 |
|
Reply
| |
I have found numerous problems in studies one hears about in the mainstream media, so I thought a thread on this topic would be valuable for those who read this newsgroup. I will update with future posts to this thread, but I want to begin the thread now, because I just read a study about how potatoes lower cholesterol and TGs - if you eat the entire potato. What does "low cholesterol" mean - here we have a language problem that you see all the time. In Ancel Keys' famous book, "Seven Countries" (Keys is regarded as the founding father of the heart disease/high cholesterol claim), he states that mortality was lowest in those whose cholesterol was between 200 and 220, and this was among people who were consuming quite a bit of oxidized cholesterol, though heart attacks were less frequent among the peoples of those nations who ate more antioxidant-rich foods, less homogenized dairy, etc.
I agree with Keys about the 200 to 220 range being best - in general. The problem is that if you do a study on people who are eating a particular kind of diet, let's say one rich in foods that act as oxidizing agents (e.g., refined, highly unsaturated oils), the potatoes may indeed by a very good choice, whereas for people on a diet that is low in foods that act as oxidizing foods (and abundant in antioxidant-rich foods), potatoes may not be especially healthy. In fact, if those people only have access to potatoes that are a bit green, then they may be quite an unhealthy choice.
Let's generalize: in order for this kind of study to be of any use, the researchers should specify what kind of diet the subjects were eating and what the potatoes were substitiuted for (assuming the subjects didn't just eat potatoes along with what they usually did). It would also be important to do all kinds of tests on the subjects to see if they already had pathological processes going on in their bodies, if they had high levels of markers for oxidative stress, etc.
In the case of potatoes, I don't see that they would do anything to perpetuate my health, though I could see that if someone ate a typical Western diet, and substituted boiled potatoes for cookies with farily high PUFA content, there could be the kind of results they report. Until more about all of these kinds of issues are known, it's not clear what to make of these findings.
This is why I propose a new nutritional science, one based on whole diets rather than introducing one food for several weeks (and this is another major problem with most of these studies, that is, they look for certain markers in the short term). Raw demographic data is already available, which went a long way towards making the case (for me) that saturated fatty acids can't be "bad;" otherwise, there would be very high rates of heart disease among coconut consuming Asians, rather than the very low rates we can see in the demographic data. However, to design an optimal diet in the context of availability and budget constrainst faced by many or most people, it likely would be necessary to do experiments on animals. Such experiments would be complete within a few years, would be inexpensive, and would not require any markers. We would simply note which diet allowed the animals to live longests. In science, especially these days, it seems like the simplest and cheapest things to do are the things that never get done! |
|
 First
Previous
2-10 of 10
Next
Last
|
|
Reply
| |
Most people are not aware that the foundations of biology, medicine, and nutrition are so "shaky." For example, in the book titled “The Billion-Dollar Molecule�?(1994) by Werth, Mark Murko, who sought to delineate structures of proteins, states:
“…not all the equations we use to describe those
interactions are accurate. Some of them are fudge factors. Some of them are thought to be correct even though the experimental data
they’re based on are wrong, only nobody knows that because nobody’s gone back and double-checked the experiments. Some are pure guesses. There are assumptions, biases. There’s user error. There’s imprecision in the hardware and software.�?BR>
Page 303. And on page 209, it is said that the chemist Joshua Boger thinks biology is “too mushy.�?Boger states:
“I mean, what are the basic concepts of biology and how sure are we of them? Well, there aren’t any, hardly. It isn’t that the people are stupid, it’s that the data isn’t there.�?
Those who have attempted to build proper foundations, such as Gilbert Ling, have been largely ignored, and proper funding has been witheld when he sought it for important experiments (see his book, "Life at the cell and below-cell level" if this interests you, or visit his web site at www.gilbertling.org).
So what are these "sciences" based upon? Untested "models," assumptions that appeared reasonable to people who wrote the textbooks, markers that correlate with clinic symptoms (usually called "diseases" or "syndromes"), or flawed experiments that are still be cited (some are still cited in the professional literature, such as the 1930 Burr & Burr "essential fatty acid" experiment on rats, even though it was refuted in 1948).
