Attack on Mothers
125 Comments Posted June 19, 2007 06:51 PM (EST)
Read More: Breaking Living Now News, Robert F. Kennedy
The poisonous public attacks on Katie Wright this week--for revealing that her autistic son Christian (grandson of NBC Chair Bob Wright), has recovered significant function after chelation treatments to remove mercury -- surprised many observers unfamiliar with the acrimonious debate over the mercury-based vaccine preservative Thimerosal. But the patronizing attacks on the mothers of autistic children who have organized to oppose this brain-killing poison is one of the most persistent tactics employed by those defending Thimerosal against the barrage of scientific evidence linking it to the epidemic of pediatric neurological disorders, including autism. Mothers of autistics are routinely dismissed as irrational, hysterical, or as a newspaper editor told me last week, "desperate to find the reason for their children's illnesses," and therefore, overwrought and disconnected.
But my experience with these women is inconsistent with those patronizing assessments. Over the past two years I've met or communicated with several hundred of these women. Instead of a desperate mob of irrational hysterics, I've found the anti-Thimerosal activists for the most part to be calm, grounded and extraordinarily patient. As a group, they are highly educated. Many of them are doctors, nurses, schoolteachers, pharmacists, psychologists, Ph.D.s and other professionals. Many of them approached the link skeptically and only through dispassionate and diligent investigation became convinced that Thimerosal-laced vaccines destroyed their children's brains. As a group they have sat through hundreds of meetings and scientific conferences, and studied research papers and medical tests. They have networked with each other at meetings and on the Web. Along the way they have stoically endured the abuse routinely heaped upon them by the vaccine industry and public health authorities and casual dismissal by reporters and editors too lazy to do their jobs.
Many of these women tell a story virtually identical to Katie Wright's -- I have now heard or seen this grim chronology recounted hundreds of times in conversations, e-mails and letters from mothers: At 2-1/2 years old, Christian Wright exceeded all milestones. He had 1,000 words, was toilet-trained, and enjoyed excellent social relations with his brother and others. Then his pediatrician gave him Thimerosal-laced vaccines. He cried all night, developed a fever and, over the coming months, this smart, healthy child disappeared. Christian lost the ability to speak, to interact with family members, to make eye contact or to point a finger. He is no longer toilet trained. He engaged in stereotypical behavior--screaming, head-banging, biting and uncontrolled aggression, and suffers continuously the agonizing pain of gastrointestinal inflammation.
After hearing that story a couple dozen times, a rational person might do some more investigation. That's when one encounters the overwhelming science -- hundreds of research studies from dozens of countries showing the undeniable connection between mercury and Thimerosal and a wide range of neurological illnesses. In response to the overwhelming science, CDC and the pharmaceutical industry ginned up four European studies designed to disguise the link between autism and Thimerosal. Their purpose was to provide plausible deniability for the consequences of their awful decision to allow brain-killing mercury to be injected into our youngest children. Those deliberately deceptive and fatally flawed studies were authored by vaccine industry consultants and paid for by Thimerosal producers and published largely in compromised journals that neglected to disclose the myriad conflicts of their authors in violation of standard peer-review ethics. As I've shown elsewhere [see http://www.robertfkennedyjr.com/], these studies were borderline fraud, using statistical deceptions to mislead the public and regulatory community.
The CDC and IOM base their defense of Thimerosal on these flimsy studies, their own formidable reputations, and their faith that journalists won't take the time to critically read the science. The bureaucrats are simultaneously using their influence, energies and clout to derail, defund and suppress any scientific study that may verify the link between Thimerosal and brain disorders. (These would include epidemiological studies comparing the records of vaccinated children with those of unvaccinated populations like the Amish or home-schooled kids who appear to enjoy dramatically reduced levels of autism and other neurological disorders.) The federal agencies have refused to release the massive public health information accumulated in their Vaccine Safety Database (VSD) apparently to keep independent scientists from reviewing evidence that could prove the link. They are also muzzling or blackballing scientists who want to conduct such studies.
Ironically, it is the same voices that once blamed autism on "bad parenting," and "uninvolved" moms that are now faulting these mothers for being too involved.
Due to this campaign of obfuscation and public deception, Thimerosal-based vaccines continue to sicken millions of children around the world and potential treatments -- like the chelation that benefited Christian Wright -- are kept out of the hands of the mainstream doctors now treating autistic kids with less effective tools. Like thousands of other mothers of autistic children, Katie Wright knows what sickened her child. Her efforts to spare other families this catastrophe, deployed with a cool head and calm demeanor, are truly heroic. Maybe it's time we all started listening. Maybe it's time to start respecting and honoring the maternal instincts and hard work of Katie and her fellow mothers by aggressively funding the studies that might verify or dispute them.
Wednesday, June 20, 2007
Ease Those Bug Bites with Easy Herbs
A timely post for all those NASTY bugs that LOVE to bite me and my kids!
Ease Those Bug Bites with Easy Herbs
c. 2000, Susun S Weed
Summertime means insect bites and stings. Ouch! Take a leaf from Susun S. Weed's storehouse of natural remedies: Soothe, heal, and prevent bites with safe herbal remedies that grow right where you live, north or south, east or west, city or country. The best natural remedies for insect bites are right underfoot.
