Книга - The Healthy Thyroid: What you can do to prevent and alleviate thyroid imbalance

The Healthy Thyroid: What you can do to prevent and alleviate thyroid imbalance
Patsy Westcott


Thyroid health is an increasingly common concern. This updated edition (formerly titled 'Thyroid Problems’) is a clear and practical guide to symptoms, treatment options and self-help measures for those who have, or think they may have a thyroid related problem.Sales Handles:• It’s estimated that 1 in 10 women have a thyroid imbalance**, but as symptoms are diverse the problem is often unresolved. This book shows how to identify a thyroid problem, relieve symptoms, and obtain treatment.The symptoms of a thyroid imbalance include Chronic Fatigue, Weight Gain, Mood Swings, as well as dried out skin and hair, changes in libido and menstrual problems.This new edition has been fully re-structured and includes a large amount of new material to reflect the needs of today’s readers.Contains detailed information about natural health and complementary treatments to help relieve symptoms.Gives the low-down on thyroid hormone tests and other orthodox medical procedures that may be offered.Is an informative yet simple book that provides a ‘patients-eye’ view of thyroid imbalance so readers can better understand their doctors.Discusses the links between sub-clinical thyroid problems (the most common sort – that cause longterm problems but are hard to pin down) and other conditions such as depression, obesity.









The Healthy Thyroid

What you can do to prevent and alleviate thyroid imbalance

Patsy Westcott










Copyright (#ulink_abef7951-cd85-5e73-900d-a192fb7148a1)


Thorsons Element

An imprint of HarperCollinsPublishers 1 London Bridge Street London SE1 9GF

www.harpercollins.co.uk (http://www.harpercollins.co.uk)

and Thorsons are trademarks of HarperCollinsPublishers Ltd

First published as Thyroid Problems by Thorsons 1995 This revised edition published by Thorsons 2003

© Patsy Westcott 2003

Patsy Westcott asserts the moral right to be identified as the author of this work

A catalogue record of this book is available from the British Library

All rights reserved under International and Pan-American Copyright Conventions. By payment of the required fees, you have been granted the nonexclusive, nontransferable right to access and read the text of this e-book on-screen. No part of this text may be reproduced, transmitted, downloaded, decompiled, reverse engineered, or stored in or introduced into any information storage and retrieval system, in any form or by any means, whether electronic or mechanical, now known or hereinafter invented, without the express written permission of HarperCollins e-books.

HarperCollinsPublishers has made every reasonable effort to ensure that any picture content and written content in this ebook has been included or removed in accordance with the contractual and technological constraints in operation at the time of publication.

Source ISBN: 9780007146611

Ebook Edition © FEBRUARY 2016 ISBN: 9780007392001

Version: 2016-02-29




Contents


Cover (#u0535c377-2389-5393-9fd3-8684c68caf81)

Title Page (#u6db5d4a5-30e0-54e9-a8a9-5bde68ade9a7)

Copyright (#uef7609f7-cd5a-5612-96b0-0a24c59c61ee)

Chapter 1 The Hidden Illness (#u65240409-fee6-5ca0-99f0-041fe3b840c6)

Chapter 2 Understanding Thyroid Problems (#uc48c3bc0-3e37-5339-894f-6b52376257ba)

Chapter 3 The Out-of-Balance Thyroid (#u1eab7076-5671-5856-b91e-6e1c6a33bfd3)

Chapter 4 Getting a Diagnosis (#litres_trial_promo)

Chapter 5 Treatment Options (#litres_trial_promo)

Chapter 6 I Just Want to Feel Normal Again (#litres_trial_promo)

Chapter 7 Integrated Treatment: Complementary Therapies (#litres_trial_promo)

Chapter 8 The Eyes Have It: Thyroid Eye Disease (#litres_trial_promo)

Chapter 9 Thyroid Problems and Reproduction (#litres_trial_promo)

Chapter 10 The Menopause and Beyond (#litres_trial_promo)

Chapter 11 Questions and Conundrums (#litres_trial_promo)

Glossary (#litres_trial_promo)

Resources (#litres_trial_promo)

Index (#litres_trial_promo)

Acknowledgements (#litres_trial_promo)

About the Publisher (#litres_trial_promo)





CHAPTER ONE The Hidden Illness (#ulink_50cc9465-e776-5c0e-9fb6-ae3ab7e20490)


Thyroid disease is common and affects women more frequently than men.



Many books and articles on thyroid problems for both the general public and medical profession begin with these or similar words. But this bland statement barely begins to suggest the number of women afflicted by thyroid problems or the impact of thyroid disorders on our lives. In fact, according to a review in the British Medical Journal, taken together, underactive and overactive thyroid conditions represent the most common hormonal problem – and this problem overwhelmingly affects women.

In terms of statistics alone, thyroid problems in women deserve to be taken seriously:



• Four out of five people with thyroid disorders are women.

• One in 10 women will develop a thyroid disorder at some stage in her life.

• Between one and two in 100 women in the UK will develop an underactive thyroid (hypothyroidism), a condition 10 times more common in women than men.

• Two out of every 25 women – and one in 10 past the menopause – have so-called mild thyroid failure that is considered borderline on blood tests. These ‘subclinical’ problems are linked with nagging ill health, such as fatigue, mood swings and overweight, as well as more serious medical problems such as depression, heart disease and osteoporosis.

• Overactive thyroid conditions (hyperthyroidism) are also common in women, affecting between five in every 1000 to one in 50 – or 10 times more women than men.

• One in every 100 people in the UK will develop an autoimmune thyroid disorder, when the body turns against itself to cause the thyroid to become either underactive or overactive. Autoimmune disorders, including those affecting the thyroid, are estimated to be the third biggest killer after heart disease and cancer.

• Having a personal or family history of autoimmune disorders, such as diabetes or rheumatoid arthritis, gives you a 25 per cent greater risk of developing a thyroid disease than someone without such a history.

• Hashimoto’s thyroiditis – an autoimmune disorder causing an underactive thyroid – may account for up to one-third of such cases in this country and is five times more common in women than men.

• Graves’ disease – an autoimmune condition causing an overactive thyroid – is 15 times more likely to affect you if you are a woman.

• Goitre (a swollen or enlarged thyroid gland) is four times more common in women than in men.

• Thyroid nodules or lumps are also more common in women – estimated to affect about one in 20 women.

• Thyroid cancer, although rare, is also more likely to develop if you are a woman.




Only as Healthy as Your Thyroid?


Thyroid problems can affect a woman at any age or stage in life – from the teens to retirement. Throughout this time, they are a source of much ill health and unhappiness. During the reproductive years and after the menopause, they can exacerbate other female health problems as well as create a host of debilitating symptoms that affect every system of the body:



• Thyroid problems can cause menstrual disturbances, such as heavy or absent periods, and worsen problems such as premenstrual syndrome (PMS).

• Thyroid problems are an underrecognized cause of fertility problems and miscarriage.

• During pregnancy, thyroid disorders are the most common hormonal problem.

• Even a mild shortage of thyroid hormone during pregnancy may affect the unborn child’s future IQ (intelligence quotient). Research shows that children, aged seven to nine, whose mothers had untreated hypothyroidism during pregnancy scored about seven points lower on IQ tests.

• According to US research, women with faulty thyroid function are more likely to give birth to babies with defects of the heart, brain or kidney, or have abnormalities such as a cleft lip or palate, or extra fingers.

• Babies whose mothers have an underactive thyroid have an increased risk of heart problems – even if their mothers are being treated for the condition. Yet, at the time of writing, the NHS still does not routinely test thyroid function in pregnancy.

• One in 10 young women have thyroid problems after giving birth, with symptoms such as depression, tiredness and a lack of zest that cast a shadow over the first months of parenthood. Such symptoms are often misdiagnosed as ‘the baby blues’, thus depriving women of treatment that would help.

• Later in life, thyroid disease becomes even more common. An estimated one in 10 women over 40 may have undiagnosed thyroid disease, which is particularly worrying as thyroid problems are associated with an increased risk of two very significant causes of female ill health in later life: heart disease and osteoporosis (brittle-bone disease).

• One in five women over 60 suffer thyroid problems. With the ‘baby-boomers’ reaching this age, thyroid disorders will become an increasingly major health challenge.

• Thyroid disease in older women is more likely to be ‘silent’, producing few or vague symptoms. But compared with, say, high blood pressure – another ‘silent’ disease with serious consequences – thyroid problems are far less likely to be suspected or tested for.



These facts and figures alone put thyroid disease on a par with conditions like diabetes, estimated to affect one to two in every 100 people, and breast cancer, which strikes one in eight women. However, thyroid problems attract only a fraction of the research funding given to these high-profile conditions, and have until only recently relatively poor media coverage. That this is now beginning to change was reflected by an editorial in the prestigious British medical journal The Lancet that declared ‘you’re only as healthy as your thyroid’.




Are Times Changing?


During the writing of the first edition of this book more than seven years ago, there was little awareness – even among journalists specializing in women’s health – of just how common thyroid problems are and of the misery they can cause. A small request for help placed in The Guardian newspaper resulted in a deluge of phone calls: 200 over two days.

