Lectins, Viruses and Pleomorphic Bacteria – The Missing Links
We cannot fully understand how disease develops and how to properly treat it without a return to cellular physiology. New information concerning viruses, intracellular bacteria, and dietary lectins unlocks many of the mysteries of the past and gives us new direction in our approach to “idiopathic” conditions.
Below is the transcript of a lecture given during the North American Veterinary Conference in January of 2013. Of course, I love to talk more than write so “you really had to be there”. But…this papers covers most of the important points, with the exception of a few new items I added to the PowerPoint in the days immediately preceding the talks. For example, the science behind wheat’s harm is in a dynamic state and we are learning more and more every day exactly why today’s wheat is harmful for everyone and every living thing that consumes it.
I will be writing more about a very special lectin, WGA (wheat germ agglutinin), mitochondrial DNA (“It’s bacterial!!!”) and the science of epigenetics in the near future. In the meantime, Google those terms for more insight into how wheat and the other members of the “big 4” do their harm as well as how and why we react the way we do.
Hope these help,
Dogtor J
Lectins, Viruses, and Pleomorphic Bacteria – The Missing Links
John B. Symes, D.V.M.
Beltline Animal Hospital, PC
Mobile, AL
Introduction
The role of viruses, bacteria and lectins in the development of disease has been one of the most intriguing topics that I have studied in all of my years as a veterinarian. I include lectins, particularly those derived from dietary sources, because there is a fascinating interaction between these three entities that helps to explain many of mechanisms involved in the conditions we still refer to as “idiopathic”, a term to which I now take exception. The only concept that irritates me more is “autoimmunity”, a term that implies our immune system does not know what it is doing. I wholeheartedly disagree with the latter premise and a better understanding of viruses, bacteria and lectins supports my dissent.
What are Lectins?
In my quest for solutions to “idiopathic” problems, the study of these antibody-sized proteins yielded answers to many of the questions that were haunting me as I tried to explain how my recommended dietary changes could possibly yield such phenomenal results. Lectins are carbohydrate-binding proteins or glycoproteins of non-immune origin that are ubiquitous in nature. Plants, animals and even bacteria produce these remarkable entities. The latest research has identified both extracellular and intracellular lectins in mammalian cells. Although the true role of lectins is still under investigation, we know that these proteins play numerous important roles in the health of man and his animals.
For example, lectins serve to bind circulating glycoproteins to cells, such as those in the liver, in order to facilitate their removal. Our body produces lectins that are involved in immune responses (e.g. mannose-binding lectin), the adhesion of cells, and the removal of pathogens through binding to carbohydrates on their surfaces. In the case of neurons, the oligodendrocyte produces two different lectins, one that helps nourish its neuron and another that can kill that same neuron. Bacteria produce lectins that enable them to adhere to tissue. Finally, certain foods contain lectins that can do serious harm to susceptible individuals. Therefore, there are “good” and “bad” lectins in nature – those that promote health and others that contribute to the disease process.
For the purposes of this discussion, the focus will be on those dietary lectins that have been directly linked to illness in animals and man. The most common sources of damaging lectins are the gluten grains (wheat, barley, rye), dairy products (cow’s milk), legumes (e.g. soy, peanuts, beans), and corn. The nightshade family (tomatoes, potatoes, peppers, eggplant and tobacco) also contain potentially harmful lectins, most of which are inactivated by cooking but to which some individuals can become quite sensitive (e.g. arthritis). For example, uncooked wheat flour and legumes are considered toxic (injurious) while heating these same foods removes most, but not all, of the harmful lectins.
Fermentation, sprouting, and soaking have also been employed to help remove these pro-inflammatory proteins. However, I frequently tell people to think “peanut allergy” when considering the degree of sensitivity that some individuals develop to these proteins. I suggest any food that requires processing (cooking, fermentation) in order to be made safe to consume may cause problems in the most sensitive individuals even when that processing has occurred. Remember: Lectins are antibody-sized, which makes them virtually impossible to eliminate altogether except through avoidance.
