Appendix: Oxidative Stress and Lung Disease, Diabetes

Appendix A: Oxidative Stress & Lung Disease

For current smokers, former smokers and people with respiratory health concerns, a key cause of shortness of breath is inflammation. Inflammation in the lungs is similar to inflammation in other parts of your body — tissues swell with fluid and become stiff. If you’ve ever sprained an ankle, knee or shoulder, you know how your damaged joint swelled and stiffened for a period of time after the injury. The pressure of the swelled tissue feels uncomfortable, like someone squeezing you. The stiffened joint makes it hard to move, restricting your activity. Well, now imagine those same effects happening to your airways… no wonder it’s hard to breathe!

So what causes lung inflammation? Researchers believe a leading cause of inflammation in the lungs is “oxidative stress” created by prolonged exposure to cigarette smoke. You see, a single puff of cigarette smoke contains 10,000,000,000,000,000 pro- oxidative molecules known as “free radicals.”

Free radicals from cigarette smoke are destructive particles that travel like shards of glass into the lungs and nick up the smooth lining of the lungs called the epithelium and expose cells of the epithelium and surrounding muscle tissue to the toxic chemicals in cigarette smoke. Over time, the damage done by the constant barrage of free radicals permanently alters lung tissue, causing it to malfunction. As a result of this damage, your lungs become inflamed when lung cells sense a threatening presence (i.e. bacteria, fungi or other “alien” inhaled particles).

Imagine invading bacteria are inhaled into your lungs (the aliens). Proteins in lung cells called cytokines that are charged with keeping a lookout for troublemakers (radio listeners) sense the invasion and panic. The cytokines start signaling other cytokines, sending out thousands of messages (calls flooding police stations). The message-receiving cytokines in turn call even more cytokines and so on… all putting out alerts for the body to produce white blood cells (policemen) to come and attack the invading aliens. The cells that produce white blood cells receive thousands, tens of thousands, hundreds of thousands, millions of messages from the cytokines to rush to the lungs as fast as possible and take care of the invaders. Soon the lung tissues, as the cytokines and white blood cells gather for the fight, become swelled with the particles and fluids from these defenders of the peace, all running around in a panic about the invading bacteria. They’ve brought enough ammo to wipe out millions of the invaders… but guess what? There may only be a hundred of the bacteria molecules.

You see — it’s a false alarm. An act. An overreaction. Cigarette smoke has messed up lung cells’ ability to appropriately detect and respond to invading bacteria. Instead of cytokines accurately sensing the number of invading bacteria/fungi and sending out signals for a proportional response to kill them, the cells fear there is a massive attack and respond with overwhelming force. The problem with this overreaction is that when lung tissues swell with fluid and become stiff, the airways narrow, and it becomes harder to breathe.

How can you stop or reduce inflammation? Pulmonology researchers and practitioners are in an ongoing search to find effective ways to reduce oxidative stress, relieve inflammation, and prevent/ reverse /minimize the damage done by cigarette smoke and other inhaled toxic agents.

If you currently smoke, the number-one step you can take to reduce inflammation is to quit. Permanently. Plain and simple, it’s the single best first step you can take. Outside of smoking cessation, physicians can and often do prescribe some combination of short-acting bronchodilators and corticosteroids for use when patients are experiencing uncomfortable shortness of breath. These medications force open the airways by shutting off the production of cytokines and similar signaling agents in the body… but only for a short time.

These pharmaceutical solutions do very little to resolve inflammation long term, and they unfortunately come with common dissatisfying side effects such as persistent dry-mouth.

Physicians often also prescribe antibiotics to help patients and others with respiratory conditions defeat upper respiratory infections caused by bacteria & fungi. Antibiotics do help relieve immediate shortness of breath symptoms by killing off infectious bacteria & fungi, but again, this is only a short-term fix. Antibiotics do not relieve inflammation over the long term.

There are some very specific, research-proven action steps you can take on your own to reduce oxidative stress, alleviate inflammation, reduce shortness of breath and feel better for the long run, including:

  • Engage in a regular cardiovascular & strength training exercise program
  • Increase antioxidant & key nutrient intake from food
  • Increase antioxidant & key nutrient intake from dietary supplements
  • Ensure you are receiving adequate exposure to direct sunlight
  • Practice proven breathing techniques & airway clearing techniques


Appendix B: Oxidative Stress & Diabetes

Type-2 diabetes (often referred to as adult-onset diabetes) is the most common form of the disease and affects over 150 million people worldwide. And scientists project that diagnoses of the disease will double within the next 14 years. Diabetes is considered a metabolic disorder where the body’s process to absorb, utilize and store blood sugar (glucose) becomes disrupted.

What causes the disruption of this process?

Researchers believe it is oxidative stress created by a combination of poor diet and physical inactivity. Poor diet contributes to the development of diabetes through high consumption of pro-oxidant-laden foods (saturated fats are the primary culprit) and low consumption of antioxidant-rich foods (unsaturated fats, fruits, vegetables, nuts, whole grains). Physical inactivity contributes to the development of diabetes by reducing the body’s ability to efficiently produce and/or utilize the low level of antioxidants and antioxidant precursors consumed through food.