Revisiting thyroid problems now, has anything changed? The good news is that there has been a shift in knowledge and attitudes. A great deal more is becoming understood in terms of how thyroid problems are caused and how they may best be treated. And certainly, many more people are now aware of thyroid disease than in 1995.

Part of this new awareness is thanks to a number of books drawing attention to the wide-ranging effects of thyroid problems and the misery they can cause. The advent of the Internet has also done much to fill the information gap. There are now several excellent websites where women with thyroid problems can get information and communicate with others who have the same condition. This is good news for the millions of women living with a faulty thyroid.

However, in other aspects, the changes have been pitifully few. Thyroid disease is still a ‘Cinderella’ disorder, despite being the cause of so much depression, tiredness, discomfort and feeling well below par. Even nowadays, women often soldier on for long periods before anyone takes their complaints seriously – hardly surprising given that the average medical student only has a lecture or two on thyroid problems, if they’re lucky. And although there are more post-training courses for interested doctors, endocrinology (the study of hormones) is still not a core subject in most basic medical courses.

Like their ‘sisters’ in 1995, many of the women interviewed for this new edition had struggled on for months, even years, with crippling symptoms before being diagnosed. Once diagnosed, they had to cope with unsympathetic doctors and endure treatments that were uncertain, took time to get right and sometimes didn’t work at all.

Just like seven years ago, many women also spoke of the dilemmas posed by treatment – how long it had taken for medications to start working, the uncertainty of their effects, the agony of deciding whether to opt for surgery or radioiodine therapy, or whether different forms of medication might be more effective. All related stories of how difficult it was to obtain relevant information and how alone they felt with this unpredictable disease.

Others told poignant stories of how the disease had affected their daily lives and relationships in the face of the pressures of holding down a job while battling overwhelming fatigue, the difficulties encountered with partners, friends and children who did not always understand why the person they loved had undergone such a major personality change, of being overweight or underweight, of the self-consciousness endured because of bulging eyes, thinning hair and thickened skin, and the effects these had on their self-esteem. Some described the heartache of not being recognized by friends they had not seen for some time.

These physical problems are often dismissed as trivial but, in a world where the pressure to look young and attractive is intense, they can become the cause of a huge amount of distress and self-loathing. They can also lead to other women’s health problems such as eating disorders.




Tip of the Iceberg?


In recent years, it has become apparent that thyroid problems may be even more common than ever imagined. The availability of more sophisticated methods of testing thyroid function has revealed that many seemingly healthy women with apparently normal thyroid function have, in fact, abnormal levels of hormones and antibodies against the thyroid gland. This also suggests that the cases of thyroid disease identified and treated may be only a fraction of what is actually out there.

Since 1995, such cases of mild or low-grade thyroid disease have received a great deal of attention in the medical and public media. Medical journals, such as the influential New England Journal of Medicine, have carried major articles on subclinical thyroid disease, while the shelves of bookshops now carry stacks of books about thyroid problems aimed at the general public. Many put forward the view that hidden thyroid problems are a factor in a host of conditions reaching epidemic proportions in the 21st century, including:

• Chronic fatigue

• Depression, anxiety and mood swings

• Difficulty in losing weight

• Eating disorders

• Menstrual problems

• Fertility problems, miscarriage and premature births

• Perimenopausal and menopausal problems

• Changes in libido

• Heart disease

• Osteoporosis

• Ageing.



There is much controversy surrounding the issue of mild thyroid disease – or should it be called early or pre-thyroid disease? Despite being more widely recognized, there is little consensus on its significance and whether or how it should be treated. No one truly knows how important it is as a cause of ill health or how often it might lead to full-blown thyroid disease. Other questions remain, too: Should it be tested for in the absence of symptoms? Should women with symptoms suggestive of thyroid problems, such as tiredness and depression, be treated even if blood tests are apparently normal? Should widespread thyroid screening be introduced and, if so, at what age and how often should testing be performed?

Just as in 1995, there is a lot of debate, but no definitive answers.




Why Me?


Almost every woman included in this book wanted to know why she, in particular, had developed a thyroid disease. Unfortunately, there are no simple answers to this question. Despite its prevalence, the experts themselves still do not fully understand what causes the thyroid to misbehave. As with so many illnesses, one of the most pressing questions is whether nature or nurture lies at the root of the problem.

The cracking of the human genome, the inherited ‘database’ of some 40,000 to 50,000 genes containing all of the instructions for life, has led to an explosion of genetic research – and some interesting insights into the origin of certain kinds of thyroid problems. Some of the genes involved in certain kinds of thyroid cancer have been identified as well as other possible ‘candidate’ genes that may lead to an increased risk of developing an autoimmune thyroid disease.

However, although genes undoubtedly play a role, they are not the whole story. As with any illness with a genetic component, possessing one or more of these predisposing genes may give you a tendency to develop a particular problem – in this case, thyroid disease – but it is your environment and individual lifestyle that may yet determine whether you actually will.




The Immune Connection


The role played by the immune system in triggering a number of thyroid disorders remains a controversial topic. Autoimmune thyroid disease, which underlies both hypo- and hyperthyroidism, is caused by failure of a fundamental mechanism: the body’s ability to recognize its own organs and tissues as belonging to itself.

If the body fails to recognize itself, it produces self-attacking proteins – known as autoantibodies – to destroy its own tissue. Experts are becoming increasingly aware of a number of diverse thyroid problems due to the production of such autoantibodies, including:



• Hashimoto’s thyroiditis, which causes an underactive thyroid

• Graves’ disease, which causes an overactive thyroid

• Myxoedema, or generalized swelling of the skin and other tissue

• Subclinical hypo-/hyperthyroidism, mild or hidden thyroid under-/overactivity

• Thyroiditis, or inflammation of the thyroid

• Postpartum thyroiditis, or inflammation of the thyroid after childbirth

• Thyroid eye disease (TED).




Putting the Clues Together


Women, as we already know, are much more likely than men to develop thyroid disease. Many of those interviewed for this book added, almost as an afterthought, ‘My mother (or sister, or daughter) has thyroid problems, too.’ In particular, Graves’ disease and Hashimoto’s thyroiditis seem to cluster in families. In the past, this was dismissed as a coincidence. Recently, however, the new science of molecular genetics has led a number of researchers to look for an underlying inheritance factor in the development of autoimmunity. It is now generally agreed that as much as 10–15 per cent of us inherit an immune system with the potential to turn against itself.

Nevertheless, the development of thyroid problems is not just a matter of inheriting a faulty set of genes. Many people possess autoantibodies and do not go on to develop full-blown thyroid disease. In fact, it is estimated that only about one in 10 of those with an inherited tendency to develop thyroid antibodies will actually have thyroid problems.

One of the main aims of research, therefore, is to discover the possible triggers of thyroid problems. We know that the immune system can be damaged by many aspects of the 21st-century lifestyle that seem to have potential roles in the development of thyroid disease. Pollution, ageing, diet, stress, viral and bacterial infections, and habits like smoking and drinking are just some of the factors being explored by scientists in the hopes of finding out why the thyroid becomes faulty. Since 1995, much more information has been accrued on the roles these factors may play in triggering thyroid disease – and one important risk factor could simply lie in being female.




The Hormone Connection


The thyroid gland is involved in virtually every bodily process, including those of the reproductive system, and thyroid disease is linked to a number of specifically female problems (see Table 3.1).

Table 3.1 Links between thyroid disorders and the reproductive system






The first clue that something may be wrong with the thyroid gland is often when a woman consults the doctor on a ‘woman’s problem’, such as menstrual irregularities, difficulty in getting pregnant, miscarriage, postnatal depression or menopausal symptoms. It is also increasingly recognized that thyroid problems may be confused with or aggravate the symptoms of women’s problems such as PMS and the menopause.

With so many women’s problems being linked to thyroid disease and, conversely, so many thyroid problems being associated with the reproductive cycle, could it be that the female hormones play a part in susceptibility to thyroid disease? The answer is most likely yes. Research suggests that the two main female sex hormones, oestrogen and progesterone, moderate the activity of the immune system – hence the preponderance of thyroid disease in women.

The involvement of hormones and the immune system could also explain why the thyroid may misbehave for the first time during pregnancy and after birth. It also provides a reason for why so many women develop debilitating postpartum thyroiditis (PPT), which is often confused with postnatal depression.

One of the most striking developments since the first edition of this book has been the increasing awareness that the brain and nervous system, the immune system and endocrine (hormonal) system, all previously thought to be completely separate systems, do not work in isolation. This has led to the development of new fields of study such as psychoneuroendocrinology and psychoneuroimmunology, which are dedicated to exploring the body-mind connection and the way in which each ‘talks’ to the other.




With Women in Mind


This book is an exploration of these and other issues. Chapter 2 looks in detail at the thyroid gland and how it works to enable readers to understand the links between the thyroid and other body systems, and why – when it goes wrong – there may be such wide-ranging effects. The chapter also outlines some of the latest thinking on the immune system and the part it plays in thyroid problems.

Chapter 3 examines all the things that can go wrong with your thyroid, and explores some of the latest theories for how thyroid problems arise in an attempt to answer that nagging question, ‘Why me?’ There is also more detailed information on thyroid nodules (lumps) and thyroid cancer. Despite being one of the simplest forms of cancer to treat, survival rates in the UK have, until now, lagged woefully behind those of other countries.