Plantain, also called ribwort, pig's ear, and the band-aid plant, is a common weed of lawns, driveways, parks, and playgrounds. Identify it by the five parallel veins running the length of each leaf. (Most leaves have a central vein with smaller ones branching out from it.) You may find broad leaf plantain (Plantago majus), with wide leaves and a tall seed head, or narrow leaf plantain (Plantago lanceolata), with long thin leaves and a small flower head that looks like a flying saucer. Many Plantago species have seeds and leaves that can be used as food or medicine. A South American variety (Plantago psyllium) is used to make Metamucil.(TM)
How to use plantain? Make a fresh leaf poultice. Pick a leaf, chew it well and put it on the bite. "Like magic" the pain, heat, and swelling -- even allergic reactions -- disappear, fast! (Yes, you can dry plantain leaves and carry them in your first aid kit. Chew like you would fresh leaves.)
Poultices ease pain, reduce swelling, and help heal. No wonder they're the number one natural choice for treating insect bites, bee and wasp stings.
Mud is the oldest and simplest poultice. Powdered white clay, which should be mixed with a little water or herb tea, can be applied directly to the sting as soon as possible. Clay can be kept on hand at all times and is less likely to contain fungal spores than the real thing. Finely ground grains such as rice or oatmeal, or bland starchy substances like mallow root, grated potato, or arrowroot powder also used as soothing poultices to ease itching and pain from insect bites.
Fresh-herb poultices are a little more complicated, but not by much. Just find a healing leaf, pluck it, chew it, and apply it directly to the sting/bite. If you wish, use a large leaf or an adhesive bandage to hold the poultice in place. Plantain, comfrey (Symphytum uplandica x), yellow dock (Rumex species), wild geranium (Geranium maculatum), wild mallow (Malva neglecta), chickweed (Stellaria media),and yarrow are only a few of the possiblities.
In the woods, you can take a leaf from a tree, chew it and apply that to the bite. Any tree will do in an emergency, but if you have a choice, the best leaves are those from witch hazel, willow, oak, or maple. Play it safe: Learn to recognize witch hazel (Hamamelis virginia) and willow (Salix species) leaves before you chew on them. Maple (Acer) or oak (Quercus) leaves are easier to recognize and safer to chew -- unless you live where poison oak grows. If uncertain, avoid all shrubs and any trees with slick or shiny leaves. If the leaf you are chewing tastes extremely bitter or burns your mouth, spit it out at once.
To repel ticks, mosquitoes, and black flies, try a diluted tincture of yarrow (Alchellia millefolium) flowers directly on all exposed skin. A recent US Army study showed yarrow tincture to be more effective than DEET as an insect repellent.
If you've spent the day in an area where lyme disease is common, take a shower right away and scrub yourself with a bodybrush. Have a friend check you out for ticks. Also, it takes the tick some time to make up its mind where to bite, so most are unattached and will wash off.
"If the worst happens and I do get a bite, I help my immune system by taking a daily dose of 2-6 dropperfuls of Echinacea tincture. I avoid Goldenseal as I believe it could have adverse effects. If I have symptoms, I use a dropperful of St. Joan's wort (Hypericum) tincture three times a day to help inactivate the lyme's organism."
Ease Those Bug Bites with Easy Herbs
c. 2000, Susun S Weed
Summertime means insect bites and stings. Ouch! Take a leaf from Susun S. Weed's storehouse of natural remedies: Soothe, heal, and prevent bites with safe herbal remedies that grow right where you live, north or south, east or west, city or country. The best natural remedies for insect bites are right underfoot.
Plantain, also called ribwort, pig's ear, and the band-aid plant, is a common weed of lawns, driveways, parks, and playgrounds. Identify it by the five parallel veins running the length of each leaf. (Most leaves have a central vein with smaller ones branching out from it.) You may find broad leaf plantain (Plantago majus), with wide leaves and a tall seed head, or narrow leaf plantain (Plantago lanceolata), with long thin leaves and a small flower head that looks like a flying saucer. Many Plantago species have seeds and leaves that can be used as food or medicine. A South American variety (Plantago psyllium) is used to make Metamucil.(TM)
How to use plantain? Make a fresh leaf poultice. Pick a leaf, chew it well and put it on the bite. "Like magic" the pain, heat, and swelling -- even allergic reactions -- disappear, fast! (Yes, you can dry plantain leaves and carry them in your first aid kit. Chew like you would fresh leaves.)
Poultices ease pain, reduce swelling, and help heal. No wonder they're the number one natural choice for treating insect bites, bee and wasp stings.
Mud is the oldest and simplest poultice. Powdered white clay, which should be mixed with a little water or herb tea, can be applied directly to the sting as soon as possible. Clay can be kept on hand at all times and is less likely to contain fungal spores than the real thing. Finely ground grains such as rice or oatmeal, or bland starchy substances like mallow root, grated potato, or arrowroot powder also used as soothing poultices to ease itching and pain from insect bites.
