In this saga dealing with the little known consequences of hypothyroidism, let’s now look at the scalp, hair and nails. As already seen for the skin, they can tell us much about the existence of a defective thyroid function.

There is often an abnormal hair loss all over the scalp, in contrast to the more localized loss on the front and on the top of the head due to an excess of androgens in men, typically the consequence of an inherited predisposition. Failing hair growth can of course also result from other causes, such as an iron deficiency, which needs to be systematically examined. If detected in time, the hair loss from hypothyroidism can generally be reversed and some re-growth achieved, which is of great consolation to patients correctly diagnosed and treated. Other patients can often suffer from alopecia areata, when sudden, sometimes brutal hair loss occurs, causing patches to appear on the scalp. This is typically linked to autoimmune issues and may suggest an autoimmune thyroiditis, causing hypothyroidism.

Sometimes there is a loss of hair in the eyebrows and eyelashes. The loss in the outer part of the eyebrows only occurs in some patients but when this symptom is observed, a diagnosis of hypothyroidism is assumed (a symptom known as “pathognomonic”).

As far as nails are concerned, I think they represent an excellent indication of thyroid status, although this information is often masked by other factors that can also cause a weakening of the nails. These other factors cover a large array of nutrient deficiencies from calcium to zinc but also various vitamins and unsaturated fatty acids. Hypothyroid patients often complain of brittle nails, and of their nails easily splitting or cracking. They are unable to let them grow by themselves, or they must constantly file them down to remove the small bumps that keep appearing.

Overall, when it comes to hair and nails, we talk about dryness: dry and breaking nails, dry hair that breaks and splits and is often flat and lifeless. The hairdresser may sometimes be the first one to notice the initial signs of deterioration in thyroid function...

Anaemia represents a very interesting marker to start the search for subclinical hypothyroidism. Indeed, the relationship between anaemia and hypothyroidism is well known and has been the subject of many publications. Please consult the conference on my website www.gmouton.com (headings Conferences – Functional Hormonology – Thyroid). The link between the two can be easily explained: Thyroid hormones are a must to stimulate the production of erythropoietin by the kidneys. This hormone, which is none other than the infamous EPO so highly publicised among athletes, in turn stimulates the activity of the bone marrow producing red blood cells that carry haemoglobin.

A strong link has also been established between hypothyroidism and iron deficiency, and because you need iron to synthesize haemoglobin, it this provides us with a second cause of anaemia, independent of the first one already explained by the kidneys (they all add up). The lack of iron as such contributes to tiredness, an issue hitting a majority of hypothyroid patients, but we'll return to this topic later.

The role of thyroid hormones in the kidneys far exceeds the necessary stimulus for the synthesis of erythropoietin. There is in fact a strong link between hypothyroidism and renal failure, which is not explained on the physiological level and therefore largely unknown by the medical profession. The relationship is none the less strong and it is sometimes maddening to see so much ignorance, especially in moderate cases when the impairment of renal function can still be recovered. Admittedly, the thyroidologists rarely speak to the nephrologists and vice-versa: and we have to ask; how many problems arise from the aberrant “compartmentalising" of the human body by the medical profession?

Let’s continue on our journey to cover all the clinical signs, symptoms and dysfunctions of the body that might betray hypothyroidism, without forgetting that no patient suffer from all of these problems at once. One symptom alone is enough to raise a suspicion, but of course, the more symptoms that are present, the greater the likelihood that the patient suffers from an underactive thyroid. However any final diagnosis must be based on objective biological evidence, which serves to support the clinical signs.

We left our discussion with kidney failure and anaemia, but these two conditions are also other linked together in fact, which we have not previously specified. We should also mention additional disturbances of the urinary tract: the frequent need to urinate especially during the night (called nocturnal pollakiuria), water retention or oedema. This last topic is of great importance as we find it in many cases and in many forms: facial puffiness, bags under the eyes, swollen eyelids (especially upon rising), swollen fingers (resulting in a difficulty to remove rings), swollen legs and ankles, etc.

