Note: Much of the analysis in this paper draws from the book “Good Calories, Bad Calories” by Gary Taubes, and the article would not have been possible without his research.

At the age of 64, after a morning playing golf, President Dwight D Eisenhower had his first heart attack. As Pulitzer Prize winning author Gary Taubes describes in his book “Good Calories, Bad Calories”, Eisenhower’s heart attack “constituted a learning experience on coronary artery disease (CAD).” After the event, his doctors, considered the top experts in the field, gave the public a “lucid and authoritative description of the disease itself,” followed by twice-daily press conferences held on the president’s condition. Soon, most of America, particularly middle-aged men, were intently aware of the dogma surrounding heart disease, dogma that continues to persist today – namely the notion that dietary fat and cholesterol are major factors in the development of CAD. Like much of the rest of the nation, Eisenhower began to avidly lower his fat and cholesterol intake.

Yet this plan of attack was somewhat counterintuitive for Eisenhower who, before his heart attack, had none of the risk factors mainstream medicine connects with CAD. His blood pressure was only seldom elevated, and his weight throughout his life remained around 172 pounds (considered optimal for his height). His total cholesterol was below normal – his last measurement before the attack was 165 mg/dl, a level that heart diseases specialists today consider safe. He had even quit smoking six years earlier in 1949.

In the time that followed, Eisenhower became a prime example of the fact that fat and cholesterol have little to do with CAD. After gaining four pounds, the ex-president reduced the amount of food he ate for breakfast, then eventually sacrificed lunch completely. His doctor was mystified at “how a man could eat so little, exercise regularly, and not lose weight.”

Even after renouncing butter, lard, cream, and replacing them with corn oil, his cholesterol continued to rise. The president was worried. “He’s fussing like the devil about cholesterol,” wrote his doctor. “He has eaten in the last week only one egg, one piece of cheese.” It got to the point where his doctor started to lie about his cholesterol levels in order to keep the president calm. At one reading, Eisenhower was told his level was 217 when it was actually 223. On his final day in office, he was made to believe his cholesterol was 209 when in reality it had soared to 259. Finally, in 1969 at the age of 78, Eisenhower died of heart disease. By that time he’d had six other heart attacks.

Clearly in Eisenhower’s case, and in the case of many other people with coronary artery disease or CAD, something other than fat and cholesterol consumption drives progression of the disease. As Taubes describes it, the long held dogma about heart disease, in which cholesterol clogging the arteries and excess body fat are viewed as culprits, “as though the fat of a greasy hamburger were transported directly from the stomach to the artery lining,” needs major revision.

In a paper published in the New England Journal of Medicine, researcher Göran K. Hansson explains that while it was previously believed that heart disease was caused by progressive narrowing of the blood vessels as smooth-muscle cells gradually formed plaque, “Recent research has shown that inflammation plays a key role in coronary artery disease and other manifestations of atherosclerosis.”^[1]

Luigi Fontan, MD, PhD, assistant professor of medicine at Washington University in St. Louis and an investigator at the Instituto Superiore di Sanita, Rome, Italy agrees. “Many years ago, atherosclerosis was thought to be related to lipids and to the excessive deposit of cholesterol in the arteries,” states the scientist. “Nowadays, it’s clear that atherosclerosis is an inflammatory disease.”^[2]

“Inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular disease,” states Savoia Schiffrin of the University of Montreal, the lead author of a review article which showed that inflammation is present in the arteries of animals with high blood pressure. “The identification of the mechanisms leading to the activation of inflammation should contribute to the development of specific therapeutic approaches to apply in hypertension [high blood pressure] and its complications.”^[3]

It’s possible that until recently, the vast majority of researchers in the field of CAD have been barking up the wrong tree – focusing on fat and cholesterol and missing the correct cause of cardiovascular disease.

Today, cardiovascular diseases are expected to be the main cause of death globally within the next 15 years, owing to a rapidly increasing prevalence in developing countries and eastern Europe. In fact, cardiovascular diseases cause 38 percent of all deaths in North America and are the most common cause of death in European men under 65 years of age and the second most common cause in women.

Increasing evidence points to the presence of bacteria in Coronary artery disease (CAD)

Coronary artery disease or CAD is driven by atherosclerosis – the accumulation of plaque in the arterial blood vessels. Atherosclerosis is gradual, often taking decades before the affected person is in danger of cardiovascular problems. Plaque is largely composed of white blood cells called macrophages which begin to gather in areas where the arteries naturally bend or curve. Many of these immune cells exhibit signs of activation and produce inflammatory cytokines – proteins that cause pain and fatigue. This, in turn, provokes an inflammatory immune response that causes further damage to the artery wall.^[4]

Over time, the plaque may calcify, or form a hardened “shell.” This reduces the artery’s ability to contract and expand and narrows the artery, thus reducing the amount of blood that can flow through it. If the plaque deposit ruptures, a blood clot can form at the site of the rupture, or pieces of the plaque can travel through the arteries until they eventually cause a blockage. A heart attack and cardiac arrest may result.

Thus, it is the release of various inflammatory substances that drives the pathogenesis of heart disease and stroke. That begs the question – what causes the release of these substances in patients with these illnesses?

It is commonly accepted that inflammation and the release of cytokines are a direct result of bacterial infection. “An inflammatory immune response—one of the body’s primary means to protect against infection—defines multiple established infectious causes of chronic diseases,” argues Dave Relman of Stanford University. “Therefore, inflammation is a clear potential link between infectious agents and chronic diseases.”^[5]

The CDC concurs, stating, “The epidemiologic, clinical, and pathologic features of many chronic inflammatory diseases are consistent with a microbial cause.”^[6]

According to Marshall, the bacteria lurking inside the macrophages of patients at risk for heart disease and stroke are cell wall deficient forms called L-form bacteria. “There is an emerging school of thought in mainstream cardiology that atherosclerosis is caused by microbes; in my opinion the same microbes which we have found to be behind the Th1 diseases [L-form and biofilm bacteria],” states the biomedical researcher.

For decades, microbiologists have realized that these pathogens are able to live undetected inside the macrophages where the immune system can no longer detect their presence. “The presence of bacterial microbes inside the cell is what triggers the immune response,” states Gabriel Nunez of the University of Michigan in a paper published in the Journal of Immunology.

These bacteria are hypothesized to cause inflammation and painful symptoms by taking control and thus modulate the activity of a protein called Nuclear Factor Kappa B. They are able to activate proteins that increase the activity of Nuclear Factor Kappa B, which subsequently moves to the nucleus or center of the cell. Once there, it turns on a variety of genes that cause the release of inflammatory cytokines and other substances. These substances include the cytokines, interferon gamma and TNF alpha, IL-6, tumor necrosis factor, and the hormone angiotensin II.

As mentioned above, as the cytokines are released, the macrophages begin to clump together at injured areas along the blood vessel wall. Since macrophages are meant to be extremely active immune cells that engulf and kill invading pathogens, Marshall sees the fact that these white blood cells begin to gather together listlessly as a key sign that the immune system is not functioning correctly.

