to do a study looking at the use of artificial sweetness in large number patients with diagnosis of Hashimoto’s hypothyroidism and patients with well differentiated thyroid cancer to see if we find any coloration consumption of artificial sweetness and those thyroid diseases.”

These data indicate eliminating artificial sweeteners from the diet can benefit patients with thyroid disease. Sachmechi told Endocrine Today that a study is underway to confirm these findings in a larger cohort. – by Samantha Costa

Source: Endocrine Today

 

Thyroid Screening Neglected in Hypercholesterolemia.

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Just half of primary-care patients with hypercholesterolemia received recommended thyroid-function screening, a new retrospective study has found.

The findings were presented here at the American Association of Clinical Endocrinologists (AACE) 2013 Scientific & Clinical Congress by Devina Willard, MD, an internal-medicine resident at Boston Medical Center, Massachusetts.

Hypothyroidism is an important secondary cause of elevated total cholesterol and LDL cholesterol. In overt hypothyroidism cases, thyroid hormone replacement treatment often normalizes the cholesterol levels. For that reason, guidelines from the AACE, American Thyroid Association, and National Cholesterol Education Program (NCEP) recommend testing for hypothyroidism.

Dr. Willard‘s study was designed to determine the rate of adherence to the guidelines by primary-care physicians. “The 50% rate of screening is a bit surprising. Although guidelines from the NCEP and [American College of Physicians] ACP state that thyroid dysfunction is [included in the] differential [diagnosis] for new-onset dyslipidemia, the practice of screening in standard clinical practice seems to often be overlooked,” she told Medscape Medical News.

Important to Treat Underlying Cause of Hyperlipidemia

Dr. Willard and colleagues reviewed charts from patients aged 18 years and older with total-cholesterol levels of 200 mg/dL and/or LDL-cholesterol levels of 160 mg/dL or above, who were seen at Boston Medical Center’s internal-medicine and family-medicine clinics for routine care during 2003 – 2011. Patients who had previously taken lipid or thyroid medications were excluded.

Of the 8795 patients newly diagnosed with hypercholesterolemia, thyroid-stimulating hormone (TSH) levels had been checked within 6 months of the diagnosis for 49%. Peripheral thyroid-function tests were also done for 18.4% of the patients.

Of the total 4349 patients who had TSH levels screened, 151 had TSH levels greater than 5 mIU/L and 74 had TSH levels over 10 mIU/L. Of these 225 patients (with TSH levels >5), 50.7% received levothyroxine treatment, Dr. Willard reported.

Of those 114 patients treated with levothyroxine, 75.4% did not receive a lipid-lowering agent within 1 year, possibly because correction of their hypothyroidism resulted in improvement of their lipid panel and correction of the dyslipidemia, she said.

The clinical implications of the findings are identifying a treatable cause of dyslipidemia and saving on the potential costs of long-term management of cholesterol-lowering therapy in many individuals, as well as reducing risk for cardiovascular events, Dr. Willard told Medscape Medical News.

She added, “We agree with the guidelines… It is important to treat the underlying and potentially reversible cause of dyslipidemia. However, we would conclude that more research is needed to better assess the cost/benefit effectiveness of having these guidelines be universally adopted.”

Source: medscape.com

 

 

Challenge the Establishment — Dispelling Five Common Health and Fitness Misconceptions .

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fasting

 

In life we take many things for granted. People are told to go on a low fat diet and do some aerobic training, and yet they still gain body fat. Your blood work shows slightly altered cholesterol and thyroid levels and right away you’re told to go on medication. The trainer at your local gym rips out a copy of Everyday Stretches (reproduced from a 1987 poster) and says: “Do this before your next workout.”

If you’ve been spinning your wheels and going nowhere in your pursuit for optimal health and fitness, then stop! Doing something simply because you’ve been told to is not good enough.

It’s time to question authority and challenge the establishment!

Five Common Health and Fitness Misconceptions

Let’s start by dispelling five common health and fitness misconceptions. Dare I suggest that…

1.      A high fat intake can actually lower body fat!

Two reasons: a) If low fat is consumed, your body retains body fat as a protective/survival mechanism, and b) a high fat intake upregulates key (lipase) enzymes, which not only break down dietary fat but also body fat.

Of course, a high fat and high carb diet will result in body fat accumulation so this only applies to a low carbohydrate intake.

