low sodium / high sugars: Perhaps you lot already... - Thyroid UK

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low sodium / high sugars


Perhaps you lot already know this, but I didn't know a low sodium level can go with an underactive thyroid. Anyway, this is a good example of very clear explaining (though I'm not familiar with the website).


My sodium is low and my GP told me that this can make blood glucose show false highs - the readings are high when the sugars actually aren't. I have type 1 diabetes and my BGs have been running high for ages. Now that I've searched, it seems that it's the other way round: high blood glucose can cause false low sodium readings. (So on the blood count, low sodium does go with high sugar, but she had it backwards. Or she was right and I have it backwards?)

I'm not dehydrated and haven't got water retention swelling, and kidney function is always fine on regular tests, so I looked at the possible causes of low sodium and was interested to see hypothyroidism. As far as I know I *have not* got anything wrong with thyroid function this year.

I was also interested to see chronic pain can cause it - but it says severe, and mine isn't that bad these days (I have fibromyalgia). At least I wonder what counts as severe. Now I want to know the mechanism by which pain lowers sodium!

8 Replies

I note you also have fibromyalgia and one of our deceased Advisers also ran the Fibromyalgia Research Foundation. This link may be helpful. His Fibro patients only recovered with T3 I believe:-


muddlemand in reply to shaws

Thanks @shaws, I think I've read that before and it was probably you that linked to it. :) Is it you that sometimes mentions it's possible to be hypothyroid even with all blood results ok, including antibodies?

I have made a choice to ignore that possibility for the time being - all my bloods show that my thyroid is fine, and for the moment, I have enough variables to consider without this one more. Besides, I can't afford much private testing and getting this on the NHS seems like a battle too far. One chooses one's battles, you know.

... So ... assuming my thyroid really is ok, I have to assume it isn't the cause of FM in my case. (For now!) - FM is neurological anyway, isn't it? or at least, it can (should) be identified by MRI. Perhaps that isn't cause, only indication.

And just to confuse things more, I have the diagnosis of FM but am not 100% certain that it's a correct diagnosis. I have never had the tender points which are usually part of the criteria.

Vasopressin, the antidiuretic hormone (ADH), is synthesized as a peptide prohormone in neurons in the hypothalamus, to help regulate the amount of water in the body by controlling how much water is excreted by the kidneys. When water excretion by the kidneys is decreased, this retains more water in the body, and dilutes the sodium. Pain, stress, exercise, a low blood sugar level, and some disorders of the heart, thyroid gland, kidneys, or adrenal glands can stimulate the release of vasopressin from the pituitary gland, triggering the alteration in sodium levels.

So low sugars can cause higher sodium - but that wouldn't mean high sugars lower sodium, necessarily?

Do you know why pain and stress trigger more ADH to be released? It seems counterintertuitive to me, I'd have expected these things which (thinking as a layperson) increase adrenaline, to make us wee more rather than less (the extreme of adrenaline/stress being wetting yourself in terror!). Hypoglycaemia also triggers adrenaline, the anxiety/panic symptom. So I see that the list you give are all stresses, but I don't understand why they would make us retain water. VERY layperson reasoning, I know.

None of this is falsely high or low readings, though, of either sodium or sugars. Actually changing levels is different from making them look higher/lower than they are.

Whether we would wet ourselves in terror or not, is a function of the limbic system - responsible for a variety of functions including emotion, behavior, motivation etc. Bladder control requires an interplay of brain regions, and the pontine micturition centre, an area of the brain stem, is in constant contact with the bladder so that when pressure is building, it makes the preliminary decision to void. However, the prefrontal cortex can override the desire to urinate by sending an inhibitory signal to the brainstem, but under stressful conditions the inhibitory signals from the frontal lobe can themselves be overridden by the limbic system, a combination of brain areas that controls the famous “fight or flight” response. When we become stressed or anxious, electrical signals from the limbic system become so intense that the brainstem has trouble following the frontal lobe’s commands, and that’s why many people urinate more frequently before exams or going to the dentist say. In life-threatening situations, the limbic system’s orders become so urgent that the bladder empties outside of one's conscious control.

Exactly why pain and stress in particular trigger more ADH is above my intellectual pay grade, but by way of an explanation, it's useful to understand how it is triggered. The most important variable regulating antidiuretic hormone secretion is plasma osmolarity - the concentration of solutes in blood. Osmolarity is sensed in the hypothalamus by neurons known as an osmoreceptors, and those neurons, in turn, stimulate secretion from the neurons that produce antidiuretic hormone.

When plasma osmolarity is below a certain threshold, the osmoreceptors are not activated and secretion of antidiuretic hormone is suppressed. When osmolarity increases above the threshold, the osmoreceptors recognize this as their cue to stimulate the neurons that secrete antidiuretic hormone. Antidiuretic hormone concentrations rise steeply and linearly with increasing plasma osmolarity. Osmotic control of antidiuretic hormone secretion makes perfect sense: walking across a desert, the sun beating down, we'd begin to lose a considerable amount of body water through sweating. Loss of water results in concentration of blood solutes - plasma osmolarity increases and antidiuretic hormone is secreted, allowing almost all the water that would be lost in urine to be reabsorbed and conserved. Secretion of antidiuretic hormone is also stimulated by decreases in blood pressure and volume, conditions sensed by stretch receptors in the heart and large arteries. Changes in blood pressure and volume are not as sensitive a stimulator as increased osmolarity, but are nonetheless potent in severe conditions eg loss of 15-20% of blood volume by hemorrhage results in massive secretion of antidiuretic hormone.

Another potent stimulus of antidiuretic hormone for obvious reasons, is nausea and vomiting, both of which are controlled by regions in the brain with links to the hypothalamus.

I'm a T1. Low sodium doesn't cause falsely elevated BG. You're right. She's wrong.

muddlemand in reply to G2G2

Oh dear! I know doctors are human and can get muddled about details - and GPs have a huge amount of info, can't possibly memorise every single bit. In theory they should add "if I remember right..." or something... I look at doctors as resources, some are great for information but bad at empathy, so I see those as useful textbooks, others have a great bedside manner but may be technically less perfect. I'm quite new to this GP so i suppose it's good to find out now.

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