What causes this immune dysfunction? Again, L-form bacteria are the likely culprits. In a recent discovery, Marshall used molecular modeling software to show that some species of bacteria are able to create substances that bind into the vitamin D Receptor (VDR) and slow its activity.^[7] Since the VDR, a fundamental receptor of the body, controls the activity of the innate immune system and the activity of the antimicrobial peptides, patients infected with the pathogens become immunocompromised.

“Think about it for a minute,” says Marshall. “If you were a persistent pathogen, wouldn’t it seem a good idea to disable your host’s ability to produce the antimicrobial peptides [and slow the innate immune system]? And if you discovered that disabling just one receptor, the VDR, would get rid of [many types of AMPs], wouldn’t you try to evolve a mechanism for doing that?”^[8]

Because of this immune dysfunction, Marshall believes that the weakened macrophages which clump together in patients’ developing heart disease are eventually killed by the L-form bacteria living inside their walls. As described above, dead macrophages may eventually build up and form part of the plaque that perpetuates cardiac disease. If the immune system were able to function correctly it might be able to clear away developing plaque, but “When the immune system is compromised it simply can’t clear away the obstruction,” states Marshall.

The failure of the immune system to function correctly would also mean that other pathogens besides L-form bacteria are able to persist in the body more easily. One of the most common co-infections found in patients with heart disease and stroke is Chlamydia pneumoniae (CP) – a species of bacteria that dwells exclusively within other cells such as macrophages and traffics cholesterol out of the macrophage cell membrane.

While CP may certainly cause additional symptoms in patients with heart disease, rather than being the cause, it is more likely a pathogen that “comes along for the ride” once the immune system is compromised – a co-infection. This is supported by the fact that CP and Mycoplasma have been detected in control subjects as well as people with heart disease. However, people with plaque have been shown to harbor greater levels of CP and Mycoplasma. Those with the worst plaque levels have markedly higher levels of the pathogens – particularly high in areas of plaque formation.^[9]

It should be mentioned that conditions such as cardiac arrhythmia and mitral valve prolapse, which are not necessarily tied to the amount of plaque in the arteries, have also been tied to bacterial infection (see cases discussed below). Conditions such as atrial fibrillation, congestive heart failure, ventricular enlargement, and valve disease probably may be associated with CAD, but also may result from the direct impact of L-form bacteria and the associated inflammation on heart tissue.

The fact that patients with sarcoidosis, a lung disease caused by L-form bacteria, often show signs of heart disease strongly indicates that their heart problems result from the same pathogenesis. According to the Cleveland Clinic, any cardiac structure may be affected in patients with sarcoidosis. The most frequent diagnoses include heart blockage, infiltrative cardiomyopathy (heart muscle disease) with blood pressure dysfunction, angina-like chest pain and pericardial disease – an inflammatory illness that affects the sac surrounding the heart. The reality that the heart abnormalities found in sarcoidosis have been linked to a bacterial cause adds weight to the argument that all of the yet unexplained forms of heart disease are the result of bacterial infection.^[10]

C-Reactive Protein (CRP)

Another substance released by the immune system in response to L-form bacteria is C-reactive protein or CRP. Interestingly, CRP is actually used diagnostically by doctors to predict future cardiovascular events. “Plasma levels of circulating inflammatory molecules, such as CRP [and the cytokine] interleukin-6 (IL-6), have been shown to be predictive of future cardiovascular disease,” states Paolo Pauletto of the Università di Padova in Italy.^[11]

In fact, nearly all patients with heart disease display high levels of CRP. CRP is elevated on hospital admission in about 90% of patients who have a heart attack preceded by angina. According to Pauletto, high levels of CRP persist in most patients even after they have left the hospital, and at the three-month follow–up mark elevated CRP is associated with subsequent recurrent plaque instability and heart attack.

“CRP is part of the body’s reaction to bacterial infection.”In a 2003 article published in the Journal of the American Medical Association, Howard Sesso and team showed that among 20,525 females enrolled in the Women’s Health Study, levels of CRP predicted the development of hypertension, during a follow-up of 7.8 years.^[12] This data has been recently confirmed by researchers at Kuopio University Hospital in Finland who showed that, during a follow-up period of 11 years, middle-aged men with CRP levels greater than 3.0 mg/l are at increased risk of developing hypertension as compared to those with CRP levels below <1.0 mg/l.^[13]

Yet most of these researchers still fail to link elevated CRP to the presence of bacteria. “They [the researchers in the above studies] are so near and yet so far,” states Marshall. “CRP is part of the body’s reaction to bacterial infection.”

L-form bacteria are passed through blood transfusions

Since it has become abundantly clear that everyone acquires L-form bacteria as they age, it is almost certain that a person who receives a blood transfusion will also acquire new species of L-form bacteria – particularly because L-form bacteria have been detected on multiple occasions inside the red blood cells of both healthy and diseased subjects.^[14][15] The L-form species a person might acquire through a blood transfusion intermingle with the species they already possess – further blocking the activity of the VDR and increasing their risk for CAD.

Indeed, Dr. Barnaby Reeves and colleagues from the University of Bristol studied data on more than 8,500 UK patients who underwent heart surgery between 1996 and 2003.^[16] They found that patients who had received red blood cell transfusions were around three times more likely to suffer a heart attack or stroke due to complications caused by not enough oxygen reaching key organs. Patients who received blood transfusions also had an increased risk of infection, readmission to hospital, and death compared with heart patients who did not receive blood.

“Red blood cell transfusion appears to be harmful for almost all cardiac surgery patients and wastes a scarce commodity and other health service resources.”The risks associated with blood transfusions were not influenced by a patient’s age, hemoglobin levels or the extent of their disability at the time of transfusion. Writing in the journal Circulation, Dr. Reeves and team conclude: “Red blood cell transfusion appears to be harmful for almost all cardiac surgery patients and wastes a scarce commodity and other health service resources.”

Sadly, up until this study, blood transfusions were mistakenly thought to reduce the risk of cardiovascular problems among heart surgery patients by increasing the amount of oxygen in the blood stream and over half of all heart surgery patients in the UK receive blood transfusions.

Vitamin D and CAD

The rate of CAD will also continue to rise until physicians fully comprehend the role that vitamin D supplementation plays in driving all forms of chronic disease. Recent molecular modeling research has indicated that the form of vitamin D derived from supplements and sun (25-D) is a secosteroid. At levels over 20 ng/ml, 25-D begins to bind and inactivate the vitamin D receptor in the same fashion as the substances created by bacteria.^[17] As a result, the activity of the innate immune system and the antimicrobial peptides are reduced, and the transcription of at least a thousand genes (which are also transcribed by the VDR) is thwarted.

As the immune system slows, less bacteria are killed. This often makes the patient feel better temporarily. Why? Because it is when L-form bacteria die that they cause the most problems for the host. The immune system releases numerous cytokines in response to their death, not to mention the fact that the body is forced to deal with the toxins they once harbored and the remains of the cells they once inhabited. All of the above mean that patients taking high levels of vitamin D experience temporary drops in inflammation – drops that are mistakenly picked up by doctors and researchers as a sign that the substance is slowing or preventing disease.

