For some, digestion can play a big role. The whole issue of paleo diet addresses a number of items - potential food sensitivities like gluten/gliaden, casein and soy. Food additives such as MSG and glutamates and also blood sugar.
In my own case, though sex has never been a trigger, the vagal aftermath of sex can precipitate PAC runs that could initiate afib. My own experience has been that optimal magnesium supplementation will fix this problem.
More background Mg++/K+ & insulin information is here, with some interesting sections copied & reposted:
From [
www.afibbers.org]
Autonomic Nervous System
Mg is required for activity by the cholinesterase enzymes(13). One of these, acetyl cholinesterase degrades acetylcholine, the neurotransmitter substance for the PNS and for the first part of the sympathetic nervous system (SNS), specifically the nicotinic receptors of the SNS. In fact, deficiency of magnesium and excess calcium both increase the release of acetylcholine. Deficiency of either magnesium or calcium prolongs the effect of acetylcholine(58). Mg deficiency translates to enhanced vagal tone further augmented by too much or too little Ca.
Catecholamine-O-methyltransferase (COMT) and monoamine oxidase (MAO) catabolize (break down) norepinephrine (NE), the neurotransmitter for the rest of the SNS. However, unlike acetylcholine but like glutamate, neuronal reuptake of discharged norepinephrine is a major mechanism for terminating sympathetic neurotransmission (see glutamate discussion above). MAO catabolizes this NE, while COMT is more active in catabolizing extracellular circulating (humoral) catecholamines secreted by the adrenal gland(30). Both are part of the SNS. COMT requires Mg as a cofactor(28,29). Neuronal reuptake also requires ATP (and Mg). Low Mg
translates to higher sympathetic tone(105). These enzymatic shortfalls might produce an exaggerated response of either the PNS or the SNS at transition or crossover points, a time when many VMAF episodes arise, e.g., lying down or bending over. The neurotransmitter substance or hormone secreted on each occasion is not degraded or removed, resulting in a prolonged over response. For example, cocaine blocks dopamine reuptake leaving more dopamine in the synaptic cleft, which results in over timulation of the D2 receptors (causing schizophrenic episodes)(106).
Sexual activity triggers some episodes for many afibbers(72). In addition to MAO breakdown of dopamine within neurons (neuronal reuptake) COMT breaks down circulating dopamine, an important hormone produced at this time. The dopamine no doubt triggers automaticity (associated with beta-1 receptors) in ectopic foci with a resulting increase in PACs (see EP discussion below)(107). The over responding vagus causes a shortening of the AERP. Mg deficiency in this scenario (independent of K) may be causative in bedtime episodes and even some more typically adrenergic episodes.
GERD
The alkaline tide precedes the start of any meal. This is caused by gastric cell secretion of H and Cl into the lumen for digestion of food and simultaneous extrusion of K and HCO3 into the blood. This more alkaline blood causes bicarbonaturia (HCO3 in urine) to lower this pH (blood pH is tightly controlled between 7.35 and 7.45). Unfortunately, K(54) as well as Mg(104) are cations lost in the urine (kaliuria and magnesuria respectively) along with the anion HCO3. This lowers blood K, although not necessarily below lower limit of normal. Furthermore, there is evidence that high vagal tone may sustain basal gastric acid hypersecretion in some persons and temporary hypersecretion during stress in others(49). Some cases of GERD (gastroesophageal reflux disease) and non-ulcer dyspepsia (NUD) probably result in transiently low K via the constant steady alkaline state (in plasma) that accompanies the slightly hyperacidic state (in the stomach). The K/H pump also rectifies this increase in blood pH. H goes into the blood and K comes into the cells. Again this requires cardiac muscle cells to maintain their intracellular K concentration against a greater gradient. Also, greater concentration of K within renal tubule cells contributes to increased renal secretion of K into urine. Normally the concentration of K within heart muscle cells is 150 millimoles/liter (v. four mm/l outside the cell), a considerable gradient (almost 40:1) to maintain(9). Ingested protein stimulates more HCl secretion (and a stronger alkaline tide and greater kaliuria).
Other suggested mechanisms for GERD related episodes of LAF include stimulation via irritation of the vagus nerve during episodes of reflux and/or gastric distention. Some VMAFers associate their episodes with GERD(72). Curiously, many of them prefer to sleep on their right side (right lateral decubitus position). Vagal tone is increased while in this position(67). This is because the heart is slightly higher (v. the left side position) relative to the carotid baroreceptor. This pressure receptor in the neck senses more hydrostatic pressure and signals the vagus nerve to increase tone (bad for a VMAFer). However, the preference may be because this position promotes gastric emptying (our stomachs pass their contents to the right and dump them into the duodenum) and possible relief for a GERDer.
Dysinsulinism
Those with impaired glucose metabolism hyper respond with insulin (produced by the beta cells of the pancreatic islets) to a carbohydrate meal (target cells are insulin resistant). The ensuing hypoglycemia (low blood glucose) stimulates release of glucagon (produced by alpha cells of the pancreatic islets) and catecholamines with consequent hyperglycemia (high blood glucose) with a kind of yo-yo effect(72). Catecholamines but especially glucagon stimulate glycogenolysis (breakdown of glycogen, the storage form of glucose) and gluconeogenesis (release of glucose from cells that store glycogen), most notably from the liver. Gluconeogenesis involves enolase and magnesium is required as a cofactor(91). In fact five of the other eight steps in gluconeogenesis also require Mg(94). It appears that Mg is critical to the proper function of glucagon and catecholamines in this area.
There is an epidemic of overweight/obesity in the Western world, especially here in America. Syndrome X (or Metabolic Syndrome = includes high blood pressure, obesity, diabetes, high blood insulin and triglyceride levels) represents the far end of the spectrum of this disorder of carbohydrate metabolism. Useful laboratory tests include serum hemoglobin A1C, which will detect large swings in blood glucose levels over the preceding three months. Fasting blood glucose and then an OGTT (oral glucose tolerance test) are the best tests to diagnose impaired glucose tolerance and diabetes mellitus. Mg deficiency plays an important role in this process (see
insulin section above).
Postprandial (after a meal) reactive hypoglycemia (PRH) is defined as low blood sugar (less than 3.3 mmol = 60gm/dl) concurrent with symptoms (dizziness, depression, sweating, weakness, hunger, anxiety)(82,83,89). LAF has recently been added to this list(84,85,86). Although the oral glucose tolerance test (OGTT) is not abnormal