The Emerging Energy Paradigm, Simplified
This post contains the narration to this slideshow:
Why do people with myalgic encephalomyelitis, or chronic fatigue syndrome, have less energy than healthy people – even on relatively good days? On bad days – after overexertion – everything goes haywire, but why do they have less energy on ordinary days?
Several bits of recent research converge on an answer to this basic question. These studies include four metabolomic analyses that have gotten a lot of press. They’re not easy for most people to read, so this is a simplified account.
The chain of events starts with some agent – a molecule or cell – that’s circulating in the bloodstream. This agent provokes cells into producing less energy – and probably several other changes, too.
We know that the cause of this problem is in the bloodstream because labs have put cells from ME/CFS sufferers in healthy people’s blood, and the cells turned healthy. And blood from people with ME/CFS makes cells from healthy people sick.
We also suspect that this agent is not a small molecule, because researchers filtered out large ones and got a different effect.
No one knows what this agent is – or how or why it gets produced. But, being in the bloodstream, it goes throughout much of the body, and it interacts with many different cell types. It probably provokes a host of changes in these cells; possibly it leads to most or all of the symptoms in ME/CFS.
By the way, one researcher has suggested that cells in ME/CFS resemble those of a hibernating worm; another argues that they resemble the effects of sepsis and starvation. Ugh.
In any case, the metabolomics studies agree that the healthy process of energy production, using glucose, fails at an early stage. And this happens before much fuel is produced. The fuel in our cells is a molecule named ATP, and our cells engage in a long, complex chain of processes to make ATP bit by bit. Unfortunately, in ME/CFS this chain gets broken fairly early, before much fuel has been produced.
This failure leaves a lot of a molecule called pyruvate hanging around, and it gets turned into lactate. Just by itself, lactate inhibits the production of more fuel, and it reduces the force of muscles. Add that to the broken chain of fuel production, and you have a triple whammy.
But our cells are resourceful and can use alternatives to pyruvate to make ATP. And people with ME/CFS depend on these alternatives, which include free fatty acids from fat, amino acids, and protein from muscles. Unfortunately, employing these alternatives is slower and less efficient, and that (plus the bad effects of all that lactate) translates into lower energy, even on good days, in ME/CFS.
So that’s it: a mysterious molecule or cell in the bloodstream provokes cells into screwing up the normal process of making fuel. Thus, people with ME/CFS have to depend on an inferior method of producing energy.
Now, even if this scenario is correct, then many basic questions remain to be answered:
• What is this molecule or cell that’s wreaking such havoc?
• What happens on bad days, after overdoing it – the so-called Post-Exertional Malaise (when everything goes haywire, including energy production)?
• How do other ME/CFS symptoms fit in with this?
• Why do people with ME/CFS have more energy (but still not a normal amount) for months or years but less at other times?
• And, above all, how can any of this be treated?
In a future presentation, I’ll go into more detail about the ways our cells produce energy and the implications for ME/CFS.