This seeming wellness is illusory. As immune function decreases, the L-form and biofilm bacteria at the heart of CAD and other chronic diseases are able to spread with much greater ease, making the patient much more ill over the long-term.

Why then are we repeatedly told by mainstream medicine that vitamin D is beneficial for people with CAD? Simply because the molecular models showing that 25-D acts as an immunosuppressive secosteroid are very new. Until they gain acceptance, doctors continue to cling to a model of vitamin D that is no more complicated than “vitamin in, benefit out.” Since mainstream medicine doesn’t yet recognize the role that bacteria play in the pathogenesis of CAD, studies continue to tout vitamin D’s benefits without realizing that they are only promoting the use of a steroid.

In the same vein, we are often told that vitamin D deficiency is a risk factor for CAD. Again, misunderstanding reigns supreme – namely, mainstream medicine fails to realize that the low levels of 25-D seen in patients with CAD are very likely not causing the disease, but are simply a result of the disease process. As patients accumulate L-form bacteria, the level of the active vitamin D metabolite 1,25-D rises as a result of bacteria-induced blockage of the VDR. As described by Marshall in his newly published paper “Vitamin D discovery outpaces FDA decision making,”^[8] blockage of the VDR affects numerous feedback pathways – resulting in a downregulation of the body’s level of 25-D. This means that what is commonly interpreted as a deficiency is probably nothing more than a marker of L-form infection.

Nevertheless, studies still continue to incorrectly tie vitamin D “deficiency” to CAD – a recent example being the report just published in a Journal of the American Heart Association which found that patients with vitamin D “deficiency” have double the risk of experiencing a cardiovascular event. However, rather than indicating a deficiency, the low levels of vitamin D observed among the subjects strongly suggests that L-form bacteria are downregulating their levels of measured 25-D.^[18]

The fact that vitamin D has been artificially added to the food chain, and patients are routinely told to take extra amounts of the substance is putting the entire American public at greater risk for CAD. The same can be said for immunosuppressive drugs such as corticosteroids, and a variety of supplements that also slow activity of the immune system. The frequent use of beta-lactam antibiotics, which are quite effective at killing classical strains of bacteria, but actually cause the formation of L-form bacteria, is another practice that must be re-evaluated if we are to effectively conquer CAD. The use of different antibiotics or combinations of antibiotics should be investigated as a means to kill classical strains without promoting L-form creation.

Re-examining the role of dietary fat and CAD

Despite abundant evidence pointing to the presence of a host of microbes in people with heart disease and stroke, much of mainstream medicine still fails to recognize the role of pathogens in causing these forms of illness.

During the time that the role of bacteria in heart disease is gradually gaining acceptance, many doctors continue to blame heart disease and stroke on risk factors previously described – namely diet and cholesterol – the same factors that physicians have been blaming for decades.

This misunderstanding has led to major problems in the field of cardiology, where doctors, oblivious to the pathogens likely making their patients sick, tend to over-emphasize the role of diet, exercise and cholesterol when advising their patients about treatment and medications. Often patients, rather than the bacteria causing their disease, are blamed for the development of CAD. This proves frustrating for many patients who, like Eisenhower half a century ago, develop heart disease and stroke despite significant efforts to keep their weight and cholesterol intake under control.

It follows that for every study showing a connection between fat and CAD there are other convincing studies which demonstrate that dietary fat actually plays a very small role in the progression of heart disease, and that the substance has, for the most part, been incorrectly linked with CAD due to biased research efforts and a tremendous amount of consensus thinking.

The confusion largely boils down to the efforts of one man who, through large public campaigns during the 1960s and 70s, was able to convince the government that it should recommend a diet low in fat in order to help the average American avoid CAD. This man was Ansel Keys. Sadly, Keys’ ability to tie excess fat to heart disease was largely based on popular support (the public and the media were drawn to the idea that heart disease could be prevented by dieting) rather than evidence obtained from reliable research studies.

Keys arrived at his hypotheses linking dietary fat to CAD after studying seven distinct populations around the world who ate diets relatively low in fat and also seemed to have a lower incidence of CAD. In light of today’s understanding of CAD it is very likely that those populations were simply passing around less L-form bacteria. Furthermore, researchers at the University of California, Berkeley, found that Keys had chosen only six countries for his comparison though data was available from 22 countries. When all 22 were included in the analysis, the link between fat and heart disease vanished.

In fact, Keys’ theory implicating diet as the cause of heart disease appeared on the cover of Time Magazine in 1984 despite the fact that, at the time, only two studies had directly tested the connection. One of these studies actually proved Keys wrong. It was a British trial, in which the fat content of the meals of a group of men who had previously suffered from heart attacks was reduced to 1/3 of it’s previous level. A control group continued to eat a normal diet. After three years the average cholesterol levels dropped from 260 to 235, but the recurrence of heart disease in the control and experimental groups was essentially identical. “A low-fat diet has no place in the treatment of myocardial infarction,” the authors concluded in 1965 in the Lancet.

The largest diet-heart trial ever carried out in the United States was not even included in medical or political debates about the best diet for the America public. Because the results opposed what was becoming the consensus view on diet and CAD, they went unpublished (they were later published in a small cardiology journal that very few people read). The trial, which included 9,000 residents of various mental hospitals, found that men on a low-fat diet had a slightly lower risk of heart attacks, although women did not. Overall, patients who had eaten a low-cholesterol diet were associated with a greater risk of heart disease. Of the patients eating the diet, 269 died during the trial, compared to 206 eating the normal hospital food.

One ironic story is that of the Anti-Coronary Club Trial formed in 1966, part of whose eleven hundred members took a pledge to eat what the New York City Health Director at the time deemed a “prudent diet.” Less then 30% of calories on the diet came from fat. Although the diet seemed to prevent heart disease in the short term, just nine months later, an article revealed that 26 members of the Club had died during the trial compared to only six of the men whose diet had not been “prudent.” Eight members of the Club died from heart attack, but none of the controls. This appeared to be “somewhat unusual” the leaders of the study acknowledged.

During the 1980s, British epidemiologist Geoffrey Rose did a series of experiments connecting diet to CAD. According to his calculations, only one man in every fifty might expect to avoid a heart attack by virtue of avoiding saturated fat for his entire adult life. “Forty nine out of fifty would eat differently every day for forty years and perhaps get nothing out of it. The bottom line: It’s clearly important to eat a healthy, well rounded diet, but despite the fact that the vast majority of the medical community still preach a diet low in fat to those at risk for CAD, unless the underlying bacterial cause is addressed, there is little hope that a low-fat diet will curb progression of the illness.

Solidifying the consensus view

What our current generation fails to realize, is that up until about a decade ago, there was a fervent debate between those researchers who believed that fat and cholesterol are at the root of heart disease and a host of prestigious researchers who did not. Unfortunately, in 2000, the National Institutes of Heath held what Taubes described as a “consensus” conference that put a stark end to these years of debate.

