Nah, this time I actually meant her candy line...no candy for me but weird Russian drugs? Sign me up! Lol!
Somehow inhibiting carnotine transport with Meldonium is producing almost exactly the opposite effects of whatever is inhibiting the carnotine transport in MECFS. I wonder if it's a different part of the pathway? It seems so from what I've read so far but I'm no expert. It just seems odd that inhibition on the one hand of MECFS causes extreme fatigue and neurological problems and inhibiting it on the Meldonium side causes an enhancement in athletic performance to the point where it has become a banned substance in sport.Carnitine transport has already been shown to be deficient in CFS patients.
I do not see a benefit in further limiting fatty acid metabolism.
I recommend steering clear of mildronate/meldonium, I strongly suspect it would make things worse.
literature review showed that Meldonium is an effective anti-ischemic drug with further applications in immunomodulation and in the treatment of neurodegenerative disorders and bronchopulmonary diseases.
Meldonium is a structural analogue of the carnitine precursor, gamma-butyrobetaine. Carnitine is a key regulator of fat metabolism, since it is required to transport fatty acids into the mitochondria for fatty acid breakdown via beta-oxidation. Meldonium affects carnitine metabolism by inhibiting its biosynthesis and transport and this protects mitochondria from an overload of Fatty Acid metabolites. Meldonium also increases gene expression related to glucose metabolism and thereby stimulates the aerobic oxidation of glucose (2).
Meldonium decreases the beta-oxidation of fatty acids and shifts cellular metabolism towards the oxidation of carbohydrates, which requires far less oxygen per ATP molecule than beta-oxidation of fatty acids. This sparing of oxygen could be of huge benefit under hypoxic conditions. The most obvious benefits have been seen in the treatment of ischemic heart disease, but there is evidence to suggest that Meldonium could be equally beneficial under the low oxygen conditions induced by intense endurance exercise (3).
One review (4) of the effects of Meldonium on exercise performance listed the following benefits:
- Decreased levels of lactate and urea in blood
- Improved economy of glycogen: level of glycogen increased in the cells during the long-lasting exercise
- Increased endurance properties and aerobic capabilities of athletes
- Improved functional parameters of heart activity
- Increased physical work capabilities
- Increased rate of recovery after maximal and sub-maximal loads
- Activates CNS functions and protects against stress
Hmmm...and yet Sharapova has been using it for just shy of a decade.that four to six weeks is a common course
CNS Drug Rev. 2005 Summer;11(2):151-68.
Mildronate: an antiischemic drug for neurological indications.
Sjakste N1, Gutcaits A, Kalvinsh I.
Mildronate (3-(2,2,2-trimethylhydrazinium)propionate; MET-88; meldonium, quaterine) is an antiischemic drug developed at the Latvian Institute of Organic Synthesis. Mildronate was designed to inhibit carnitine biosynthesis in order to prevent accumulation of cytotoxic intermediate products of fatty acid beta-oxidation in ischemic tissues and to block this highly oxygen-consuming process.
Mildronate is efficient in the treatment of heart ischemia and its consequences. Extensive evaluation of pharmacological activities of mildronate revealed its beneficial effect on cerebral circulation disorders and central nervous system (CNS) functions. The drug is used in neurological clinics for the treatment of brain circulation disorders. It appears to improve patients' mood; they become more active, their motor dysfunction decreases, and asthenia, dizziness and nausea become less pronounced.
Since the brain does not utilize fatty acids as fuel other mechanisms of action of mildronate in CNS should be considered. Several reports indicate the possible existence of an alternative, non-carnitine dependent mechanism of action of mildronate. Our recent findings suggest that CNS effects of mildronate could be mediated by stimulation of the nitric oxide production in the vascular endothelium by modification of the gamma-butyrobetaine and its esters pools. It is hypothesized that mildronate may increase the formation of the gamma-butyrobetaine esters. The latter are potent cholinomimetics and may activate eNOS via acetylcholine receptors or specific gamma-butyrobetaine ester receptors.
This article summarizes known pharmacological effects of mildronate, its pharmacokinetics, toxicology, as well as the proposed mechanisms of action.
While Grindeks has previously stated that the drug can provide an “improvement of work capacity of healthy people at physical and mental overloads and during rehabilitation period,” the company said that it believes the substance would not enhance athletes’ performance in competition and might even do the opposite.
Somehow inhibiting carnotine transport with Meldonium is producing almost exactly the opposite effects of whatever is inhibiting the carnotine transport in MECFS.