To be honest, these conditions don’t just come from weakness in the kidneys, but also a lack of combustion of metabolic waste, which is the role of fat burner played by the active thyroid hormone T3. It comes from the activation of the enzyme that fixes L-Carnitine on fatty acids, allowing them to be imported into the small factories that produce energy in the form of ATP (the mitochondria).

In the same vein we find many hypothyroid patients suffering from what we call tunnel syndromes, which are due to the compression of small bones and ligaments through which certain nerves pass. The most well known example of this is carpal tunnel syndrome where the median nerve is compressed resulting in tingling and pain in the fingers, especially at night. It is totally unnecessary to operate on these patients (often bi-laterally): the correction of the underlying hypothyroid condition is usually sufficient to cure them!

We progress to the next disorder, an absolute classic of insufficient thyroid function: hypercholesterolemia (high cholesterol)is all too often "treated" with statins when a simple rebalancing of thyroid function normalizes cholesterol levels almost every time, as long as a good diet is also implemented. As with the other cited links, you will find all the scientific evidence on my website www.gmouton.com (under “Conferences – Functional Hormonology – Thyroid)

As a logical continuation of this, let’s now tackle, the cardiovascular disease, as their relationship with hypothyroidism is well recognized; whether atherosclerosis (blocked arteries), coronary artery disease (whereby the coronary arteries are specifically affected), and hypertension. It is interesting to note that hypertension resulting from a thyroid weakness primarily affects primarily the diastolic blood pressure (the lower value when your blood pressure is taken). One can easily guess the stimuli leading to these problems: an accumulation of cholesterol and various metabolic wastes, water retention and even an increase in homocysteine (hyperhomocysteinaemia, is a well-known risk factor).

Still following the role of thyroid hormones as the key metabolic activator, there can be an increase in triglycerides (known as hypertriglyceridemia), a type of fat exclusively produced from sugars and starches. This is yet another cardiovascular risk factor plus, for some, an increased tendency to develop type II diabetes, as a consequence of insulin resistance.

Moreover, clinicians see a familiar link with hypoglycaemia, which can derive from an underactive thyroid (as in adrenal insufficiency). It must be reiterated that these feelings of hunger and general weakness should not lead to the intake of fast releasing sugars, nor even starchy foods eaten on their own. A handful of nuts (almonds, walnuts) or a small tin of sardines will resolve this “moment of weakness”!

To conclude the previously discussed issues concerning the negative impact of hypothyroidism on vascular health, blood pressure, and cardiovascular risks factors (cholesterol, triglycerides, homocysteine, glucose, insulin), we should not be surprised by the anti-atherogenic effect of corrective thyroid treatment, as highlighted by many publications. For more details, I refer you to the heading “Conferences – Functional Medicine – Thyroid” on my website www.gmouton.com (free download).

Continuing with the cardiovascular system, there is another symptom largely unknown, but indeed published (and where I have had to deal with a flagrant case). This is the lengthening of the QT interval seen during an electrocardiogram, an anomaly that disappears with the correction of the thyroid status. Here again is a cardiovascular factor that may worry your cardiologist, as not all of them are aware of the possible connection with the thyroid gland. Yet more bitter fruit from the division of medicine into specialties too independent from one another.

We now turn to the effects of hypothyroidism on the nervous system. I want to first highlight the importance of drowsiness: patients often say that they fall asleep anywhere, as soon as they cease their activities. Sleep can be extended (until 10:30 or even 12 noon). Sleep is deep, with a very difficult morning awakening, requiring much time...and several coffees. It is not at all unusual to encounter simultaneously one of these symptoms and its direct opposite (as has already been discussed with weight gain and weight loss). In all scenarios, sleep is reported as non-restorative and the patient wakes up as tired as they were when they went to bed, without any improved motivation or vitality.

A typical manifestation of mild cases of hypothyroidism is to overload the agenda, preferring multiple activities, often messy and inefficient as a result. This compensatory hyperactivity energises patients because it stimulates thyroid function (just as sports activity of moderate intensity does, and often sought by such patients for this reason). However, once the engine stops, it results in total collapse and we know patients whose overflowing activity during the day is crushed once they are home. They can scarcely drag themselves from the sofa to their bed and have no energy whatsoever to prepare a decent evening meal. As far as their Sundays are concerned, I'm sure I don't need to spell it out, hence the notion of the Sunday Syndrome.

