Grouppe Kurosawa: Can the Flu And the Common Cold Be Cured? (print)

Can the Flu And the Common Cold Be Cured?
Unlikely. But there is something you can do to prevent these viruses
from making you really sick.

Can the Flu and the Common Cold be cured? Unlikely. But there is something you can do to prevent these viruses from making you really sick.

A cure for the common cold is not likely. Most “cold viruses” are rhinoviruses, a group of respiratory viruses that includes over 100 members. Due to something called “genetic drift” this number is always increasing. Immunologically, these viruses are sufficiently different to make the development of one, all encompassing, vaccine very difficult if not impossible. The same is true of influenza viruses. They change their structure over time which makes the development of one, all encompassing, vaccine impossible. Nevertheless, there is something you can do to prevent rhinoviral and influenza virus infections from making you really sick. Rhinoviruses and influenza viruses both infect the lungs, but they are a world apart in terms of toxicity. Rhinoviruses are not unlike plant pollen. They are intrinsically harmless, but the immune response they stimulate is not. Influenza viruses, on the other hand, are deadly if the immune response does not control them appropriately. In either case, natural medicines can interfere with the ability of both viruses to infect cells in the lung. In this essay, we will review the infection cycle for both these viruses and suggest treatment approaches that can be adopted by anyone with access to a drug store or grocery market.

Two of the most heralded natural preventative medicines for the common cold are chicken soup and vitamin C. Both of these natural medicines do alleviate some of the symptoms of respiratory infections. Vitamin C must be taken in large doses (over 1 gram/day) to see any results, and the effectiveness of chicken soup probably has more to do with the fact that it is served hot than the actual content of the soup. Contrary to a common myth, exposure to cold temperatures has absolutely nothing to do with becoming infected with a respiratory virus. Scientists have been administering volunteers nose drops full of rhinoviruses for 50 years and there is no necessary correlation between prolonged exposure to cold temperatures and susceptibility to viral infections. It is actually very difficult to intentionally make a person sick, even with huge doses of viruses. Stress, on the other hand, whether it is due to cold temperatures or emotions, does play a role in the susceptibility to viral infections, and many other diseases for that matter. However, most stressors are highly individualized. Some people are intrinsically sickly while others rarely become ill. If one persons immune system is better than anothers, it is probably not due to genetic factors. With few exceptions, what is or is not stress is strictly in the eyes of the beholder. Burns and hypothermia are obvious examples of physical events that are stressors regardless of how they are perceived, but these types of injuries are extreme and uncommon. Under most situations, the immune system is perfectly capable of eliminating both rhinoviruses and influenza viruses from the body in relatively short order. This is why flu vaccines are only offered to the elderly, a population that has an intrinsically sluggish immune response to many pathogens.

First we will discuss rhinoviral infections. With one exception, all rhinoviral strains can be categorized by their binding affinity for one of two cellular receptors. Macrophages, large white blood cells that ingest and destroy cellular debris and microorganisms, have two different rhinoviral receptors on their membranes. One of these receptors is called ICAM-1 and it represents the cellular binding site for 90% of all rhinoviruses. Rhinoviruses do not actually grow in macrophages, but they do activate them to secrete a long list of inflammatory hormones that contribute to the common symptoms associated with a “cold”. Rhinoviruses also cause an influx of neutrophils, white blood cells that are one of the first lines of defense against bacterial and viral infections, into the lungs. Once localized in the lungs and nasal passages the neutrophils secrete additional factors that increase inflammation, airway constriction, and the flow of mucous. Rhinoviruses cause respiratory infections because they induce a highly exaggerated immune response to their own presence. This is due to the nature of their cellular receptors, and the high concentration of these receptors on white blood cells and cells lining mucous membranes. Healthy people are exposed to rhinoviruses all the time, and their immune system quietly takes care of the intruders without inducing cold symptoms. Children are particularly susceptible to colds because their immune systems are not fully developed. Although rhinoviral infections are often considered harmless from a pathological standpoint, this is not true for children. Rhinoviruses cause bronchitis, croup, bronchopneumonia, asthma attacks, and crib death. The relationship between crib death and subacute respiratory infections is only now becoming understood. Most asthma attacks in children have also been linked to rhinoviral infections. Fortunately, the severity of rhinoviral infections can be controlled without too much effort.