“The NIH Consensus Conference officially gave the appearance of unanimity where no unanimity existed.”While those researchers who supported the view that fat and cholesterol are to blame for CAD were given ample time to speak, those researchers who opposed the idea were not even invited. “The NIH Consensus Conference officially gave the appearance of unanimity where no unanimity existed,” states Taubes. “After all, if there had been a true consensus,” one of the researchers involved later explained, “you wouldn’t have had to have a consensus conference.”

When the dietary guidelines laid out by the researchers at the NIH conference reached the public and their doctors, fat and cholesterol became, as they are considered today, the “recognized” causes of CAD. Not surprisingly, with bacteria missing from the picture, and these low fat, low cholesterol guidelines in place, the incidence of CAD has continued to escalate.

Even before the NIH consensus conference, political pressure to agree with the mainstream view affected much of the research on fat and CAD. “It’s hard to avoid the suspicion that once the government began advocating fat reduction in the American diet it changed the way many investigators in this science perceived their obligations,” states Taubes. “Those who believed that dietary fat caused heart disease had always preferentially interpreted their data in the light of that hypothesis. If the evidence didn’t support the recommendations, the task was to interpret it so that it did.”

Weight gain and/or serum cholesterol elevation may not cause CAD but instead be a result of the disease process.

Despite the fact that bacteria rather than dietary fat seem to be at the root of CAD, there is no denying that people at risk for heart disease or stroke are often overweight. Enter one of the greatest misunderstandings still held by modern medicine, surely the misunderstanding that led Keys and other researchers down the wrong path. It’s the idea that excess fat causes heart disease, when, according to the Marshall Pathogenesis, weight gain in patients with CAD is a result of the illness itself, and a sign that the patient is indeed infected with large quantities of L-form bacteria.

The above is true because weight gain and obesity are also greatly affected by L-form bacterial load and the composition of bacteria in the gut. Research by Gordon at Washington University in St. Louis has shown that the species of bacteria in the gut determine how effectively a person gleans calories from food.^[19] When a person becomes infected with L-form bacteria, it seems probable that the immune system is less able to keep bacteria in the gut under control and in the proper balance for optimal health. Species that are extremely effective at extracting calories from food from the host’s digestive tract seem to thrive while other “healthier” species of bacteria are pushed to the wayside. In this manner, many patients infected with L-form bacteria may tend to gain weight even when they are not eating high amounts of calories.

Armed with this understanding, it becomes suddenly clear that heart disease, stroke, and obesity are all likely to be the result of the same pathogenesis. Obesity doesn’t cause heart attacks or strokes – rather the diseases develop simultaneously, due to accumulation of L-form bacteria and the immunosuppression, inflammation, and metabolic changes that results. For example, many cases of heart disease have been associated with insulin resistance, hypoglycemia, and intense cravings for carbohydrates – all of which lead to weight gain and less energy for exercise.

“It’s the first evidence of a potential mechanistic link between abdominal fat and systemic inflammation.”Then again, excess fat does become a place where L-form bacteria take hold, meaning that staying slim might offer some benefit to people with heart disease. Take the recent study by researchers at Washington University School of Medicine in St. Louis who confirmed that fat cells inside the abdomen secrete cytokines – a compelling sign that they are infected with L-form bacteria. “It’s the first evidence of a potential mechanistic link between abdominal fat and systemic inflammation,” states Luigi Fontana, M.D., who headed the study.^[2]

When the team sampled blood from the portal vein in obese patients undergoing gastric bypass surgery, they found that visceral fat in the abdomen was secreting high levels of the inflammatory cytokine IL-6. “The portal vein is filled with blood that drains visceral fat,” says Fontana. “Portal vein blood had levels of IL-6 that were 50 percent higher than blood from the periphery. These data support the notion that visceral fat produces inflammatory cytokines that contribute to insulin resistance and cardiovascular disease,” says Fontana.

Interestingly, increased IL-6 levels in the portal vein were also correlated with concentrations of CRP – the substance previously discussed which is part of the immune system’s response to bacterial infection.

Researchers at The University of Texas M.D. Anderson Cancer Center and The University of Texas Health Science Center at Houston also obtained study results confirming that fat cells do indeed produce CRP, a substance they describe as “a protein that is linked to both inflammation and an increased risk of heart disease and stroke.”^[20] So it comes as no surprise then that overweight individuals are generally shown to have higher levels of CRP.

Carbohydrates and the metabolic syndrome

The metabolic syndrome is a combination of medical disorders including high blood pressure, obesity and elevated tryiglycerides, that increase the risk of developing cardiovascular disease and diabetes. According to a recent article in Cardiology Diabetology, “The metabolic syndrome, together with insulin resistance and their consequences, are basic factors in pathogenesis of atherosclerosis.^[21] The syndrome, which occurs very frequently in our population, has a significant association with chronic viral and bacterial infectious agents.” In fact, according to lead author of the paper, Zahra Sanjdideh, elevated levels of CRP, IL-6, and TNF-alpha (which are released by the immune system in response to bacterial infection) have been shown to exacerbate the condition.

Several recent studies suggest that a diet low in carbohydrates may help patients better manage symptoms of the metabolic syndrome, namely by influencing a patient’s level of the hormone insulin.^[22][23]

The insulin resistance often observed in patients with CAD may be a direct result of bacterial infection. According to Marshall, the VDR is responsible for transcribing the gene that creates insulin receptors. When the VDR is dysregulated by bacterial ligands and high levels of 25-D, insulin receptor expression (manufacture) can be affected.

Patients who consume high levels of carbohydrates tend to experience surges of glucose, leading to higher blood sugar, which also causes inflammation. This additional inflammation may take away resources from the immune system as it is forced to deal with substances such as reactive sugar molecules that produce AGEs (advanced glycation endproducts).^[24]

This may be why several recent studies have found that weight loss among obese subjects can reduce inflammatory markers such as CRP in some people.

In this sense, a diet low in carbohydrates, which may lead to weight loss, could impact a person’s level of inflammation. “In obese, insulin-resistant persons, a calorie-restricted diet, moderately lower in carbohydrate and higher in unsaturated fat, is as efficacious as the traditional low-fat diet in producing weight loss and may be more beneficial in reducing markers for cardiovascular disease risk, states Gerald Reaven of Stanford University.^[25] However, in the long run, beneficial effects would be minimal without addressing the bacteria at the heart of the disease process.

Cholesterol levels appear to have little impact on CAD

There’s also no denying that cholesterol levels tend to rise in people with CAD. The question is why. Do cholesterol levels rise because of the fact that people are eating more of the substance, thus clogging their arteries? Or does cholesterol rise simply as a result of the disease process? Could it be that high cholesterol is simply a sign that a person is accumulating the L-form bacteria responsible for causing heart disease, just as low levels of the vitamin D metabolite 25-D in patients with most chronic diseases is not a sign of deficiency but rather an indication of L-form bacterial infection and immune dysfunction?