Let’s continue in the neurological domain with hearing disorders: tinnitus, loss of hearing, vertigo, Ménière's disease…We find an almost complete range of pathologies of the inner ear; even if the ENT doesn't necessarily make the connection!

Patients can be affected by a wide range of muscle disorders: cramps (at night, but not necessarily, also during exercising) contractures, or true myopathy (muscle inflammation with marked increase of specific enzymes, CPK, detected during a blood test). The tendency for muscle contractions can sometimes cause acute blockages: torticollis, back pains, lumbagos that are in fact paralysing for patients, condemning them to stay on their sofas… The scale of these muscle contractions should always be an alert to look for an underactive thyroid, correction of which will constitute the only way to achieving lasting relief.

So, what about the infamous fibromyalgia, a label stuck a little too easily on the back of hyperalgesic patients? What if, once again, it is another low blow from the thyroid?

From the beginning of the 20th century, endocrinologists had already noticed the link between thyroid insufficiency andarthritic joint pain; it is in fact one of the most constant symptoms! Other studies, this time dating from the end of the last century, show the prevalence of rheumatoid arthritis to be three times higher in patients with thyroid dysfunction.

For around fifteen years now, several authors have associated fibromyalgia with an insufficient level of active thyroid hormone T3. Whilst the first articles on this subject came out between 1997 and 2003 in minor medical journals, it was the renowned Journal of Rheumatology that published a study in 2004, the results of which established a conclusive link between fibromyalgia and autoimmune thyroid disease. You will find all these references on my website www.gmouton.com, under the heading “Conferences – Functional Hormonology – Thyroid” (free download).

Also in the neurological field, it appears that thyroid hormones exert a neuroprotective effect towards axonal pathologies (axons are the nerve fibres, the long slender extensions of the neurons that transmit messages to other neurons). Some can even see the demyelination of the neurons as a complication of autoimmune thyroid disease. When the myelin sheath (this insulation that protects axons just like the colourful plastic sheaths that insulate electrical cables) is attacked by autoantibodies, multiple sclerosis ensues, anautoimmune disease affecting the nervous system. However, the link between MS and autoimmune thyroid disease has been well published, as is the fact that in some experimental models of demyelination, thyroid hormones improve and accelerate remyelination….

We stay in the neurological sphere to list a series of dysfunctions and proven pathologies for which an association with hypothyroidism has been the subject of scientific publications. Namely these are mood disorders, depression, manic depression or bipolar disorder, cognitive impairment, lack of concentration, memory loss, melancholy, anxiety, panic attacks, dementia, and most psychoses. It is also well recognized in the world of psychiatry that thyroid hormones can dramatically improve the efficacy of drug treatment with antidepressants or psychotropic drugs.

One might also wonder about the possibility of a therapeutic effect of thyroid hormones in their own right, instead of first prescribing drug treatments. It is not uncommon to see some psychiatrists prescribe T3 and I would say that, in general, in patients suffering from severe depression, they tend to go for a very high dosage!

How many patients receive antidepressants to treat their depression when in reality they are suffering from undiagnosed hypothyroidism? I do not pretend that this is an absolute rule, but a search for other signs and symptoms that could suggest a thyroid insufficiency is of the utmost importance to avoid missing the true diagnosis. We must look for these too often unaccounted for links, especially if the root cause of the depression or anxiety is at the level of the thyroid. This will yield much better results, as is the rule in medicine when you treat the underlying cause!

Some authors even go so far as to claim that bipolar disorder doesn’t exist as such and that it is “always” a symptom reflecting hypothyroidism. I wouldn’t go that far but, in my clinical experience, I must admit that it has very often been the case…

It is now time to consider the consequences of hypothyroidism on other organs such as the gallbladder and liver. Hypothyroidism is a very common cause of gallstones and there is also a clear link with concomitant hypercholesterolemia. Surprisingly, it is often the removal of the gallbladder or cholecystectomy that will reveal thyroid disease. It must be said that any surgery can lead to the awakening of a latent hypothyroidism, undoubtedly due to the trauma that this act represents. In the medical literature the frequent occurrence of thyroid failure following car accidents that have caused "whiplash" or whiplash syndrome has been cited, because the thyroid horns can be “broken” at the time of the injury to the cervical spine.