Chapter 4 tackles the problem of getting a proper diagnosis. It includes a description of the various tests that may be performed, and explores the issue of what is normal and the difficulties involved in interpreting thyroid function tests.

Chapter 5 describes the available treatments, including medications, surgery and radiotherapy, and explains how they work, including their pros and cons. It also covers the debate over newer – and the revival of older – forms of treatment, and how you can work with your doctor to find the treatment that is right for you.

Chapter 6 covers the different ways you can help yourself, such as by paying attention to what you eat, making sure you get the right amount of exercise and managing stress, as well as how to come to terms psychologically with having thyroid disease.

Chapter 7 looks at how complementary therapies can help you manage your thyroid problems. These therapies are much more widely accepted now than when the first edition of this book was written, and many doctors and healthcare practitioners now acknowledge the part these therapies can play alongside conventional medical treatment.

Chapter 8 is devoted to thyroid eye disease, a particularly devastating condition about which too little is known, even now, and includes the still controversial issue of how it should be treated.

Chapter 9 describes how thyroid problems can affect you at different points in the female reproductive cycle, and includes important new information on how thyroid problems can affect menstruation, fertility, pregnancy and life after childbirth.

Chapter 10 looks at the problems that may be caused by thyroid disease at around the menopause and as we get older.

Chapter 11 investigates some of the major issues in thyroid disease and the advances made in our current understanding of the disorder, as well as takes a peek into the future at possible new treatments.

Finally, there is a glossary of terms relevant to thyroid disorders, and a list of books, websites and organizations that may prove helpful.

The more you know about the way your body works, the better able you will be to help yourself if something goes wrong. The objective of this book is to provide the information you need to help yourself, to work with your doctor to get the best treatment for your problems, and to feel more in control of your body and your life – something that women with thyroid problems often feel they have lost.

This book does not intend to tell you what to do or replace medical advice. There is a great deal of controversy surrounding thyroid problems – how they come about and how they should be dealt with. The main areas of debate have been outlined in this volume to give you an idea of what different experts think so that you can make up your own mind about how to live with your thyroid problems.





CHAPTER TWO Understanding Thyroid Problems (#ulink_1b285420-203e-509c-b445-055de784363b)


To better understand what can go wrong with your thyroid, it is necessary to know something about how the gland works. This chapter attempts to reveal why we have a thyroid gland, and looks at the way the thyroid interacts with other systems of the body, including the immune system.



The thyroid is one of 10 glands that make up the endocrine (hormonal) system. From the moment we are conceived until the time of our death, our bodies are under the influence of a cocktail of hormones produced by this system. As this system is so finely tuned, when anything happens to disturb its delicate balance, the repercussions ricochet throughout the rest of the body.

The hormones produced by glands are chemical messengers that are carried around the bloodstream to act on cells and tissues that are often far from their site of origin. Their job is to ensure that we have the correct concentrations of metabolites – vital nutrients (such as sugars and fats), vitamins and minerals (such as calcium, sodium, potassium and iodine), enzymes and other factors essential to life – in the bloodstream.

Each gland has a specific function, but also works with the other glands to keep our body in a state of chemical balance (homoeostasis). One recent, exciting discovery is that not only do hormones interact with each other, but they also exchange messages with other chemicals produced by the brain and nervous system. Research is beginning to uncover more and more links between these major interacting systems, and to throw more light on the way hormones and chemicals produced by the nervous and immune systems work together. This, in turn, is helping to clarify the connection between mind and body as reflected by a diverse number of conditions, including thyroid disease.




Key Sites


The glands themselves are situated at key locations throughout the body (see Figure 2.1). Together they produce over 50 different hormones – so-called ‘mighty molecules’ – that have widespread effects on us from cradle to grave. As hormones cannot be stored in large quantities in the glands, the brain programmes their manufacture by means of a complex biochemical cycle that uses a series of checks and balances to ensure that hormone levels are maintained according to your body’s needs.

In addition to the endocrine glands themselves, other organs contain pockets of glandular tissue that produce hormones. One of these is the hypothalamus, a region of the brain that is both part of the nervous system and a gland.

Not surprisingly, with such a complicated system, things can go wrong. Broadly speaking, when a gland ceases to function as it should, it results in two categories of problems: the gland becomes underactive and produces too few hormones; or it becomes overactive and produces too many.




Balancing the Body


The whole endocrine system is controlled by a series of ‘feedback loops’, which slow or stop a gland from working when enough hormone has been produced, and turn it back on again when more is needed – like a central-heating thermostat (see Figure 2.2). If the blood levels of any of the essential chemicals are low, special sensory cells are able to pick up a signal that






Fig 2.1 The endocrine system






Figure 2.2 The pituitary gland and the hypothalamus in the brain work together to produce a hormone that stimulates the thyroid. The thyroid gland draws iodine from the blood in order to make T3 and T4. Sensors in the TSH-secreting cells of the pituitary detect rising levels of thyroid hormones and quell further secretion. When levels fall, the pituitary releases more TSH, which stimulates the thyroid to start making more hormones.

prompts them to release hormone. This hormone, in turn, acts on other cells to release more of the needed chemical into the bloodstream. When enough chemical has been produced, the sensory cells switch the system off, which stops further hormone release. In this way, the body’s chemical balance is constantly maintained.

The system is exquisitely sensitive: food, exercise, stress, illness, changes in body chemistry such as a shortage or excess of certain nutrients, pregnancy, ageing, even the time of day or year, can affect the balancing mechanism and, with it, the amount of hormones our glands secrete.

Most hormones act only on specific tissues and not all the cells in the body. They do this by latching on to structures called ‘receptors’, which lie studded about the surface of or within cells, rather like a key fits into a lock. This enables hormones to be transported around the bloodstream to specific locations. Receptors are also important because, as we shall see, if the wrong chemical – such as an autoimmune antibody – attaches itself to a receptor, like a thief using a master key to get into your house, it can cause havoc and destruction.




The Thyroid Gland


The thyroid is a small, soft, butterfly-shaped gland that weighs just 15–20 g (


/


–


/


oz) and is about the size of a plum, yet it is also the largest pure endocrine gland in the body. It lies across the front of the windpipe (trachea) just below the larynx, or voice box (see Figure 2.3). Its two lobes, or sections, lie on either side of the Adam’s apple and are joined together by a narrow bridge of tissue called the isthmus.

You may just be able to detect its outline if you look in the mirror and stretch your neck. If you take a sip of water and swallow, you may be able to see it moving up and down. If you can’t see it, you may be able to feel it with your fingers. (But don’t worry if you can’t see or feel it – not everyone can.)

The thyroid develops in the womb during the first weeks of life from a small piece of tissue at the root of the tongue. As the fetus grows, the tissue moves down the neck to rest at its adult position. By the time the fetus is just 12 weeks old, the thyroid has already started to work.

The thyroid is made up of two types of hormone-secreting tissue: follicular cells and parafollicular cells. The follicular cells, which make up the greater part of the thyroid, are hollow spheres surrounded by tiny capillary blood vessels, lymphatic vessels and soft connective tissue. Each follicle is filled with a yellow, semifluid, protein-containing material called thyroglobulin (TG) which, when broken down, interacts with






Figure 2.3 The thyroid gland lies across the windpipe in the throat.

iodine stored in the thyroid to produce thyroid hormone (TH). The parafollicular cells lie on their own or in small clusters in the spaces between the follicles and secrete another hormone – calcitonin.




A Tale of Two Hormones


The thyroid’s main purpose is the production, storage and release of thyroid hormone. Although referred as a single entity, there are, in fact, two thyroid hormones: thyroxine (T


) and triiodothyronine (T


), which carry four and three atoms of iodine, respectively.

T


is four times more potent than T


and works eight times more quickly. Yet, T


is about 50 times more abundant in the bloodstream than T


. This is because, although small amounts of T


are converted to T


within the thyroid gland itself, most T


is produced outside of the thyroid by a process called monodeiodination, which strips away one of the iodine atoms from T


. This allows the body to produce T


as needed – like changing your five-pound notes into one-pound coins for the parking meter.




All Under Control


Like all of the glands in the body, the thyroid is regulated and controlled by the pituitary gland, the small, pea-sized gland attached to the brain often referred to as the ‘master gland’. The pituitary gland orchestrates the entire hormonal symphony but is, in turn, driven by the hypothalamus, to which it is joined by a short stalk of nerve fibres. This hypothalamic – pituitary – thyroid gland connection is a key junction through which chemical messages are carried to and from the brain and the body.

Levels of thyroid hormone are regulated by a feedback loop that operates between the hypothalamus, pituitary and thyroid glands. Anything that increases the body’s need for energy – such as a fall in temperature or a bout of exercise – will provoke the hypothalamus to secrete a chemical messenger called thyrotropin-releasing hormone (TRH) to trigger the pituitary to secrete a messenger chemical called thyrotropin or thyroid-stimulating hormone (TSH), which stimulates the thyroid to secrete thyroid hormone. As the thyroid releases increasing amounts of TH, chemical messages are eventually passed on to the hypothalamus to inhibit production of TRH and, in turn, TSH.

This chemical round-robin means that TSH levels are a highly sensitive indicator of thyroid activity and can provide an early clue that the thyroid is not working as it should. This is why the TSH test is a key investigation in checking the health of your thyroid (see Chapter 4).




