Hi all. I have been struggling with fatigue, unplanned weight loss ( only a little) and bowel issues overall. GP had only been able to diagnosis me with Non Alcohol Fatty Liver. GP does not think it is thyroid related but I cannot help but feel it is. They have not advise on treatments but only with a plan to monitor things. In the mean time I am really struggling. Any ideas on what I can do to help with symptoms with me amazing?
Thanks
Maybe this will be of interest?
OK - I know that most members will wonder why on earth the researchers only measured TSH and not Free T4 and Free T3.
However, given current NICE guidelines encourage leaving patients until their TSH reaches 10, this paper's observation that non-alcoholic fatty liver disease (NFLD) and liver fibrosis rates rise with TSH above 2.5 should be seen as undermining that NICE recommendation.
I doubt many members will be surprised.
J Clin Med. 2021 Jun 29;10(13):2907.
doi: 10.3390/jcm10132907.
TSH Levels as an Independent Risk Factor for NAFLD and Liver Fibrosis in the General Population
Alba Martínez-Escudé 1 2 , Guillem Pera 1 3 , Anna Costa-Garrido 1 4 , Lluís Rodríguez 1 5 , Ingrid Arteaga 1 6 , Carmen Expósito-Martínez 1 7 , Pere Torán-Monserrat 1 3 , Llorenç Caballería 1 3
Affiliations
• PMID: 34209831
• DOI: 10.3390/jcm10132907
Abstract
Thyroid hormones may be a risk factor for the development of non-alcoholic fatty liver disease (NAFLD) and its progression to liver fibrosis. The aim of this study is to investigate the relationship between thyroid stimulating hormone (TSH) levels, NAFLD, and liver fibrosis in the general population. A descriptive cross-sectional study was performed in subjects aged 18-75 years randomly selected from primary care centers between 2012 and 2016. Each subject underwent clinical evaluation, physical examination, blood tests and transient elastography. Descriptive and multivariate logistic regression analyses were used to identify factors associated with NAFLD and fibrosis. We included 2452 subjects (54 ± 12 years; 61% female). Subjects with TSH ≥ 2.5 μIU/mL were significantly associated with obesity, atherogenic dyslipidemia, metabolic syndrome (MetS), hypertransaminasemia and altered cholesterol and triglycerides. The prevalence of NAFLD and liver fibrosis was significantly higher in subjects with TSH ≥ 2.5 (μIU/mL). We found a 1.5 times increased risk of NAFLD, 1.8 and 2.3 times increased risk of liver fibrosis for cut-off points of ≥8.0 kPa and ≥9.2 kPa, respectively, in subjects with TSH ≥ 2.5 μIU/mL compared with TSH < 2.5 μIU/mL (control group), independent of the presence of MetS. These findings remained significant when stratifying TSH, with values ≥ 10 μIU/mL.
Keywords: liver fibrosis; metabolic syndrome; non-alcoholic fatty liver disease; obesity; thyroid function; thyroid stimulating hormone; transient elastography.
pubmed.ncbi.nlm.nih.gov/342...
Full paper freely available here:
And this:
The focus, as so often, appears to be on cholesterol but knowing about ongoing research can have some interest.
Thyroid. 2020 Feb 26. doi: 10.1089/thy.2020.0071. [Epub ahead of print]
Thyroid hormone analogues: an update.
Zucchi R1.
Author information
Abstract
The development of thyroid hormone (TH) analogues was prompted by the attempt to exploit the effects of TH on lipid metabolism, avoiding cardiac thyrotoxicosis. Analysis of the relative distribution of the a and b subtypes of nuclear thyroid hormone receptors (TRa and TRb), showed that TRa and TRb are responsible for cardiac and metabolic responses, respectively. Therefore, analogues with TRb selectivity were developed, and four different compounds have been used in clinical trials: GC-1 (sobetirome), KB-2115 (eprotirome), MB07344/VK2809, and MGL-3196 (resmetirom). Each of these compounds was able to reduce LDL cholesterol, but a phase 3 trial with eprotirome was interrupted because of a significant increase in liver enzymes and the contemporary report of cartilage side effects in animals. As a consequence, the other projects were terminated as well. However, in recent years TRb agonists have raised new interest for the treatment of non-alcoholic fatty liver disease (NAFLD). After obtaining excellent results in experimental models, clinical trials have been started with MGL-3196 and VK2809, and the initial reports are encouraging. Sobetirome turned out to be effective also in experimental models of demyelinating disease. Aside TRb agonists, TH analogues include some TH metabolites that are biologically active on their own, and their synthetic analogues. 3,5,3'-triiodothyroacetic acid (Triac) has already found clinical use in the treatment of some cases of TH resistance due to TRb mutations, and interesting results have recently been reported in patients with the Allan-Herdon-Dudley syndrome, a rare disease caused by mutations in the TH transporter MCT8. 3,5-diiodothyronine (T2) has been used with success in rat models of dyslipidemia and NAFLD, but the outcome of a clinical trial with a synthetic T2 analogue was disappointing. 3-iodothyronamine (T1AM) is the last entry in the group of active TH metabolites. Promising results have been obtained in animal models of neurological injury induced by b-amyloid or by convulsive agents, but no clinical data are available so far.
PMID: 32098589
DOI: 10.1089/thy.2020.0071
ncbi.nlm.nih.gov/pubmed/320...
Thank you. My TSH is suppressed due to taking T3 and my cholesterol is spot on. Its very strange this has shown up now. Perhaps years of non diagnosis and lack of treatment had caught up with me now, although strange since I have been treated since 2017. All a little odd. Thanks again
I’m just dropping this info into the mix for consideration.
