Effects of low-carbohydrate diet therapy in overweight subjects with autoimmune thyroiditis: possible synergism with ChREBP

Abstract

The thyroid is one of the metabolism regulating glands. Its function is to determine the amount of calories that the body has to burn to maintain normal weight. Thyroiditides are inflammatory processes that mainly result in autoimmune diseases. We have conducted the present study in order to have a clear picture of both autoimmune status and the control of body weight. We have evaluated the amount of either thyroid hormones, or antithyroid, or anti-microsomal, or anti-peroxidase antibodies (Abs) in patients with high amounts of Abs. In a diet devoid of carbohydrates (bread, pasta, fruit, and rice), free from goitrogenic food, and based on body mass index, the distribution of body mass and intracellular and extracellular water conducted for 3 weeks gives the following results: patients treated as above showed a significant reduction of antithyroid (−40%, P<0.013), anti-microsomal (−57%, P<0.003), and anti-peroxidase (−44%, P<0,029) Abs. Untreated patients had a significant increase in antithyroid (+9%, P<0.017) and anti-microsomal (+30%, P<0.028) Abs. Even the level of anti-peroxidase Abs increased without reaching statistical significance (+16%, P>0064). With regard to the body parameters measured in patients who followed this diet, reduction in body weight (−5%, P<0.000) and body mass index (−4%, P<0.000) were observed. Since 83% of patients with high levels of autoantibodies are breath test positive to lactase with a lactase deficit higher than 50%, this fact led us to hypothesize a correlation with carbohydrate-responsive element-binding protein and therefore a possible role of carbohydrate metabolism in the development and maintenance of autoimmune thyroiditis associated with body weight increase and slower basic metabolism.

Full text:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5028075/?report=classic#pq=Qs4Ixc

Thanks, downloaded for perusal later.

Hypothyroid is often blamed on low carb diets when obviously the vast majority of cases, like all diseases, occur in people eating low fat. Probably why my hypERthyroid didn't get blamed on my diet.

Nevertheless I'm still fine tuning and so far it appears diet, exercise and light exposure don't appear to relate to its dysfunction, but daylength might.

I was relatively stable on 20mg carbimazole for a long time before the thing suddenly crashed. Went high again without the drug and needed 40mg to stop the tremors and pounding heart, then went back to 20mg and after a few weeks went low. Reduced to 10mg and went high. Back to 20mg but had some 5mg prescribed (which can be split into 2.5) so next time I went low I reduced to 15mg but only lasted about a week before going back to 20 again. Bloody frustrating so maybe this paper or some of its references may help find out why the variation which appears to occur in winter.

Or maybe it's the Brussels sprouts. Or the purple sprouting broccoli. Grrrr.

OK paper not directly relevant but interesting, and led to these

http://www.cell.com/cell-metabolism/fulltext/S1550-4131(06)00238-5

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC409910/

about ChREBP, which is involved in glucose and fat sensing and processing, which led to

https://www.jstage.jst.go.jp/article/endocrj/55/4/55_K07E-110/_article

but I haven't got beyond the abstract yet.

More stuff that dieticians will never have heard of, no doubt, to read some of them you'd think the endocrine system hadn't been discovered yet.

"Insulin can't make you gain weight, it doesn't have any calories!" or words to that effect. They dismiss the effects of insulin as "the insulin fairy" yet praise someone calling herself Plant-Based Pixie. Then they claim to be scientific.