The Calcium Connection


The thyroid is crucial in maintaining the strength and density of our bones. The parafollicular cells of the thyroid produce the hormone calcitonin, which is involved in regulating calcium levels in the body. As well as being the main mineral used for making bone, calcium is needed to trigger impulses in nerve and muscle cells.

Calcitonin acts with another hormone – parathyroid hormone (PTH) – produced by the parathyroid glands, four tiny glands that lie behind the thyroid. Whenever calcium is needed, PTH raises the levels of calcium in the blood by stimulating the release of calcium from bone, increasing the reabsorption of calcium from the kidneys and converting vitamin D into a hormone that increases gut absorption of calcium. Once calcium levels have been increased, the thyroid releases calcitonin to suppress the release of calcium from bone.




The Incredible Thyroid


Although the thyroid is only a small gland, the hormone it produces is responsible for an incredible number of biological processes. In fact, it would be fair to say that TH is essential for the health of virtually every cell in your body. Cell growth, muscle strength, body temperature, appetite, cholesterol levels, mood and memory all depend on thyroid hormone. Likewise, your heart, liver, kidneys, reproductive organs, hair and skin all require TH to function properly.

So widespread is the activity of TH that, indeed, in Victorian times, doctors believed the thyroid was vital to life. Although it is possible to live without a thyroid, provided you receive thyroid-hormone replacement therapy, they were not that far from the truth. Thyroid hormone is unique in that, throughout the whole of our lives, it acts within almost every tissue in the body and is vital for general health and wellbeing.




A MATTER OF ENERGY


The main job of thyroid hormone is to regulate your metabolism – the rate of your body’s cell activity. It does this by activating mitochondria, the tiny cellular ‘powerhouses’ that produce energy. The process of metabolism – the word literally means ‘change’ – among other things, controls your appetite and maintains your body temperature, whatever the external environment.

Your metabolism determines the rate at which your cells burn oxygen, a process involved in every activity of life – from breathing and sleeping to eating, talking and moving around – as well as all the activities of your internal organs, such as the beating of your heart, the digesting of your food, the functioning of your reproductive organs and, most important of all, the working of your brain.




A LIFETIME OF ACTIVITY


Thyroid hormone is active when the embryo is still in the womb, where it plays a crucial part in helping each of the millions of cells in our bodies to become more specialized. It is this process, known as differentiation, that turns tadpoles into frogs and a human embryo to develop from a tiny cluster of cells into a fully grown baby.

At the other end of life, the thyroid is thought to play an equally important role in the control of ageing.




THE GROWTH FACTOR


In the womb and after birth, thyroid hormone is vital for both mental and physical growth. With somatotrophin (STH) from the pituitary, it determines the length and strength of your bones. During childhood, lack of TH stunts growth by preventing the bones from growing and maturing. TH is also crucial for the normal development of the brain and nervous system in both the unborn and newly born infant. During pregnancy, low levels of T


can affect brain development, resulting in mild-to-severe mental deficiencies. In the past, the term used to describe these defects was ‘mental cretinism’.




BREAST DEVELOPMENT


Thyroid hormone may also be involved in the development of our breasts. Studies in mice have shown that TH affects prolactin, another pituitary hormone. In breastfeeding women, this hormone is involved in stimulating the production of milk. It is also thought that breast pain that is not premenstrual breast tenderness and swelling may be linked to thyroid problems.




PROTECTION AGAINST STARVATION


When it works properly, the thyroid plays a crucial part in keeping your body weight more or less stable. Increasing the amount you eat, especially of starchy foods or carbohydrates, increases metabolism and boosts the production of the active thyroid hormone T


. Dieting, on the other hand, decreases metabolism, causing the body to produce less T


.

This is almost certainly a mechanism that has evolved to protect us from starvation. It is a known fact that when the body is deprived of food, it turns down the rate of metabolism. This is one of the mechanisms thought to have enabled the survival of the babies who, incredibly, were found still alive after several days trapped under the rubble of the Mexican earthquake in the 1980s. This same mechanism also explains why the thyroid becomes sluggish in women with eating disorders such as anorexia, bulimia and excessive dieting. The brain correctly perceives these states as starvation and turns down thyroid activity to conserve energy. This is how a thyroid problem can play havoc with your appetite and your weight.




PROTECTION AGAINST INFECTION


The thyroid is a vital part of the body’s immune-defence mechanism. It stimulates the production of special white blood cells, known as T cells and B cells, to help the body fight against disease. Chronic liver and kidney disease, acute and chronic illness, starvation and diets too low in carbohydrate lower the production of T3. It is thought that this may be part of an adaptive process to help the body defend itself against illness.




FLUID BALANCE


The thyroid plays a vital role in a myriad other bodily processes. It helps to maintain the body’s fluid balance by controlling the mechanisms by which water and chemicals enter and leave the cells – one reason why bloating is troublesome if you have an underactive thyroid.




VITAMIN POWER


In the liver, thyroid hormones are needed to convert beta-carotene (the pigment that gives orange, yellow and red fruits and vegetables their colour) into vitamin A. In the past few years, beta-carotene has sparked considerable interest as one of the three key antioxidant vitamins (the other two are vitamins C and E) that play a crucial role in protecting the body against degenerative diseases, such as cancer and heart disease, and those associated with ageing.




INTERACTIONS WITH OTHER HORMONES


Thyroid hormone needs to be present for other hormones to function in various parts of the body. Most important for women, it acts in concert with the female sex hormone oestrogen to modulate reproduction. This is why thyroid malfunction can sometimes be a cause of reduced fertility and other reproductive problems.




Manufacturing Thyroid Hormone


The mineral iodine – a trace element found in soil and food – plays a central role in the manufacture of thyroid hormone. Iodine is needed for cells to work properly. To produce hormone, the thyroid absorbs iodine and, through a process involving enzymes, combines it with the amino acid tyrosine. More enzyme reactions convert this into T


and T


, which are then stored by the thyroid within a protein called thyroglobulin (TG). When thyroid hormone is then needed in the body, enzymes break down this TG to release the T


and T3 into the bloodstream.




Transporting Thyroid Hormone


Most of the thyroid hormone in the body is carried around the bloodstream attached to special transport proteins, especially thyroid-binding globulin (TBG). Once the bound thyroid hormone reaches its destination, it is released from the protein binding so that T


can be converted to T


and ready for use by the cells. A tiny amount – around 0.03 per cent of T


and 0.3 per cent of T


– remains unattached to float freely about in the blood. Although only a small quantity, free-floating T


does not have to be released from any binding and so is immediately available for use by the cells.

Certain conditions, such as taking the Pill, can raise the levels of protein in the blood and, in the past, thyroid tests which measured total levels of T


and T


were not always accurate because of some confusion in interpreting results. Today’s blood tests measure levels of both free-floating T


and bound T


as well as thyroid-stimulating hormone, which provide a much more accurate indication of thyroid function.




What Can Go Wrong?


The most common thing to go wrong with the thyroid is autoimmune thyroid disease, when the body turns against its own tissues and tries to destroy them. Over a period of time, this causes the thyroid to become either overactive (hyperthyroidism) or underactive (hypothyroidism). The result is Graves’ disease, the most common form of hyperthyroidism, and thyroiditis, the most common form of hypothyroidism.

But why should a mechanism designed to protect our body and keep it healthy go so drastically wrong? To find the answer, it is necessary to delve deeper into the fascinating science of immunology.




Immune Reactions


The body’s defence system normally provides a formidable barrier against attack by ‘foreign’ invaders such as viruses, bacteria and parasites. Although the way it works is still not fully understood, what is known is that many actions depend on two kinds of lymphocytes (white blood cells) – T cells and B cells – responsible for fending off attackers from outside.

When the body is under attack by invaders, the immune system sends T cells to the affected site to find out what is happening. There are two types of T cells: helper cells and killer cells. Helper cells help the immune system by identifying antigens, a chemical substance that marks the invaders as ‘foreign’. Once the helper cells have recognized a foreign antigen, killer cells are despatched to attack and destroy them. To protect the body against future attack by the same foreign invaders, killer T cells retain a ‘memory’ of their antigen. If the body is threatened again by the same invader, these killer T cells are quickly activated and sent in for the kill. This entire process is known as cellular immunity.

B cells work in a similar way except that they fight off an attack by producing protein antibodies known as immunoglobulins; these are produced specific to the invader. When the immune system identifies a particular invader, B cells are stimulated to produce a large quantity of a specific immunoglobulin that will attach itself to the invading antigens and immobilize them. Once this has happened, the antigens are devoured by other white cells called phagocytes. This process is known as humoral immunity.




The Enemy Within


Under normal circumstances, the immune system does not turn against itself because our own cells are coded to allow our T cells and B cells to recognize them as ‘self and refrain from attacking them. Scientists still do not know exactly why this normal recognition process fails. One theory is that, in some cases, a foreign antigen – say, a protein on a virus – escapes the immune system’s surveillance by disguising itself as one the body’s own cells. As the immune system cannot distinguish this disguised protein from its own tissue, it allows the invader access to the cells.