How Lectins Do Their Harm
Adhesion to surface receptors of target cells and interference with the attachment of growth factors necessary for cellular integrity is the accepted mechanism in most cases of lectin damage. However, a question remains how much cellular damage is done through the actual entrance of these inflammation-provoking proteins into the cells resulting in interference with normal intracellular lectin function. Highly toxic plants such as mistletoe and ricin have a more complex lectin structure than that of our typical dietary lectins and the attachment of their lectin (the B chain) allows its component toxin (the A chain) to enter the cell and interfere with ribosomal function.
On the other hand, the current literature typically describes the pathomechanism of the damage done by the less toxic lectins of “the Big 4” (e.g. wheat germ agglutinin or WGA) as being like a lock-and-key, in which the circulating lectin serves as a key that biologically “unlocks” the cell to which it attaches. All complex cells, plant or animal, have carbohydrates that project from their cell membranes. These serve as receptors (docking stations) to which circulating lectins and other glycoproteins attach. When the right “key” comes along, its attachment can initiate a cascade of events in that cell wall that can lead to a number of different outcomes, ranging from the attraction of the immune system and cell death to the production of hormones and chemicals or the multiplication of that cell. It is still unclear as to whether this damage is due primarily to a blocking action of regulatory or promotional compounds or whether the actually lectins enter the cell as they do in ricin or mistletoe toxicity.
Once I found that these harmful lectins (especially those from “the Big 4” – gluten grains, dairy, soy and corn) could cause inflammation and tissue damage all by themselves – without an immune response – food intolerance really started to make sense. The immune response we observe is actually secondary to damage done by lectins, which helps to explain why we see such a variation in the measurable response in different individuals challenged by these provocative proteins. Some will respond with an outpouring of antibodies yielding positive tests while others will not, thus helping to explain the negative test results in individuals who ultimately respond quite well to an elimination diet despite those negative tests. For example, a significant number of gluten intolerants are not “allergic” to wheat and the typical IgE testing done by veterinarians and medical doctors will often yield false negatives when trying to identify those who should avoid gluten-containing grains.
It then becomes quite clear that lectins play a major role in what we label as “autoimmune disease”. Personally, as I stated at the outset, I do not like nor do I use that term anymore unless I put it in quotes as that term implies that the immune system is attacking its own host’s tissues for no good reason. I contend that this does not happen…ever. I believe the immune system always responds appropriately. We simply do not always comprehend why the immune system does what it does. The inflammation being incited by lectins is a prime example of this.
As stated, lectins are antibody-sized. How would we know they are present when they are, in fact, that small? We can’t see them in a routine tissue sample. It would take biochemical analysis or, again, antibody testing to determine whether they are involved. Therein lies the rub. Not everyone responds with what we might call an “appropriate” response (one that we can detect readily). We just have to know that these lectins can and do cause changes in the individual cells of the body (e.g. neurons, nephrons, blood cells, liver, etc) of susceptible individuals.
As a result of studying food intolerance for over a decade, I have concluded that the “big 4” – gluten (from wheat, barley, and rye), dairy, soy and corn – are not healthy for anyone. They are simply better tolerated by some than others. This is the very nature of “spectrum disorders” among individuals, ranging in affliction from the “best of the best” to the “worst of the worst”. The least sensitive take years and years to become affected, often finally yielding to chronic inflammatory conditions such as arthritis, IBS, or hepatitis. On the other hand, the “worst of the worst” are exemplified by peanut allergy. One whiff can result in anaphylaxis. Now that’s sensitivity!
My area of special interest is the dietary control of epilepsy and other neurological disorders. Are lectins involved in central nervous system diseases? The answer is a resounding “yes”, as my findings strongly suggest. It is very clear that our neurons have a true aversion to gluten as this particular glycoprotein has been tied to just about every neurodegenerative and neuropsychiatric disorder known to man? Can gluten kill neurons? Yes, indeed! If an inquiring individual were to do an Internet search for “gluten, neurons”, they would find numerous relevant articles. How the lectins of gluten damage and kill neurons is the interesting thing to study with the answers being found in the more obscure mechanisms of cellular physiology and how that cell responds to challenges. A review of the roles of viruses and bacteria in this fascinating process helps to complete the big picture.
