My heart pounds, blub blum blub blum, as I lie in bed with closed eyes. A few minutes ago it seemed normal, quietly doing its job while I went about mine. Now its beat is loud, annoying, demanding, incessant. Listen to me, listen to me. I get out of bed.
Almost everyone I know with CFS deals with this pounding heart, and none of our doctors have any idea what is causing it. Nor do they know how to stop it. I’ve noticed over the years the things that often ameliorate it:
• doing yoga inversions, especially supported shoulderstand. • doing a few vigorous yoga poses, like upward facing bow (a backbend – not recommended for beginners) that open the hips and the chest • eating plain yogurt or goat cheese
This weekend I clicked on the link to a website written by a cardiologist who has been familiarizing himself with Dr. Yasko’s research on methylation defects in chronic and understands how to explain it. In reading over Dr James Roberts discussion of methyl cycle genomics in heart disease, I suddenly had an aha! moment. I understood how my own methylation genetics have created Pounding Heart at Rest.
Over the last few days I’ve been working to wrap my mind around these ideas. Here’s what I’ve come up with.
A pounding heart is a normal reaction to vigorous activity such as running. The demand (stress) of movement stimulates the SNS [sympathetic nervous system] to release adrenaline and noradrenaline (or if you prefer the British terms, epinephrine and norepinephrine) as well as the hormone cortisol. When the activity stops, the heart rate slows and soon returns to normal as the PNS [parasympathetic nervous system] brings the body back to homeostasis.
Certain methylation cycle defects lead to excess stimulatory activity and insufficient inhibitory recovery, and I have just about all of them. The main culprit is CBS – not the television station (even though watching TV late at night is rather stimulatory) -- but an enzyme known by that name whose job is to funnel metabolites of the methylation cycle out of the system. Meet Cystathionine Beta Synthase, a hardworking supporter whose job is to funnel homocysteine into cystathione so that the next enzyme can make cysteine and alpha keto glutarate (AKG) both of which are used for other important things. My CBS is overly enthusiastic due to a certain genetic variant known as a SNP or polymorphism. This simply means that one of the normal amino acids on the gene has been replaced by a different one, and this can happen in all of the genes if you are (CBS +/+) or half of the genes if you are (CBS +/-). I happen to have the latter variant, half of my genes. I also have other variations further upstream that intensify the imbalance.
Imagine CBS as a worker on an assembly line. If she does her job five or ten times faster than everyone else, a bottleneck will develop and then trouble will result. The enzyme that is supposed to pick up some homocysteine for recyling before CBS grabs it must also works overtime. Unfortunately, this enzyme, called BHMT, has just the opposite genetic variant in my body: it works more slowly. The net result is that my enthusiastic CBS makes lots more cystathionine than it should.
This has multiple effects. Upstream, there is not enough homocysteine getting recycled back into methionine so that it can be used to make SAMe which can then be used to make DNA, RNA, protein, lipids, creatine and creatinine. Hence, on lab tests, homocysteine, methionine, SAME, and creatinine are low, and I crave red meat whenever I try vegetarian diets.
But the downstream effects are worse, many times worse. Here’s what Dr. Roberts has to say:
The 10-fold up regulation in CBS generates sulfur breakdown products (sulfite and sulfate, which stimulate the stress/cortisol “fight or flight” response), excess ammonia (in the process wasting BH4 which is used up detoxifying ammonia), hydrogen sulfide (producing “brain fog”), and alpha-keto glutarate (leading to “excitotoxicity”). The G6PDH enzyme system may be affected, leading to abnormalities in sugar control. Methylation intermediates will “fall through this drain”, so the entire system suffers; our defenses against viral invasion and toxicity suffer. Co-Q10 and Carnitine generation will fall off due to impaired methylation, and ATP levels fall, robbing you of energy.
If this is all you want to know, skip to the end. If you want more details, read on:
1. The excess cystathionine is converted to cysteine and alpha keto glutarate (AKG). AKG is excitatory; when there is too much, the inhibitory GABA (the receptors that Valium binds) can’t operate properly to balance the excitation.
2. If this weren’t enough trouble, a byproduct of the conversion is ammonia – that stinky stuff used in oven cleaner, Phew!, toxic even in small amounts.
3. Of course the body has ways to detoxify ammonia. But in doing so, it uses up a very important enzyme known as BH4. BH4 makes non-toxic byproducts from ammonia and arginine, and helps us make the important feel-good neurotransmitters dopamine and serotonin. When BH4 stores are low, instead of getting non-toxic byproducts, we get lots of free radicals (peroxynitrite and superoxide) that go about damaging cell membranes until they are neutralized by anti-oxidants. And mood disorders can result because there isn’t enough BH4 to make all the right amounts of feel-good neurotransitters.
4. The excess cysteine gets converted to taurine rather than to glutathione. The lack of glutathione impacts the function of the immune system and lowers the ability of the body to detoxify heavy metals.
5. The abundance of taurine is less problematic, for taurine has lots of good uses in the body. It is important in the visual pathways, for the brain and nervous system, and for cardiac function. It facilitates the passage of sodium and potassium ions into and out of cells, electrically stabilizes the cell membranes, and functions as an inhibitory (calming) neurotransmitter. It conjugates bile acids for efficent fat absorption & solubilization. Not bad for one amino acid.
6. A byproduct of the conversion to cysteine and taurine is hydrogen sulfite, also known as the brain fog molecule, the one responsible for the foul smell of farts and cooked hard-boiled eggs. Here’s what a Wikipedia article says about the toxicity of hydrogen sulfide (H2S)
a broad-spectrum poison ... although the nervous system is most affected...which forms a complex bond with iron in the mitochondrial cytochrome enzymes, thereby blocking oxygen from binding and stopping cellular respiration. Since hydrogen sulfide occurs naturally in the environment and the gut, enzymes exist in the body capable of detoxifying it by oxidation to (harmless) sulfate.
HBOT (hyperbaric oxygen therapy) is particularly efficient in helping remove toxic hydrogen sulfide, which is why most people with CFS have a positive response to this therapy, but also why it doesn’t last: we have not been poisoned by breathing exogenous H2S but rather by our own excessive production of it.
In the body, H2S acts as a vasodilator (which can explain the prevalence of orthostatic intolerance in people with excessive H2S production) and in the brain increases the response of the NMDA receptor (which Martin Pall has shown is responsible for chemical hypersensitivity in those of us with CFS and MCS.)
7. And if all this isn’t enough, we get lots of neurotoxic sulfite, which overwhelms the SUOX enzyme that uses molybdenum to convert it into the less toxic sulfate.
8. Even if we support the SUOX enzyme into converting sulfite to sulfate, we have an abundance of sulfate, which stimulates the fight, flight, freeze response. We produce SNS neurotransmitters adrenaline and noradrenaline as well as cortisol, until the adrenals get too exhausted to produce high amounts of cortisol. All these stress hormones lead to a pounding heart.
Do you have sensitivity to sulphur products: sulpha-drugs, foods high in sulfur, or sulfites added to wine and dried fruits? Leave a comment below.
Why do people always assume the most confusing and theoretical hypothesis for CFS is the one that applies.
Most patients with POTS, CFS and OI have parasympathetic withdrawal and sympathetic excess, decreased norepinephrine reuptake and inappropriate peripheral vasoconstriction, stomach or splanchnic vasodilation and cerebral vasoconstriction or decreased cerebro-autoregulation.
And these findings are based on real science published in reputable medical journals.