Fresh-herb poultices are a little more complicated, but not by much. Just find a healing leaf, pluck it, chew it, and apply it directly to the sting/bite. If you wish, use a large leaf or an adhesive bandage to hold the poultice in place. Plantain, comfrey (Symphytum uplandica x), yellow dock (Rumex species), wild geranium (Geranium maculatum), wild mallow (Malva neglecta), chickweed (Stellaria media),and yarrow are only a few of the possiblities.
In the woods, you can take a leaf from a tree, chew it and apply that to the bite. Any tree will do in an emergency, but if you have a choice, the best leaves are those from witch hazel, willow, oak, or maple. Play it safe: Learn to recognize witch hazel (Hamamelis virginia) and willow (Salix species) leaves before you chew on them. Maple (Acer) or oak (Quercus) leaves are easier to recognize and safer to chew -- unless you live where poison oak grows. If uncertain, avoid all shrubs and any trees with slick or shiny leaves. If the leaf you are chewing tastes extremely bitter or burns your mouth, spit it out at once.
To repel ticks, mosquitoes, and black flies, try a diluted tincture of yarrow (Alchellia millefolium) flowers directly on all exposed skin. A recent US Army study showed yarrow tincture to be more effective than DEET as an insect repellent.
If you've spent the day in an area where lyme disease is common, take a shower right away and scrub yourself with a bodybrush. Have a friend check you out for ticks. Also, it takes the tick some time to make up its mind where to bite, so most are unattached and will wash off.
"If the worst happens and I do get a bite, I help my immune system by taking a daily dose of 2-6 dropperfuls of Echinacea tincture. I avoid Goldenseal as I believe it could have adverse effects. If I have symptoms, I use a dropperful of St. Joan's wort (Hypericum) tincture three times a day to help inactivate the lyme's organism."
Saturated Fat Attack
I LOVE this article....scientific and REAL.
Saturated Fat Attack
Can One Meal Containing Saturated Fat Really Be that Bad?
Or Why You Don't Need Vegetable Oil in Your Carrot Cake and Milk Shake to Protect Your Arteries by Chris Masterjohn
Newspapers around the world have recently published the results of a study indicating that a single meal rich in saturated fats will disrupt the functioning of your arteries and contribute to the inflammation of your blood vessels. The Associated Press story by Joe Milicia1 was heard round the internet, and reported in papers throughout the world.
The news article quoted the Kansas City cardiologist Dr. James O'Keefe as claiming the study showed that "when you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward."
Dr. Nicholls, the lead author of the study that generated such an amazing amount of attention in the press, was quoted as saying that his research showed the "need to aggressively reduce the amount of saturated fat consumed in the diet." The article then clarified that this meant reducing our intake of beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, and replacing them with safflower oil, sesame oil, sunflower seeds, corn and soybeans. Amazingly, this study had the power to make sweeping conclusions about over 15 different foods!
The study in question was published by a team of researchers led by Dr. Stephen J. Nicholls of the Australian Heart Research Institute in the Journal of the American College of Cardiology entitled, "Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function."2
Reality Check
In reality, none of the dire conclusions reported in the press is justified by the study. There was no clearly discernable effect of any type of fat on arterial function, and those consuming saturated fat had the best arterial function at all time points measured.
In fact, the researchers did not even study the inflammation occurring in the blood vessels of the people eating the meals. Instead, they performed an interesting experiment on isolated cells in which they found high-density lipoprotein (HDL) isolated from people eating safflower oil to have greater anti-inflammatory power than HDL isolated from people eating coconut oil. They attributed this observation to the saturation of fat that the study subjects consumed without a shred of evidence, and overlooked the more plausible explanation that these effects were due to the large difference in vitamin E contents of the two diets.
Study Design
The researchers fed fourteen adults a meal of carrot cake and a milk shake on two separate occasions one month apart, once made with highly saturated coconut oil and once made with highly polyunsaturated safflower oil. Both oils were non-hydrogenated, organic, unrefined and virgin.3
The researchers, who were blinded to which meals the subjects were receiving, took each of three types of measurements at three different time points: first, after an overnight fast and before the meal was administered; second, three hours after the meal was administered; third, six hours after the meal was administered.
The first type of measurement they took was the levels of various constituents in the subjects' blood: total cholesterol, LDL, HDL, triglycerides, insulin and free fatty acids.
The second type of measurement they took was of various parameters of blood flow, including the total amount of blood flow through the subjects' forearms and the degree of "flow-mediated dilation" in their brachial arteries. Flow-mediated dilation is the ability of a blood vessel to dilate to rush blood to an area that has been deprived of oxygen. To measure it, researchers use pressure to stop blood flow through an artery and then test to what extent the artery reacts once the pressure is released by dilating to increase the return of blood to the blood-deprived area. With this type of test, the more the blood vessel dilates when pressure is released, the better shape it is believed to be in.