Inflammation From Within


Another way in which the immune system can go awry is when an invader triggers an overzealous immune response, unleashing a flood of cell proteins called cytokines; these cause inflammation and increase the production of antibodies, which turn against the tissue in question and destroy it.

Both Graves’ disease and Hashimoto’s thyroiditis are caused by T and B cells that infiltrate the thyroid, triggering inflammation and the production of thyroid autoantibodies. Depending on which autoantibodies are produced, this will lead to either overproduction or underproduction of thyroid hormone.

Autoantibodies can attack virtually any of the body’s tissues or organs and not just the thyroid, causing a range of diseases in which the tissues become inflamed and are gradually destroyed. These include rheumatoid arthritis, where autoantibodies destroy the joints; Addison’s disease, where autoantibodies damage the adrenals; multiple sclerosis, where autoantibodies are directed against the nervous system; and diabetes, where autoantibodies turn against the pancreas.

It is now established that all of us possess autoimmunity to some degree but, in some people, the immune system seems to have a particular tendency to turn against itself. This might explain why having one autoimmune disorder can put you at an increased risk of developing another. It may also be why, if you have developed an autoimmune thyroid disorder, it is important to be on the look-out for other autoimmune problems.

Three-quarters of cases of autoimmune disease occur in women. What exactly triggers the immune system in women to attack itself more frequently than in men?




The Family Factor


The tendency for autoimmune diseases to run in families provides one clue. It suggests that a faulty gene or genes may be partly to blame. Indeed, scientists have identified a handful of so-called ‘susceptibility’ genes that render some of us more vulnerable to autoimmune attack. They have also pinpointed several areas – ‘susceptibility regions’ – on chromosomes, the 23 pairs of rod-like structures that carry our genes, that appear to confer a greater risk of autoimmunity.

Many autoimmune diseases, including autoimmune thyroid disease, are strongly associated with a gene for human leukocyte antigens (HLA) found on chromosome 6. Another susceptibility gene, CTLA-4 (cytotoxic T lymphocyte-4), is also involved. Both these genes are known as immune-modifying genes – they alter the way in which your immune system behaves. As well as susceptibility genes, researchers are also finding genes that are specifically involved in autoimmune thyroid problems. These ‘thyroid-specific genes’ are thought to work hand-in-hand with susceptibility genes to trigger an autoimmune attack against the thyroid.

As to why women are at greater risk than men, scientists have come up with an intriguing theory that suggests that it may be connected with the continued presence of foreign cells from a fetus in the mother’s bloodstream – and vice versa. Another way to acquire cells that aren’t your own is from a twin, even one you didn’t know you had, because it is now known that a number of pregnancies start out as twin pregnancies, but soon lose one of the embryos. Says Dr J. Lee Nelson, the American scientist who pioneered this theory, ‘Our concept of self has to be modified a little bit. We’re not as completely self as we thought we were.’




Deciphering the Clues


The presence of thyroid autoantibodies in your bloodstream is an important clue that there has been an immune attack on your thyroid. In fact, it was by studying Graves’ disease that scientists acquired some of the earliest clues of what was going on in autoimmunity. The chief culprit in Graves’ disease is an antibody, first discovered in the blood of Graves’ patients as long ago as 1956, dubbed ‘long-active thyroid stimulator’, or ‘LATS’, because in animals, it stimulated thyroid activity for longer than thyroid-stimulating hormone (TSH).

Later researchers identified LATS as a type of immunoglobulin G, the main antibody in the bloodstream and, because it stimulates thyroid production by locking onto the TSH receptor, they renamed it TSHR-Ab. This autoantibody is now thought to be responsible for the thyroid overactivity in Graves’ disease, and to play a key role in the development of thyroid eye disease by overstimulating certain cells that line the eye sockets.

A similar process is involved in Hashimoto’s thyroiditis except that, in this case, the rogue antibodies are directed against thyroglobulin (TG), the protein molecule in which thyroid hormone is stored, and thyroid peroxidase (TPO), a key enzyme involved in the early stages of manufacturing thyroid hormone. The autoantibodies block receptors on both TG and TPO, thereby causing underproduction of thyroid hormone.





CHAPTER THREE The Out-of-Balance Thyroid (#ulink_e0ce419a-802f-5ef1-a7d4-d5446e3dbf97)


Given the wide-ranging action of the thyroid, it is hardly surprising that, when something goes wrong, it affects the entire body. Exactly what these effects are depends on whether your thyroid becomes underactive or overactive.

Hypothyroidism, or the underactive thyroid, can produce a long and bewildering list of symptoms (see Table 3.4, page 42). Most of these are non-specific and easily attributable to some other disorder or simply fatigue – one reason why it often takes so long to get a diagnosis. As Camille recalls:

I noticed that my mental energy had gone right down, but I kept rationalizing. The tiredness was dreadful, but I persuaded myself it was because I was overdoing it. I kept saying to myself, ‘If only I’d taken two weeks off at Christmas, I wouldn’t be feeling so tired’. It was only the hair loss that got me in for a test.

Clare has a similar story:

I just thought I was putting on weight. I put on two-and-a-half stone in as many years. Yet, despite going to Weight Watchers and not cheating, I couldn’t shift it. In retrospect, there were other clues. I developed coarse skin but, because I’d had a baby, and my hands were in and out of sterilizing solution, I just thought it was that. My periods were irregular and I was tired all the time, but I put that down to working and having a family. It was sheer vanity that drove me to the surgery in the end.

Jennifer, who developed an underactive thyroid after the birth of her second child, remembers:

My energy levels fluctuated from day to day. I would start the week feeling fine but, by Tuesday, I would be completely exhausted and have to take the day off. I managed to drag myself through Wednesday and Thursday, and Friday I had off. I would spend the weekend in bed. I was so depressed, I would sometimes just lie there and cry. I had constant headaches and sore throats, my muscles ached, my nails were brittle, and I was always getting flu. I couldn’t concentrate; my memory was appalling. I was so cold that, even in the summer, I had to take a hot-water bottle to bed. Our sex life went completely downhill.

The key characteristic of hypothyroidism is that all your systems slow down as a result of metabolism running on near-empty. Your appetite decreases and what you do eat is converted into energy more slowly. You gain weight and feel permanently cold. The smallest task becomes a supreme effort. Your muscles feel weak and stiff, and ache on the slightest exertion. Just walking up the road can leave you exhausted and breathless. You may experience muscle cramps. Your heart beats more slowly and your pulse is slowed while blood pressure rises. Digestion takes longer and you become constipated. You may also experience joint pain and stiffness. Your kidneys work more slowly, leading to water retention and tissue swelling (oedema). Your liver also slows down, resulting in a rise in levels of ‘bad’ LDL cholesterol and other blood fats known as triglycerides. You may succumb to every passing minor infection as the lack of thyroid hormones takes its toll on your immune system. Cuts and bruises take a long time to heal because of the fragility of your blood vessels. You feel miserable, washed out and overwhelmed with fatigue. As Christine observes, ‘It is total; every body system is affected. People often say, “I just feel so ill, but I can’t put my finger on it.”’




Appearance Matters


One of the most distressing aspects of hypothyroidism is the effect on your looks. Even though you have no appetite, the weight piles on unstoppably. Your hair becomes dry, brittle and thin; your skin becomes dry, coarse and puffy. Your waistband nips, your rings become tight and you feel bloated. These symptoms are the result of an autoimmune attack called ‘myxoedema’, where the cells become ‘leaky’, leading to fluid accumulation and mucus deposition beneath the skin. You may become pale due to anaemia, and your complexion may take on a slightly yellowish hue due to the buildup of the yellow pigment beta-carotene in your blood.

Carol, who was initially diagnosed with depression and went for many years before her underactive thyroid was diagnosed, recalls:

I developed nasty sores on my skin, mainly on my arms, but also on my upper thighs, stomach, and neck. It took five years to find out this was a combination of a side-effect from the antidepressants and poor skin-healing due to my thyroid problem.

You may also develop a goitre (see page 56) or, alternatively, your thyroid may shrivel up (atrophy).




Tired All the Time


These physical symptoms are compounded by an almost overwhelming exhaustion, as Maggie, who developed an underactive thyroid after the birth of her first child, relates:

I felt totally paralysed for three days. I was so weak I could barely walk around. That slowly improved, but I still felt slow – the way I imagine an old person must feel. I had no appetite, but even so, the weight piled on. On one occasion, I was actually vomiting for three days and I still put on a pound! I was freezing cold all the time and had to keep the heating turned up high. My face was puffy; I looked as though I had been crying. My head felt as if it was full of cottonwool. I couldn’t focus properly – if I looked at the TV and then tried to look at a newspaper, everything was blurred. I had noises in my ears. I slept very badly. I had pain and tingling in my hands that woke me up. I was also suffering from terrible constipation. I started losing my hair, but I just thought that was the normal hair loss that happens after pregnancy, but what was strange was that I didn’t have to shave my legs or pluck my eyebrows. I felt as if my whole appearance was changing. The smallest task seemed enormous – I had trouble just walking to the corner of the road. Things came to a head when we went for a walk with some friends we were visiting. I was dragging myself along at my usual snail’s pace, several yards behind. Being unable to keep up with the others really brought it home to me that it was more than just the after-effects of having a baby. Something was seriously wrong.

