How Your Thinking Affects Your Health Part 2 of 3

Theoretical physicist Dr. David Bohm

Theoretical physicist David Bohm explained how virtually all thought has physiological correlates, and that the meaning we assign to material events serves as the link between energy and matter. He refers to thought as energy, and he refers to matter in this case as the body. Meaning that is simultaneously mental and physical can serve as the link or bridge between two realms. This link is indivisible, like two sides of a continuous Mobius strip. Information contained in thought, on the mental side, is at the same time a chemical activity of the material side. (A Mobius strip is a continuous one-sided surface formed by rotating one end of a rectangular strip 180° and attaching it to the other end.)

The Basic Biochemistry of a Stressful Thought:

The hypothalamic pituitary adrenal axis (HPA) (Cacioppo and Tassinary, 1999)
1) A stressful thought appears in the frontal cortex.
2) The frontal cortex triggers the hypothalamus to secrete a peptide known as
corticotropin-releasing factor (CRF) within seconds.
3) The CRF then acts on the anterior pituitary.
4) Then, within about fifteen seconds, the anterior pituitary releases adrenocorticotropic
hormone (ACTH) into the bloodstream with the adrenal glands as the target organs.
5) The ACTH then almost immediately reaches the adrenal glands.
6) Then, within a couple of minutes, the ACTH causes the adrenal cortex to secrete
several hormones including cortisol into the bloodstream.
7) The release of cortisol into the bloodstream triggers the pituitary to increase or
decrease ACTH, depending on the cortisol level. This particular feedback loop gets
interrupted during extreme emotional distress, resulting in continued release of cortisol
into the bloodstream.
8) The increased sympathetic activity in the ANS then signals the adrenal medulla to
secrete epinephrine (Epi) into the bloodstream.

One of the reasons that knowledge of the HPA axis is important is because it helps explain medical as well as psychological problems. For example, the HPA axis has been found to become altered downward as a result of chronic emotional distress in childhood.

There are actually two major stress-response systems—the sympathetic-adrenal-
medulla system and the hypothalamic-pituitary-adrenal cortex system.

In addition to the HPA axis (above), what follows below is the action of the
hypothalamic-adrenal medullary system. This system works as follows:
1) The hypothalamus activates the ANS.
2) ANS activation, including the action of NE, results in sympathetic arousal.
3) Sympathetic arousal results in release of the various stress-related hormones
such as catecholamines, epi, and NE.

Neuropsychology researchers are now able to study the effects of specific thoughts and feelings on brain function through positron emission tomography (PET). PET involves using a radioactive tracer to track the activity of neurotransmitters in the brain. Neurotransmitters are biochemicals that act to transmit or inhibit nerve impulses. Another useful tool to explore the effect of thoughts and feelings on physiology is the fMRI. This scanner allows researchers to observe and follow subtle shifts in oxygenation and perfusion in different areas of the brain. An older method, electroencephalography (EEG) allows researchers to pinpoint electrical activity deep within the brain by triangulating from electrodes attached to the scalp. EEG is like NF without a feedback signal or target algorithm for learning purposes.
Depression is immunosuppressive and results in the following: an inflammatory response, increased leukocytes, especially monocytes and neutrophils. There are increased indicators of T-cell activation. There are increased levels of positive acute phase proteins such as C-reactive protein (CRP). There is a secretion of pro-inflammatory cytokines such as IL-6, IL-8, and other indirect indicators.

Sympathetic arousal can create a 300-fold increase in the production of epi. Epi increases natural killer (NK) cells. NK cells and their activity diminish with a high allostatic load, but increase with normal daily stressors, from which the ANS returns to homeostasis. Normal daily stressors from which we rapidly recover actually improve immune function.

Allostasis refers to the deleterious effects of stressors and the adaptation to them. One type of allostatic load is the result of being repeatedly exposed to multiple novel stressors. A second type of allostatic load is the result of a lack of adaptation to those novel stressors. A third type is associated with a prolonged response that is due to delayed shut down of the stress hormone response system. A forth is due to an inadequate response, such as inadequate secretion of glucocorticoid, which in turn leads to elevated levels of inflammatory cytokines. Those cytokines are normally kept in check by the glucocorticoids.

There is no clear dividing line between a person’s philosophy and physiology. —William James

No thought, no emotion, is without biochemical, electrochemical activity; and the activity leaves no cell untouched. —Jeanne Achterberg, Ph.D.

Thoughts are electrochemical events, taking place within nerve cells, and these chemical changes inevitably invoke parallel chemical and hormonal changes throughout the body. —Alastair Cunningham, Ph.D.

Here is still another way our emotions have profound physiological effects on neurotransmitters and hormones. The heart is innervated by both the sympathetic and parasympathetic branches of the autonomic nervous system. Parasympathetic fibers innervate the heart via the vagus nerve and release the neurotransmitter, acetylcholine (Ach) on sinoatrial (SA) node cells. ACh has an effect on the depolarization of SA nodal cells, slowing their firing rate. The increased parasympathetic stimulation has a negative chronotropic effect, slowing the heart rate (HR).

Increased HR is the result of the release of increased NE from the sympathetic fibers that innervate the heart. Emotional distress increases sympathetic activity and decreases parasympathetic activity, sometimes resulting in tachycardia.

Sympathetic activation also results in NE being released on the heart’s ventricular cells, which leads to more forceful contractions. This increased sympathetic activation leads to increased HR, increased contractility, and increased vasoconstriction in all the major arteries. This is a good thing when we need to physically escape actual danger every once in a great while. However, emotional distress on a regular basis causes these same effects, and that chronicity is pathogenic to the entire cardiovascular system and beyond.

The baroreceptors provide a feedback mechanism that helps us remain normotensive throughout the day. Based on the results observed in the growing number of fMRI studies of meditating Buddhist monks, it is likely that increases in allostatic load involve changes in the brain that could likely impair baroreceptor function, knocking out our best protection against spikes in blood pressure (BP).

Emotional distress results in an alpha-adrenergic-mediated vasoconstriction in the entire GI tract, the kidneys, and the liver. Any negative impact on renal function can interfere with the ability to regulate BP through fluid balancing. The release of angiotensin results in fluid retention and vasoconstriction, further contributing to hypertension. Antidiuretic hormone (ADH) (vasopressin) serves to increase the water permeability of the collecting ducts in the kidneys, causing additional increased vasoconstriction, systemically. It is possible that anxiety sometimes decreases renal function. It is also possible that since anxiety is known to raise blood pressure, it could actually improve renal function by way of increased renal oxygenation and perfusion. It is known that the renal arteries are not very responsive to alpha-adrenergic-mediated vasoconstriction. During sympathetic arousal, skeletal and heart muscle receive increased oxygenation and perfusion while the GI tract receives less.