On the hepatic level, you should know that the vast majority of enzymatic reactions occurring in the liver are hampered in case of thyroid weakness, whether it is protein synthesis (for example, like sex hormones binding globulin or SHBG) or all of the detoxification reactions. In some hypothyroid patients, we can even see abnormally low levels of liver enzymes, transaminases and gamma-GT, a deficit that should arouse suspicion. Again, the opposite is also true, and given the essential role of thyroid hormones in lipid degradation, we can observe overloaded hepatocytes, expressed by the increase in transaminases. It is non-alcoholic steatohepatitis (NASH), also provoked by the excessive consumption of fructose. Links between hypothyroidism and hepatocellular carcinoma (liver cancer) on one hand, and Chronic Hepatitis C on the other hand, have been published and are probably the consequence of diminished immune defences…

The next step concerns the intestines, starting by the impressive prevalence (up to 15% of cases) of autoimmune thyroiditis in patients with celiac disease (severe allergy to gluten). In the United Kingdom nutritionists go as far as to prohibit gluten for all patients with autoimmune thyroid disease, considering they are all, more or less, suffering from an allergy to gluten cereals! In any case, the guidelines of the medical authorities are telling: “we must always look for celiac disease in case of autoimmune thyroiditis and vice versa”.

Remaining focused on the subject of the intestinal mucosa, you should know that it hosts a crucial enzymatic reaction: the conversion of betacarotene into Vitamin A, the result of a reaction controlled by the enzyme betacarotene-15-15-dioxygenase, which is predominantly expressed in the intestinal mucosa. Consequently, this becomes an interesting marker for anyone suffering at this level and therefore of leaky gut syndrome. Even more stunning, this enzymatic conversion is accelerated by thyroid hormones! There is clinical evidence of this enzyme control, namely the orange hue of the palms and/or sole of the feet that can be seen in some hypothyroid patients due to the accumulation of beta-carotene. All of these are published: visit my website www.gmouton.com and the heading “Conferences – Functional Hormonology – Thyroid” (free download).

Thyroid hormones also activate several enzymes that are involved in the metabolism of vitamin B2 or riboflavin, in particular converting riboflavin into its active physiological form, flavin adenine dinucleotide or FAD. This enzymatic cofactor plays a key role in many enzymatic reactions, including the recycling of homocysteine, hence the propensity to hyperhomocysteinaemia that we have already mentioned as being a cardiovascular risk factor.

Let‘s now look at all the signs and symptoms likely to reveal a thyroid weakness in children. This is not intended in any way to suggest prescribing thyroid hormones for the little ones, unless it is an absolute necessity of course, but rather to support thyroid function if need be. For example, it may be a matter of giving iodine, often deficient in children, just as long as the deficiency is clearly established by a urine test (as I am not in favour of giving iodine blindly). Let’s also not forget the use of ultra sound of the thyroid to assist us to identify an abnormal gland (one lobe only) or hypotrophy (meaning too small, less than 2 to 3 ml per lobe).

The first thyroid doctors, a century ago, knew well (in reality better: there were no blood tests!) the clinical aspect of hypothyroidism, especially in children. They are constipated, with bouts of diarrhoea, when blocked stools ferment to the point of making the cork 'pop' by its liquefaction. Their abdomen is abnormally sensitive, even painful at the right iliac fossa (the ileocecal valve bursting with intestinal yeasts). The tonsils and / or adenoids appear inflamed, enlarged to the point of making breathing and swallowing difficult.

Hypothyroidism causes looseness of tendons explaining diminished tendons reflexes (these being the ones that are evaluated with a small hammer). It is therefore not surprising to find some flat feetin children suffering from hypothyroidism. Thyroid hormone powerfully activates growth so we wouldn’t be surprised to find a growth delay: a child too small for his age (according to the height and weight curves) should arouse suspicion about the possibility of hypothyroidism, even if there are no other symptoms present. This is a diagnosis not to overlook, because correction could restore proper growth.