June said, ‘I thought everyone else was going too fast. I didn’t realise it was me that was slow.’

In some cases, the tiredness associated with an underactive thyroid is so troublesome that a number of doctors believe that ME/CFS (myalgic encephalomyopathy/chronic fatigue syndrome) and fibromyalgia (pain in the soft tissue and muscles accompanied by exhaustion) may be a result of undiagnosed hypothyroidism. In the absence of hard evidence from studies, there is much debate over this issue. In the US, Dr John Lowe, an expert in fibromyalgia, believes there is a clear link between the two conditions (Clinical Bulletin of Myofascial Therapy, 1997; see also www.thyroid.about.com). In the UK, Dr Charles Shepherd has found that hyper- and hypothyroid problems are associated with ME/CFS. Most conventional doctors tend to pooh-pooh the idea, but many current texts on the thyroid, especially those coming from America, consider the idea to have merit.




The Senses


An underactive thyroid can affect your senses as a result of tissue swelling. You may experience headaches, migraine or blurred vision. You may become slightly deaf or hear constant noises in the ears (tinnitus). Your voice may become deep and husky due to thickening of the vocal cords. Swelling and thickening of the tissues around the wrists and ankles can compress the nerves, causing pins-and-needles in the hands and feet or numbness, a condition known as carpal – tarsal, or carpal tunnel, syndrome. This can make it difficult to use a keyboard or perform other everyday tasks. Thickening of the neck tissue may cause snoring. Digestion may be impaired as the muscular contractions (peristalsis) that propel food through the gastrointestinal tract slow down. Sluggish bowels can cause constipation.




Menstrual Disturbances and Subfertility


Menstrual problems and subfertility – difficulty conceiving and/or maintaining a pregnancy – are both associated with an underactive thyroid (see Chapter 8). It may also be difficult to conceive because your sex life has ground to a halt. When doing anything is an effort, it may be impossible to summon up the energy for sex, especially if you are feeling unattractive due to various physical changes.

If hypothyroidism is a result of pituitary malfunction, you may begin to produce milk from your breasts even though you are not lactating, a result of an abnormal production of the milk-producing hormone prolactin by the pituitary.

Lyn, who was diagnosed with hypothyroidism after the birth of her second baby, says, ‘I was very irritable and my lack of libido didn’t help my marriage.’




Effects on the Heart


One of the most serious consequences of hypothyroidism is that the heart, like every other system in the body, slows down. Sluggish thyroid function causes excess LDL cholesterol to accumulate in the bloodstream, which can lead to atherosclerosis – narrowing and ‘furring’ of the arteries – causing insufficient oxygen to reach the muscles of the heart.

Clues that your heart may be affected include shortness of breath on exertion or, sometimes, chest pain (angina). Another symptom of atherosclerosis is pain in the calf on exertion (intermittent claudication), caused by furred arteries in the leg.

Tests may reveal a slow pulse rate (under 60 beats a minute), unusual in everyone except trained athletes, low blood pressure, unusual in everyone except the very young and/or very fit, and raised levels of ‘bad’ LDL cholesterol and other blood fats called triglycerides.




Mental Effects, Depression and Mood Swings


Mental sluggishness is a commonly reported effect of hypothyroidism. Your brain feels like cottonwool, and you find it difficult to pay attention, to concentrate and to remember. There may be a time lag while you try to recall events, and even familiar names or facts can be elusive – a mental state typically described as ‘feeling in a fog’.

One of the biggest bones of contention is the relationship between thyroid problems, depression and mood swings. In a letter to the British Medical Journal (October 2000), consultant psychiatrist Martin Eales outlined his belief that faulty thyroid function – including so-called mild or subclinical thyroid problems – is a significant factor in triggering depression and the failure of some people to respond to treatment with antidepressants, and can aggravate mood swings in manic-depression (known medically as bipolar disorder). This idea receives some support from the fact that antithyroid peroxidase antibodies, associated with hypothyroidism, have been found in people with manic-depression. In rare instances, there may be more severe mental disturbances, such as paranoia (feelings of persecution). These symptoms – at one time cruelly described as ‘myxoedematous madness’ – quickly disappear once treatment to correct the underactive thyroid is begun.




A Matter of Chemistry


To understand these links, it is necessary to look more closely at the chemistry of the brain and some of the discoveries that have been made concerning how the brain and body ‘talk’ to each other. Depression has been found to be linked to changes in both the hypothalamus-pituitary-thyroid axis and the hypo – thalmus – pituitary – adrenal axis – two key hormonal circuits that link the brain and the body.

A major step towards understanding depression came with the discovery that the condition is linked to a shortage of the brain chemical serotonin, sometimes called the ‘happiness hormone’. This led to the development of a new class of antidepressants called selective serotonin reuptake inhibitors (SSRIs) which, as the name suggests, selectively block serotonin receptors to cause levels of serotonin – and feelings of wellbeing – to rise. These drugs, of which Prozac is the most well known, are now considered the standard treatment for depression.

Recently, researchers found that people who are depressed tend to have raised levels of thyroxine (T


). At the same time, they have disturbances in their body clock causing lower daytime levels and a lower-than-normal night-time surge of thyroid-stimulating hormone, thought to be due to lack of serotonin. This is yet another example of how the brain and body communicate. Some doctors also suggest that the activity of T


is also reduced, although this is not as yet supported by any clear evidence.

A number of psychiatrists, particularly in the US, have found that a T


plus antidepressant ‘cocktail’ helps lift depression faster in the 30–40 per cent of people who seem to be resistant to antidepressants. Interestingly, adding the more usual thyroid treatment, T


, has not proved effective, which suggests that the ability to convert T


to T


in the brain may be damaged in depressed people. Although most studies were carried out with the older tricyclic antidepressants that are not as widely used these days, it is thought that adding a dash of T


to an SSRI might be equally effective.




Sorting It All Out


It may not always be easy for you – or your doctor – to distinguish between depression and hypothyroidism because the two conditions have many symptoms in common. In fact, some doctors surmise that an underfunctioning thyroid may be an indicator of depression. Others think that depression can put you more at risk of developing thyroid antibodies by impairing immune function, which may, in turn, lead to hypothyroidism.

Carol’s story is fairly typical:

I felt extremely fatigued, had trouble getting up in the morning and wanted to sleep all day. Sometimes I took a day or two off work and did just that – slept for 24 hours. I was also very tearful and had problems concentrating, making decisions, even thinking. I couldn’t watch TV or read – it was too much effort. I took about three months off work. I had a nice GP at the time and he diagnosed depression. I had a feeling it was something more physical as I didn’t feel depressed in the way it was described in the books. I wanted to do things, but I had no energy. I took antidepressants for five years. They helped my mood, which enabled me to return to work, but I had little energy for anything else.

Table 3.1 Symptoms common to both hypothyroidism and depression




Table 3.2 Clues to help you to determine whether you have hypothyroidism or depression




DEPRESSION OR THYROID?







Christine, whose underactive thyroid went undiagnosed for years, urges women not to be fobbed off with a diagnosis of depression if the symptoms don’t improve with antidepressant treatment. She was one of the few who developed myxoedema coma, a potentially life-threatening condition in which body temperature drops severely, brought on by untreated hypothyroidism. It can also cause low blood sugar and seizures, and lead to death. The coma can be triggered by cold, illness, infection or injury, and drugs that suppress the central nervous system. Although rare, it can still happen, as Christine recalls:

After years of to-ing and fro-ing to the doctor, I was referred to a psychiatric unit and diagnosed as chronically depressed. I was prescribed lithium [a drug used to treat manic-depression]. Within six months, I was comatose – my body grinding to a halt and my kidneys failing. I heard the doctors talking outside my room saying it should never have happened.

Although such an occurrence is extremely rare, it does underline the importance of persistence and of getting a proper diagnosis.




Why Does the Thyroid Become Underactive?


There are two main types of hypothyroidism: primary, when the thyroid is the source of problems; and secondary, when a fault in the hypothalamus or pituitary has a knock-on effect on the thyroid.



• Primary hypothyroidism can be brought on by:

• thyroiditis (inflammation of the thyroid), a feature of Hashimoto’s thyroiditis (see page 49) and postpartum thyroiditis (PPT)

• surgical or medical treatment for an overactive thyroid (see Chapter 5) or surgery and/or radiotherapy for certain kinds of cancer

• prescription medications and over-the-counter drugs containing iodine (iodides), such as lithium for treating manic-depression, and some cough remedies

• congenital (inborn) problems affecting the thyroid, such as absence or abnormal development of the thyroid or errors of metabolism (see Chapter 9).

• Secondary hypothyroidism is caused by failure of the hypothalamic – pituitary – thyroid hormonal axis leading to deficient secretion of hormones by the hypothalamus or pituitary, caused by:

• known damage to the hypothalamus or pituitary as a result of previous surgery, meningitis, trauma or radiation to the brain

• the development of tumours or cysts.




Variable Symptoms


Although many of the symptoms of an underactive thyroid are common to both primary and secondary hypothyroidism, there are some suggestive differences that either you or your doctor may notice.

Table 3.3Clues to help you determine whether you have primary or secondary hypothyroidism







Is Your Thyroid Underactive?


Symptoms of hypothyroidism are not always easy to detect. Table 3.4 lists some symptoms that you may experience, that others may notice or that your doctor may detect.