“Whether they’re high or low, either our cholesterol levels directly increase mortality or they’re the symptom of an underlying disorder that itself increases our risk of disease,” states Taubes. Although not enough research has been done on the subject at the moment to arrive at a definite answer, the results of numerous studies show that the later may very well be the case.

Over the years, multiple large studies have shown that reducing cholesterol levels in patients at risk for CAD has little, if any, effect on mortality.

In 2001, the Cochrane Collaboration published a systematic review that analyzed 27 of the most rigorous studies to test the ability of reduced or modified diets to prevent cardiovascular disease. Together the trials accounted for around 10,000 subjects followed for an average of three years each.

“The review concluded that the diets, whether low fat or cholesterol lowering, had no effect on longevity and had no “significant effect on cardiovascular events.””The review concluded that the diets, whether low fat or cholesterol lowering, had no effect on longevity and had no “significant effect on cardiovascular events.” Five years later Cochrane published another review, which again examined multiple risk factors including lowering blood pressure and cholesterol in order to see if the substances affected heart disease and mortality. This time around they analyzed the results of 39 trials involving over 900,000 patients, and once again found that the “pooled effects suggest multiple risk factor intervention has no effect on mortality.”

Similarly, the results of the Framingham study, one of the largest studies on cardiovascular disease conducted to date, found that for both men and women over 50 years of age, life expectancy showed no association with cholesterol levels. The likelihood of suffering a fatal first heart attack was no less for those with a cholesterol level of 180 mg/dl than it was for those with 250. In fact, those Framingham residents whose cholesterol declined over the first 14 years of observation were more likely to die prematurely than those whose cholesterol remained the same or increased.

Then there’s the MONitoring heart disease study or MONICA conduced by the World Health Organization in the 1970s which has been described as “far and away the biggest international collaborative study of cardiovascular disease ever carried out.” By the late 1990s, MONICA had recorded 150,000 heart attacks and analyzed 180,000 risk factor records. The results? Heart disease mortality was declining worldwide but that decline was independent of cholesterol levels, blood pressure, or even smoking habits.

Many studies today continue to obtain the same results. Take. for example, a study conducted just a few months ago by researchers at the University of Oxford in Britain, whose study results indicated that lower cholesterol levels were not linked to reduced stroke deaths.^[26] The team, which analyzed 61 previous studies involving almost 900,000 adults, conducted mostly in western Europe and North America, found no relationship between total cholesterol levels and risk of stroke death, especially at older ages and among people with higher blood pressures.

“I think all we can say is that we don’t really understand what’s going on here,” team leader Sarah Lewingston said in a phone interview. “And we need to know more about cholesterol and more about stroke sub-types to find out what’s going on.”

Furthermore, the current view that lowering cholesterol will decrease the mortality rate among patients with CAD fails to take into account the complex role that the substance plays in the body. For example, cholesterol is used by the body to synthesize all of the body’s nuclear receptors – receptors that are at the heart of immune function. It is also the substance from which all the body’s hormones, including estrogen, testosterone, and progesterone is derived from. Until further research is conducted, particularly research that factors the role of bacteria into the pathogenesis of heart disease, it could be argued that due to its myriad roles in the body, removing cholesterol from the diet may have numerous side effects on other bodily pathways and processes which have yet to be revealed.

Statins modulate the activity of the immune system

Nevertheless, a large number of patients at risk for heart disease or stroke are prescribed statins – drugs that are marketed as cholesterol lowering agents. There’s no question about the fact that statin medications can effectively lower cholesterol. The concerns are twofold: does lowering cholesterol actually benefit patients with CAD? And most importantly, are the effects of statins on patients with heart disease even related to their ability to lower cholesterol?

In an article in the Lancet, researcher David S. Grimes asks the question – are statins analogues of vitamin D? “Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues,” states Grimes. “This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D.”^[27]

Grimes is on the right track because while statins are not exact analogues of vitamin D, recent molecular modeling research has revealed that they do bind the same receptors as the vitamin D metabolites 25-D and 1,25-D. These receptors include the Vitamin D Receptor, the glucocorticoid receptor, and the alpha and beta thyroid receptors. Together these nuclear receptors transcribe the bulk of the body’s genes.

Each of the statins has a different affinity for these key receptors. Some exert strong effects on the VDR while others don’t. Simvastatin has a very strong affinity for the VDR. Lovastatin and Pravastatin also bind the receptor. The other three statins (atorvastatin, fluvastatin, and rosuvastatin) bind the glucocorticoid and thyroid receptors only (often with affinities that are quite high). Despite the fact that they don’t bind the VDR directly, they still affect the immune system.

Unfortunately, there is no data on whether statins activate the nuclear receptors (function as agonists) or inactivate them (function as antagonists). Although scientists can only speculate at the moment, one thing is certain – because each of the six statins have such different affinities for the receptors they bind, they each work in different ways and influence the transcription of different genes. “Look at the molecular data,” states Marshall (see chart). “Simvastatin, rosuvastatin and atorvastatin work vastly different ways. They may each benefit people under different conditions but we have no way of knowing exactly how at this point.”

The most compelling evidence for the hypothesis that statins benefit patients with heart disease via their effects on the nuclear receptors rather than through their cholesterol-lowering properties comes from the recent ENHANCE trial. The trial tested the effects of a new cholesterol-lowering medication called Zetia on patients with cardiovascular disease. It found that Vytorin, a combination pill that combines Zetia with the statin Zocor, proved better than the statin alone at reducing levels of cholesterol. But to everyone’s surprise, Vytorin failed to slow the growth of fatty plaques in the arteries, and it may have actually made plaque formation worse.

It turns out that unlike the statins, which block the liver from making cholesterol, Zetia stops the intestine from absorbing cholesterol in food. So if both the statins and Zetia effectively lower cholesterol, why does Zetia have no effect on plaque formation? It’s almost certain that unlike the statins, Zetia does not bind the nuclear receptors. It follows, then, that the statins almost surely work by binding the nuclear receptors, rather than by lowering cholesterol.

Sadly, mainstream cardiologists remain oblivious to the effects of statins on the nuclear receptors, or the possibility that the effects of statins on patients with cardiovascular disease are not even related to their cholesterol-lowering abilities. Naturally, they remain greatly perplexed by the results of the ENHANCE trial. Rather than further investigate the actions of either the statins or Vytorin, the American College of Cardiology recently hosted a conference in which they encouraged doctors to only prescribe Vytorin as a last resort. Nearly half of the 30,000 cardiologists in the United States attended the conference, many of them heard the panel’s recommendations firsthand. The New England Journal of Medicine made a similar recommendation about the drugs in a recent editorial.

Side effects or immunopathology?

Statins have been shown to effectively decrease the incidence of cardiovascular events among subjects ages 30 -80 who already suffer from heart disease, presumably through their anti-inflammatory, rather than their cholesterol lowering effects. A 2008 meta-analysis by researchers at McGill University also found that statins substantially reduce all-cause mortality among elderly patients.^[28]

According to some researchers, these positive results have prompted many doctors to over-prescribe statins to people who probably don’t need them. It has also been argued that there is also a trend among medical professionals to prescribe statins at higher doses than necessary. Such scientists feel tendency of doctors to over-prescribe statins poses a problem, as statins have been shown to have a wide range of side effects – perhaps because they affect so many of the body’s receptors in ways yet unknown. “Statins are small, agile molecules so they act on numerous receptors,” states Marshall.

