In some cases, what you hear about in the media is just "hype." In other words, the resesarchers say that a finding is "promising" and "may lead to an eventual cure for disease X." But it may get reported as "a cure for disease X appears to be just around the corner." An example of this is:

"'Research Uncovers Signaling Pathways Related To Brain-immune System Links'

New research on signaling pathways in immune cells bolsters evidence of connections between the central nervous system and the immune system. The findings may also advance the scientific foundation for a potential HIV treatment that may block the virus that causes AIDS... Because macrophages are a reservoir for HIV, a strategy that denies the virus entry into those immune cells may be important in combating HIV infection."

Source: http://www.sciencedaily.com/releases/2006/05/060515230947.htm

If you read the whole report you see that they observed some molecular phenomenon, then tried to fit the square peg into the round hole. If a virus was damaging, destroying, or rendering dysfunctional macrophages, then it would be detectable, just as what happens to macrophages when there is too much oxidized cholesterol in the body is detectable (and the entire "disease process" is clear). Instead, these researchers are assuming that the textbook models and claims are accurate, and so they come to tentative conclusions (notice how many times "may" is used in these kinds of reports/studies) that don't consider the process as a whole, and in this case their conclusions are inconsistent with basic observation. There is not a great deal of macrophage dysfunction or destruction in a person "infected with HIV," though after taking toxic drugs for many years there can be all kinds of damage done to the body. So what are they talking about?

If I asked them to cite one piece of scientific evidence (where controls are used and a few hundred people or more are involved) that demonstrates that within even a year of "HIV infection" there is massive macrophage death and/or dysfunction, what would they cite? I have yet to find such evidence for such claims as theirs. Moreover, the "proof is in the pudding" when it comes to "diseases." If they can't "cure" it (and they've had 25 years now), then they have failed. I'd like to see others with fresh ideas that are focused on the process as a whole get proper funding, but instead those who mouth the dogma seem to get the lion's share of it.

Another problem in these kinds of studies, that is, ones that appear to be so specific and focused on molecular-level phenomena is that many researchers, who are often highly specialized in their research, may be so fixated on one gene or protein, for example, that they don't realize that even if it were easy to change, inhibit, or enhance genetic or protein expression, it is likely that the long-term consequences will be worse than doing nothing at all. For example:

"A gene commonly involved in cancer onset, c-myc, has been found to have a role in the immune system's normal function according to a study published today in Blood."

Source: http://www.sciencedaily.com/releases/2006/05/060515100316.htm

A good example of how many research scientists "miss the forest because the trees get in the way" is the following:

"The cellular activity of PI-103 was traced to its ability to cooperatively inhibit both the p110á subunit of PI3 kinase and a downstream molecule called mTOR that also plays a critical role in cell growth. Although both of these molecules are members of the same signaling cascade, the researchers found that they must be concurrently inhibited because of a regulatory feedback loop that renders a monospecific inhibitor ineffective. Importantly, dual inhibition of p110á and mTOR with a low dose of PI-103 elicited no drug-related toxicity and was highly effective against human gliomas transplanted into mice."

Source: http://www.sciencedaily.com/releases/2006/05/060516075929.htm

Now this sound like they are incredible geniuses, to be sure, but what have they to show for it? You can go back many years and find reports like this, and nothing ever seems to come of the "momentous discoveries." The simple reality is that such aberrant cellular signaling is due to the fatty acids people are now consuming in much of the world (and low intake of antioxidant-rich foods, etc.). Yes, you can then inhibit what should never have been enhanced in the first place, but you risk "side-effects" that are worse than the "disease" that you were originally trying to "cure."

Also note that they are trying to inhibit cell growth, and yet in other studies, researchers with similar or the same credentials argue that arachidonic acid is "essential" because it stimulates cell growth (as does the Mead acid, but not as potently). One does not need to have any credentials, however, to realize that growth needs to take place at certain times and to a certain degree (or else cancer can result, among other deleterious possibilities). Yet in many studies the researchers never talk about what the thresholds are, and thus to say that something is "good" or "beneficial" because it "stimulates growth," without any context, is worse than meaningless - it can lead people to do things that are very dangerous.

A very common problem with many studies is that they focus on "markers," which again is indirect and possibly totally wrong. The most obvious example of this involves measuring serum cholesterol (or LDL) levels and then claiming that X "lowers the risk of heart disease." Especially now, because it's known that oxidation of cholesterol/LDL is the main problem, such a claim is very misleading, and could cause cancer rates to rise, because low LDL has this effect in most people. This approach is based upon a statistical evaluation of this marker and rates of one "disease." They hardly ever consider the possibility that "high" cholesterol (between 200 and 220) may be best for overall mortality (as Ancel Keys himself noted in his 1979 "Seven Countries" book). Today, many "beneficial" claims are made for fish oil, yet if one only looks for markers of AA damage, one can miss the damage done by omega 3 fatty acids in fish oil. For example:

J Biol Chem. 2005 May 13; [Epub ahead of print]

Regiochemisry of neuroprostanes generated from the peroxidation of docosahexaenoic acid in vitro and in vivo.

Yin H, Musiek ES, Gao L, Porter NA, Morrow JD.

Departments of Pharmacology and Medicine, Vanderbilt University Medical Center, Nashville, TN 37235.

