Quote from hillcountry on May 24, 2020, 7:06 pm

Hi y'all - I survived the Gominak D3-B-complex protocol with some early sleep-benefits but not much else. Reading a post by Josh on another site led me to reconsider, which then led me to review the Marshall Protocol perspective again. I excerpted a few portions of the linked page to give a quick overview of their understanding. I think it will provide some insight regarding "Vit A" as well. I'll poke around and see where they're at on the question. Hope y'all find it useful in some way.

https://mpkb.org/home/pathogenesis/vitamind#supplemental_vitamin_d_tends_to_be_immunosuppressive

Ramifications of a simplistic understanding of vitamin D metabolism

Numerous studies have identified patient populations that are “deficient” in vitamin D. Patients suffering from obesity, schizophrenia, fibromyalgia, multiple sclerosis, autism, etc. all seem to be suffering from vitamin D deficiency. One could list hundreds of such studies.

Although it is not unheard of, few seem to explore the possibility that a low 25-D is the result of disease. Perhaps it is because researchers conceptualize vitamin D as they might a resource which gets used up and needs to be replenished – not unlike gasoline when a car runs low. This metaphor is not at all apt, because vitamin D is regulated like the steroid it is.^35) 36)

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Large segments of the population are consuming vitamin D at historic levels. Like the first-line treatment for many autoimmune diagnoses, the corticosteroid Prednisone, vitamin D temporarily reduces symptoms of disease, but long-term use dramatically increases the odds of disease relapse.³⁷⁾

In practice, widespread and systematic supplementation of vitamin D may serve to drive a kind of self-fulfilling prophesy. When whole populations are given large amounts of vitamin D, the only members of that population who remain “deficient” are those whose immune systems are fighting disease by actively downregulating 25-D. In other words, the more rigorously vitamin D is added to milk, juice, snack bars, and breakfast cereals, the less likely it is that someone has low levels of vitamin D but no chronic disease.

Supplemental vitamin D given to healthy people

According to the Marshall Pathogenesis, limited amounts of vitamin D may be helpful for a time to healthy people. Because the body is able to properly regulate the VDR, ingested vitamin D is rapidly converted into 1,25-D, which activates the VDR. This may explain the one (barely) significant finding from a 2011 Cochrane systematic review.³⁸⁾ (Publication bias may have also tilted the findings towards intervention.) However, this is certainly no basis for forced fortification.

Marshall Protocol and vitamin D

As opposed to certain treatments which employ sunshine or light therapy, patients on the Marshall Protocol (MP) use the VDR agonist, olmesartan, and pulsed, low-dose antibiotics to gradually eliminate the Th1 pathogens. Patients on the treatment must refrain from supplementing with vitamin D or eating any foods that contain vitamin D. These measures allow 25-D levels to drop to a point where the VDR can most optimally activate the innate immune system.

Because the vitamin D metabolites are dysregulated in chronic disease, most patients on the MP also become sensitive to light. Although light sensitivity improves as the Th1 pathogens are killed, most patients must avoid bright sunlight and block bright light in the eyes with special sunglasses during the healing process. However, once the Th1 pathogens have been killed and the vitamin D metabolites have re-stabilized, patients are able to tolerate sunlight and bright lights once again.

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However, bacteria create ligands, which like 25-D, inactivate the VDR and, in turn, the innate immune response. This allows the microbes to proliferate. In response, the body increases production of 1,25-D from 25-D, leading to one of the hallmarks of chronic inflammatory disease:

a low 25-D and a high 1,25-D.

This pattern is a result of the disease process rather than a cause. For a variety of reasons, neither increased consumption of vitamin D nor the body's synthesis of additional 1,25-D is ultimately effective at combatting infection.

Supplemental vitamin D show no consistent effects on infection

In studies on acute respiratory tract infection³⁾, tuberculosis⁴⁾ and overall infections⁵⁾, the effects of vitamin D have been mixed (and largely unsuccessful) in terms of reducing infectious burden.

A complete evaluation of the above-mentioned studies, and the differences between them that can help explain the different results, is not suited for this article. However, on a general basis, one of the reasons for differing effects may be that vitamin D works differently in relatively healthy people as compared to sick people. Thus, vitamin D supplementation may give a marginal benefit in preventing infections in healthy people (see section below), but not in sick people. As of today (Dec 2012) we are not aware of any studies that have shown an actual reduction in infections in sick people (for instance tuberculosis or COPD) by vitamin D supplementation, as measured by culture or genetical detection methods. Furthermore, a general trend seems to be that apparent beneficial effects on infection in healthy people are not seen in individuals who have 25-hydroxyvitamin D levels within the normal range⁶⁾⁷⁾⁸⁾, adding, as a side point, further weight to the mega dose vitamin D supplementation craze being without merit.