Table 3.4 Symptoms suggestive of hypothyroidism







Life in the Fast Lane: Hyperthyroidism


Overproduction of thyroid hormones – hyperthyroidism – is caused by an overactive thyroid. The state of being hyperthyroid, called thyrotoxicosis, is sometimes easier to spot than hypothyroidism, partly because there may be rather dramatic mental and physical effects. However, symptoms are not always obvious, but may just creep up on you. It may only be when someone else comments on how you have changed or when your doctor notices some signs that the condition is diagnosed.

Whereas an underactive thyroid slows your body down, an overactive one speeds it up, causing your metabolism to race uncontrollably. As Jan, who has Graves’ disease, the most common cause of hyperthyroidism, describes it:

I’d had a lot of trouble in my marriage and a lot of stress generally after I left. The first thing I noticed was that I was full of energy. I couldn’t sit still, I had to be working, working out, cooking or doing something with the kids all the time. I started to drink to try and slow myself down. As time went on, I couldn’t sit down long enough to think and I became totally exhausted. My muscles started to waste away, even though I was exercising so much. My periods stopped. I had bouts of breathlessness, which were diagnosed as asthma. I couldn’t think straight, my mind was so overactive. I felt as if my head was full of twittering sparrows and I had what I can only describe as an ‘electrical buzzing’ in my head.

As Jan’s account illustrates, when the thyroid becomes overactive, the body burns energy at a tremendous rate. If you are affected, you can eat like an elephant without putting on weight; in fact, more often than not, you will lose pounds instead.

As the gland continues to step up production, you may feel constantly hot and sweaty, and find yourself stripping off and throwing windows open, even on cold days. You may also notice a change in bowel habits – needing to go more often and sometimes having diarrhoea, a symptom so common that it’s not unusual for hyperthyroidism to be first diagnosed at a gastroenterology clinic. Some of those affected experience a raging thirst and pass large amounts of urine, similar to that seen in people with undiagnosed diabetes.

Anyone who has been around someone with an overactive thyroid can’t fail to notice their boundless ‘get up and go’. Sufferers pace like caged lions, talking 19 to the dozen, yet are unable to muster any concentration. Their energy never flags for a second, even at bedtime. Recalls Louise, 38:

I couldn’t settle for the jumble of racing thoughts that were flying around my brain. My sex drive increased, too – I wouldn’t leave my husband alone.

Louise’s experience echoes that of many others, and is thought to occur because of the increased turnover of male-type sex hormones – androgens – which control the libido and are converted into the female hormone – oestrogen – in the body.




Mood Swings


Wildly swinging moods are a key feature of thyroid overactivity. One minute you are optimistic and on top of the world, the next you are plunged into the depths of despair. Nervousness and anxiety are also characteristic, probably as a result of increased sensitivity to the effects of the stress hormone adrenaline, which triggers the body’s ‘fight or flight’ reaction. Unfortunately, some find that when they report symptoms to their doctor, they are seen to be a cause rather than an effect of their problem. Just as people with an underactive thyroid may find themselves dismissed or treated with antidepressants, it has been known for those with hyperthyroidism to be referred for psychiatric help for manic-depression.




Appearance Matters Too


An overactive thyroid can affect your physical appearance. Your skin becomes thin, pink and moist; you tend to flush easily, and your palms may become red and sweaty. Your hair becomes fine and flyaway, and falls out while your nails become thin and flaky.

A number of those with Graves’ disease develop thyroid eye disease (see Chapter 8) and some will also develop an infiltrating skin disorder causing the skin on the front of the shins to become lumpy, red and thickened skin in the front of the shins – a condition also known as pretibial myxoedema. These symptoms can appear years before or after the thyroid becomes overactive.

Some people with hyperthyroidism develop thyrotoxic tremor – a constant, fine trembling that is most noticeable when the hands are stretched out. This is thought to be due to an oversensitivity to adrenaline. Maria, 35, a freelance photographer, recalls that this tremor was the first thing she noticed when her thyroid became overactive:

I first became aware of the problem when I noticed that I wasn’t able to hold my camera steady. I couldn’t hold a pen straight to write either, and I started having palpitations. My heart beat so fast that, on one occasion, I was convinced that I was going to have a heart attack. I was losing weight rapidly: I went from my usual eight-and-a-half to nine stone to seven-and-a-half stone, even though I was eating like a pig. And I was irritable and bad-tempered.




Bone, Heart and Other Muscles


Like hypothyroidism, untreated hyperthyroidism can damage the heart. The palpitations Maria describes are a common feature, caused by an overactivity of the heart muscle that causes the pulse to accelerate; this can lead to palpitations and an irregular heartbeat, called atrial fibrillation (see Chapter 10), especially in older women. Breathlessness is another common symptom and this, too, is sometimes misdiagnosed as asthma or bronchitis. The slightest exertion can bring on an attack.

An overactive thyroid can also disturb your body’s calcium balance, accelerating the natural rate of bone loss. Bone is a living tissue that is constantly being built up and broken down. Thyroid overactivity speeds up the breakdown part of this natural cycle. This, in turn, can lead to thinning of the bones (osteopenia) and an increased risk of osteoporosis when you are older.

Weakness as a result of wasting of the muscles is another problem for about half of all hyperthyroid sufferers. As Sarah remembers:

I am a marathon runner, but I just couldn’t run at all. If I got down on the floor, someone had to help me up.

Very rarely – and particularly in those who are Asian – people with an overactive thyroid can experience periodic paralysis, attacks of profound muscle weakness or paralysis brought on by eating sugary or starchy foods. This is due to a disturbance of the body’s ability to maintain a constant concentration of potassium in the blood.




Menstrual Problems and Pregnancy


Hyperthyroidism, too, can be responsible for menstrual problems, including PMS. Although not as likely to affect fertility as an underactive thyroid, it is nevertheless associated with a number of complications during pregnancy (see Chapter 9).




The Goitre Connection


As with an underactive thyroid, an overactive one can also cause a goitre (see page 56). If the doctor listens through a stethoscope, it may be possible to hear the blood surging turbulently through the vessels in the goitre, a noise known as ‘thyroid bruit’ (a bruit is the sound made in the heart, arteries or veins when the blood flows at an abnormal speed).




Is Your Thyroid Overactive?


The symptoms of hyperthyroidism can often sneak up insidiously. Table 3.5 lists some of the clues that you or others may notice, or that your doctor may detect.




Why Does the Thyroid Become Overactive?


Hyperthyroidism may also be primary, when something goes wrong with the thyroid itself, or secondary, when the fault lies with the hypothalamus or pituitary.

Primary hyperthyroidism can be due to:

• Graves’ disease, caused by autoimmunity (see page 50)

• Thyroiditis (inflammation of the thyroid), caused by autoimmunity (see page 52)

• Nodular thyroid disease, for example, toxic multinodular goitre (Plummer’s disease), characterized by the development of multiple lumps, or a ‘hot’ nodule (toxic adenoma), where a single lump becomes overactive (see page 57)

• Postpartum thyroiditis, wherein problems develop after giving birth (see Chapter 9)

• Excess iodine either from the diet (from food or, in some instances, herbal supplements) or from medications (such as the drug lithium, used to treat manic-depression; amiodarone, a drug used to treat irregular heart beat; and interferon, used to treat certain types of cancer)

Table 3.5 Symptoms suggestive of hyperthyroidism




• Overdosage of thyroxin treatment for hypothyroidism. On rare occasions, hyperthyroidism can be a consequence of people with an underactive thyroid accidentally or intentionally taking too much medication, a condition known as thyrotoxicosis factitia.



Secondary hyperthyroidism can be brought on by:

• Faulty pituitary function, on rare occasions due to a pituitary tumour, leading to an abnormal production of thyroid-stimulating hormone (TSH), thereby causing the thyroid to produce too much hormone

• Cancer-related problems. In extremely rare instances, hyperthyroidism may be the result of a thyroid cancer that has spread.




Autoimmune Thyroid Problems

Hashimoto’s Thyroiditis


In adults, the most common reason for the thyroid to become underactive is autoimmunity. Hashimoto’s thyroiditis (Hashimoto’s disease) – named after Hakuru Hashimoto, the Japanese doctor who originally described it in 1912 – is the most common type of autoimmune hypothyroidism. The other type is called ‘spontaneous atrophic hypothyroidism’, where the thyroid wastes away and shrinks. This is more likely to affect older women.




THE SYMPTOMS


At first, although you may not feel ill. You may develop a small, painless goitre and, as time goes on, this may become tender and feel uncomfortable when you swallow. Curiously, when the disease first develops, you may develop symptoms of an overactive thyroid (see page 48). This is only temporary, however. As the disease progresses, the thyroid becomes increasingly less active, and the typical signs and symptoms of hypothyroidism eventually set in.




Graves’ disease


For six to eight out of 10 women, hyperthyroidism is a result of Graves’ disease, another autoimmune condition that is the mirror image of Hashimoto’s disease. It is most common between the ages of 20 and 40, but it can be seen in girls as young as five and, very occasionally, in the infants of sufferers.

