The lipid profile is a group of tests that are often ordered together to determine risk of coronary heart disease such as heart attack or atherosclerosis. The lipid profile typically includes:
In many of the diseases the Marshall Protocol (MP) treats, patients may present with elevated cholesterol. Traditionally, it has been assumed that the elevated cholesterol is causing or contributing to the disease process. However, the alternate hypothesis is no less plausible; in certain inflammatory diseases, the body may be deliberately upregulating levels of cholesterol in order to better manage the disease process. Increasing evidence suggests that this alternative explanation may be true.1 2 For example, a 2010 study found that several bacterial taxa in the oral cavity and the gut correlated with plasma cholesterol levels3, and another study found that high cholesterol protects against endotoxemia.4
Both “good” and “bad” forms of cholesterol play pivotal roles in fighting infection, for example, scavenging endotoxins that are released during destruction of pathogenic bacterial forms. While higher levels of total cholesterol are associated with some forms of cardiovascular disease in some patient populations, a number of statistically significant inverse correlations have been found between total cholesterol and various diseases including chronic heart failure, respiratory and gastrointestinal diseases, and various acute infections.
Thus, high cholesterol levels among patients on the MP are not seen as a problem but as a sign of the inflammatory response to infection. This means that MP patients do not need to take any measures to lower cholesterol. Over time, as the MP medications work to gradually lower infectious agents causing inflammation, it is expected that cholesterol will return to a normal range. In this same vein, statins, in particular, should not be used to lower cholesterol, because they have effects on the same receptors as olmesartan, which may prevent the drug from working effectively.
The statins (or HMG-CoA reductase inhibitors) along with other drugs, such as cholestyramine (Questran), comprise the class of hypolipidemic drugs. Hypolipidemic drugs are prescribed - sometimes aggressively so - to lower cholesterol levels in people with or at risk of cardiovascular disease and certain inflammatory diseases such as sarcoidosis. Statins are prescribed even though their full mechanisms of action remain unclear. One strong possibility is that statins exert their effects via the body's nuclear receptors, which are intricately connected to innate immune function.
The statins have a range of documented negative effects, some of which may be immunopathological. Because statins may interfere with the Marshall Protocol, these drugs are contraindicated.
Statins interfere with the actions of Olmesartan, as they are a very similar molecule, and compete with Olmesartan for many of Olmesartan's molecular binding sites. The actions of statins on the Nuclear Receptors are therefore competitive with Olmesartan, as they reduce or negate Olmesartan's therapeutic activities.
As the 2008 ENHANCE trial illustrates, while high cholesterol is correlated with increased incidence of diseases, lowering cholesterol does not appear to improve human health.5 Indeed, there is some evidence this type of intervention does the opposite.6
While there's no doubt plasma lipoproteins function primarily in shuttling lipids among tissues and organs:
Cumulative evidence suggests that lipoproteins may also prevent bacterial, viral and parasitic infections and are therefore a component of innate immunity. Lipoproteins can also detoxify lipopolysaccharide and lipoteichoic acid. Infections can induce oxidation of LDL, and oxLDL in turn plays important anti-infective roles and protects against endotoxin-induced tissue damage. There is also evidence that apo(a) is protective against pathogens. Taken together, the evidence suggests that it might be valuable to introduce the concept that plasma lipoproteins belong in the realm of host immune response.
R. Han 7
Many epidemiological and clinical observations are in accord with the laboratory studies.16 Statistically significant inverse correlations have been found between total cholesterol and various diseases (i.e. higher cholesterol is correlated with lower disease incidence):
Higher levels of cholesterol are also associated with lower prevalence of disease in systems susceptible to infections including the respiratory system and the gastrointestinal tract. A meta-analysis of 19 cohort studies including 68,406 deaths, found an inverse correlation between total cholesterol and mortality from respiratory and gastrointestinal diseases.24
According to the widely accepted belief, high LDL cholesterol promotes the development of atherosclerosis, and, therefore, cardiovascular disease. However, there is a great deal of contradictory evidence.25 26 27
The pathophysiologic understanding of chronic heart failure has made significant advances over the last decades. Counterintuitively, high levels of plasma cholesterol are associated with better survival, perhaps because plasma lipoproteins are able to scavenge lipopolysaccharide, a cell-wall component from gram-negative bacteria. A number of similar features are present in patients who have sepsis.
S. von Haehling et al.41
There is some evidence that lower serum cholesterol concentrations (as a surrogate for the totality of lipoproteins) relate to impaired survival in patients with chronic heart failure (CHF). Inflammation is a feature in patients with CHF and increased lipopolysaccharide may contribute substantially. We postulate that higher concentrations of total cholesterol are beneficial in these patients. This is potentially attributable to the property of lipoproteins to bind lipopolysaccharide, thereby preventing its detrimental effects.
M. Rauchhaus et al.42
[My physician] remarked on my astounding cholesterol improvement in the last year (from 311 to 191 mg/dL, and my triglycerides are down from 129 to 68 since 1 year ago) and he explained that this could be from weight loss (no, weight has been stable except for slight recent gain since adding Bactrim) or change of diet (no), or exercise (no). I told him the only thing I've done differently is the MP. Cue the skeptical look.
I got my blood work results today…. My triglyceride level went from 450 down to 125 without statins, change of diet or exercise…. I don't have problems with my heart rhythms any longer and having my count drop like that was pure joy.
Dolores P. Rosner (martysfolks), MarshallProtocol.com
I went to see my doctor yesterday and she told me the results of my blood tests were all normal so I am pleased about that. My cholesterol is normal and it looks like the MP has done the trick as I stopped taking statins almost a year ago.
Lipid-lowering treatment to the end? A review of observational studies and RCTs on cholesterol and mortality in 80+-year olds Abstract
People aged 80 or older are the fastest growing population in high-income countries. One of the most common causes of death among the elderly is the cardiovascular disease (CVD). Lipid-lowering treatment is common, e.g. one-third of 75–84-year-old Swedes are treated with statins [ 3]. The assumption that hypercholesterolaemia is a risk factor at the highest ages seems to be based on extrapolation from younger adults. A review of observational studies shows a trend where all-cause mortality was highest when total cholesterol (TC) was lowest (‘a reverse J-shaped’ association between TC and all-cause mortality). Low TC (<5.5 mmol/l) is associated with the highest mortality rate in 80+-year olds. No clear optimal level of TC was identified. A review of the few randomised controlled trials including 80+-year olds did not provide evidence of an effect of lipid-lowering treatment on total mortality in 80+-year-old people. There is not sufficient data to recommend anything regarding initiation or continuation of lipid-lowering treatment for the population aged 80+, with known CVD, and it is even possible that statins may increase all-cause mortality in this group of elderly individuals without CVD.