The markers that correlate can then be examined in an epidemiological context and advice given to the public by "public health experts." Let's take an example: there is a big increase in heart attack deaths among men in their 40s and 50s. Researchers notice that these men have higher serum cholesterol levels (though there are other markers they ignore for whatever reason or are totally unaware of), and so they put the word out that lowering cholesterol is something everyone should do. They don't know why this is the case, nor do they know if this advice will do more harm than good, but they do know that there is a correlation, and they have nothing else, so they "run with it." The fact that the fathers and grandfathers of these men ate plenty of cholesterol and saturated fatty acids and did not die of heart attacks apparently never dawns on them. Now, there are plenty of studies that introduce a concept that is as insidious as they come, scientifically. For example, many researchers, assuming that "high cholesterol is bad," use this notion as a "surrogate endpoint," meaning that they don't care whether lowering cholesterol results in a much higher mortality rate, either from heart disease or in general. As long as the result was that the cholesterol levels of the subjects was lowered by the agent used, they can say that the experiment was a great success and that the agent (usually a drug) should be marketed to people with "high cholesterol," the definition of which changes from time to time.
Fortunately, there is now plenty of molecular level evidence and better understanding of the effects of oxidizing activity on biological systems to understand the exact mechanism, rather than relying on speculation. Read my post: How polyunsaturated fatty acids (PUFAs) cause "heart disease." if you want more information about this particular phenomenon.
One of the most important goals of this newsgroup is to point out to people that they do not have to rely on the models, markers, correlations, etc., but, if they are willing to put some time into it, learn about the exact mechanisms involved.
|
|
Reply
| |
Here's an interesting take on some experimental data:
QUOTE: The study found that by weight category, in-hospital mortality rate was 6.3 percent for underweight, 4.6 percent for healthy weight, 3.4 percent for overweight and 2.4 percent for obese patients, according to the study published in the American Heart Journal... UNQUOTE.
The researcher's interpretation was:
QUOTE: "The study suggests that overweight and obese patients may have a greater metabolic reserve to call upon during an acute heart failure episode, which may lessen in-hospital mortality risk," says Fonarow...
Copyright 2007 by United Press International. All Rights Reserved. UNQUOTE.
This could be accurate, but what exactly is meant by "metabolic reserve" here? Are the patients being given too little food? Or are their bodies being traumatized in some way by the medical "professionals" that handle them? It would be a good idea to take levels of various known markers, which might lead to the development of a formal hypothesis.
Source: http://www.sciencedaily.com/upi/index.php?feed=Science&article=UPI-1-20070109-17444100-bc-healthwrap.xml
In another study:
QUOTE: Tests on volunteers showed that black tea significantly improves the ability of the arteries to relax and expand, but adding milk completely blunts the effect. Supporting tests on rat aortas (aortic rings) and endothelial (lining) cells showed that tea relaxed the aortic rings by producing nitric oxide, which promotes dilation of blood vessels. But, again, adding milk blocked the effect. UNQUOTE.
This demonstrates the problem with various nutritional studies, and that is if you just isolate one variable for study, you may be led (by the findings) to conclude that this or that food is unhealthy. In this case, among peoples who drink tea with milk one might find totally opposite effects than among peoples who don't use milk in their tea. Moreover, whether this effect of tea (wihtout milk) is "beneficial" may depend upon whether your cells contain arachidonic acid, how much iron is in your diet, etc. Obviously, a researcher who wanted to make a particular food might be able to design his or her study in such a way as to make a food appear healthy or unhealthy, regardless of what the scientific reality actually is.