Cellular Response and Adaptation
It seems logical to me that living entities (e.g. viruses and bacteria) inside the cell would be among the things that determine the response of that cell to the challenge by lectins, carcinogens, and other chemicals/pollutants/preservatives, etc. For example, it has been described in the literature that a cell can have as many as ten different responses to a lectin challenge, ranging from cell death (apoptosis) to tumor formation. I have to believe that part of the mechanism involves the presence of adaptive bacteria and viruses found inside that cell. After all, that is what viruses do in nature – they facilitate adaptation (as well as cause variation in nature). Some even help bacteria adapt (the bacteriophage).
The phenomenal thing to see is that our very DNA contains these adaptive viruses. Researchers now estimate that up to 45% of the genetic information in our double stranded DNA are actually viral codes, some active and some extinct. This is what retroviruses, in particular, do. They infect the cell and incorporate their genetic information into our DNA. These are now known as HERVS – human endogenous retroviruses – and they are said to comprise approximately 8% of our nuclear genetic material. That is why these particular viruses are often involved in cancer and why cancer can be “genetic” (inherited). This “genetic” information can then be transmitted vertically to offspring.
As heretical as it may seem, I am now convinced that cancer itself is an adaptive process. I believe the viruses that “cause” cancer are simply adapting to the challenges (e.g. carcinogens) that man keeps throwing at them. When all else fails, they cause the cell (the one they are designed to protect) to start growing out of control in order to ensure the survival of that cell and the virus itself. Thus, I now view a tumor as a “protective cocoon”. Is this a radical idea? Yes, indeed. Does it make sense once it is understood that viruses are vital to the normal function of plants and animals (including man) and that their main purpose is to facilitate adaptation? It certainly does to me, especially when we examine the stages leading up to cancer formation.
The hot topic in today’s cancer circles is inflammation and how cancer typically arises in areas of chronic inflammation. One of the oldest and most well-known examples has been the development of osteosarcoma at a previous fracture site. This appears to occur even more frequently when metal implants are involved in the fracture repair. Other examples are cancer of the lungs, skin, prostate, breast, uterus, ovaries, liver and kidneys, all of which must cope with significant inflammation over the course of their functional lives. Once we grasp the concept of cellular adaptation and identify the culprits that force our cells into changing cell types (e.g. carcinogens, lectins, repetitive trauma, hypoxia, malnutrition), then it is not hard to see why cancer – often referred to as “the end game of immune-mediated diseases” – arises in such areas.
The relationship of cigarette smoking to the development of lung cancer is the perfect example. Our upper airways are lined with rather delicate, tall, slender cells that possess hair-like projections (cilia) for sweeping out impurities. However, under the influence of the heat and toxins associated with smoking, these cells begin to undergo a metamorphosis, changing from the original ciliated columnar epithelial cell into a cell that is more skin-like. This process is known as squamous metaplasia and is considered a pre-cancerous change. The interesting thing to note is, if the individual stops smoking in time, the process reverses. The big question on the minds of those who smoke should be “When is it too late to quit?” I suggest that the primary warning sign of that time approaching is when the smoker’s cough develops, which is reflective of the loss of the cilia, with coughing acting as the back-up mechanism to the sweeping action of those valuable cilia. Yes, there comes a time in the metaplasia of that respiratory cell during which it can no longer support those cilia.
The fascinating question to then ask is “What is responsible for metaplasia?” It has been known for years that the mitochondria play a vital role. Although many are aware that the mitochondrion is the powerhouse (battery) of the cell, most do now know that the DNA of that organelle is thought to be bacterial in origin. Evolutionary scientists believe that bacteria were engulfed by primitive cells (the endosymbiotic hypothesis) and became the part of the cytoplasm of eukaryotic cells that we call mitochondria. I found this theory interesting, but…the take-home message for me was that mitochondrial DNA (mtDNA) was bacterial DNA. And since mitochondria are described as being very dynamic, I had to question whether there was an ongoing influence of extracellular bacteria on the mtDNA in a fashion similar to that of retroviral influence on the nuclear DNA.