“The lipase enzyme is a naturally occurring enzyme found in the stomach and pancreatic juice, which is also found within fats in the foods you eat.

Lipase enzyme digests fats and lipids, helping to maintain correct gall bladder function. As such, these constitute any of the fat-splitting or lipolytic enzymes, all of which cleave a fatty acid residue from the glycerol residue in a neutral fat or a phospholipid. The lipase enzyme controls the amount of fat being synthesized and that which is burned in the body, reducing adipose tissue (fat stores).

The lipase enzyme belongs to the esterases family of proteins. The lipase enzyme is found widely distributed in the plant world (beans and legumes), as well as in molds, bacteria, milk and milk products, and in animal tissues, especially in the pancreas.

In sufficient quantities of lipase enzyme production, lipase can help use fat-stores to be burned as fuel. Indeed, lipase is a rate-determining enzyme, which not only activates the burning of stored body fats but also effectively inhibits fatty acid synthesis, or fat storage!

Hormone-Sensitive Triacyclglycerol Lipase, as it is also known, actually stimulates lipolysis in fat tissues, safely raising blood fatty acid levels, which ultimately activates the beta-oxidation pathway in other tissues, such as liver and muscle. In the liver, lipolysis leads to the production of ketone bodies that are secreted into the bloodstream for use as an alternative fuel to glucose by peripheral tissues.”

2.      Reduced thyroid levels (i.e. TSH levels above 5) for a lean individual following a low-carb diet may be normal and healthy!

Now before you throw your chair at the computer, hear me out. As Dr. Ron Rosedale notes in the excerpt below, reduced thyroid levels are not necessarily synonymous with hypothyroidism. Your body chooses to lower thyroid hormones due to an increased efficiency of energy use and hormonal signaling. It is yet another example of how your body adapts and should not be viewed as abnormal.

The knee-jerk reaction in many cases would be thyroid medication, which could potentially decrease your lifespan.

“Metabolic rate and temperature has long been connected with longevity. Almost all mechanisms that extend lifespan in many different organisms result in lower temperature. Flowers are refrigerated at the florist to extend their lifespan. Restricting calories in animals also results in lower temperature, reduced thyroid levels, and longer life.

It should be noted that reduced thyroid levels in this case are not synonymous with hypothyroidism. Here, the body is choosing to lower thyroid hormones because the increased efficiency of energy use and hormonal signaling (including perhaps thyroid) is allowing this to happen.

Anything will dissolve faster in hot water than cold water. Extra heat will dissolve, disrupt and disorganize. This is not what I try to do to make someone healthy. It is commonly advised to increase metabolism and increase thermogenesis for health and weight loss.

Yet how many of you would put a brand of gasoline in your car that advertised that it would make your engine run hotter? What would that do to the life of your car? It is not an increase in metabolism that I am after; it is improved metabolic quality.”

3.      Low cholesterol levels will promote aging.

Cholesterol is the raw material for many hormones. If you lower your cholesterol you will also lower your hormone production … and if you lower hormone production, you increase aging! To make matters worse, low cholesterol has been associated with a broad complex of emotional, cognitive and behavioral symptoms including aggressiveness, hostility, irritability, paranoia, and severe depression.

There is also an increase in deaths from trauma, cancer, stroke, and respiratory and infectious diseases among those with low cholesterol levels.

Furthermore, a study in the British medical journal, Lancet, indicates that elderly men die earlier with low blood cholesterol levels.

“The human organism is in a state of dynamic equilibrium, know as homeostasis. One of the main roles in normal homeostasis belongs to multiple feedback loop mechanisms.

Cholesterol is the precursor or the building block for the basic hormones: pregnenolone, DHEA, progesterone, estrogen, testosterone.

Deterioration of the reproductive function, one of the most striking endocrine alterations occurring in aging, is related to a complex interplay of factors. Target organs may become less sensitive to their controlling hormone or may break them down at a slower rate. Hormone levels may change; some increasing, some decreasing and some remaining unchanged.

Many of the diseases that middle-aged persons begin experiencing including depression, abdominal weight gain, prostate, breast and heart disease, are directly related to hormone imbalances.

Conventional doctors are prescribing drugs to treat depression, elevated cholesterol, angina and other diseases that may be caused by hormone imbalance.

A few years ago we found out that some patients who had high cholesterol levels before hormonorestorative therapy (HT) were free of cholesterol problems during therapy. We started pondering as to why this had happened?

