Putting The Cart Before the Horse: The Child Obesity And Thyroid Study

A new study on childhood obesity has hit the headlines. Doctors at the Regional Hospital of Bolzano in Italy measured serum free T3, free T4 (two types of thyroid hormones, TSH (thyroid-stimulating hormone, thyrotropin), performed a thyroid ultrasound, and measured antithyroid antibodies in a group of overweight and obese children. There are some rather questionable conclusions from this study which are drawing most of the attention, and which we will get to in a minute, but some of the other correlations deserve a bit of attention first. To quote:

Results: A total of 23 children (12.4%) showed antithyroid antibodies and an ultrasound pattern suggestive of Hashimoto’s thyroiditis (group A). Of them, 20 (10.8%) showed antithyroid antibodies and normal ultrasound (group B). A total of 70 subjects (37.6%) showed absent antithyroid antibodies and an ultrasound pattern suggestive of Hashimoto’s thyroiditis (group C), and 73 children (39.2%) showed no thyroid antibodies with normal ultrasound (group D). TSH was higher in groups A and C compared with groups B and C, and controls

Notice that out of the overweight children only 39% (group D) had both normal thyroid structure, antibodies, and hormones! More than half of the kids have thyroid abnormalities.

It is very well established that underactive thyroid causes weight gain, and overactive thyroid causes weight loss and wasting. A study that came out just this March found that even small increases in TSH (levels of TSH have an inverse relationship to the thyroid hormones you need to function, and which are replaced in the deficient) WITHIN what has historically been considered normal, are associated with weight gain. Now imagine if the thyroid changes are the CAUSE of the weight gain, as any experiment with altering thyroid hormone levels would support. Then the "mystery" of increasing childhood obesity would be much less of a puzzle, or at least, an avenue towards treating it would be clear.

The Claim

The doctors behind the childhood obesity study however, do not believe that thyroid problems are the cause of the obesity however, but rather, reverse the proposition, and suggest that obesity is the cause of the thyroid problems (seen here on the BBC and Reuters for example).


Why the cause, rather than the result? Well Hashimoto's thyroiditis, the most common cause of thyroid insufficiency in the US, and a major cause throughout the world, is an autoimmune disorder. Continual attack by the immune system causes the thyroid to swell and interferes with thyroid function. Hashimoto's disease is generally diagnosed in no small part through the detection of antibodies and while the study found that no less than 12.4% of the children in the study had the classic signs of Hashimoto's disease (a rather large number by the way, if the sample is representative) many of the children had a swollen thyroid like Hashimoto's disease, but lacked the antibodies.

There was reason to think that the thyroid was indeed swollen and abnormal (and not just naturally bulky) because one of the thyroid hormones was out of balance, and TSH levels [which when high, indicate insufficient thyroid (T3 and T4) hormones], were elevated over controls, and moreover, correlated with the degree of obesity.

In other words, a full 37.6% of the overweight and obese children looked as if they might have a hypothyroid problem, and tests were pointing to the appropriate associated hormone levels, BUT the doctors could not detect an autoimmune attack on the thyroid. Because they cannot detect an attack on the thyroid the doctors behind this study suppose that a "low-grade inflammation state" CAUSED by being overweight is making the thyroid malfunction.

Other Explanations Perhaps?

Doubtless, you can see how this novel theory might be incorrect, but the problem is worse than this. Your adaptive immune system, the portion of your immune system that can learn from past attacks and which vaccines are designed to train, is divided into two sections, the cell-mediated, or Th1-type immune response, and the humoral or Th2-type response. Both portions of your immune system work together to defeat viruses, bacteria, fungi, and other immune threats, but each is better at attacking certain types of threat. The Th2 system for example, produces antibodies, and is better at attacking bacteria, while the Th2 system includes T-cells that recognize and destroy a cell when it has been "hijacked" by a virus. Because each of the two 'wings' of the immune system are better at fighting separate threats, your body will tend to 'turn up' either Th1 or Th2 when it is under attack, and will 'turn down' the less effective half of the immune system.

The thing is, while Hashimoto's disease is recognized by antibodies, part of the Th2 system, the better portion of the cellular damage is caused by "a cell mediated autoimmunity induced by Th1 cytokines". The test for Hashimoto's disease thus is able to detect that there is a problem, when the Th1 portion of the immune system is able to recruit the Th2 to attack one's own body. Even when it recruits the Th2 system however, the Th1 remains dominant in Hashimoto's disease. To quote:

The above findings suggest that a Th1 pattern of immune response characteristic of cellular immunity is dominant in HT (Hashimoto's thyroiditis), whereas the predominance of Th2 cytokines in GD (Graves' Disease) indicates a humoral pattern of immune reaction.

This study that I just quoted also helps to highlight the importance of thyroid disease as a cause, rather than as an effect of obesity. Both Hashimoto's thyroiditis and Graves' disease are autoimmune disorders where the immune system attacks the thyroid gland.

Hashimoto's disease, where the Th1 portion of the immune system is dominant, causes hypothyroid, with the body not getting enough of the T3 and T4 thyroid hormones. A shortage of T3 and T4 thyroid hormones will turn down a person's metabolism, and just as one would expect, Hashimoto's disease tends to make those who suffer from it become overweight.