For example, a recent meta analysis by researchers at the Massachusetts College of Pharmacy and Health found that intensive-dose (higher than usual) statin therapy was associated with a reduced risk for important cardiovascular events, but was also associated with an increased risk for statin-induced adverse events.^[29]

Similarly, as described by Uffe Ravnskov in a comment published in the British Medical Journal, the recent IDEAL trial, which compared patients taking the statin simvastatin to patients taking the statin atorvastatin, found that almost 90% of participants in both groups had side effects.^[30] Almost half of them were recorded as serious. The authors of the IDEAL trial did not comment on these findings, nor did they inform readers about the nature of these events.

In his 2004 book Overdosed America, Dr. John Abramson argues that pharmaceutical companies are distorting medical knowledge by encouraging doctors to prescribe statins to sections of the population that do not benefit from their effects. “Too many people — healthy women of any age and men over 65 — are taking statins without proof they need them,” states Abramson.^[31]

In a 2007 Lancet article, Abramson and Wright argue that no proof exists showing that statins prevent heart attacks or strokes in healthy people, nor do they work as agents of primary prevention in women or in people over age 65.^[32]

Abramson argues that guidelines which encourage physicians to prescribe statins are created by experts who have financial ties to the drug companies that make the drugs being considered in the process. 59% percent of the experts who formulate the official guidelines on statins have such financial ties. For example, in a meta-analysis of statins in the October Lancet, 13 out of 14 studies were commercially sponsored. The one that was not commercially sponsored showed distinctly lesser benefit from statins.

Then again, it’s quite possible that the symptoms researchers such as Ravnskov attribute to the side effects of statins may actually be due to another cause.

Take, for example, the recent uproar surrounding Pfizer Inc.’s Lipitor, also called atorvastatin. It’s the world’s best-selling statin, with revenues of $12.6 billion in 2007. However, the drug is causing some women to experience what researchers are referring to as serious cognitive side effects.

“This drug makes women stupid,” Orli Etingin, vice chairman of medicine at NewYork-Presbyterian Hospital, declared at a recent luncheon discussion sponsored by Project A.L.S. to raise awareness of gender issues and the brain.

Researchers at the University of California at San Diego are nearing completion of a randomized controlled trial examining the effects of statins on thinking, mood, behavior, and quality of life. As part of a separate project the team is also collecting anecdotal experiences of patients, good and bad, on statins. They’ve found that in about 5000 people to date, memory problems are the second most common side effect, after muscle aches.

“We have some compelling cases,” says Beatrice Golomb, the study’s lead researcher.

While it’s possible that the mental symptoms observed among women taking Lipitor could be due to unexplainable side effects of the drug, something else might be going on.

That something else may very well be immunopathology – or the immune system’s response to bacterial death. Women who are prescribed statins are almost certainly infected with L-form bacteria, as the pathogens and other biofilm bacteria (collectively called the Th1 pathogens) are responsible for causing the inflammation that leads to high cholesterol.

As patient reports from the Marshall Protocol site confirm, the Th1 pathogens seldom infect only one area of the body, and everyone in the population acquires them as they age. This means that many women prescribed statins for high cholesterol very likely have these bacteria in their brains as well.

Aside from mild episodes of brain fog or memory loss, most women on statins are probably unaware of the that fact their brains may harbor Th1 pathogens, largely because it’s not until these bacteria are killed that the host becomes acutely aware of their presence.

When the immune system targets the Th1 pathogens, it releases a host of inflammatory molecules in response to their death, which along with the toxins released by the bacteria as they die, and the debri from the cell they once inhabited, cause a rise in symptoms in the area in which the bacteria are been killed (immunopathology).

As described above, Marshall’s recent molecular modeling research has made it abundantly clear that while statins do lower cholesterol, their main actions on the body come not from their cholesterol lowering properties but from the fact that they bind the nuclear receptors – a class of receptors intrically connected to the activity of the innate immune system.

These are the same receptors activated by Benicar – the ARB medication used by patients on the Marshall Protocol (a medical treatment described later in this paper). Benicar activates and enables the innate immune system via the Vitamin D Receptor (VDR). In fact, drugs such as Benicar that bind and activate the nuclear receptors can be so effective at turning on the innate immune system that they enable some people to kill the Th1 pathogens even without the help of antibiotics.

Despite the fact that Lipitor doesn’t bind the VDR directly, it still affects, and could very likely activate, the immune system because it binds both the glucocorticoid and thyroid receptors with a very high affinity in both cases. Could this mean that those women who experience a rise in cognitive symptoms from Lipitor are simply feeling the effects of bacterial die-off in the brain as the statin allows their immune system to target pathogens in that area more effectively?

It’s possible that this same pattern of events may be repeating itself on a much larger scale. Perhaps most, or all, of the side effects attributed to statins are actually symptoms of immunopathology – caused by bacterial die-off in all areas of the body, not just the brain. If muscle aches are the number one side effect attributed to statins, could that simply mean that the drugs cause immunopathology in people who’s muscles are infected with the Th1 pathogens? While much more research is needed on the issue, it’s food for thought.

If the above scenario proves true, then statins may actually be the very helpful drugs. But until more research is conducted on exactly how each statin affects the nuclear receptors, patients may want to consider taking an ARB medication in place of a statin. ARBs bind the same nuclear receptors as statins, but are recognized as agonists of the receptors and are already known to have excellent safety profiles. The public generally knows less about ARBs because they have yet to be promoted by drug companies with the same zeal as statins.

As discussed above, patients on the MP take an ARB called Benicar. Since the benefits of Benicar on the cardiovascular system have been widely studied, the MP discourages people from taking statins – at least until the effects of each individual statin on the immune system are better researched and it is confirmed that the two types of drugs do not interact.

The bottom line: high cholesterol does not appear to be a risk factor for cardiovascular disease, and the ability of statins to prevent cardiovascular events has nothing to do with their ability to lower cholesterol. The side effects of statins may actually be a result of immunopathology. Those patients with high cholesterol should start the Marshall Protocol, which will allow them to kill the L-form bacteria driving the progression of their disease. Once this happens, cholesterol levels will naturally return to the correct range.

Using the MP to treat cardiovascular disease

The Marshall Protocol is a medical treatment that appears to effectively kills L-form bacteria, and while not enough people with CAD have completed the treatment to provide exact data on recovery, those patients with cardiovascular issues on the treatment are, for the most part, currently claiming improvement and recovery. “We have not specifically studied atherosclerosis,” states Marshall, “although we have shown that patients’ general cardiac health returns at the same time as their other chronic diagnoses go into remission.”