Source: http://www.sciencedaily.com/releases/2007/01/070108191523.htm |
|
Reply
| |
I found a study that is typical of many nutritional studies on dietary fat sources. This is what they "found:" QUOTE: After 4 wk, both PHSO and IE fats significantly elevated both the LDL/HDL ratio and fasting blood glucose, the latter almost 20% in the IE group relative to POL. Fasting 4 wk insulin was 10% lower after PHSO (p > 0.05) and 22% lower after IE (p < 0.001) compared to POL. For the postprandial study the glucose incremental area under the curve (IAUC) following the IE meal was 40% greater than after either other meal (p < 0.001), and was linked to relatively depressed insulin and C-peptide (p < 0.05). UNQUOTE. PHSO stands for partially hydrogenated soybean oil and IE stands for a new kind of fat, cooked up in labs, called "interesterified fats ," which some companies have decided to sell as a "healthy alternative" to oils deemed to be "trans fat." POL stands for palm olein, which is obtained from plam trees, and is commonly used for frying in some parts of the world, but not in the USA. So what is wrong with the study? I will address some of the problems. We don't know who these subjects are. Are they young and healthy college students or are the geriatric individulas with all kinds of health issues? In any case, raising LDL and lowering HDL may not be a "bad" thing. If cholesterol is not oxidized, then there is no reason to fear LDL and no reason to want particularly high HDL. However, elevating glucose levels does seem to be something that should be regarded as negative. What they should have done is to measure a marker of oxidative stress, which would indicate whether the causative mechanism was excess free radical activity or not, since this is a major issue with fat source that have more than small amounts of unsaturated fatty acids. Fortunately, I found a study that did just this, and here are the results of that one: QUOTE: There was a significant increase in myocardial catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities with no significant change in myocardial thiobarbituric acid reactive substances (TBARS) only in group PO 5 as compared to group C. There was no light microscopic evidence of tissue injury. A significant rise in myocardial TBARS and depletion of myocardial endogenous antioxidants (SOD, CAT and GPx) along with significant myocyte injury was observed in control rats subjected to ischemia-reperfusion (C IR). Hearts from palm olein oil fed rats subjected to ischemia-reperfusion (PO 5 IR and PO 10 IR) were protected from increase in TBARS and depletion of endogenous antioxidants as compared to C IR group. No significant myocyte injury was present in the treated groups. UNQUOTE. They concluded that: QUOTE: The present study demonstrated for the first time that dietary palm olein oil protected rat heart from oxidative stress associated with ischemic-reperfusion injury. UNQUOTE. "TBARS" are molecules that are markers for oxidative stress, and PO stands for plam olein here. Note that they don't tell us what the control diet consisted of, so we can only assume it was rich in linoleic acid, since that is common in dry animal feed. It could be corn, soybean, safflower, or sunflower oil (or a combination), for example. They are clear about their notions concerning the role of free radicals in this context, however. For example: QUOTE: Palm olein oil (PO), obtained from refining of palm oil is rich in monounsaturated fatty acid and antioxidant vitamins and is widely used as oil in diet in many parts of the world including India. UNQUOTE. Source of the first study: Nutrition & Metabolism 2007, 4:3. On the internet: http://www.nutritionandmetabolism.com/content/4/1/3/abstract Source of the second study: BMC Pharmacology 2004, 4:29. On the internet: http://www.biomedcentral.com/1471-2210/4/29 |
|
Reply
| |
Here is an abstract of a recent study that is likely to mislead or confuse people who are trying to do their own research, but who are not as familiar with this topic as someone like myself is. First, they say that PUFAs play and "important role" in causing and preventing cancer, but they don't specify exactly what they mean. In particular, to say that PUFAs prevent cancer is at best a gross distortion of the scientific literature on this subject. If they mean that in a lab one can do things to tumor cells that do not occur in the body, leading to cancer cell death, then there is no reason to mention this, because it cannot help anyone at this point, and clearly does not "prevent
cancer.
Secondly, they tell us that some types of cancer cells have less PUFA content than normal cells. This is interesting because it's certainly reasonable to view cancer as an adaptation to stressful conditions, and PUFAs are a destabilizing substance. In an important sense, the body is a cooperative colony of cells, and under conditions that are too stressful, it makes sense that certain "checks" against adaptation to the conditions that would lead to a dangerous situation (that is, out of control growth we call "cancer") would be discarded.
Next, they talk about exposing the cancer cells to AA or DHA at 100muM. This is a very high dose, and is basically akin to poisoning the cells. Obviously, if you get cancer and poison yourself, you will also poison the cancer, to some degree at least. This is confirmed by the mechanism for this "positive" result, which is lipid peroxidation - free radical damage. Notice that they do not specify exactly how a practical treatment could be devising using this information. While it is certainly possible that the complete text of this study exhibits a more reasonable interpretation of their experimental results, I doubt it, because this abstract makes little sense to anyone who has done as much research as I have on this subject, and I fear that such "studies" as this will lead various "experts" to suggest that people consume more dietary PUFAs. The evidence suggests that this is the way to become afflicted with cancer (or some other very dangerous condition), not to avoid it.
