Thank you so much for the feedback. Truly appreciate that. While short term stress can be adaptive, prolonged stress can lead to cortisol dysfunction. In this case I suppose by "too much" you mean prolonged stress. For instance during a prolonged stressful condition like starvation the body may respond by releasing cortisol and ketones to provide energy. One study by Britta Kubera et al. Rise of ketone bodies with psychosocial stress in normal weight men found that social stress increased ketones in normal weight men that was associated with an increase in ACTH, norepinephrine, epinephrine. However, they could not detect a rise in ketones in obese men for the same study.

Thank you very much and take care of your health.

Thank you very much.

Thank you

Thank you very much. Truly appreciate your valuable response. There are quiet interesting observations around the management of ME/CFS. "NICE" GUIDELINES emphasizes that exercise goals should be set by patients and should not be driven by treatment plan. The NICE guidelines for example also states" Tell people about the risk and benefits of physical activity and explain that some people with ME/CFS have found that they can make their symptoms worse, for some people it makes no difference and others find them useful" I find it confusing that they also admit some also find it useful. This is an interesting disorder with divided opinions. The guideline also proceeds to say that if physical activity is offered then it should be overseen by physiotherapist or an ME/CFS specialist team. www.nice.org.uk/guidance/ng206/chapter/Recommendations#managing-mecfs Thank you very much.

@@jamesedwardschalktalk Thank you so much for your interest, and you're absolutely right. I am an ME/CFS patient myself, who become severe (bedbound for 4 years now) precisely after pushing through exercising, so this subject resonates particularly with me. The main point I think is that GET is sometime seen as a treatment as if the main driver of the condition was deconditioning (with not enough questioning why one becomes house or bedbound and consequently deconditioned as a result). An interesting test that captures the hallmark of ME/CFS is the 2-day cardiopulmonary exercise test, where the VO2max is lower on the second day, as opposed to healthy controls. This would indicate a malfunctioning aerobic metabolism. I will post a link to this study, I hope it is of interest. I posted another few links but I suspect they might have been classified as spam by youtube, as I cannot see them on this comment section anymore. Personaly, given the variability in the prognosis and in the symptoms, I am inclined to believe that ME/CFS is currently a label for a subset of potentially different pathophysiologys that will eventually require different treatments. Sorry for the long message and apologises if I caused any inconvenience, but I honestly just want to raise awareness about this condition. Take care and thank you again :)

Thank you so much. Glad it was helpful.

So nice of you

My pleasure!

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Thanks

Denosumab targets receptor activator of nuclear factor kappa ligand (RANK-L). By binding to RANK-L they prevent them from activating RANK receptors on osteoclast. This reduces bone resorption and reduces calcium mobilization from the bone matrix into the blood. It is often used as a second line agent in the treatment of osteoporosis. But it is recently approved for the management of malignancy associated hypercalcemia if bisphosphonates become refractory. It has serious implications if used in children. Thank you

@@jamesedwardschalktalk Thank you so much.

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Thank you very much for your valuable response and also for watching. Regarding your question: In fact that is a great question and there has been some proposed mechanisms: 1. In hypothyroidism there may be accumulation of mucopolysaccharides in the interstitial spaces that increases the oncotic pressure in that space. This tends to decrease arterial blood volume which triggers the release of ADH, increased expression of aquaporin 2 channels and excessive water reabsorption. 2.It has also been proposed that hypothyroidism may lead to an increased peripheral vascular resistance from a reduction in endothelial relaxing factor and also from the decreased arterial volume explained above. This decreases the cardiac output , renal flow and GFR ie the excretion of water decreases. Again the low metabolic state in Hypothyroidism can decrease the activity of Na/K Atpase which can decrease sodium and water reabsorption Hope this was useful. Thank you. Cheers!

@@jamesedwardschalktalk Thanks a lot.

Its a pleasure! Thank you.

Thanks for watching!

@@jamesedwardschalktalk my pleasure