Finally, the researchers extracted HDL from the subjects' blood at each time point. They incubated isolated endothelial cells from human umbilical veins with the HDL at various concentrations. After the incubation period, they added an inflammatory chemical called tumor necrosis factor-alpha (TNF-a) to the cells, which stimulates the production of adhesion molecules with long-winded names like intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), which are believed to play a role in the adhesion of immune cells to arterial plaque. HDL has been shown to inhibit the expression of these inflammatory molecules, and the researchers conducted this part of the study to see whether how you eat can affect how much potential HDL has to inhibit the expression of these presumably harmful adhesion molecules.
The researchers claimed to generate two findings:
Flow-mediated dilation decreased more strongly after the coconut oil meal than after the safflower oil meal. From this, they concluded that "consumption of saturated fat impairs . . . endothelial function."
When cells were incubated with HDL taken from subjects after they ate the coconut oil meal, the expression of the inflammatory adhesion molecules in response to TNF-a stimulation was increased compared to cells incubated with HDL taken from fasting subjects. By contrast, when cells were incubated with HDL taken from subjects after they ate the safflower oil meal, the expression of inflammatory molecules in response to TNF-a stimulation was decreased compared to cells incubated with HDL taken from fasting subjects. From this, the authors concluded that "consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins."
Although both of these conclusions are more conservative than the statements written in the Associated Press article, neither of them is justified by the study.
Let's take a closer look at each.
Flow Mediated Dilation
The researchers claim that consumption of the saturated fat meal impaired flow-mediated dilation (FMD). They did indeed show that at the three-hour mark the decline in FMD was almost twice as great in the coconut oil group as it was in the safflower oil group. Yet the FMD was actually higher in the coconut oil group than in the safflower oil group at every point along the way! The reason? When the subjects were fasting, those who were about to eat the coconut oil meal had 33 percent better FMD than those who were about to eat the safflower oil meal. Even at the three-hour point, when FMD had declined the most, it was still 9 percent higher in the coconut oil group than in the safflower oil group.
There are two ways we could look at this paradoxical situation. Figure 1 shows the changes that took place in FMD three and six hours after the meals, relative to the FMD before the meals (called "baseline"). You can see that for both the coconut oil meal and the safflower oil meal, FMD declined substantially at the three-hour mark, although the rate at which it declined was nearly double after the coconut oil meal.
Figure 1. Percent change in the degree of flow-mediated dilation (FMD) compared to baseline values.
Group Baseline Three Hours Six Hours
Saffllower Oil No Change 17 percent lower 8 percent lower
Coconut Oil No Change 32 percent lower 10 percent lower
Now let's look at these findings another way. Figure 2 compares the relative degree of FMD of the coconut oil group with that of the safflower oil group. Here you can see that the FMD is higher (a good thing) in the coconut oil group at every single time point during the study.
Figure 2. Comparison of the degree of flow-mediated dilation (FMD) in the coconut oil group to that in the safflower oil group at three time points.
Baseline 3 hours 6 hours
33 percent higher in coconut oil group 9 percent higher in coconut oil group 29 percent higher in coconut oil group
Thus, we have to ask: is consumption of coconut oil rather than safflower oil the reason for the greater decline of FMD in the coconut oil group? Or, is the reason for this decline the simple fact that the people who ate the coconut oil meal started out with a higher value of FMD in the first place, and therefore, so to speak, had more to lose?
There are two reasons that the latter scenario might be true: first, the decline in FMD after a meal might not even be a function of the FMD; second, a randomly high sampling error for the FMD before the meal could result in what is called "regression to the mean."
In the first case, it could be that eating carrot cake and drinking a milkshake, whether made with safflower oil or coconut oil, depresses FMD to a certain point regardless of fasting levels. For example, eating the meal might depress FMD to about 5 percent, regardless of whether the person's fasting level was 6 percent or 9 percent.
In such a scenario, a person whose fasting level is 9 percent would experience a 44 percent decline in FMD, while a person whose fasting level is 6 percent would experience only a 17 percent decline in FMD.
Thus, if the effect of a meal on FMD is not a function of fasting FMD, the coconut oil group, which by random chance had a 33 percent higher fasting FMD, would exhibit a greater relative decline than the safflower oil group for no other reason than that they started off with substantially better FMD in the first place!
Regression to the Mean
The authors themselves admitted a very similar explanation in the journal article, writing that "it is possible that 'regression to the mean' may have contributed to some of the FMD reduction observed after consumption of the saturated fat." The concept of "regression to the mean" is essentially this: if by random sampling error an initial value tends to be higher than the mean, a second value will tend to be closer to the mean. Thus, a decline in values could result simply from the first value being randomly high.
Yet was this caveat noted in the press? Of course not. Instead, we were told that when we eat saturated fat, "damage to the vessels happens immediately afterward," and thus we must "aggressively reduce the amount of saturated fat consumed in the diet."
No one warned us that if when fasting, by random sampling error we happen to have a higher-than-average value of FMD, rapid but unmeaningful FMD reduction will occur after we eat due to "regression to the mean." No one warned us that we must "aggressively reduce the amount of random sampling error" lest we suffer statistically indicated arterial dysfunction with one, single meal.