Robert James Graves, a charismatic Irish physician, gave his name to the illness. In 1835, he wrote a paper outlining all the symptoms now recognized as Graves’ disease in the UK and USA. In Europe, the same condition is often called ‘von Basedow’s disease’, after Dr Carl A. von Basedow, a private practitioner in Germany, who described the illness in 1840. Graves was the first to make the connection with pregnancy – the women he wrote about were all pregnant (see Chapter 9).




Confusing Symptoms


Graves’ disease may be associated with all the classic symptoms of hyperthyroidism but, according to the UK-based endocrinologist Dr Anthony Weetman, these can be extremely variable. Writing in the New England Journal of Medicine, Weetman explains that both age and duration of thyroid overactivity play a part in determining which symptoms predominate. In over half those affected, nervousness, fatigue, rapid heart beat, heat intolerance and weight loss are key symptoms. However, in the over-50s, weight loss and loss of appetite are more common. Atrial fibrilliation is rare among the under-50s, but affects up to a fifth of those over 50. And while 90 per cent of younger women have a firm, diffuse goitre, only 75 per cent of the over-50s do. Glucose intolerance (inability to metabolize glucose) and, more rarely, diabetes can accompany Graves’ disease, and if you have diabetes, the condition will increase your need for insulin.




Is It Really Graves’ Disease?


Graves’ disease has been called the ‘great masquerader’ because it doesn’t always produce the typical symptoms of an overactive thyroid. Confusingly, the condition can take a relapsing-remitting form in which the thyroid swings from overactivity to normal to underactivity and back to overactivity again. Even more curiously, 5 per cent of those with Graves’ disease become hypothyroid over time, sometimes becoming lethargic and passive, and unable to do anything but lie in bed all day. Patricia, 34, who was diagnosed with an overactive thyroid two years ago, recalls:

In the past, I was always a very active person. I love sports and would be out playing tennis or squash or doing aerobics four or five times a week. A couple of years ago, I began to feel completely worn out. I started to put on weight. My muscles ached all over and I felt fluey. I really struggled to get through each day. I was backwards and forwards to the doctor for about six months but, each time, I was diagnosed as having flu or a virus.

My mother suffers from an underactive thyroid so when my neck began to swell, I asked the doctor if I could have a thyroid problem. He said no. He thought it was a problem with my ears, because my job involves a lot of flying abroad. Eventually, I saw an ENT specialist, who felt my neck and said, ‘Are you being treated for your thyroid problem?’ Two days later, I was back at the hospital having tests, which showed I had an overactive thyroid. My symptoms weren’t at all typical, which I guess is why it took so long to get a diagnosis.

Such symptoms tend to be more common in older women who develop an overactive thyroid and who may be labelled depressive or thought to be suffering from a hidden cancer. This type of hyperthyroidism – known as apathetic thyrotoxicosis – can be particularly tricky to detect, which can lead to delays in diagnosis. But a diagnosis is important as this kind of apathy is a sign that the body’s metabolism has reached the point of burnout and in need of urgent treatment to bring the thyroid under control.




Thyroiditis


Thyroiditis is inflammation of the thyroid. There are three different types:



• Viral or subacute thyroiditis is the result of a virus infecting the thyroid, although no single virus has yet been identified as the culprit. It tends to be especially common between the ages of 20 and 50. The condition usually resolves within two to five months, although one or two out of 10 of those who get it will have a recurrence. Symptoms may include:

• swelling, pain and tenderness of the thyroid

• flu-like symptoms and/or a raised temperature

• symptoms of thyroid overactivity (see page 43) lasting for two to four weeks, sometimes followed by symptoms of hypothyroidism.

• Autoimmune thyroiditis is yet another autoimmune effect on the thyroid. Mild autoimmune thyroiditis can affect as many as one in five women who are otherwise healthy, often without their even being aware of it. In a small number – about one in 10 – the disease may progress to overt hypothyroidism. The condition tends to run in families, so if you have a family history of this condition (see page 129), the doctor may suggest testing for thyroid antibodies.

• Postpartum thyroiditis (see Chapter 9).




Triggers and Causes


Hashimoto’s thyroiditis, Graves’ disease and most kinds of thyroiditis are autoimmune conditions. What triggers the immune system to see the thyroid as its enemy in such cases? All have a genetic component, yet studies of identical twins show a relatively low genetic effect; clearly, environmental and lifestyle factors must play key roles. Research has been mainly aimed at Graves’ disease, but there is reason to believe that similar mechanisms may be involved in other autoimmune types of thyroid disease.




Could Infection Play a Part?


Because the immune system is commonly triggered by infection, the hunt has been on for some time to identify a possible specific infection that might trigger autoimmune thyroid problems. One of the most intriguing suggestions, described by US surgeon Mr David V. Feliciano in the American Journal of Surgery in November 1992, was that Graves’ disease might be sparked off by a food-poisoning bug known as Yersinia enterocolitica, a distant relative of the plague bacteria.

Although Y. enterocolitica has not proved to be as significant as Feliciano suspected, a study published in the journal Clinical Microbiology and Infection in 2001 reported that patients with Hashimoto’s thyroiditis also had a 14-fold increase in Y. enterocolitica antibodies – so the question is still open.




Is Stress to Blame?


Over the past few years, there has been increasing evidence that, in a number of illnesses, the immune system is weakened by negative mental states such as fear, tension, overwork, anxiety and exhaustion – in a word, stress. So, could stress be responsible for autoimmune thyroid problems? The answer seems to be yes, especially in the case of Graves’ disease.

Doctors in the 19th century observed that Graves’ disease often followed a period of severe emotional stress – a frightening episode or ‘actual or threatened separation from an individual upon whom the patient is emotionally dependent’. One 19th-century doctor, Bath-based physician Caleb Hillier Parry, described the onset of symptoms in the patient ‘Elisabeth S, aged 21’:

[She] was thrown out of a wheelchair in coming fast down hill, 28th April last, and very much frightened, though not much hurt. From this time she has been subject to palpitation of the heart, and various nervous affections. About a fortnight after this period she began to observe a swelling of the thyroid gland.

Today, Dr Mark Vanderpump, secretary of the doctors’ organization the British Thyroid Association, observes:

When compared with people without thyroid disease or patients with toxic nodular goitres, patients with Grave’s more often give a history of psychological stress before the onset of hyperthyroidism through immune suppression followed by immunological hyperactivity. The same phenomenon is seen post pregnancy as well when the immune system is suppressed during pregnancy and relapse follows delivery.

In Norway and Denmark, the incidence of hyperthyroidism increased during the first years of the Second World War. In their book Thyroid Disease: The Facts, Drs R.I.S. Bayliss and W.M.G. Tunbridge mention research showing a significant rise in the incidence of Graves’ disease in Northern Ireland since the start of political troubles in 1968. More recently, researchers reported a dramatic fivefold increase of Graves’ disease in eastern Serbia during the war in the former Yugoslavia.




Significance of Life Events


Back in 1991, a team of Swedish researchers found that those developing Graves’ had often suffered an unhappy event in the recent past. The death of a close relative or friend was reported by 15 per cent of Graves’ patients compared with 10 per cent of a control group. The disease was also more likely to strike those who were divorced or less happy with their jobs – suggesting that long-term anxiety, unhappiness and other negative feelings could be a factor.

In 1998, Japanese researchers reported in the journal Psychosomatic Medicine that women diagnosed with Graves’ disease were seven-and-a-half times more likely to have experienced stressful life events although, curiously, the same finding did not hold true for men. In 2001, another study, reported in the journal Clinical Endocrinology, found a five-and-a-half-fold increase in ‘life events’ in individuals with Graves’ compared with those with toxic nodular goitre and those without thyroid problems. Intriguingly, in this study, people with Graves’ had also experienced more happy – but still potentially stressful – events like a promotion, a pay rise, getting engaged or married, or having a baby.

None of these studies prove conclusively that stress is to blame for triggering Graves’ disease, but they do suggest a significant connection. However, fewer connections have been found linking stress with Hashimoto’s thyroiditis. Clearly, more research is needed to unravel the precise mechanism by which stress may tip the thyroid into overactivity and to determine whether it is a factor in thyroid underactivity.




Smoking


Smoking has long been a known risk factor for the thyroid eye disease Graves’ ophthalmology (see Chapter 8). However, its role in Graves’ disease has been less clear. Nevertheless, the evidence is beginning to stack up. In the 1998 Japanese study mentioned above, smoking was found to be an independent risk factor for women developing Graves’. This finding was echoed in a Danish study, published in the journal Thyroid in January 2002, in which 45 per cent of women diagnosed with Graves’ disease were current or former smokers, compared with 28 per cent of those with toxic nodular goitre and 23 per cent of those with autoimmune hypothyroidism.





Конец ознакомительного фрагмента. Получить полную версию книги.


Текст предоставлен ООО «ЛитРес».

Прочитайте эту книгу целиком, купив полную легальную версию (https://www.litres.ru/patsy-westcott/the-healthy-thyroid-what-you-can-do-to-prevent-and-alleviat/) на ЛитРес.

Безопасно оплатить книгу можно банковской картой Visa, MasterCard, Maestro, со счета мобильного телефона, с платежного терминала, в салоне МТС или Связной, через PayPal, WebMoney, Яндекс.Деньги, QIWI Кошелек, бонусными картами или другим удобным Вам способом.