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Health news updates

Posted by Richard on March 6, 2007

Back in September, I warned you to start taking vitamin D supplements as the days grew short. I hope you did, and I hope it helped you avoid the flu this winter. The February issue of Life Extension Magazine (yes, I’m a bit behind in my reading) has an article that goes into much greater depth regarding the connection between seasonally low levels of vitamin D and high rates of influenza. It includes information about how vitamin D helps protect you:

In the past few years, several independent researchers have shown that vitamin D significantly enhances the genetic expression of antimicrobial peptides in human monocytes (precursors to macrophages), neutrophils, and other immune system cells.15,1617-19

For Dr. Cannell, these various clues led to one inescapable conclusion: vitamin D—which is produced when the skin is exposed to summer sunlight, and which, conversely, declines in winter—plays a critical role in our vulnerability to influenza infection. In fact, vitamin D must surely be Hope-Simpson’s mysterious “seasonal stimulus.” Dr. Cannell consulted a number of leading vitamin D researchers, all of whom agreed with his conclusions. They include researchers from such venerable institutions as the National Institutes of Health and the Harvard School of Public Health. One of these scientists, Dr. Michael F. Holick, has been studying vitamin D for three decades.1,7,20

In an interview with Life Extension, Dr. Holick alluded to the special relationship between vitamin D and the body’s primary immune system defenders, the macrophages. “What intrigues me the most,” Dr. Holick noted, “is that we’ve always known that macrophages activate vitamin D.” The form of vitamin D generated through the skin’s interaction with ultraviolet B radiation (from sunshine or artificial sources) is a pre-hormone. It must be converted in the body to its active hormone form, called 1,25-dihydroxyvitamin D3. An intermediary form, known as 25-hydroxyvitamin D, is the major circulating form of vitamin D, and is measured to determine vitamin D status.20

Most of this activation of vitamin D occurs in the liver and kidneys. However, the fact that macrophages facilitate the conversion of circulating vitamin D to its active form,20 and that activated vitamin D in turn regulates the activity of macrophages, suggests an important relationship between the two. These antimicrobial proteins help to destroy invading infectious microbes. With their broad-spectrum activity, they are capable of killing everything from bacteria to viruses. They have been shown to be an important part of the respiratory tract’s defense against invaders, and likewise show promise in fighting the influenza virus.

Life Extension Foundation has also taken aim at the shoddy supplement study I wrote about last week, issuing a consumer alert entitled "Another Flawed Attack against Antioxidants." Among other issues, LEF looked at the ridiculously wide range of nutrient dosages in the studies:

The JAMA review that attacked the value of antioxidants included vitamins A, C, E, and selenium and evaluated these very basic nutrients in a very wide & inconsistent dosage range:

Supplement

Dose range

Vitamin A (synthetic)

1,333200,000*** IU

Alpha Tocopherol (synthetic)

105,000 IU

Vitamin C (synthetic)

60 – 2,000 mg

Selenium (natural)

20 – 200 mcg

As an example of the strange decisions made by the JAMA authors as to which studies to exclude or include in their analysis, they selected a single dose study*** of patients using 200,000 IU of vitamin A, who were subsequently followed for 3 months.8

LEF also found that the authors misrepresented some of the included studies, attributing deaths that didn’t happen, and seem to have intentionally omitted a long list of studies that demonstrated positive benefits from antioxidants from their cherry-picked (68 out of 815) sample. LEF characterized the JAMA study as an "irrational and highly biased attack," and quoted several other respected scientists who dismissed this study as deeply flawed.
 

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