Inflammation in the Test Tube
Contrary to the Associated Press report's claim that "fewer inflammatory agents were found in the arteries" after the safflower oil meal than before it, the researchers did not measure any type of inflammation in the arteries of the test subjects. Instead, they incubated isolated umbilical vein endothelial cells with HDL taken from these subjects at various time points before and after the meals, and then stimulated these isolated cells to produce inflammatory adhesion molecules by adding a compound called TNF-a to them. Finally, they measured whether HDL isolated after the different meals had a different ability to lower the amount of adhesion molecules released after stimulation with TNF-a.
The researchers found that cells incubated with the HDL isolated from subjects after they had eaten the coconut oil meal produced more adhesion molecules (ICAM-1 and VCAM-1) after stimulation with TNF-a than did cells incubated with HDL isolated from fasting subjects, and that cells incubated with HDL isolated from subjects after they had eaten the safflower oil meal produced fewer adhesion molecules after stimulation than did cells incubated with HDL isolated from fasting subjects. In other words, eating safflower oil seemed to make the HDL a more powerful anti-inflammatory agent, while eating coconut oil seemed to make the HDL a less powerful anti-inflammatory agent.
There are a number of problems with the large leap of logic it takes to conclude from this finding that a meal rich in saturated fat causes inflammation. First, we are neither test tubes nor petri dishes, but complex organisms with many different chemical and electrical feedback systems that do not exist in laboratory dishes. The researchers could have directly measured the levels of ICAM-1 and VCAM-1 in the subjects' blood, but that is not what they chose to study.
Second, the researchers only studied the anti-inflammatory potential of HDL. They could have incubated the cells with whole plasma to measure the total anti-inflammatory capacity of the blood, but they chose not to, for the simple reason that they were only trying to answer one small question about HDL and not look at the bigger picture.4
Virgin coconut oil is rich in very powerful polyphenols,5 some types of which have been shown to decrease expression of TNF-a and adhesion molecules,6, 7 and which are carried by water-soluble proteins in the blood and not by HDL.8 Thus, virgin coconut oil's contribution to the anti-inflammatory capacity of the blood could be primarily in the non-HDL fraction, whereas safflower oil's contribution to the anti-inflammatory capacity of the blood might be primarily in the HDL fraction. We simply do not have enough knowledge at this point to say for sure.
The only way to determine the effect of safflower oil and coconut oil on the total anti-inflammatory capacity of the blood is to perform the experiment by incubating the cells with whole blood. The only way to determine the effect of safflower oil and coconut oil on the actual level of inflammation in the people consuming the oils is to measure the inflammatory compounds being directly produced in their blood. This study did neither.
Finally, and most importantly, the researchers provided no evidence whatsoever that the effects they observed were due to the type of fat in the two meals. They simply assumed that the difference they observed between safflower oil and coconut oil was due to the fact that coconut oil is high in saturated fat and safflower oil is high in unsaturated fat. In doing so, they overlooked a very interesting hypothesis that could explain their results and that has substantial support in the scientific literature.
An Alternative Hypothesis: Vitamin E
The difference between safflower oil and coconut oil does not stop at the relative degree of fatty acid saturation. Figure 3 shows the difference in vitamin E content between the two oils. Safflower oil is 77 times higher in alpha-tocopherol and 47 times higher in total tocopherols.9
Figure 3. Typical tocopherol (vitamin E) content of coconut oil and safflower oil.
Tocopherol Coconut Oil Safflower Oil
Alpha-tocopherol 5 mg/kg 387 mg/kg
Beta-tocopherol -- --
Gamma-tocopherol -- 174 mg/kg
Delta-tocopherol 6 mg/kg 240 mg/kg
TOTAL tocopherol 11 mg/kg 801 mg/kg
Source: (Enig, 2000).
Is it plausible that the difference in vitamin E content of the oils could account for the difference in the expression of adhesion molecules in the isolated cells? Absolutely.
A recent review of alpha-tocopherol's role in regulating gene expression listed the suppression of the gene that codes for ICAM-1 as one of its functions.10 In fact, Chinese researchers performed a very similar experiment to the one we have been discussing, wherein they incubated endothelial cells taken from human umbilical veins with vitamin E instead of HDL. They found that incubating the cells with alpha-tocopherol, gamma-tocopherol and mixed tocopherols all inhibited the ability of oxidized LDL to induce ICAM-1 expression in the cells in a dose-dependent manner.10 Another group found vitamin E to reduce both ICAM-1 and VCAM-1 in the heart cells of rats.11
Vitamin E suppressed ICAM-1 and VCAM-1 levels in vivo in rabbits, although the effect on VCAM-1 was not statistically significant.13 In humans, the combination of vitamins E and C, but not vitamin C alone, decreased blood levels of ICAM-1 after six months. When the supplementation was stopped, blood levels of ICAM-1 returned to their initial levels. A similar effect was seen on VCAM-1, but it was not statistically significant. Unfortunately the researchers did not study the effect of vitamin E alone.14
Vitamin E travels in the blood associated with lipoproteins, including HDL.15 When endothelial cells are incubated with vitamin E-enriched HDL, they selectively take up vitamin E from the HDL at ten times the rate at which they take up the HDL particles themselves.16
It is therefore reasonable to suggest that the high vitamin E content of safflower oil led to an enrichment of the subjects' HDL particles with vitamin E, which was then taken up by the endothelial cells where it suppressed the expression of adhesion molecules.