In our opinion, when the production of hormones starts to decline our body tries to correct this problem by increasing the production of cholesterol. A similar situation happens to women during pregnancy. When a female’s body needs more hormones for herself and her baby, cholesterol levels are elevated significantly. If a woman’s body is unable to increase the production of cholesterol the risk of an abortion and miscarriages is increased.

Another situation is a low level of cholesterol. If your total cholesterol is less than 160, you have nothing to worry about. Wrong opinion!

A low level of cholesterol means a low production of basic hormones (because of a limited amount of building blocks). Patients with a low level of hormones have life problems that include suicides, criminal behavior, depression, attention deficit disorder, cancer at young age, etc. Low cholesterol is a marker for poor underlying health.

When patients take cholesterol-lowering drugs (CLD) we can surmise that hormonal production will decrease. That’s why many patients on CLD have severe fatigue, fibromyalgia-like pain, depression, high risk of cancer, suicides, weight gain and impotency.

Normally our body tries to keep a normal ratio between different hormones: DHEA/cortisol, estrogen/progesterone, female/male hormones. When we have a malfunction in a feedback loop mechanism we start to have the problems related to the imbalance of hormones (for example: male or female dominance, estrogen dominance, etc.).

Once again, when the production of hormones starts to decline, our body tries to correct the deficiency of hormones by the extra production of cholesterol. It looks like the elevation of total cholesterol serves as a compensatory mechanism for hormonal deficiency.”

Source

4.      Aerobic training can increase body fat.

Specifically, long distance, low intensity, rhythmic-type aerobics done for a long duration/distance on a frequent basis can signal your body to store fat.

Your body prefers fat for fuel at lower intensities. It adapts to aerobic activity by storing fat (usually in the hips and thighs) to become more efficient for future use. The more fat you store, the more you can use.

Furthermore, aerobics are associated with increased cortisol levels without a concomitant increase in testosterone (as occurs during strength training) disrupting an optimal testosterone:cortisol ratio. In fact, average testosterone levels are significantly lower in endurance athletes. This, of course, equates to a decrease in muscle and strength along with an increase in (android) body fat, i.e., midsection fat.

5.      Static stretching will make you weak.

This has been well documented in the literature, and yet a typical warm-up usually contains some form of (you guessed it) static stretching. The classic Bob Anderson style of stretching before exercise tends to sedate muscles, and research shows that it will decrease power and strength by as much as 30 percent for up to 90 minutes. By that time, your workout is over!

Sometimes you need to take a sledgehammer and crush what’s written in stone!

We’ve been told to reduce fat in our diets, lower our cholesterol levels, improve reduced thyroid production with medication, perform aerobic training almost daily, and definitely start each workout with some static stretching.

Dare I suggest otherwise?

You better believe it!

Source: Mercola.

Subclinical hyperthyroidism unrelated to overall, CV mortality.

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The associated health risks for subclinical hyperthyroidism in patients aged at least 65 years are not entirely clear. However, data presented at the 82nd Annual Meeting of the American Thyroid Association suggest that the disease was not linked to overall or cardiovascular mortality.

“[Older patients with subclinical hypothyroidism] They are a group with a high prevalence of subclinical thyroid dysfunction and a high prevalence of comorbidities that make their management more complex,” researcher Anne R. Cappola, MD, ScM, associate professor of medicine at Penn Medicine and physician at the Perelman Center for Advanced Medicine in Philadelphia told Endocrine Today.

Cappola said there are two clinical implications.

“One, thyroid function testing should be repeated in older people with subclinical hyperthyroidism to confirm testing prior to initiating management. Two, older people with subclinical hyperthyroidism are at increased risk of atrial fibrillation,” Cappola said.

The Cardiovascular Health Study (CHS) was used to examine the 5,009 community-dwelling patients aged 65 years and older who were not taking thyroid medications. According to data, the serum thyroid-stimulating hormone and free thyroxine concentrations were measured in banked specimens at visits between 1989 and 1990, 1992 and 1993, and 1996 and 1997.

Within the CHS, researchers identified 70 patients with an average age of 73.7 years (60% women, 24% not white) with subclinical hyperthyroidism based on their first TSH measurement. They studied the persistence, resolution and progression of the disease during a 2- to 3-year period.

Using Cox proportional hazard models, researchers were able to determine the link between subclinical hyperthyroidism and CV risk and total mortality after more than 10 years of follow-up, with 4,194 euthyroid patients used as a reference group.