The Role of Bacteria and Viruses
Interestingly, it has been recently discovered that intracellular bacteria (pleomorphs, cell wall deficient bacteria, mollicutes) do interact with the mitochondria of the cell to affect cellular differentiation. How they do this is still being investigated but there are two hypotheses: 1) Intracellular bacteria enter the cell, start to multiple and begin to consume the cell’s energy, placing an unusual demand on the cell’s mitochondria and forcing them to adapt, leading to cellular differentiation; and 2) The DNA of intracellular bacteria actually become an active part of the mtDNA, thus facilitating metaplasia in a more direct way. It’s a fine point but one that is intriguing to consider knowing that the DNA of mitochondria is bacterial in origin (whereas that of the nuclear DNA is viral).
So, it appears that we have a “tag-team” of bacteria and viruses working together to facilitate adaption in the cell. Applying this model to our smoker, under in the influence of heat, tar, nicotine and the other 4,000 toxins it contains (including 43 known carcinogens), bacteria from the respiratory tract enter the cell and affect the mitochondria through one or both of the two mechanisms described above and the cell starts to undergo metaplasia. The flattening and toughening of the ciliated columnar epithelial cells continues until the cilia are lost. Again, if the individual stops smoking in time, the process reverses and disaster is avoided. But if the insults continue, the cells persist in their metaplastic transformation and cancer develops…if the individual has the cancer-“causing” virus in their nuclear DNA. If not, they end up like Aunt Edna who smoked 6 packs a day her entire life and died of emphysema or COPD (which we now know are a veritable Petri dish of atypical bacteria, including Mycoplasma and Chlamydia).
But…knowing that we are all subject to multiple carcinogens throughout our lives, starting at birth, why don’t we all suffer from cancer and develop it early in our lives? Once again, there is another part of the “syndrome” that is necessary – a weakened immune system. Yes, we are all killing cancer cells right now (hopefully). The immune system recognizes when a cell is trying to do something inappropriate or harmful and sends in the cavalry. This, I believe, is what we (incorrectly) label as an “autoimmune response”. Once again, I contend that the body knows exactly what it is doing each and every time it takes action. We simply don’t understand what it is doing sometimes and I believe that what we call “autoimmune disease” is one of those times.
It is rather easy to see how this would apply to common medical conditions such as rheumatoid arthritis, chronic active hepatitis, and pancreatitis if we look at the immune assault as “housecleaning”, during which the immune system is taking out the garbage (lectins, toxins, bacteria and cellular debris) from the war that has been going on in that tissue for years and years. But does this principle apply to other immune-mediated diseases? Is it part of the pathomechanism of those “idiopathic diseases” with which we are all too familiar, such as lupus, epilepsy, MS and other neurodegenerative diseases (e.g. Alzheimer’s, Parkinson’s, and ALS)
Many viruses have a distinct affinity for the central nervous system. The two most common brain tumors in veterinary medicine are the oligodendroglioma and astrocytoma, both of which are likely to be viral neoplasms involving those cells that control many of the supportive functions of the neuron, including the production of the myelin sheath and the control of neurotransmitter levels (glutamate). If there are viruses in those cells capable of generating tumors, then through “reverse engineering”, we can see that there are going to be processes (e.g. “autoimmune”, immune-mediated disease) taking place that precede the formation of these tumors. These are the means by which the immune system controls the tumor production…until it is overwhelmed by all the toxins we are throwing at it and our failure to provide adequate nutrition.
Latent viruses are involved in many of the disease “syndromes” with which we are afflicted, including epilepsy and cancer. I like to use cancer as the parallel to illustrate the difference between “causes” and “triggers”. For example, carcinogens alone do not “cause” cancer nor do the viruses they challenge. Thus, it is hard to point the finger at either as the “cause” of cancer. It is the marriage of carcinogens and viruses that causes cancer. I am convinced that the public will be told in the (near) future that all cancer is ultimately viral. Researchers have been saying this for years and years. After all, it is what some viruses do… incorporate their DNA into that of the host only to have that cell reproduce out of control at a later date. It is those ugly chemicals and pollutants we call carcinogens that trigger these viruses into turning the DNA into a cell factory.