It is however not certain, in spite of some reported benefits in a few studies, that any level of supplementation is beneficial in terms of reducing infection. The studies are still too few to draw firm conclusions, and publication bias, as in any field science, may skew the overall results. Another factor which makes the reported benefits doubtful is that not all studies have reported an actual reduction in infection, but merely symptom-based outcomes. Symptom based outcomes are relevant, but in light of the symptom reducing effects therapies that are immune suppressive may have, it is not clear that symptom reduction in the vitamin D supplementation studies are due to an actual reduction in infection. Further, most of the symptoms in upper respiratory tract infections are caused by the body's own immune response, and not the infectious agents⁹⁾.

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One of the abiding weaknesses of studies on the effects of vitamin D on health is that researchers simply do not follow subjects consuming the secosteroid for a sufficient period of time. Instead, they tend to track subjects over the course of weeks, months, or one or two years, during the period of time when study participants are usually feeling the palliative effects of the steroid.

This practice is a mistake as it does not account for the long-term immunosuppressive effects of a steroid. For example, the U-shaped relationship between vitamin D levels and long-term outcome in large cohort ²²⁾

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Many vitamin D studies suffer from methodological errors including bias inherent to using self-selected subjects and insufficient followup, but perhaps their most egregious liability comes in mistaking correlation for causation. ²³⁾  It's undisputed that a wide array of studies point to the fact that 25-hydroxyvitamin D (25-D) – typically referred to in the media as vitamin D – is low in people with numerous chronic inflammatory diseases. However, these studies fail to prove that low 25-D causes disease. Even so, some studies assume that doubling serum levels of 25-D would drastically reduce mortality.²⁴⁾

In fact, molecular science has revealed that the levels of the vitamin D metabolites through a series of intricate and carefully controlled feedback pathways, mechanisms that belie the simplistic first-order mass-action model used to guide the short-sighted vitamin studies. Also, epidemiological evidence suggests that while 25-D is low in chronic disease, 1,25-D (1,25-dihydroxyvitamin D) tends to be very high, an observation which is at odds with the theory that vitamin D deficiency causes or exacerbates disease.

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…observational studies show that populations which avoid vitamin D consumption have naturally low levels of 25-D and remain healthy with such levels.

• healthy Chilean women– A study which tested the level of 25-D in 90 “healthy, ambulatory Chilean women” showed that 27% of the premenopausal and 60% of the postmenopausal women had 25-D levels under 20 ng/ml.²⁶⁾
• healthy Saudi medical students– A 2012 study collected data from 95 male and 103 female students with an average age of 19.5 years old. In 100% of the students, the vitamin D level was considered low. The mean 25-D level was 26.83 nmol/L in males and 16.03 nmol/L in females.
• healthy Bangladeshi women– A study on healthy Bangladeshi women found that approximately 80% of the women had a level of 25-D under 16 ng/ml.²⁷⁾ A separate study of premenopausal Bangladeshi women came to a similar conclusion.²⁸⁾
• healthy Chinese infants– In a 1992 study, healthy full-term infants from China had serum concentrations of 25-D ranging from an average of 5 ng/ml to 14 ng/ml.²⁹⁾
• healthy Omani women– A 2011 study of 41 apparently healthy women (ages 18-45 years) working at the Royal Hospital, Muscat, Oman found that all study subjects had 25-D levels below 50 nmol/L.³⁰⁾
• young healthy adults in western India– Among young healthy adults from the western part of India, the average serum level of 25-D indicated vitamin D “deficiency”: 17.4 ng/ml.³¹⁾
• healthy Saudi Arabians– Severe hypovitaminosis D is widespread and more common in non-diabetics than diabetics in Saudi adults.³²⁾ Nevertheless, this 2010 study's authors conclude a bit bizarrely, “The study further underscores the need for vitamin D fortification of the Saudi diet, and the promotion of vitamin D supplementation in both groups.”
• healthy lactating mothers– Even when lactating mothers take all but exceedingly high levels of vitamin D – 6,000 IU which is 15 times the United States' Recommended Daily Intake – the vitamin D content in breast milk remains very low.³³⁾ This is confusing for advocates of vitamin D supplementation who would think that breastfeeding mothers would give their infant extra levels of vitamin D during formative stages of growth.

The Vitamin D Council, an organization that advocates vitamin D supplementation, stated:

One of the great mysteries in human biology is the fact that most human breast milk is deficient in vitamin D. How could Nature overlook such an important nutrient in the “perfect food”?

Vitamin D Council