I have nafld, developed 3-4 yrs ago. I’ve had no thyroid since 1986 and well balanced on T3 only.
However I have polycystic ovarian disease which as I age causes heart, diabetes and nafld. My cholesterol is ok and I’m vegetarian.
There appears to have been too little research/ understanding into PCOS and aging- mainly all research has been directed at fertility and diabetes.
Bella
Have you had an HBA1C test done amongst the other tests? Was just wondering whether it had shown you to be pre-diabetic?
Insulin resistance is a biggie when it comes to NHFLD—and there is a link between taking thyroid hormones and insulin resistance. I also spotted you had some luck with an anti Candida diet? As anti-Candida diets generally reduce carbohydrate intake, I was wondering if that’s what had made the difference then—reducing your carbohydrate intake?
Thank you. Yip, all clear. Only raised markers were liver and reduced iron again. I did the anti- candida programme 2 years ago. Did wonders. Might give it a go again. Thanks.
Hihave you been tested for coeliac disease, my son prior to his coeliac diagnosis had NFLA flagged up by his GP, also his liver enzymes were raised. Following his diagnosis and his cessation of eating foods containing gluten both NFLD and raised liver enzymes disappeared.
His doctor thought his NFLD was due to alcohol consumption because he was a student, but he was almost teetotal because beer/ lager gave him severe stomach upsets.
Good luck getting to the bottom of your troubles, if you are completely gluten free already this will obviously not apply. 
Hi SAUK. I think Jazzw has a point about insulin resistance, HBA1C can be normal as can fasting glucose, it’s your fasting insulin that tells you if there is a problem and this is not a blood test that GP’s are happy to do. Thyroid, insulin resistance and fatty liver are all connected. I have recent read an excellent book on the subject and it explains the link to hypothyroidism. The book is called The Blood Code by Dr Richard Maurer. If you think this might be you then you could try the Keto diet and intermittent fasting (you can just do a window of eating e.g. 8 hours in a day) as both of these treat insulin resistance.
KETO DIET! There is a very good presentation by a doctor if you Google it. I forgot his name, but he seems to be very knowledgeable on the subject of non Alcoholic fatty liver. He suggests this is why so many people have “ belly fat” and thyroid issues. Too many simple carbohydrates!and too much sugar. I have started on this diet he suggests, and I’m amazed how much better I feel already, after 3 days. I’m not hungry after a simple drink that anybody with a blender can make, for breakfast. Chopped kale that’s been frozen, blueberries ( frozen), a cup of water, and a cup of plain keifer .( like liquid yogurt) It’s worth a try. I have yet to totally commit to the KETO diet. I’m slowly working my way into it. Try it. It can’t hurt, and it may be just the thing you need .
I have NAFLD. NAFLD is a lifestyle disease. 1/3 of people have it and it is related strongly to obesity. Systemically it can result in insulin resistance, which in turn can lead to fatigue, weight gain and elevated uric acid / gout. I have not seen any documented evidence of it causing weight loss. Weight loss = something else.... and the something else could be equally responsible for the fatigue.
I completely ignored mine for years because I didn't want to change my lifestyle and was convinced it was not the cause of my problems. Then I was diagnosed with two low grade cancers (my something else), had my thyroid lopped out (as one was thyroid cancer) and realised that I had to simplify the profile of conditions affecting me to get a grip of the remaining chronic cancer I have to live with (Lymphoma)
NAFLD is best tackled by reducing alcohol to close to zero (I do 2 units a week) and removing meat from 50% of your meals. An emphasis on plant based is very helpful. So tackle this and you will have a better picture of whether there is a something else.
In my searches I have found two points of interest. In one paper, which I've not been able to dig out for you, I found a statistical correlation between T3 levels and NAFLD. Lower levels = increased risk. People who are hypothyroid are much more likely to get it. But it is not an "on/off" type of switch. Hyper people still get it. So getting thyroid hormones correct is likely to help. The improvement to my liver enzymes has been since taking direct T3. I did not get an improvement on Levo (in fact it got worse).
If your NAFLD is giving you gout be very wary of taking Allopurinol. It is very bad for liver enzymes and trashes your thyroid hormones. This is personal experience and also documented in about three independent papers. If it interests you I'll dig them out.
Cortisol also has a big effect on NAFLD, which has been shown by this paper: sciencedaily.com/releases/2... .Since thyroid hormones affect cortisol it is probable that the findings in relation to T3 are connected to NAFLD via this pathway. The paper I have not been able to relocate on T3 thought it was a more direct effect on liver metabolism. In any case checking your cortisol levels would be prudent.
Hope this helps.
This makes so much sense what your saying. Because I was diagnosed with NASH when I was dosed with T4 sole after my TT. Now that I'm on combo withT4 with T3 the sonogram showed that there was a big improvement. I'm also a vegetarian but have been for years . But no doubt that being gluten dairy free plays a role with this. Exercise is also said to be very helpful.
Hi CaptainBeOS, I understand from reading another book called The Obesity Code by Jason Fung (I’m busy trying to understand all this at the moment) - that high cortisol is also linked to high levels of insulin, there is a whole chapter on Cortisol and Insulin and Thyroid, it shows how they are all linked. It talks about NAFLD being reversible by reducing sugar and particularly fructose, there is lots of science and studies to back this up. Basically similar to what you are saying that by cutting alcohol you are reducing sugar and you can further heal NAFLD by intermittent fasting and drastically reducing carbs. I think you might find it an interesting read.
Hashimotos and Fatty Liver.
Reversing fatty liver on LCHF
Fatty!!
Alcohol 
Hashimotos and Alcohol
