The real revolution in the prevention and treatment of heart disease will come with increased understanding of the role played by the autonomic nervous system in the genesis of ischemia and its measurement through the tool of heart rate variability (HRV).
We have two distinct nervous systems: the first, the central nervous system (CNS), controls conscious functions such as muscle and nerve function; the second nervous system, the autonomic (or unconscious) nervous system (ANS), controls the function of our internal organs. The autonomic nervous system is divided into two branches, which in a healthy person are always in a balanced yet ready state. The sympathetic or “fight-or-flight” system is centered in our adrenal medulla; it uses the chemical adrenaline as its chemical transmission device and tells our bodies there is danger afoot—time to activate and run. It does so by activating a series of biochemical responses, the centerpiece of which is the glycolytic pathways, which accelerate the breakdown of glucose to be used as quick energy as we make our escape from the bear chasing us.
In contrast, the parasympathetic branch, centered in the adrenal cortex, uses the neurotransmitters acetylcholine (ACh), nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) as its chemical mediators; this is the “rest-and-digest” arm of the autonomic nervous system.
The particular nerve of the parasympathetic chain that supplies the heart with nervous activity is called the vagus nerve; it slows and relaxes the heart, whereas the sympathetic branches accelerate and constrict the heart. I believe it can be shown that an imbalance in these two branches is responsible for the vast majority of heart disease.
Using the techniques of heart rate variability (HRV) monitoring, which gives a real-time accurate depiction of autonomic nervous system status, researchers have shown in multiple studies5 that patients with ischemic heart disease have on average a reduction of parasympathetic activity of over one-third. Typically, the worse the ischemia, the lower the parasympathetic activity.6 Furthermore about 80 percent of ischemic events are preceded by a significant, often drastic, reduction in parasympathetic activity.7
By contrast, those with normal parasympathetic activity, who experience an abrupt increase in sympathetic activity (such as physical activity or an emotional shock), never suffer from ischemia.
In other words, without a preceding decrease in parasympathetic activity, activation of the sympathetic nervous system does not lead to MI.8 Presumably we are meant to experience times of excess sympathetic activity; this is normal life, with its challenges and disappointments. These shocks only become dangerous to our health in the face of an ongoing, persistent decrease in our parasympathetic, or life-restoring, activity.
The decrease in parasympathetic activity is mediated by the three chemical transmitters of the parasympathetic nervous system: ACh, NO, and cGMP. It is fascinating to note that women have stronger vagal activity than men, probably accounting for the sex difference in the incidence of MI.9 Hypertension causes a decrease in vagal activity,10smoking causes a decrease in vagal activity,11diabetes causes a decrease in vagal activity,12 and physical and emotional stress cause a decrease in parasympathetic activity.13 Thus, all the significant risk factors suppress the regenerative nervous system activity in our heart.
On the other hand, the main drugs used in cardiology upregulate the parasympathetic nervous system. Nitrates stimulate NO production while aspirin and statin drugs also stimulate the production of ACh along with NO—that is, until they cause a rebound decrease in these substances which then makes the parasympathetic activity even worse.
Beta-blockers work by blocking the activity of the sympathetic nervous system, the increase of which is a central factor in the etiology of MI.
The bottom line: the risk factors for heart disease and the interventions used all affect the balance in our ANS. Whatever effects they may have on plaque and stenosis is of minor relevance.
HOW HEART ATTACKS OCCUR
So what is the sequence of events that leads to an MI? First comes a decrease in the tonic, healing activity of the parasympathetic nervous system—in the vast majority of cases the pathology for a heart attack will not proceed unless this condition is met. Think of those who are always pushing themselves, who never take time out, who have no hobbies, who constantly stimulate the adrenal cortex with caffeine or sugar, who do not nourish themselves with real food and good fats, who do not incorporate a regular pattern of eating and sleeping into their daily lives.
Then comes an increase in the sympathetic nervous system activity, usually a physical or emotional stressor. This increase in sympathetic activity cannot be balanced because of chronic parasympathetic suppression. The result is an uncontrolled increase of adrenaline, which directs the myocardial cells to break down glucose using aerobic glycolysis. Remember that in a heart attack there is no change in blood flow as measured by the pO2 in the cells. This step shunts the metabolism of the heart away from its preferred and most efficient fuel sources, which are ketones and fatty acids. This explains why heart patients often feel tired before their events. This also explains why a diet liberal in fat and low in sugar is crucial for heart health.
As a result of the sympathetic increase and resulting glycolysis, a dramatic increase in lactic acid production occurs in the myocardial cells; this happens in virtually 100 percent of MIs, with no coronary artery mechanism required.14,15 As a result of the increase in lactic acid in the myocardial cells, a localized acidosis occurs. This acidosis prevents calcium from entering the cells,16 making the cells less able to contract. This inability to contract causes localized edema (swelling), dysfunction of the walls of the heart (hypokinesis, which is the hallmark of ischemic disease as seen on stress echoes and nuclear thallium stress tests), and eventually necrosis of the tissue—in other words, a heart attack. The localized tissue edema also alters the hemo-dynamics of the arteries embedded in that section of the heart, resulting in shear pressure, which causes the unstable plaques to rupture, further block the artery, and worsen the hemodynamics in that area of the heart.
Please note that this explanation alone explains why plaques rupture, what their role in the MI process is, and why they should indeed be addressed. Notice also that this explanation accounts for all the observable phenomena associated with heart disease and is substantiated by years of research. The true origin of this epidemic of heart disease could not be more clear.
NOURISHING THE PARASYMPATHETIC NERVOUS SYSTEM
If heart disease is fundamentally caused by a deficiency in the parasympathetic nervous system, then the solution is obviously to nurture and protect that system, which is the same as saying we should nurture and protect ourselves.
Nourishing our parasympathetic nervous system is basically the same as dismantling a way of life for which humans are ill-suited. This means avoiding the excesses of industrial civilization. The known things that nourish our parasympathetic nervous system are contact with nature, loving relations, trust, economic security (a hallmark of indigenous peoples the world over) and sex—this is a whole new world of therapy for ailing hearts.