According to data, of the patients with subclinical hyperthyroidism who participated in follow-up thyroid testing or were taking thyroid medication at the time of follow-up (n=44), 43% persisted; 41% became euthyroid; 5% progressed to the point of overt hyperthyroidism; and 11% began taking thyroid medication.

“Our study provides additional supportive data in both estimates of persistence of subclinical hyperthyroidism and risk of cardiovascular effects,” Cappola said.

  • Source: Endocrine Today.

 

 

 

 

 

Endocrine Society revises recommendations for thyroid disease during pregnancy, postpartum.

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The Endocrine Society has revised its 2007 Clinical Practice Guideline on the management of thyroid disease in pregnant and postpartum women. Updates include recommendations regarding diagnosis and treatment before, during and after pregnancy.

“Pregnancy may affect the course of thyroid diseases, and conversely, thyroid diseases may affect the course of pregnancy,” Leslie De Groot, MD, a researcher from the University of Rhode Island, said in a press release. “Pregnant women may be under the care of multiple health care professionals, including obstetricians, nurse midwives, family practitioners and endocrinologists, making the development of guidelines all the more critical.”

Key updates

According to the release, revisions include:

  • Caution should be used in the interpretation of serum free thyroxine levels during pregnancy and each laboratory should establish trimester-specific reference ranges for pregnant women using a free T4 assay. The non-pregnant total T4 range (5 mcg/dL to 12mcg/dL or 50 nmol/L to 150 nmol/L) can be adapted in the second and third trimesters by multiplying this range by 1.5-fold. Alternatively, the free T4 index appears to be a reliable assay during pregnancy.
  • Propylthiouracil (PTU), if available, should be the first-line drug for treatment of hyperthyroidism during the first trimester of pregnancy because of the possible association of methimazole (Tapazole, King Pharma) with congenital abnormalities. Methimazole may also be prescribed if PTU is not available or if a patient cannot tolerate or has an adverse response to PTU. Recent analyses by the FDA indicate that PTU may rarely be associated with severe liver toxicity. For this reason, clinicians should change treatment of patients from PTU to methimazole after completion of the first trimester.
  • Breast-feeding women should maintain a daily intake of 250 mcg of iodine to ensure breast milk provides 100 mcg of iodine per day to the infant.
  • Once-daily prenatal vitamins should contain 150 mcg to 200 mcg iodine in the form of potassium iodide or iodate — the content of which is verified to ensure that all pregnant women taking prenatal vitamins are protected from iodine deficiency.
  • Since thyroid receptor antibodies (thyroid receptor stimulating, binding or inhibiting antibodies) freely cross the placenta and can stimulate or inhibit the fetal thyroid, these antibodies should be measured before 22 weeks gestational age in mothers with 1) current Graves’ disease; 2) a history of Graves’ disease and treatment with radioactive iodine (I-131) or thyroidectomy before pregnancy; 3) a previous neonate with Graves’ disease; or 4) previously elevated thyroid-stimulating hormone receptor antibodies.
  • In women with thyroid-stimulating hormone receptor antibodies, at least two- to threefold the normal level and women treated with antithyroid drugs, fetal thyroid dysfunction should be screened for during the fetal anatomy ultrasound (18 to 22 weeks) and repeated every 4 to 6 weeks or as clinically indicated. Evidence of fetal thyroid dysfunction could include thyroid enlargement, growth restriction, hydrops, presence of goiter, advanced bone age or cardiac failure.
  • Women with nodules ranging from 5 mm to 1 cm in size should be considered for fine-needle aspiration (FNA) if they have a high-risk history or suspicious findings on ultrasound. Women with complex nodules ranging from 1.5 cm to 2 cm in size should also receive an FNA. During the last 6 weeks of pregnancy, FNA can reasonably be delayed until after delivery. Ultrasound-guided FNA is likely to have an advantage for maximizing adequate sampling.

Up for debate

The committee charged with updating the guidelines, however, did not reach a consensus on screening recommendations for all newly pregnant women. For instance, some members recommended screening all pregnant women for serum TSH abnormalities by the ninth week or at the time of their visit, whereas others supported aggressive case finding to identify and test high-risk women.

A full summary of the changes between the 2007 and the 2012 recommendations can be found in the August issue of the Journal of Clinical Endocrinology and Metabolism.

Source: Endocrine Today.