Yet one question remains: why would the HDL taken from subjects after they ate the coconut oil meal be less effective at suppressing the expression of adhesion molecules than HDL taken from subjects when they were fasting? The one study I've found on the effect of a meal on the distribution of vitamin E in the blood15 suggests that the fraction of vitamin E in HDL actually declines temporarily after a meal when the meal is relatively low in vitamin E, but rises if the meal is high in vitamin E. It may be, then, that the vitamin E content of HDL declined after the coconut oil meal not because of the coconut oil itself but because any low-vitamin E meal reduces the amount of vitamin E in circulating HDL. On the other hand, the safflower oil meal may have been high enough in vitamin E to make the vitamin E content of HDL rise.
The only way to actually know would be to directly measure the vitamin E content of the HDL particles after the meal. Although the researchers who conducted the study we have been discussing measured the amount of protein, phospholipid, triglyceride and cholesterol in the HDL particles that they extracted, they unfortunately did not measure the amount of vitamin E in these particles.
The foregoing is, of course, a hypothesis. I have not shown conclusively that the effects observed in the study must have been due to vitamin E; I have simply shown that this is a plausible explanation. Further research would be needed to confirm or refute the hypothesis.
Likewise, it is an unconfirmed hypothesis that the effect observed was a result of the consumption of saturated fat. This unfortunately did not stop the researchers from titling their paper "Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function" as if they had actually shown this to be the case.
So Which Oils Should We Eat?
If it turns out to be true that the difference in the protective effect of HDL in the test tube was in fact due to the high vitamin E content of safflower oil and the low vitamin E content of coconut oil, that does not mean we should avoid coconut oil. It does not even mean we should eat safflower oil.
These findings simply reflect the fact that coconut oil is not a good source of vitamin E. Coconut oil is still the best source of medium-chain fatty acids, which boost metabolism and support the immune system, and virgin coconut oil is rich in powerful antioxidant polyphenols.
Polyunsaturated fatty acids such as those found in safflower oil actually deplete the body of vitamin E and thereby increase the body's need for vitamin E--this is basic textbook biochemistry.17 Safflower oil may raise the amount of vitamin E in lipoproteins immediately after a vitamin E-rich meal, but what is the long-term effect on vitamin E status of an excessive intake of polyunsaturated fats?
It makes sense then that the best way to obtain vitamin E would be from sources that are high in vitamin E but low in polyunsaturated fat. Unrefined palm oil is an excellent example of such a source.
Palm oil is only 9 percent polyunsaturated, compared to safflower, which is 75 percent polyunsaturated. In terms of the absolute amount of vitamin E, compared to safflower oil, palm oil has a somewhat lower level of alpha-tocopherol, more than double the gamma-tocopherol, and large amounts of tocotrienols, which are another important part of the vitamin E complex that are completely absent in safflower oil. The combined absolute value of tocopherol and tocotrienol forms of vitamin E is 46 percent higher in palm oil than safflower oil.9
When one takes into account the high polyunsaturated fat content of safflower oil, which increases the need for vitamin E, the advantage of more saturated palm oil becomes obvious: the ratio of vitamin E to polyunsaturated fatty acids in palm oil is 12 times greater than the same ratio in safflower oil!
Yet newspapers the world over carrying the Associated Press article told us to reduce our intake of palm oil and other saturated fats "aggressively."
Dire Warnings
We've been told that this study shows that when "you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward." We've been told that it shows we must "aggressively reduce the amount of saturated fat consumed in the diet." We've been further told to throw out the beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, replacing all these fats with safflower oil, sesame oil, sunflower seeds, corn and soybeans.
These dire warnings are based on a study that couldn't differentiate the effect of coconut oil from the effect of random sampling error on flow-mediated dilation and that showed people consuming coconut oil to have better flow-mediated dilation at all time points than people consuming safflower oil; they are based on a study that could not differentiate between the effect of saturated fat and the effect of vitamin E on the capacity of HDL to prevent inflammation in isolated, laboratory-cultured cells; and they are based on a study that tells us nothing about the amount of inflammation going on within the people consuming the meals, who are much more complex than globs of isolated laboratory-cultured cells.
Further research should uncover whether the effects seen in the test tube are due to vitamin E, to saturated or unsaturated fats, or to other causes entirely, and what relevance these observations in the test tube have for real, living people.
In the meantime, traditional animal fats, tropical oils and olive oil remain our best bet for avoiding the modern diseases that suspiciously ascended to prominence soon after researchers began heralding seed oils like safflower oil as a healthy alternative to traditional, saturated fats.
We can, however, draw two conclusions from the present study to make life safer for all of us and to advance the public health. First, always avoid random sampling error before you eat; otherwise, it would take only a single meal for "regression to the mean" to result in statistically induced markers of arterial dysfunction immediately afterward. Second, if you do eat a meal high in saturated fats, resist the urge to extract your HDL and throw it into the nearest petri dish. Chances are there's a researcher just waiting for your defenseless lipoproteins with a pipette full of inflammatory chemicals, and at that point, all hope of preventing cell-to-cell adhesion is lost.
