Oxidative Stress

People who suffer from high blood pressure have been shown to have higher levels of the byproducts of oxidative stress as well as an inability to produce adequate levels of intracellular antioxidants, which help to neutralize the unstable molecules that cause oxidative stress.

The results are an early disturbance of the endothelial cells that line the vessels, and this represents compelling evidence of the root causes for hypertension. These sensitive cells experience injury and stress, just as all other cells in the body. However, these cells’ ability to self-repair from exposure to toxins, mechanical injury, exposure to pro-inflammatory cellular “waste” products, and infiltration from “bad cholesterol” have broken down.

The weight of oxidative stress causes a shift in the REDOX potential, and the cell is unable to maintain balance. The result is cell death, cell dysfunction, or cellular defensive adjustments.

Cell death requires replacement. In youth, the body easily adjusts. With age, this cellular renewal slows down and sometimes results in scar formation. This is the beginning of arterial plaque, or hardening of the artery.

Cellular dysfunction can also cause abnormal signaling by REDOX molecules, producing a stress response that can create constriction and cause an elevation in blood pressure. Defensive adjustment leads to inflammation and further infiltration of immune cells and expansion of plaque formation that can harbor clots and may eventually even lead to stroke and heart attack.

Solutions are found in balancing the diet with fewer sugars and more complex carbohydrates. Additionally, maintaining proper weight and having daily exercise along with supplementing REDOX signaling molecules can create a balanced physiology and prevent the damage to the vessels from oxidative stress.

The number-one killer in the industrialized world is coronary artery disease (CAD). The arteries of the muscle of the heart are very susceptible to oxidative stress. The oxygen and nutrient requirements of the heart muscle cells are massive. The heart never rests! Thus, these vessels are critical lifelines for the heart muscle to be able to function.

Blockages cause major troubles for the cells. The body has established vast pathways of vessels and capillaries and to provide the needed “interstate” arteries as well as the tiny side “roads.”

Blockages (see HYPERTENSION) cause oxidative stress in the cardiac muscle cells. This oxidative stress can cause REDOX chemical reactions, which result in malformed proteins—proteins that fail to produce the contractions (muscle squeezing) necessary to pump blood throughout the body.

Oxidative stress in the muscle cells causes a chemical imbalance inside the cells (NAD(P) oxidase, and a breakdown in the mitochondria’s (cellular power plants) ability to create energy via electron chain transport system. This buildup (like rusting) and oxidative stress, coupled with a lack of ATP (energy) being produced by the muscle cell, causes weakness in contraction ability. Cells can actually die from exhaustion as well. Some cells weaken so much that they dilate (enlarge), resulting in heart enlargement (congestive heart failure).

Treatment is challenging. Symptomatic treatment may include stretching the vessels open with balloons placed in the arteries through angioplasty/angiography, which can be life-saving. Best, however, is to get at the heart of the problem (pun intended), by decreasing oxidative stress. Obesity, hypertension, and elevated blood lipids are REDOX mediated issues that respond to foundational lifestyle changes and supplementation of REDOX signaling molecules.

Alzheimer’s disease, an age-associated dysfunction of brain cells that is degenerative in nature, is clearly connected to oxidative stress. Highly specialized brain cells are slower to replace themselves and warrant the body’s protection. The brain has mechanisms that aid this—the blood-brain barrier, for example, and the myelin sheath surrounding nerve fibers are protective of nerve cells.

Damaged mitochondria in combination with chronic oxidative stress often result in the body’s inability to correct imbalances of cellular waste and toxins. Glutathione (a potent antioxidant produced by the body) plays a role in cleaning up but is ineffective without the presence of certain REDOX signaling molecules to help neutralize oxidizing free radical toxins.

This deficiency, usually from sluggish, damaged mitochondria, can be genetically predisposed but may also (especially when manifest in the earlier years) result from habitual smoking, insufficient diet, and stress. Additionally, brain cells have naturally high levels of certain fatty acids, which are especially susceptible to oxidation. The vast blood supply that normally serves the brain is a key factor in the input of oxygen and nutrients and the outtake of waste. Any brief restriction of the blood supply to brain tissue is devastating, and even minor chronic deficiency of good circulation is equally debilitating to the ability of brain cells to maintain balance away from the oxidative zone.

Age-related macular degeneration (MD) perfectly exemplifies the devastation of oxidative stress on specialized tissues. Retinal cells (those affected by MD) have rich oxygen demands, and are injured easily by toxins. Tremendous circulatory strength helps to eliminate the products of cellular combustion, which are large. This oxidative stress load (from cellular combustion) can grow as we get older. Age-induced narrowed circulation along with slower cellular metabolism and energy production by the mitochondria compound the problem. It is this uncorrected oxidative exposure that results in macular degeneration.