Nocturnal enuresis (bedwetting) is a very interesting sign: these children most often sleep very deeply and the wakening normally triggered by the feeling of a full bladder (especially given the frequent need to urinate or pollakiuria) doesn’t happen. So many family dramas could be avoided if only in all those cases a proper diagnosis was made early….

Maternal hypothyroidism can have adverse effects on the foetus and there is a strong relationship with a relative decline in IQ (compared to what would have happened under normal circumstances). Unfortunately also found in these undetected and untreated cases can be developmental brain disorders. Links with attention deficit and hyperactivity have been demonstrated and published. In an animal model (rats) where maternal hypothyroidism was induced via the administration of an anti-thyroid drug, the offspring displayed hyperactive type behaviour.

All the references for the publications cited in these blogs about the thyroid can be found under the heading “Conferences – Functional Hormonology – Thyroid” when you visit my website www.gmouton.com (free to download).

To finish this penultimate blog, let’s briefly discuss how to specifically identify hypothyroidism in the "fathers", by describing the male symptoms, especially as we will dedicate the next and final blog to all the manifestation of hypothyroidism occurring in the “mothers” (and believe me, an entire blog dedicated to this subject is necessary!).

Hypothyroid men will often complain of a low libido, premature ejaculation, or erectile dysfunction. These problems have typically driven biological research to examine the level of male sex hormones, therefore conspiring to completely miss an underactive thyroid. Even more interesting is the fact that the medical literature clearly attests that the correction of an underactive thyroid may improve all these “male” complaints…

I devote a grand total of 33 slides to the topic of signs and symptoms of hypothyroidism in women (see heading “Conferences – Functional Hormonology – Thyroid” on my website www.gmouton.com; free to download)! The subject is really of great importance because it is the whole ensemble of female reproductive life that is at stake.

Let’s start with all the possible and imaginable menstrual abnormalities and symptoms! Typically, periods can be too far apart, with cycles exceeding 30 days or those that could even go up to several months. The ovarian dysfunction (or the pituitary dysfunction from where the instructions originate) can sometimes go as far as anovulation and as a result there is no longer a period. We must also not forget the plethora of cases of "early menopause" at 42 or 45 years old, which more often than not reveal an underactive thyroid. If corrected in time, menstruation returns as though nothing had happened until the normal age of the menopause, giving longer protection against cardiovascular disease.

Make no mistake, cycles can also be shortened: it is indeed the case that symptoms can slip towards either extreme…. Hypothyroid patients often complain of heavy periods (menorrhagia), both in amount of blood loss and duration. Many cases of painful periods (dysmenorrhoea) and an increased frequency of PMS (premenstrual syndrome) are often noted and exacerbated in hypothyroid patients. Other factors contribute to premenstrual complaints besides the lowering of thyroid activity. These include deficiencies in vitamin B6 (or pyridoxine), magnesium, zinc, and dihomo-gamma-linolenic acid (DGLA), an omega 6 fatty acid that constitute one of the two precursors to anti-inflammatory prostaglandins (along with the omega 3 fatty acid EPA).

All these disturbances of ovarian function of course do not help promote fertility. However, the loss of fertility – even infertility in worst cases – result from several other phenomena linked to thyroid insufficiency, especially the lack of growth, starting with the tremendous need for new tissue growth triggered by the implantation of the fertilized egg in the uterine wall.

I must also mention the risk of foetal loss, or miscarriage, typically occurring between the sixth and tenth week of pregnancy, when the need for thyroid hormones in pregnant women significantly increases and cannot be satisfied by a gland already pushed to its limits. There is an increased risk of obstetric or neonatal complications, not to mention the occurrence of premature contractions (see blog 5/9 relating to muscular issues) and therefore a risk of premature delivery.