A Better Experiment
A major drawback of the current study is that it could not distinguish between the effect of the saturation of the fats that the study subjects consumed and the amount of vitamin E in their diets. One way to conduct an experiment while avoiding this pitfall would be to use palm oil, which is very rich in vitamin E despite being a highly saturated fat.
A better experiment would use three groups: one fed palm oil alone, a second fed a mixture of coconut oil and olive oil, and a third fed olive oil alone. This experiment would be able to differentiate between the effects of saturated fat and those of vitamin E because the dietary fat of the first and second groups would be similarly and highly saturated but the first group would receive 15 times as much vitamin E as the second group. Conversely, the second and third groups would receive similar amounts of vitamin E, but the dietary fat of the third group would be much lower in saturated fat.18
If HDL isolated from the first group was much more effective at inhibiting the expression of adhesion molecules by stimulated endothelial cells than HDL isolated from the second and third groups, this would support the hypothesis that it is the vitamin E content of the diet rather than the saturation of the dietary fat that is operative. If, on the other hand, HDL isolated from the first group was no more or less effective than HDL isolated from the second group but considerably less effective than HDL isolated from the third group, this would support the hypothesis that the saturation of the dietary fat rather than the amount of vitamin E is operative.
But even these findings would be tenuous. HDL is only one constituent of many in the blood, and the functioning of an artery within a living human is much more complex than the functioning of a mass of cells in a petri dish upon which a researcher has dropped solutions of isolated chemicals with a pipette. The ultimate test to teach us which oils to eat is which oils are consumed by the people who live the longest, are the healthiest, and have the best quality of life.
Anthony Colpo Comments on the Carrot Cake & Milkshake Study
The study discussed in this article was supported by a Pfizer Cardiovascular Lipid award. Pfizer makes over ten billion dollars per year from sales of Lipitor, the world's best-selling cholesterol-lowering drug.
Dr. Nicholls is supported by a postgraduate research scholarship from the National Heart Foundation of Australia. Co-author Dr. Rye is a National Heart Foundation of Australia Principal Research Fellow. The National Heart Foundation of Australia operates a program in which it charges a fee so that food manufacturers can display the "Heart Foundation Tick." Polyunsaturated vegetable oils and margarines contribute a significant portion of ingredients in these certified products.
Another co-author of the study, Dr. Lundman, is supported by postdoctoral scholarships from the Swedish Heart and Lung Foundation, which counts among its sponsors Unilever, the food giant that manufactures numerous vegetable oil and margarine products.
There have been numerous randomized controlled CHD prevention trials conducted since the 1960s, in which people have been given either high-polyunsaturate diets or high-saturate diets as the sole intervention. In these trials, extending up to eight years, no cardiovascular or overall mortality advantage has ever been observed that can be attributed to saturated fat restriction. In fact, a number of these trials observed poorer mortality outcomes in the high-polyunsaturate group.
Healthy subjects placed on high polyunsaturated diets for four-week periods have exhibited higher levels of free radical activity and blood clotting markers than those on high-saturated diets. In animal studies, polyunsaturated vegetable oils consistently promote cancer growth; an eight-year trial with real live humans that observed significantly higher cancer incidence in the polyunsaturated group suggests this phenomenon is not merely confined to lab rats.1 This same study, by the way, showed little difference in extent of atherosclerosis among autopsied subjects from the high-saturate and high-polyunsaturate diets. If anything, the aortas of those eating the polyunsaturated-enhanced diet tended to show more plaque build-up.
So when clueless health "experts" tell you to opt for polyunsaturated fat instead of saturated fat, ignore the living daylights out of them. Doing so could well save your life.
Anthony Colpo is the author of The Great Cholesterol Con, a no-holds-barred exposé of the farcical cholesterol theory of heart disease. Unlike the authors of the above study, Colpo has absolutely no ties to any food, drug, medical, or supplement industry groups, nor health organizations that receive money from these groups.
1. Dayton S, et al. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation, 1969; XL: II-1-63.
References and Notes
Milicia, Joe, "One High-Saturated Fat Meal Can Be Bad," Associated Press. Carried by the Washington Post. http://www.washingtonpost.com/wp-yn/content/article/2006/08/07/AR2006080700905.html. Published August 7, 2006. Accessed August 19, 2006.
Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer, DS. Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function. Journal of the American College of Cardiology, 2006; 48(4): 715-720.
David Celermajer and Jason Harmer, personal communication.
David Celermajer, personal communication.
Nevin KJ, Rajamohan T. Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem. 2004 Sep; 37(9): 830-5.
Ukil A, Maity S, Das PK. Protection from experimental colitis by theaflavin-3,3'-digallate correlates with inhibition of IKK and NF-kappaB activation. Br J Pharmacol. 2006 Jul 31; [Epub ahead of print].
Mazzon E, Muia C, Paola RD, Genovese T, Menegazzi M, De Sarro A, Suzuki H, Cuzzocrea S. Green tea polyphenol extract attenuates colon injury induced by experimental colitis. Free Radic Res., 2005 Sep; 39(9): 1017-25.