Isoprostanes (IsoPs) are isomers of prostaglandins (PGs) that are generated from the free radical-initiated peroxidation of arachidonic acid (C20-4 omega-6). IsoPs exert potent bioactivity and are regarded as the "gold standard" to assess oxidative stress in various human diseases. Analogously, autoxidation of docosahexaenoic acid (DHA, C22:6 omega-3) generates an array of IsoP-like compounds that are termed neuroprostanes (NPs). A major class of NPs identified in vitro and in vivo contain F-type prostane rings and are know as F(4)-neuroprostanes (NPs). A number of different F(4)-NP regioisomers are formed from the peroxidation of DHA. Among the eight possible regioisomeric groups, we hypothesize that 4- and 20-series NPs are generated in greater amounts than other classes because the precursors that lead to regioisomers other than those of the 4- and 20-series can be further oxidized to form novel dioxolane-IsoP-like compounds, analogous to those generated from arachidonate. Various mass spectrometric approaches, including electron capture atmospheric pressure chemical ionization mass spectrometry, were utilized to analyze NPs formed in vitro and in vivo based on their characteristic fragmentation in the gas phase. Experimental results are consistent with our hypothesis that 4- and 20-series NP regioisomers are preferentially generated. The discovery of regioselectivity in the formation of NPs will allow studies of the biological activities of NPs to focus on the more abundantly generated compounds in order to determine their role in modulating the pathophysiological consequences of DHA oxidation and oxidant stress.

The most common problem, however, is the finding of a "link," "association," or "correlation." This compounds the problem of looking for markers, adding another level of "noise" instead of just employing the scientific method. The "link," or whatever they call it, is often due to socio-economic or other "non-scientific" factors. For example, from sciencedaily.com (on 1/20/2006) was the following:

"Wine Drinkers Have Healthier Diets Than Beer Drinkers:

People who buy wine also buy healthier food and therefore have healthier diets than people who buy beer, finds a study published online by the British Medical Journal.

Studies have shown that drinking wine is associated with lower mortality than drinking beer or spirits. Some studies have also suggested that wine drinkers have healthier diets than beer or spirits drinkers, and this may explain wine's beneficial effect on health.

To study this theory, researchers in Denmark investigated the link between the purchase of beer and wine and various food items from supermarkets.

They analysed 3.5 million transactions chosen at random from 98 outlets of two large Danish supermarket chains over a six month period (September 2002 to February 2003).

Customers were categorised as "wine only," "beer only," "mixed," or "non-alcohol" buyers. Details of items bought, the number and price of the items, and the total charge for each customer's transaction were recorded.

They found that wine buyers bought more olives, fruit and vegetables, poultry, cooking oil, and low fat cheese, milk, and meat than beer buyers. Beer buyers bought more ready cooked dishes, sugar, cold cuts, chips, pork, butter or margarine, sausages, lamb, and soft drinks than wine buyers.

These results indicate that people who buy (and presumably drink) wine purchase a greater number of healthy food items than those who buy beer, say the authors. They also support findings from the United States, Denmark, and France showing that wine drinkers tend to eat fruit, vegetables, and fish and use cooking oil more often and saturated fat less often than those who prefer other alcoholic drinks.

The health benefits of drinking wine may be due to specific substances in wine or to different characteristics of people who drink other types of alcohol, they add. Thus, it is crucial that studies on the relation between alcohol intake and mortality adjust for other lifestyle factors such as drinking patterns, smoking, physical activity, education, or income."

Source: http://www.sciencedaily.com/releases/2006/01/060119232848.htm

Most of these kinds of studies are called "epidemiological," which is derived from their first use to understand "infectious diseases," which were said to cause "epidemics." I am using quotation marks here because of the fact that all factors are not controlled for, which is required by the scientific method. If you've read though some of my essays here, you realize that the fatty acids you eat can play a huge role in your health, whether you develop particular "diseases," etc., but of course there are many other factors that are rarely or never taken into account (such as the socio-economic ones). Indeed, one could argue that it is impossible to do so, yet that does not explain how a "scientist" can decide to not control for factors that have been demonstrated to be important (such as the fatty acids). I call the worst abuses of this approach "smelly socks epidemiology," because it would be easy to find an "association" between how much a person's socks smell at the end of the day to just about any "disease," and yet hardly anyone would think that the socks caused the disease, though if you substitute "sugar," "salt," "cholesterol," or any number of things most people view as "unhealthy," few question the results, and the existing dogma is reinforced.

One way to refute a supposedly scientific claim is to demonstrate that there is another explanation that accounts for all the data without any problems. It is not difficult to validate experimentally the points I've made on this site; all a researcher needs to do is to feed one group of animals the diet and supplements I suggest while feeding another group a diet that is consistent with the "typical American" diet, and then expose the animals to various "infectious diseases." If the latter group becomes ill but the former does not (or if the incidence of "disease" is much lower and/or the manifestation of it greatly attentuated) it would be clear that at least most "infectious diseases" are epiphenomenal - resulting from a combination of factors that one could avoid or manipulate to best effect.

Of course, this would then mean a loss of jobs for many very powerful people n the biomedical establishment, a huge loss of profits for companies that make certain "medicines," etc., so even if such exeperiments are performed, do not expect the mainstream media to explain to you what the implications are. As I said in another essay here, experiments like this are being done, but the researchers are not controlling for the variables that appear to play a major (if not the major) role, due to excessive "professional" specialization (since I have cited other studies which point to the roles these variables play in "disease" in several essays here).