Blindness from this condition affects millions of Americans, most commonly after the age of 65. Demographic research demonstrates that MD is more prevalent in those who smoke habitually and are frequently exposed to toxins. Studies have shown that consuming a diet rich in lutein (a potent dietary antioxidant-provoking amino acid) helps to decrease risk of MD. Supplementing the body with balanced stabilized REDOX molecules may help prevent and assist in treatment of this condition.

Osteoarthritis is a condition of uncorrected (by the body) wear and tear that leads to a breakdown in the integrity of the cartilage that lines the joint. Damaged cartilage cannot support ongoing joint movement, and this leads to deterioration and secondary inflammation. Aging can lead to sluggish mitochondria within the cartilage cells (chondrocytes). When the mitochondria are no longer able to maintain the health of the cell, chondrocytes die at a rapid rate, create pro-inflammatory cytokines, and activate certain transcription factors (NF-kB) which instigate an inflammatory response within the joint compartment lining cells (synovial sheath).

Eventually, the fluid in the joint becomes toxic and aggravates the health of the cartilage cells. The bone under the cartilage becomes mechanically and oxidatively stressed as well.

Osteoarthritis is a condition that is best addressed at its foundation—it is a REDOX condition at its core. Regular (not extreme) exercise actually promotes cartilage vitality. There are no vessels in cartilage, so it gets its nutrients and oxygen through diffusion through fluid and tissues directly, and movement promotes this transfer of resources. Maintaining healthy REDOX potential will insure the best way to create a balanced internal environment for cartilage repair and maintenance of a smooth cellular surface to lubricate a joint.

Roughly 90% of strokes are acute blockages (thrombosis) in the vessel. Because brain cells need significant and sustained blood flow to receive oxygen and nutrients, any restriction in blood supply results in serious consequences. From a REDOX perspective, maintaining brain health means maintaining the health of the cerebral vessels (see HEART DISEASE).

Recovery from stroke requires REDOX balance. REDOX signaling molecules render brain cells capable of redesigning both themselves and the interconnections necessary for them to perform critical functions. REDOX chemistry is critical in signaling the replication of neighboring cells to replace damaged ones—this process requires activation of transcription factors, which ignite cellular replication. Partially damaged cells seek to restore mitochondrial actions to rebuild the integrity of the cell membrane and allow nutrients in and waste out.

Obesity is a global epidemic primarily impacting populations of industrialized countries. In the US, obesity rates exploded after the “cola wars” of the late 1970’s and coincided with dramatic increases in sugar consumption, especially among children. Excess calorie consumption leads to weight gain and for most adults, losing the pounds can be a significant challenge.

The answer lies in REDOX chemistry. Obesity leads to a dramatic increase in oxidative stress. In studies, obese subjects show increased superoxide production, protein kinase activation, and endoplasmic reticulum stress in tissues with excessive fat cells. Lipotoxicity is a term describing the oxidative stress load of excessive fat cells in various places in the body. Lipotoxicity leads to altered sugar and fat metabolism as well as high leptin (human obesity protein that regulates appetite) levels. Eventually fat chemicals begin to accumulate in places other than the normal fat deposits—in the pancreas, liver, heart, kidney, and blood vessel walls. These chemicals block the normal function of organs and impede inter-organ and cellular messaging, resulting in signaling molecule message breakdown.

Research is now ongoing to discover an intervention to restore a healthy REDOX potential and correct the weight loss obstacle of oxidative stress. I have personally witnessed how supplementing with REDOX signaling molecules helps greatly in restoring energy levels and reducing the burden of oxidative stress. The results are encouraging.

Type 2 diabetes diagnosis rates have grown in epidemic proportions in the past 40 years, with no slowing in sight. Sedentary lifestyles coupled with diets of processed, calorie-dense foods and sugar drinks have set the stage for this condition. It is a condition based in a failure of insulin to function at a fundamental level, resulting from various forms of oxidative stress. Target tissues (liver, muscle and fat) lose the ability to receive appropriate signals from insulin.

In a healthy body, insulin binds to the tissue receptor specially designed to fit insulin. However, oxidative stress inhibits the various special steps in the “phosphorilization” of various chemical components in the Krebs cycle, and sugars cannot get transported into the cell. The cell starves for energy. Sugar levels in the blood stream (outside the cells) rise, resulting in the familiar negative symptoms of type II diabetes. Additionally, high sugar levels activate transcription factors that ignite gene expression and further insulin resistance.

Because insulin’s action is a REDOX chemical reaction, solutions can be found at this foundational level. Caloric restriction and exercise are restorative, and balancing the oxidative environment may prove helpful with REDOX signaling supplements.