Most viruses, including rhinoviruses, are harmless if they cannot enter cells in which to grow. The most notable exception to this general rule is the HIV virus. Even dead HIV viruses can cause damage to the immune system. Viruses are obligate intracellular parasites. This simply means that viruses and some other microorganisms cannot grow outside a host cell. If the entry of a virus into its respective host cell in blocked, the virus cannot increase its numbers, destroy tissues, or overly activate the immune response. The ICAM-1 protein serves as the major binding site for rhinoviruses. This protein exists on the membranes of white blood cells, endothelial cells (the cells that form blood capillaries) and various cell types in the lungs. Normally, the ICAM-1 protein is barely expressed on the membranes of cells. However, during an inflammation, they are hyper-expressed. ICAM-1 interacts with a protein called LFA-1 that is expressed on the membranes of white blood cells. The interaction between ICAM-1 and LFA-1 allows white blood cells to exit the blood and to enter the tissues, such as the lungs. As a general rule, you don’t want white blood cells entering tissues if there is no need. These cells and the inflammatory products they secrete can turn a small, localized inflammation into a major, chronic inflammatory condition. Just ask anyone with rheumatoid arthritis.
When a rhinovirus enters the lungs, it binds the ICAM-1 receptors in the lung tissues and activates the cells harboring the ICAM-1 molecule on their membrane. This induces a further synthesis of ICAM-1 proteins resulting in a hyper-expression of ICAM-1 on cellular membranes. Now the white blood cells, such as macrophages, neutrophils and lymphocytes enter the lungs in large numbers. The immune hormones these white blood cells release cause the symptoms associated with a “cold”. Rhinoviruses are not deadly, in and of themselves. However, the exaggerated immune response to these viruses can be quite deadly, such as inducing fatal asthma attacks. Influenza viruses are all potently deadly, especially in someone with a compromised immune response. The immune response that is initiated by “flu virus” is acting in defense of ones health. The opposite is true of the immune response against rhinoviruses.

Can you “defend” yourself against rhinoviral infections? The answer is yes. There actually is some truth to the late, great Dr. Linus Pauling’s claim that vitamin C can prevent a “cold”. Unfortunately, prevention requires a steady, large daily dose of vitamin C and the results are inconsistent. If you smoke or are under constant stress (who isn’t these days), you can forget about vitamin C. Both of these conditions destroy vitamin C at a rapid rate. Vitamin C is an important anti-oxidant, but other compounds are more powerful.

First, a little more background information. Rhinoviruses bind the ICAM-1 protein, which activates the cells harboring this protein on their membranes. This activation cascade forces an important genetic regulator protein to migrate from the cytoplasm (the interior of the cell excluding the nucleus where the DNA is kept) to the nucleus. When this protein, called nuclear factor kappa beta or NF-kappaB, binds the DNA in the cell, it activates a number of genes. These previously quiet genes now produce a wide variety of pro-inflammatory immune hormones. The list is long and distinguished. These hormones make the inflammation worse by attracting additional white blood cells into the lungs. Once in the lung tissue, the activated white blood cells release additional inflammatory compounds further compounding the problem. Two very simple procedures can dramatically reduce the cellular immune response to rhinoviruses.