But again, viruses and carcinogens alone are not sufficient for the individual to develop cancer. The host must also experience some degree of immune failure in order to get the “big C”. So, it is this triad of factors…viruses, carcinogens, and immune failure…that come together to yield the resulting cancer. That is what we call a “syndrome”. There are other contributing factors in this syndrome, including lectins, bacteria, trauma and hypoxia.
Epilepsy as a Model
Epilepsy is also a syndrome and parallels cancer. Most individuals are loaded with viruses that have the potential to cause seizures just as they have those that are involved in cancer. In humans, Epstein Barr (EBV) is one such Herpes virus. 50% of our children in the U.S. have Epstein-Barr by age 5 and 95 % of Americans over age 40 have this virus in their body. Many epilepsy sufferers have never been told that viruses are proven causes of seizures. The fact is that there are over 25 viruses known to causes seizures in people, many of which are ubiquitous, including Epstein Barr, Herpes simplex, measles, mumps, Coxsackie viruses, and many more. Of course, measles and mumps are in the paramyxovirus group, to which the virus of canine distemper belongs.
But why don’t 95% of Americans over 40 years of age seizures if EBV can cause them? One explanation would be that most individuals don’t have the right cofactors in place to make it happen. And there are many cofactors in epilepsy: Diet, the existence of food intolerance (e.g. celiac disease), air quality, hormonal influences (e.g. low levels of thyroid or progesterone), lifestyle choices (e.g. cigarette smoking, alcohol consumption, lack of proper sleep and exercise), and many other things that affect the immune system as well as the health of the central nervous system, liver, kidneys, and endocrine systems, all of which can play vital roles in the manifestation and severity of epilepsy.
Of all of these factors, diet is clearly the most important. This is very easy to see once we understand what is required of our brains, bodies, and immune systems in order for them to stay healthy and operate optimally. The “big 4” (gluten, dairy, soy and corn) are the “who’s who” of what is wrong with foods, as they damage our gut’s ability to absorb nutrients (e.g. celiac disease), shower our body with damaging proteins (lectins), load us up with staggering levels of “excitotoxins” (glutamate and aspartate) and pound us with pro-inflammatory bioactive phytoestrogens (isoflavones). As a result, tissue health suffers, immunity fails, enzyme systems go down, and the Pandora’s Box of viral and bacterial disease is opened wide.
Our medical histories all line up with this once the role (and ultimate purpose) of viruses and bacteria in nature and in our bodies is grasped. They are not the malicious entities that we have labeled them to be. They are our roommates and are simply doing their job. The noxious stimuli being thrown at them is the real issue. We are forcing them into becoming “pathogens”, a commonly applied misnomer. After all, how can we label a bacterium like Borrelia burgdorferi (Lyme disease) a true “pathogen” when only 5% of dogs infected with this guy will ever develop clinical signs? The same can be said of the Tuberculosis bacterium. Over 1/3 of the world’s population is now infected with TB and yet only 3.5 % have active TB at any given moment, with the main at-risk factor being cigarette smoke. Whose fault is it that the TB bacterium starts to replicate and does tissue harm? And what substance activates mesothelioma? We’ve all seen that ambulance-chasing ad for asbestos exposure victims. Would that virus have never been activated had the individual not been exposed to asbestos? Yes, some triggers are very specific. Is the virus or the bacteria really the culprit here?
In addition to the plethora of offending agents they consume, most individuals are compounding matters through poor nutrition, polluted environments, fast-paced lifestyles, overindulgence and lack of sleep. All of these things add up to the self-induced misery we see around us.
Conclusion
Our pets may not be out partying all night but the two most important factors – their horrific commercially-prepared diets and polluted environments – are wreaking havoc on their health just as they are ours. Is it really their “genetic makeup” that is cutting their lives so woefully short? Do our “genes”, as we’ve previously understood them, ultimately turn on all of us? If so, why do they wait years and years to make that turn?
Aided with the latest research concerning dietary lectins, viruses, and bacteria and our understanding of the mechanisms by which toxins and carcinogens do their harm, we can start to see what…or who…the real culprit is. As the cartoon character Pogo so wisely stated years ago, “We have met the enemy…and he is us.”
