One thing I find myself trying to explain to people who have no scientific background is how important the cellular level is, yet trying to explain this can get very "technical." However, one concept that is helpful is that of stress. Many substances have stressful effects on cells, whereas others are neutral, or may even help cells that are stressed. During pregnancy or growth, a certain amount of "stress" is required, though it needs to be strictly controlled. Some drugs for "HIV/AIDS" are growth suppressing, though to such a degree that the body cannot function correctly, and a stressful situation soon develops.
This is all obvious (or should be) to those who study cellular biology. However, what is less obvious is that many "diseases" are basically all related, in terms of causation. Here is a passage from an abstract of a study of estriol, a form of estrogen (which is a stress-inducing substance required for preganancy):
QUOTE: ...Rats were given estriol (20 mg/kg ip), and Kupffer cells were isolated 24 h later. After addition of lipopolysaccharide (LPS), intracellular Ca2+ concentration was measured using a microspectrofluorometer with the fluorescent indicator fura 2, and tumor necrosis factor- was measured by ELISA. CD14 was evaluated by Western analysis. One-half of the rats given estriol intraperitoneally 24 h before an injection of a sublethal dose of LPS (5 mg/kg) died within 24 h, whereas none of the control rats died. Mortality was prevented totally by sterilization of the gut with antibiotics... it is concluded that estriol treatment in vivo sensitizes Kupffer cells to LPS via mechanisms dependent on increases in CD14. This is most likely due to elevated portal blood endotoxin caused by increased gut permeability. UNQUOTE.
What is so interesting here is how a cellular-level stressor (estriol) causes the conditions the allow an "infectious disease" to occur and result in death to the organism. Unfortunately, because stresssful substances can be so powerful, much of the biomedical establishment is focused on developing "medicines" from these substances (or like them), rather than trying to find ways to lessen the cellular-level stressors that cause the conditions which lead to the disease. Another good example is fish oil, which is very stressful, yet because it counteracts other very stressful substances, those created when arachidonic acid is metabolized by enzymes, it is regarded by most "experts" as "beneficial." However, to determine this, only "markers" are studied, not mortality. The evidence that does exist on mortality is clear: too much fish oil means a premature death - it is just too stressful to cells.
It is also unfortunate that there is no way to seperate money from biology at this point - the two are "bound at the hip" now. But let us take a hypothetical. Let's say that there is a biologist who is considered to be the Newton or Einstein of biology. Suppose he or she tells us that all we have to do to avoid "disease" is to avoid eating and doing certain things (aside from the obvious, such as obtaining enough good quality protein in our diets)? What then? Do we still spend billions of dollars a year in taxpayer money to cure things that can be prevented easily? Would we allow ourselves to be bankrupted as a nation in order to help those with lung cancer (who were all long-time smokers) live a few more years?
In any case, the situation is similar to someone who wants to "reinent the wheel," only insists that it be a square shape. Cellular-level stress is "bad," no matter what the markers appear to suggest in the short term , and simple, inexpensive experiments can demonstrat this. Instead, one can find many studies in which it is claimed that estriol has all kinds of apparent "benefits," just as with fish oil. As I tell people, I'm going to keep cellular-level stress to a minimum, but if you want to ramp up cellular-level stress and see what happens, go ahead. Just tell me so that I can witness what the results are.
Source of the quoted passage: Am J Physiol Gastrointest Liver Physiol; Vol. 277, Issue 3, G671-G677, September 1999.
On the internet: http://ajpgi.physiology.org/cgi/content/full/277/3/G671 |
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