Links have also been established between autoimmune thyroiditis and endometriosis as well as with autoimmunethyroiditis and polycystic ovary syndrome (PCOS). Recalling the problem of diastolic hypertension occurring in hypothyroid patients (see blog 4/9), we should not be surprised by the increased risk of gestational hypertension. When this becomes associated with a leakage of proteins in the urine we then refer to it as pre-eclampsia (not to mention eclampsia which is much rarer but very serious for both mother and baby).

We must also mention the potentially adverse effects on the foetus, and mention again the consequence of reduced IQ already discussed in blog 8/9. Furthermore, it could result in a low birth weight, not only due to a possible premature delivery but also due to a lack of growth caused by the depleted delivery of thyroid hormones. Finally, in women who have just given birth, there is a significantly increased risk of autoimmune thyroiditis due to the immune disruption caused by the presence of the paternal genes. It affects up to 5% of women and is the major cause of post-partum depression…

After all this, I dare not even talk about the link (which is clear to me) with breast cancer, which is the subject of an increasing number of publications: look at the slide show on my website!

That’s it; the 'party' is over! 52 weeks and 52 blogs later, I hope you have learnt some interesting things. Without really planning the subject of the blogs, we have still managed to cover all the major areas of Functional Medicine.

Unsurprisingly, no less than 20 of my blogs have been dedicated to food, exposing the greatest myths and most common dietary errors. The significant damage caused by sugars, fructose, cereals, gluten and animal milks have all been covered. Also, attention was given to the overload of eggs (without respecting the winter break imposed by nature) and the insufficient consumption of oily fish and good quality plant oils. Many of my blogs have dealt with fats, both good and bad: let’s no longer demonize cholesterol or even animal fats in general, and let’s avoid hydrogenated vegetable oils (trans fatty acids) like the plague!

Fats also play a critical role in the lubrication of the intestinal mucosa, the gateway for absorbing all of our nutrients, especially the fat-soluble vitamins and other micronutrients that are difficult to absorb such as iron, calcium and most of the B vitamins. It is with great pleasure that I have wrung the neck of numerous myths that have misled the general public and generate tragic dietary errors and health problems.

Don’t believe anyone who says: “you become fat because you eat fats”, “a calorie is a calorie”, "calcium should always come from dairy products” or “whole grains are the base of the food pyramid”. We've had enough of all these dogmas that, in reality, have no scientific basis! They are just total nonsense that everyone repeats, including some doctors, with total disregard of the biological reality.

We are all different and from an early age it is essential to personalise dietary advice because the balance of the major food groups (proteins, fats, carbohydrates) depends on genes and even on the intestinal flora unique to each individual. For some, this flora has suffered tremendous damage by aggressive antibiotic therapy, which selects the most efficient microorganisms to digest complex sugars, which leads to greater extraction of calories for these subjects. Do not listen to dieticians who insist that you count calories, drink orange juice before breakfast and swallow a rice cake as a snack: stop the massacre...and find the right people to help you eat well.

Besides the blog on antibiotics, two others deal with the risks of drugs and their deleterious consequences for digestive health (proton pump inhibitors) and bone health (biphosphonates). Three other blogs are aimed at the correct interpretation of laboratory tests and some errors of interpretation that are all too frequent. Let’s recall the founding philosophy of Functional Medicine, which is the restoration of physiological and biochemical functions as close as possible to equilibrium. Here is a dogma that deserves to be supported: “let’s restore normality!’.

This principle clearly applies to endocrine function, both thyroid hormones (11 blogs in total) and adrenal hormones (4 blogs), and even female sex hormones after the menopause (2 blogs). This approach implies that even mild or moderate imbalance (sometimes mistakenly called “subclinical”) deserves consideration by the medical profession. Do not wait for this to be proven inadequate or for the obvious deficiency to be recognised: let’s intervene before the dysfunction has yet to cause a major illness. We will be much more effective at this stage: prevention first! Why wait for a disease that will then require medication to treat it?

To please the pharmaceutical industry? Yes, it is true, a drug can often perform miracles in a crisis and it is ideally suited to solving the most acute cases. But taken chronically, these chemical products push us little by little further away from the physiological equilibrium that is so desirable. Therefore, let’s do all that we can to make sure we don't need it!