Here is the study's abstract:
Chem Biol Interact. 2007 Jan 10; [Epub ahead of print].
"Arachidonic and docosahexaenoic acids reduce the growth of A549 human lung-tumor cells increasing lipid peroxidation and PPARs."
Trombetta, A., et al.
Polyunsaturated fatty acids (PUFAs) play an important role in both induction and prevention of carcinogenic process. It is well known that several types of neoplastic cells show decreased total PUFA content, contributing to their resistance to chemotherapy and lipid peroxidation. In the light of this, human lung cancer A549 cells, with low PUFA content, were exposed to arachidonic or docosahexaenoic acid to investigate the effect of n-6 and n-3 PUFAs on growth and elucidate underlying mechanisms. The bulk of the results showed that both n-6 PUFAs and n-3 PUFAs decrease human lung-tumor cell growth in a concentration-dependent manner, inducing cell death mainly evident at 100muM concentration. The mechanism underlying the antiproliferative effect of n-6 and n-3 PUFAs appeared to be the same, involving changes in fatty acid composition of biomembranes, production of cytostatic aldehydes derived from lipid peroxidation and able to affect DNA-binding activity of AP-1, and induction of PPAR. From these results it may be hypothesized that n-6 PUFAs, like n-3 PUFAs, are able to inhibit tumor growth. |
|
Reply
| |
The researchers of the study cited in the post above appear to have been unaware that a key experiment had already been done, with the study published in 2003. In that paper, entitled "Arachidonic acid cytotoxicity: can arachidonic acid be a physiological mediator of cell death?", the following statements are made:
"As for polyunsaturated fatt acids, which are apoptotic at 5-100uM, cell death seems to be closely linked to oxidative stress and lip peoxoditation..."
"Human plasma levels of free arachidonic acid (non-esterified) vary from 5.8 to 49.3 uM. Because of the presence of albumin, however, the actual concentration of available arachidonic acid in plasma is probably below 0.1 uM."
"Under some pathological situations, plasma levels [or arachidonic acid] can increase to 100 uM (malaria)..."
"As for the study of intravenously-injected arachidonic acid, death of rabbits, which occurs in minutes, also renders the study of specificallytriggered cytotoxicity mechanisms unfeasible."
"Arachidonic acd, nevertheless, is cytotoxic to many cells types, showing low specificity."
".. the oxidative stress caused by arachidonic acid, which is the most probable mechanism to explain its cytotoxicity, is hard to control and in many cases leads to necosis. When cells die by necrosis, they burst and release cytotoxic substances that cause inflammation."
Thus, the authors of the study cited in the post above this one should have know that because fatty acids such as arachidonic acid are so unstable, they are what one might call indiscriminate cell killers, and so it's highly unlikely that they would prevent cancer from occurring in the first place (though highly likely that they cause cancer), and are so dangerous that only if they could be targeted to kill only cancer cells would they be worth investigating further in this context. Next time a "professional" or "expert" tells you that arachidonic acid is "essential," ask him or her if he or she has read the study cited in this post.