Graves' disease on the other hand, features a dominant Th2 immune attack on the thyroid gland, and instead of causing an underactive thyroid, producing too little T3 and T4 hormones, Graves' disease induces an OVERACTIVE thyroid, that produces TOO MUCH T4 and T4 thyroid hormone. Because of the excess of thyroid hormone, Graves' disease causes people to LOSE WEIGHT.

So, just to restate and lay everything out, when the immune system malfunctions and attacks the thyroid, it produces different results depending on whether the Th1 orTh2 portion of the system is dominant in the malfunction. When the Th1 is dominant, amongst other symptoms, the person is likely to become overweight, with their metabolism depressed. When the Th2 portion of the immune system is dominant, the victim's metabolism is revved up, and the person loses weight (along with other symptoms).

In both of these cases, there is a serious malfunction, but the Th1 attack and underactive thyroid is detected when a test picks up that the OTHER, non-dominant side of the immune system is attacking the body. Diagnosis of a Th1 autoimmune attack thus depends on the detection of a secondary attack by the other half of the immune system.

Now your body is not supposed to attack itself. Might it be, that even if one portion of your immune system decides to attack your own body, that the other half of the immune system would, in some cases hold off? As everyone knows, immune reactions such as allergies can vary widely in severity. What if a person's immune system launched a more mild autoimmune attack? Might it be that only half of the immune system would go rogue?

In the Italian study, 12.4% of the overweight children had a full blown Hashimoto's type problem but 37.6% showed the signs that one might expect if half, rather than ALL of the immune system went haywire.

Yet another thing that might trigger a thyroid problem and accompanying obesity.

An AUTOIMMUNE reaction to one's own body is not the only thing that can cause thyroid swelling and dysfunction. A simple immune reaction will do the trick just fine. An immune reaction, with the victim suffering from an underactive thyroid would logically be triggered by a persistent virus, rather than a bacteria, because the Th1 portion of the immune system, which is stronger in attacking viruses, would be the portion of the immune system that would trigger thyroid suppressing damage. While my limited knowledge, and I suspect, modern medicine's limited knowledge prevent me from putting here a long list of appropriate viruses, there is one that can serve to make the point. Chronic hepatitis C, the third major type, for which there is now no vaccine is well known to cause thyroid problems, indeed including both autoimmune thyroid disease, and thyroid cancer. Hepatitis C also is a good example of how a virus could be a significant problem, and yet escape detection. Blood borne hepatitis is a major threat that can often be lethal, and both hepatitis A and B were known and identified by the 1970s, but by the middle of the decade, it had been established that neither hepatitis A or B was responsible for most blood-transfusion induced hepatitis. Despite this, nobody identified the causative virus until 1987. Hepatitis caused liver failure, a rather dramatic and distinctive outcome, and yet escaped detection for many years. The symptoms of an epidemic that tended to induce slight thyroid dysfunction or chronic thyroid infection by contrast, could be rather easily attributed to the lifestyle of those affected. There is no doubt that there is an epidemic of obesity around the globe, and while this cannot be said to constitute proof positive of an infectious cause, it is also difficult to imagine how such an illness, if it existed, would manifest itself differently.

Infectious Obesity

In fact, contagion induced thyroid illness would be only one of several mechanisms that have come to light over the past few years by which germs are able to cause weight gain.

Some viruses for example, force stem cells that COULD become fat cells to DO so, and moreover, they cause the new fat cells to take up more fat, becoming bigger.

cranial nerves VII and VIII and selected structures of the inner and middle ear. 1 Nervus vestibularis, 2 Nervus cochlearis, 3 Nervus intermediofacialis, 4 Ganglion geniculi, 5 Chorda tympani, 6 Cochlea, 7 Ductus semicirculares, 8 Malleus, 9 Membrana tympani, 10 Tuba auditiva Creative Commons Attribution ShareAlike 2.5

Damage to the chorda tympani nerve seems to make people like sweet, salty, and fatty foods more than they would otherwise, and ear infections as a small child seem to cause just this sort of nerve damage.

Another virus can double total body fat, and triple visceral fat in experimental animals, even when the infected and the control animals consume the same amount of food.

Compared to these problems, damaging and infecting a gland, preventing its proper function, is quite prosaic, even if the effects on the infected are dramatic. No fewer than 10 types of infectious agent, from viruses, to prions, to bacteria, have been found to cause obesity in experimental animals, or have been associated with obesity in humans.
Summing Up

The doctors of Bolzano may have found a new, and common type of autoimmune disease, or they may have found a mechanism by which infectious diseases induce obesity, and provided that their sample is representative, they have certainly established that many obese children have thyroid dysfunction of some sort, but to simply claim that being overweight causes the thyroid dysfunction, rather than the other way around, is remarkable........and not in a good way.

Whether the cause of this dubious conclusion is a lack of imagination, a lack of courage, or a desire to jump on the bandwagon of lifestyle modification advocacy is not clear, but the resulting failure and faulty logic is not difficult to detect.

There is a story here, and a big one likely to affect adults as much as children. History is replete with examples where science and medicine set aside, for a time, the facts and evidence in favor of moralizing and to avoid crossing past assumptions (and the distinguished people behind those false assumptions). Hopefully someone, perhaps even someone reading this, will see through the smoke of convention and punch through the sticky web of existing assumption to lead science and medicine forward against the dramatic advances of infectious illness and the ancient claws of the autoimmune.