So, as described in the main body of this report, high doses of pro-oxidant molecules (free radicals) damage the lining of cells in our vital pathways because we don’t have adequate supplies of circulating antioxidants to offset their destructive force. This allows pathogens and toxins consumed in food, beverages and the air to damage underlying cells.

In the case of diabetes, the damage inflicted by toxins and pathogens on underlying cells appears to primarily affect the cell membranes of muscle cells and their ability to recognize insulin molecules. You see, insulin is produced in our bodies to help transport glucose to the muscles and organs, so these tissues can produce energy to perform our vital functions.

The mechanisms at work here are as follows: Let’s say you want to get up, walk across the room and answer the phone. To accomplish this act, your brain sends signals to muscle cells indicating a demand for muscle movement. In turn, the muscle cells send out signals indicating a need for glucose to help produce energy in order to facilitate the muscle movement (some glucose is floating freely in the blood, and other glucose is stored in the form of fat cells). The recipient of the muscle cells’ call for glucose is the pancreas, which produces a facilitator molecule called insulin. Insulin’s job in this chain reaction is to seek out glucose, grab hold of it and hand-deliver it to the muscle cells. When insulin molecules with glucose molecules in tow show up at the muscle cells, they are supposed to signal the muscle cell wall to open up and accept the glucose molecule. Once the glucose is absorbed into the cell, it is converted into energy by the cell’s mitochondria, allowing the muscle to react to the brain’s command.

That’s how it is supposed to work. But in sedentary individuals, this process is often disrupted. In particular, two things seem to happen when we don’t regularly engage in physical activity. First, muscle cells become “insulin resistant,” meaning they either don’t recognize that insulin has arrived bearing glucose, or they don’t open up and allow the glucose in. This results in an oversupply of both free-floating glucose and insulin in our blood (since the muscle cells aren’t getting the glucose they need, they keep sending out signals for more glucose, which means the pancreas creates more and more insulin).

The second effect of this process breaking down is reduced muscle oxygen capacity. You see, the muscle cells not only need glucose to produce energy, they also need oxygen delivered from the lungs via red blood cells. Without both pieces delivered in the appropriate mix, the muscle cells can’t utilize the oxygen that has arrived. It’s sort of similar to how a combustion engine works in an automobile: Air is mixed with fuel in the engine cylinders, and when an electrical spark is introduced by a spark plug, an internal explosion is triggered, which provides the energy for the car to move. An inappropriate mix of fuel and air will cause a car engine to misfire or operate inefficiently. In human muscle cells, the inappropriate mix of glucose and oxygen reduces the cells’ capacity to utilize oxygen efficiently.

The amazing thing about regular exercise is that it appears to help re-sync the body’s energy transport/utilization process (i.e., metabolism). In other words, exercise appears to help the body self-correct how it produces and uses energy, though scientists don’t fully understand how or why.

On the diet front, shifting dietary consumption from high levels of saturated fats and sugar in diabetics to a Mediterranean-style diet high in unsaturated fats, fruits, vegetables, nuts and whole grains has been shown in multiple studies to reduce markers of oxidative stress and inflammation, lower fasting blood glucose, lower fasting insulin and reduce insulin resistance. This occurs because such a switch reduces the consumption of pro-oxidant molecules and replaces them with higher doses of antioxidant molecules.

So how do supplemental antioxidants fit into the picture? Several core nutrients discussed in this report have been studied in relation to reducing oxidative stress and inflammation in diabetic patients, laboratory animals and human tissue samples, including N-acetylcysteine (NAC), vitamin D, vitamin C, conenzyme Q10 (CoQ10), vitamin E, zinc and selenium. Many of the studies have produced promising results, however, to be fair and balanced, live human studies on these nutrients have produced conflicting results.

Here is a small sampling of live human results that have shown promise:

A 2006 study found that women who consumed 800 IU of vitamin D and 1,200 mg of calcium daily from all sources (meaning food and dietary supplements) had a 33% lower incidence of diabetes compared with women who consumed half those amounts.[1]

A 1995 study examining the supplementation of 2,000 mg of vitamin C daily in 56 non-insulin-dependent diabetic patients produced statistically significant reductions in fasting blood glucose, fasting levels of hemoglobin (hemoglobin levels are notably raised in people with poor glucose sugar control), cholesterol and triglycerides.[2]

In a 2010 study, 46 diabetic patients at risk for nephropathy (kidney disease) who were administered 1,200 mg of NAC along with a saline solution experienced a statistically significant reduction in creatinine, a protein associated with kidney inflammation, compared to study subjects who received only the saline solution.[3]

We are not so bold as to suggest that supplemental antioxidants will prevent or cure diabetes. That said, based on the body of diabetes-related antioxidant research we’ve reviewed, combining targeted antioxidants with a regular program of physical activity and a Mediterranean-style diet can be helpful in reducing oxidative stress and inflammation in this population.

[1] Pittas AG, et al. Diabetes Care. 2006 March; 29(3): 650-656.
[2] Erikkson J, et al. Annals of Nutrition and Metabolism. 1995; 39(4): 217-223.
[3] Sar F, Journal of Nephrology. 2010 Jul-Aug; 23(4): 478-482.

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