The first step is to incorporate more arginine into ones diet. Arginine is an amino acid that is found highly enriched in nuts of all kinds, including peanut butter. This sounds crazy, but it isn’t. Give us a moment to explain. There is a protein in white blood cells and other tissues called inducible nitric oxide synthetase or iNOS. The iNOS gene is normally inactive until some form of inflammatory response activates it. iNOS makes nitric oxide (NO) from the amino acid arginine. NO is a highly chemically reactive molecule that is capable of forming complexes with a host of proteins, especially those of pathogens. When a macrophage “eats” a microorganism, iNOS is activated to produce NO. NO binds the pathogen proteins and effectively neutralizes their ability to reproduce. In a perfect world, all pathogens would be killed by NO released by scavenger white blood cells. This is not true. NO kills most bacteria and fungi, but it has an unpredictable effect on most viral infections. Except rhinoviruses. NO shuts down the synthesis of rhinoviruses by neutralizing a rhinoviral protein that is absolutely essential for the production of additional virus. In the case of influenza, HIV, herpes, and possibly hepatitis viruses, NO makes the infection worse—not better. This is why web sites that provide information to people suffering from herpes warn infected people to stay away from nuts and arginine vitamin supplements.

The second step involves taking 100 milligrams or so of the potent anti-oxidant alpha lipoic acid (ALA). Actually, combining ALA with vitamin C and vitamin E would be best. When vitamin C and E neutralize free radicals, they become inactive. ALA can reactive them, thereby tremendously enhancing their therapeutic effects. ALA can neutralize an amazing array of dangerous free radicals, including hydroxyl radicals, hypochlorous acid, peroxynitrite (a highly dangerous radical that is thought to be one of the causes of dementia in AIDS), and singlet oxygen. The reduced form of ALA, dihydrolipoic acid (DLA), can scavenge superoxide radicals, and peroxyl radicals, and regenerate the anti-oxidants thioredoxin, vitamin C, and glutathione, which in turn recycles vitamin E. Powerful stuff. Science is confusing but fun once you get used to it.

Many free radicals, especially peroxynitrite, can induce the genetic regulator protein NK-kappaB, discussed previously, to migrate into the nucleus and activate a host of pro-inflammatory genes. Vitamin C can inhibit this migration, but not to the degree that ALA can do so. ALA is one of the most powerful preventative medicines a person can incorporate into their diet. And most people have never heard of it. In laboratory tests, ALA was found to strongly limit the expression of the ICAM-1 gene. In the absence of ICAM-1 expression, the rhinovirus cannot enter cells to reproduce. In addition, white blood cells cannot enter the lungs to make the inflammation worse. Remember, the immune system can’t tell the difference between a rhinovirus and an influenza virus. It just knows it is supposed to “do something”. One final, and very important point. When the migration of NF-kappaB to the nucleus is inhibited by vitamin C or ALA, the virally infected cell dies by a process called programmed cell death. This form of cell death does not cause additional inflammation, while it removes the so-called viral reservoir, the cells producing and secreting virus, from the body.

In review, rhinoviral infections can be prevented or treated with arginine and ALA or a combination of ALA and vitamin C and E. This simple combination of non-prescription products prevents the rhinovirus from infecting new cells (inhibiting ICAM-1 expression), prevents additional white blood cells from entering the lungs which makes the inflammation worse (also by inhibiting ICAM-1 expression), prevents the rhinovirus from reproducing in infected cells (by producing NO), prevents the synthesis of pro-inflammatory hormones (in inhibiting the migration of NF-kappaB into the nucleus) and induces infected cells to die by a non-inflammatory process called programmed cell death (also by preventing the migration of NF-kappaB into the nucleus).