Source of this study: Cell Biochemistry and Function. 2003; 21: 97-104, authored by Pompeia, Celine, et al. |
|
Reply
| |
The following study is the kind that nutritionists often use when they give advice. Note that there is no experimental data. For example, they say to boil eggs "softly" only, yet where is the experimental data showing that boiling the egg yolk until it is "hard" produces more oxidized cholesterol? And if it is still in the egg shell, where is the oxygen going to come from to oxidize the cholesterol? Why are the emphasizing the temperature when it is oxygen that is necessary to oxidize? They say that butter is "highly atherogenic," yet I have yet to see evidence of this, though I advise people not to cook with it and to trim the yellowed sides off butter sticks, to avoid dangerous lipid peroxidation reactions. And notice how the author talks of "trans-fatty acids" but also of "saturated fats." This is inconsistent. Is he/she talking about the molecules or about the fat source itself? Coconut oil is clearly not "atherogenic," but something like lard probably is (due to its mere 40% saturated fatty acid content, its cholesterol content, the way it is usually cooked, etc.), yet both are classified as "saturated fats." Until this highly misleading situation is rectified, one has to question the intelligence of people making these kinds of statements. Lastly, the author talks about fish oils preventing atherosclerosis and having "antioxidant" qualities. This demonstrates both a lack of knowledge of basic nutritional literature as well as ignorance of basic biochemistry. It is unfortunate that this person has some awareness of the dangers of lipid peroxidation, but then goes on to talk about fatty acids in a way that contradicts basic, undeniable biochemicals facts. The role of eggs, margarines and fish oils in the nutritional management of coronary artery disease and strokes. Constant, J. Abstract: Although egg yolk is a rich source of cholesterol, the effect of eggs in raising serum cholesterol is variable and in some subjects there is no effect whatsoever. However, oxidized cholesterol can increase atherosclerosis even with normal serum cholesterol. In order to attenuate oxidation of cholesterol in eggs, it is necessary to limit the degree of heat applied. This means that we should use only soft-boiled eggs which should be almost like water. We can also avoid egg yolk altogether and get a highly nutritious egg food from the egg white alone. The saturated fats from milk products, especially butter, are highly atherogenic. There are available many butter substitutes in the form of margarines. But many of these margarines have hydrogenated vegetable oils which result in the production of trans-fatty acids. The trans-fatty acids are as atherogenic as saturated fats. There are available, however, margarines without the trans-fatty acids. These are found only in large supermarkets. Fish oils contain N3 fatty-acids which, unlike vegetable oils which contain N6 fatty-acids, can prevent atherosclerosis and sudden death by counteracting ventricular arrhythmias, acting as antioxidants, antithrombotic, anti-inflammatory agents, and decreasing triglycerides and blood pressure. |
|
Reply
| |
Here is a report about a study that criticizes another study which concludes that antioxidant vitamin supplementation does more harm than good:
http://www.sciencedaily.com/releases/2007/02/070228172604.htm
The report begins with: "A study recently published on possible health risks of antioxidant supplements is based on flawed methodology and ignores the broad totality of evidence that comes to largely opposite conclusions..."
The whole report is worth reading, because the Linus Pauling people do a good job of pointing out some of the "shell games" played by some scientists who appear to only be interested in evidence that seems to support their ideas (many of which simply don't make sense when you examine the evidence as a whole). |
|
Reply
| |
Many of the studies you hear about in the media these days are based upon "surrogate endpoints." For example, something that "lowers cholesterol" in health college students after a few weeks on a drug or certain kind of diet is taken to mean that they are at lower risk for "heart disease." Obviously, this is a great leap of faith. Here is an abstract of a study that makes this point in the context of cancer:
Recent Results Cancer Res. 2005;166:89-98.
"Problems with using biomarkers as surrogate end points for cancer: a cautionary tale."
Schatzkin A.
Investigations employing surrogate cancer end points are especially attractive because they may be smaller, shorter, and cheaper than comparable studies with explicit cancer outcomes. For many potential surrogate end points--epithelial cell proliferation will be taken as an example--inferences are problematic because of the existence of alternative causal pathways to cancer that bypass the surrogate end point. Evaluating potential surrogates requires information on the following three questions: (1) What is the relation of the surrogate end point to cancer? (2) What is the relation of the intervention (or exposure) to the surrogate? (3) To what extent does the surrogate end point mediate the relation between intervention (exposure) and cancer? Data for these questions may derive from animal experiments, human metabolic studies, observational epidemiologic investigations (including ecologic studies), and randomized trials. Inferences to cancer from such downstream markers as colorectal adenomatous polyps and persistent human papillomavirus infection of the cervix are strong, though not absolutely unassailable. For all but these very-close-to-cancer markers, considerable caution is warranted in extrapolating from surrogate effects or associations to cancer.
|
|
|
First
Previous
2-10 of 10
Next
Last
|
|
Free Forum Hosting
Important Announcement
Return to General