Hi, Lisa and the group.
Fundamentally, a low body temperature means that the rate of heat production relative to the rate of heat loss from the body is lower than normal. Heat production in the body comes from oxidation of fuels we derive from our food. So this means that fuels are being oxidized at a lower rate than normal. That is, the metabolic rate is lower than normal.
In ME/CFS, there is published work indicating that the actual core body temperature (measured inside the body) is normal. This is very important, because it maintains the functions of the vital organs. However, the peripheral body temperature is often lower than normal in ME/CFS. This can be noted particularly by measuring the armpit temperature, as recommended by Broda Barnes. A low value here indicates that the peripheral tissues (in particular, the skeletal muscles) are operating at a lower than normal metabolic rate.
It's true that normally the metabolic rate is governed by the thyroid gland, particularly, and also by the adrenals. The thyroid hormones influence gene expression of the enzymes involved in metabolism, particularly in the mitochondria.
In ME/CFS, we know from the work of Myhill et al., as well as a lot of other published research, that the mitochondria are dysfunctional. Some PWMEs/PWCs benefit from suppleenting thyroid hormones. At the same time, many PWMEs/PWCs have normal levels of the thyroid hormones, and do not benefit from supplementing them.
In my hypothesis, the mito dysfunction stems initially from glutathione depletion (verified by lots of lab testing now), which allows rise of reactive oxygen species, which are known to inhibit both the Krebs cycle and the respiratory chain in the mitochondria. Dr. John McLaren Howard's testing at acumenlab shows that over time, several other problems arise that contribute to mito dysfunction. These include buildup of toxins that block enzymes and act as DNA adducts, interfering with gene expression. They also include disruption of levels of essential minerals and buildup of lactic acid from anaerobic glycolysis, which is accelerated to compensate for the mito dysfunction. In addition, the methylation deficit that is associated with glutathione depletion in ME/CFS causes a drop in production of certain substances needed for proper function of the mitochondria, including Co Q10, carnitine and creatine.
Under these circumstances, supplementing thyroid hormones will give limited, if any, improvement. The mitos are simply not able to respond to the thyroid hormones, because of all their problems. In these cases, I think the answer is to restore the function of the methylation cycle, which will correct the glutathione depletion.
Best regards,
Rich