Take, for example, Myrna Dee, who has been on the MP for three years and five months. Before starting the MP, she suffered from frequent chronic left-side chest pressure, deep soreness, and sudden jabs of pain around her heart – accompanied by frequent episodes of arrhythmia. “During my worst days from this inflammation I could actually feel and hear my heart make tiny odd squeaky sounds like when you rub an inflated balloon with your finger,” states Myrna. Any stress, whether physical or emotional, would increase her heart symptoms very quickly. If she spent time outdoors, especially on sunny days, her symptoms would become much worse within minutes.

Myrna’s cardiovascular symptoms have “vastly improved” during her time on the MP. Over this past year she has seldom had heart symptoms. If she does have symptoms, they are mild in comparison to what they were like before. “Now my heart only feels mild pressure and mild soreness with shorter episodes of arrhythmia. Usually this only occurs if I have had an overexposure to natural light or when my immune system is over-exuberant. At any rate, when this does occur, I have been able to control these troublesome heart symptoms successfully with Benicar,” states Myrna.

In the late 70s Freddy Ash was told he didn’t have enough oxygen flowing to his heart. A few years later he was told he had first degree blockage (95%) in the wide parts of his arteries, myopathy, and an ejection fraction of only 15%. In March of 2000 he suffered his first heart attack followed by bypass surgery. He was also diagnosed with atrial fibrillation. A few months later he suffered another heart attack and doctors were surprised to find that his bypasses had calcified and he had to have a second quadruple bypass operation. “The doctors had never seen anything like it,” says Freddie.

After starting the MP in 2005, Freddie’s atrial fibrillation disappeared – probably due to the palliative effects of Benicar. Two years later it returned according to an EKG reading, but doctors were unable to detect any difference in heart rate that would support the results of the test. “My conclusion is that the Marshall Protocol has made my heart rhythm so good that the atrial fibrillation doesn’t have an effect any more, says Freddie. Freddie’s ejection fraction has increased from around 30% to 45% and his cholesterol levels have dropped from a range of 227-250 before the MP to a range of 150-147 now. His triglyceride level has dropped from 395 to 61. He can now walk for an hour whereas, before the MP, he had difficulty walking across a room. Freddie also no longer needs the supplemental oxygen he required before the MP. Shortly after starting the MP, “They came to pick up my oxygen machine because I didn’t need it anymore,” states Freddie.

Amy E. Stevens was first diagnosed with Mitral Valve Prolapse (MVP) and several heart murmurs at the age of 17. She proceeded to live with chest pains for the next 25-26 years. “Some of them were pretty scary,” states Amy. “I have had many in which I questioned if they were not just part of an MVP reaction but part of an actual heart attack.”

“Two months ago, Amy’s EKG came back normal with a few very faint heart murmurs.”During the first two phases of the MP, as Amy’s bacteria began to die, she still felt chest pains. However, now on the third phase of the treatment, she has noted a noticeable decrease in the level and frequency of her chest pain. “Now in Phase III, I may have had one or two occurrences of chest pain, but it’s not even the same type of feeling I have experienced all my life. They are very mild and short in duration,” states Amy. “I really believe it has to do with the MP because my life hasn’t exactly been stress free and I have had many life challenges – yet still no chest pains.” Two months ago, Amy’s EKG came back normal with a few very faint heart murmurs. “I couldn’t be happier about my new healing condition,” states Amy.

Prior to starting the Marshall Protocol, Jennifer Hicks had mitral valve prolapse (MVP) and a bicuspid aortic valve. “The aortic valve had been this way since birth and caused no problems, but the mitral valve prolapse began when I was 23 following a stressful event,” states Jennifer. Symptoms Jennifer associated with her MVP included crushing chest pain under stress, heart palpitations on a weekly basis, dizziness, pain in her left arm, numbness in her fingers, and a general feeling of unwellness.

Jennifer has been on the MP two years and two months. Aside from one extreme bout of chest and left arm pain while in Phase III of the protocol when bacterial killing was at its height, her heart palpitations have been reduced by about 80%. The dizziness and numbness in her fingers is an occasional nuisance now rather than a constant problem, and the general feeling of unwellness lifted within her first six months on the MP. “My most recent EKG showed my mitral valve prolapsing only slightly, whereas before the MP it was awfully sloppy. My MVP is now considered very mild by my cardiologist,” states Jennifer.

Benicar activates the immune system and reduces inflammation in patients with CAD

Central to the Marshall Protocol is the use of a medication called Olmesartan (known as Benicar in the United States). Benicar is an Angiotensin II Receptor Blocking (ARB) drug that acts as a “VDR agonist”, or a drug that activates the VDR, thus restoring the activity of the innate immune system and the AMPs – allowing the body to once again manage infection.^[33] The angiotensin II blockage also provides numerous other advantages of patients with CAD. For example, as researchers at the University of Duisburg-Essen in Germany point out in a recent article in Kidney and blood pressure research, “In the failing heart, the local angiotensin II concentration is increased, and the extent of cardiac angiotensin II release is related to the clinical signs of heart failure.”^[34]

In addition, Benicar also binds other receptors that are involved in the inflammatory response. For example, since angiotensin II is itself a pro-inflammatory hormone that affects the release of various other inflammatory markers, when the angiotensin II receptor is blocked, the release of inflammatory mediators such as CRP, tumor necrosis factor alpha, interleukin-6, and nuclear factor-kappaB are also reduced.^[35] This means that to a large extent, ARBs protect the patient against the damaging affects of these substances and other cytokines, ameliorating much of the harm that inflammation produces in the tissues.

Michael A. Weber, MD, Professor of Medicine in the Cardiology Division at the State University of New York (SUNY), argues that ARBs have a strong list of credentials in terms of beneficial cardiovascular and metabolic effects. According to the researcher, ARBs provide the same benefits to heart patients as drugs called ACE inhibitors, which have been shown to improve outcomes and survival in patients with heart failure and people with prior history of a heart attack.^[36]

Weber explains that definitive data exists showing that the ARB medications valsartan and candesartan effectively minimize heart failure. Valsartan was used in a study called the “Valsartan Heart Failure Trial” and candesartan in another study known as the “Candesartan in Heart Failure — Assessment of Mortality and Morbidity (CHARM) trial.” In both studies, the ARB medications showed significant benefits, so much so that they are now indicated for the treatment of heart failure. No study of this scope has yet tested the effects of Benicar, the ARB used by the MP on heart failure, but as Weber states, “We always assume the possibility that what is true for one ARB will be true for others.”

A recent article in the Journal of the American College of Cardiology, which reported the results of a meta-analysis which included a total of 56,308 patients, found that ARBs reduced overall risk of atrial fibrilation by 28%.^[37] Furthermore, the ARB Candesartan has been shown to shorten the atrial refractory period, lessen the loss of rate adaptation, as well as reduce atrial fibrosis in dogs rendered prone to atrial fibrillation.^[38]

“That raises an issue as to whether there is something special about ARBs.”There have also been several studies to test the relationship between ARBs and stroke. In the four largest studies performed on the subject, ARBs proved to be better than other drugs at preventing strokes. In the LIFE study”, ARB medications proved to be more effective at reducing stroke than the beta-blocker atenolol. Similarly, the “MOSES study”, which Weber describes as “a small but well-conducted, relatively rigorous trial,” found that the ARB eprosartan was associated with a 25% relative reduction in new strokes. “That raises an issue as to whether there is something special about ARBs,” says Weber.