Influenza virus infections are an entirely different story. Anti-oxidants such as vitamin C and ALA, and supplements containing arginine can prevent influenza virus infections, but they are less than suitable treatments for preexisting infections. The influenza virus is quite complex. It reproduces so fast and mutates so quickly that extremely toxic strains of the virus can destroy 80% of the immune system in four days. One of the characteristic differences between virulent (toxic or fatal) strains of virus and non-toxic is the ability of the former to inhibit the activation of pro-inflammatory immune hormones. When we discussed rhinoviruses, we talked about inhibiting the activation of the genetic activator protein NF-kappaB. This would terminate much of the immune response against an otherwise harmless virus. Influenza virus accomplishes this trick all by itself. One of its proteins, called NS1, blocks the activation of NF-kappaB. This reduces the secretion of pro-inflammatory immune hormones and retards the activation of the immune response against the virus. NS1 induces programmed cell death in neighboring cells as well. During an HIV infection, the virus activates the NF-kappaB protein. This results in the synthesis of additional virus in addition to an activation of the immune system. As a result, the infection is never eliminated, but it is controlled for a number of years. In the case of influenza, the exact opposite is true. The flu virus prevents NF-kappaB activation, thereby inhibiting full activation of the immune system. As the virus grows, it kills the cells it infects in addition to neighboring cells. Death can come rapidly.

Now back to prevention. People who smoke or who have chronic lung infections or asthma are much more at risk for developing influenza related pneumonia. During lung infections, or in situations where the lung immune system is activated by cigarette smoke, white blood cells produce free radicals such as superoxide. Superoxide, like NO, can destroy pathogens. It can also destroy normal tissues if it is produced chronically. Superoxide, in low doses, can prevent T cells from recognizing their targets, such as virally infected cells. This unresponsiveness is commonly found in T lymphocytes isolated from tumor tissues. These unresponsive T cells can also be found in the lungs in areas of low level, chronic inflammation. This unresponsiveness in a T cell subset called TH1 results in a dramatically reduced synthesis of important anti-viral immune hormones. Recently, this unresponsiveness was traced to a failure to induce the migration of the genetic regulator NF-kappaB into the nucleus. This is an extremely important discovery. We are exposed to airborne viruses all the time. Our immune system, if not impaired by poor personal habits or chronic stress, is capable of recognizing the viruses and reacting to them. If a person smokes, the white blood cells trying to clear the tar from the lungs secrete superoxide and other free radicals into the tissues. These free radicals can inhibit T cells previously exposed to the virus from becoming reactivated if they become exposed to the virus again. The result is an impaired immune response to flu viruses and just about any other pathogen that can be introduced into the lungs. A dietary program that includes ALA, arginine, vitamin C and vitamin E can help prevent immune non-responsiveness.

Once an influenza infection begins, these anti-oxidants should not be used in high concentrations to treat the disease. In contrast to rhinoviral infections, we do NOT want to further reduce the activation of NF-kappaB. The influenza virus is toxic precisely because it does this on its own, thereby impairing the immune system from mounting an appropriate (immediate or vigorous) immune response against the virus. Low concentrations of anti-oxidants can neutralize superoxide and other free radicals without impairing the activation of NF-kappaB. Therapeutic concentrations or megadoses of vitamin C and especially ALA should be avoided at all costs when an influenza virus infection becomes symptomatic. Therapeutic anti-oxidant therapy for the flu will only make the infection worse.

The best way to fight the flu is to prevent it in the first place. The regular use of anti-oxidants plays a significant role in preventing both rhinoviral and influenza virus infections. Influenza viruses can also be inhibited by treating them with neuaminidase inhibitors. Neuraminidase is an enzyme located on the surface of the virus particles. It interacts with molecules on cells which enables the virus to enter the cells to reproduce. If neuraminidase is inhibited, the flu virus cannot reproduce. There is no disease. Two neuraminidase inhibitors are on the market as prescription drugs—Relenza and Tamiflu. They are used to reduce the severity of already established infections. We can do better than this. Numerous scientific studies have identified ornamental plants that contain very powerful natural neuraminidase inhibitors in their leaves. In the subscription version of Dr. Steve’s Natural Plants newsletter, we will tell you how to grow these plants and prepare leaf extracts for home consumption. No big deal. Really. With a little planning, you should be able to stop the flu virus in its tracks very early in the infection cycle.

If you can grow vegetables, you can make your own natural medicines.