Other studies confirm the benefits of Benicar on patients with CAD. Researchers at the Osaka Medical College in Osaka, Japan, performed a study which examined the effects of Benicar on the formation of lesions in the aortic valves of rabbits with hypercholesterolemia. The researchers divided the rabbits into three groups, all of which were fed a diet containing 1% cholesterol. One group was given 1 mg daily of Benicar during the last four weeks of the study. The team found that the rabbits given Benicar had fewer macrophages accumulate on their heart valves, and that the medication preserved the integrity of the endothelial lining (which was disrupted by cholesterol in the other rabbits) on the side of the valves prone to lesions.^[39]

Similarly, researchers at the Graduate School of Medicine in Kyoto, Japan, found that Benicar inhibits the release of inflammatory cytokines, which markedly reduced the severity of myocarditis – a condition in which the muscular part of the heart becomes inflamed. The team concluded that Benicar actually ameliorates the disease in rats.^[40]

Benicar has even been shown to help people with high cholesterol. Reseachers at Ehime University in Japan found that treatment with Benicar “significantly decreased serum glucose and cholesterol levels” in the mice administered the drug. The mice in the Benicar group also developed higher levels of neuroprotective chemicals than those in the control group.^[41]

The list goes on and on. Researchers at the Department of Internal Medicine in Germany found that Benicar significantly reduced vascular inflammation markers, including C-reactive protein, and lipid levels in patients with hypertension after only 6 weeks of therapy. “This anti-inflammatory action of angiotensin II receptor antagonists may contribute to their beneficial cardiovascular effects,” state the scientists.^[42]

A team at the Hospital of Guangdong Medical College in China found that among mice with cardiac injury, those given Benicar released significantly fewer cytokines and experienced greater proliferation of smooth muscle cells, leading the team to conclude that Benicar can improve vascular remodeling.^[43] A team at Asahikawa Medical College in Japan found that Benicar “almost totally” prevented left ventricular dysfunction.^[44]

Antibiotics

Once patients on the Marshall Protocol have begun to take Benicar every 6-8 hours they also begin a regimen of carefully chosen antibiotics in low, pulsed, doses. The antibiotics greatly weaken L-form bacteria, meaning that with the help of Benicar, the patient’s own immune system is finally able to eliminate them.

The use of antibiotics in patients with heart disease did not begin with the Marshall Protocol. Several studies have taken place where patients with heart disease and stroke have been given courses of high-dose antibiotics for months or weeks. In some instances patients’ levels of antibodies to Chlamydia pneumoniae decreased temporarily, showing that antibiotics taken in this fashion are probably able to wear away at co-infections to some extent.

Yet none of the patients in these studies experienced recovery, due to the fact that the high-dose antibiotics used by these research teams leave L-from bacteria unscathed. This is also the reason why some studies involving antibiotics and heart disease have come up with negligible results.

In an article in the British Medical Journal, David Taylor-Robinson, emeritus professor of genitourinary microbiology and medicine at the Imperial College London, laments the results of a study in which patients with heart disease failed to respond to antibiotics. Based on the increasing number of studies linking bacteria to heart disease, the researcher was sure he should have seen results. “So, is this the end of the road?” he asks.^[45]

No it’s not, replied Marshall in a letter to Robinson. “It is our experience that no single antibiotic from those cited in this editorial, namely Rifampin, Gatifloxacin or Clarithromycin has any effect on the intra-phagocytic bacteria causing the diseases we have studied,” (meaning that the team had used antibiotics that have no effect on L-form bacteria). “However, the use of Benicar along with the judicious use of combinations of [the antibiotics used by the Marshall Protocol] is showing itself capable of working miracles against chronic disease.”

Consequently, when it comes to treating heart disease and stroke using the correct antibiotics is of utmost importance. The antibiotics used by the Marshall Protocol have been carefully selected for safety, efficacy, and their ability to cover a broad range of species.

Immunopathology

Patients who use the Marshall Protocol to treat heart disease must proceed with caution due to symptoms of immunopathology, or the immune system’s response to bacterial die-off (another term sometimes used is the Jarisch-Herxheimer or “Herx” reaction). Dying bacteria release toxins into the bloodstream, stimulate the production of inflammatory cytokines, and generate temporary hormonal imbalances. This means that once a patient begins the MP, each dose of antibiotic will cause him to feel bad for the period of time it takes his immune system to deal with the consequences of CWD bacterial die-off.

Consequently, patients with CAD will experience temporary returns of cardiac symptoms while they proceed through treatment. Patients with a history of cardiac symptoms are urged to use a modified version of the Marshall Protocol in which the antibiotic that causes the strongest immunopathology is reserved for last – allowing the patient to wear away at bacteria in the heart more slowly.

Patients should be on the lookout for signs that immunopathology resembling tachycardia (rapid beating of the heart) does not become too strong, and adjust their antibiotic dose accordingly if this proves to be the case.

“The Marshall Protocol has been designed to reduce the chance of tachycardia.”However, due to the anti-inflammatory effects of Benicar and the ability to easily adjust antibiotics, the Marshall Protocol has been designed to reduce the chance of tachycardia. “Taking a cardiac medication (like a beta blocker which slows the heart), as a preventative, isn’t usually necessary. Following the MP guidelines carefully should prevent any serious cardiac rhythm disturbances,” states Meg Mangin of Autoimmunity Research Foundation.

So far, the few patients on the Marshall Protocol to experience a disturbance in cardiac rhythm were able to obtain relief by temporarily stopping their antibiotics and increasing their dose of Benicar to 40mg every four hours. Beta blockers do not interfere with the MP, however, since some patients use them to help lower their blood pressure and have not had a problem with the treatment.

Similarly, patients should be aware that if they don’t start the antibiotics at the very low levels discussed in the Marshall Protocol guidelines, or if they increase them too quickly, there is a possibility that too many cytokines (generated by bacterial die-off) could hit the heart at once, causing an event mimicking a small heart attack. However, this event has never been a problem for any MP patient thus far. “We have not seen such a case mimicking heart attack yet, as the release of cytokines on the MP is controlled, and the level set by the patient’s symptoms,” states Marshall.

Embracing the new understanding of cardiovascular disease

It is clear that unless mainstream medicine begins to take the role of L-form bacteria in the pathogenesis of CAD seriously, the rate of heart disease and stroke may continue to rise. Unless the bacteria likeley driving the illnesses are killed, even wholehearted attempts to lower fat and cholesterol intake may have little effect on mortality.

But as the immunosuppressive properties of vitamin D supplementation and statins gain further recognition, and research about L-form bacteria and chronic disease continues to evolve at a rapid rate, the notion of conquering CAD may not be far off the horizon. In that case, we may finally put an end to the cardiovascular diseases that have taken so many lives.

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