Manach C, Scalbert A, Morand C, Remesy C, Jimenez L. Polyphenols: food sources and bioavailability. Am J Clin Nutr. 2004 May; 79(5): 727-47.
Enig, Mary G, PhD, Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol, Silver Spring, MD: Bethseda Press (2000) 115; 118; 122.
Azzi A, Gysin R, Kempna P, Munteanu A, Negis Y, Villacorta L, Visarius T, Zingg JM. Vitamin E mediates cell signaling and regulation of gene expression. Ann NY Acad Sci, 2004 Dec; 1031:86-95.
Fan Y, Liu ML, Qi YY, Ren ZW. [Effect of different isofoms of tocopherols on expression of intercellular adhesion molecule-1 in human umbilical vein endothelial cells]. Beijing Da Xue Xue Bao, 2004 Feb; 36(1):70-4.
Schulte I, Bektas H, Klempnauer J, Borlak J. Vitamin E in heart transplantation: effects on cardiac gene expression. Transplantation, 2006 Mar 15; 81(5):736-45.
Koga T, Kwan P, Zubik L, Ameho C, Smith D, and Meydani M. Vitamin E supplementation suppresses macrophage accumulation and endothelial cell expression of adhesion molecules in the aorta of hypercholesterolemic rabbits. Atherosclerosis, 2004 Oct; 176(2): 265-272.
Tahir M, Foley B, Pate G, Crean P, Moore D, McCarroll N, Walsh M. Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial. Am Heart J, 2005 Aug; 150(2): 302-6.
Meydani M, Cohn JS, Macauley JB, McNamara JR, Blumberg JB, Schaefer, EJ. Postprandial Changes in the Plasma Concentration of [alpha]- and [gamma]-Tocopherol in Human Subjects Fed a Fat-Rich Meal Supplemented with Fat-Soluble Vitamins. Journal of Nutrition, 1989; 119:1252-1258.
Balazs Z, Panzenboeck U, Hammer A, Sovic A, Quehenberger O, Malle E, Sattler W. Uptake and transport of high-density lipoprotein (HDL) and HDL-associated alpha-tocopherol by an in vitro blood-brain barrier model. J Neurochem, 2004 May; 89(4): 939-50.
Harvey and Champe, eds., Biochemistry: 3rd Edition, Baltimore: Lippincott Williams and Wilkins (2005) 389.
If each meal contained 100 grams of fat, the first and second groups would receive identical amounts of monounsaturated fat (39 g), similar amounts of saturated fat (54 g and 52 g), and similar amounts of polyunsaturated fat (7 g and 9 g), while the third group would receive more monounsaturated fat (72 g), much less saturated fat (16 g), and more polyunsaturated fat (12 g). The first group would receive 117 mg of vitamin E, while the second would receive 8 mg and the third would receive 13 mg. If the second group received a supplement of 5 mg of natural vitamin E, the second and third groups would receive equivalent amounts of this vitamin. See reference 9.
About the Author
Chris Masterjohn is the author of several Wise Traditions articles and the creator and maintainer of Cholesterol-And-Health.Com, a website dedicated to extolling the virtues of cholesterol and cholesterol-rich foods. He has authored two items accepted for publication in peer-reviewed journals: a letter in an upcoming issue of the Journal of the American College of Cardiology criticizing the conclusions of a recent study on saturated fat and a full-length feature in an upcoming issue of Medical Hypotheses proposing a molecular mechanism of vitamin D toxicity. Masterjohn holds a Bachelor's degree in History and is preparing to pursue a PhD in Molecular and Cellular Biology. He is also a Weston A. Price Foundation Local Chapter Leader in West Brookfield, Massachusetts
Saturated Fat Attack
Can One Meal Containing Saturated Fat Really Be that Bad?
Or Why You Don't Need Vegetable Oil in Your Carrot Cake and Milk Shake to Protect Your Arteries by Chris Masterjohn
Newspapers around the world have recently published the results of a study indicating that a single meal rich in saturated fats will disrupt the functioning of your arteries and contribute to the inflammation of your blood vessels. The Associated Press story by Joe Milicia1 was heard round the internet, and reported in papers throughout the world.
The news article quoted the Kansas City cardiologist Dr. James O'Keefe as claiming the study showed that "when you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward."
Dr. Nicholls, the lead author of the study that generated such an amazing amount of attention in the press, was quoted as saying that his research showed the "need to aggressively reduce the amount of saturated fat consumed in the diet." The article then clarified that this meant reducing our intake of beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, and replacing them with safflower oil, sesame oil, sunflower seeds, corn and soybeans. Amazingly, this study had the power to make sweeping conclusions about over 15 different foods!
The study in question was published by a team of researchers led by Dr. Stephen J. Nicholls of the Australian Heart Research Institute in the Journal of the American College of Cardiology entitled, "Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function."2
Reality Check
In reality, none of the dire conclusions reported in the press is justified by the study. There was no clearly discernable effect of any type of fat on arterial function, and those consuming saturated fat had the best arterial function at all time points measured.
In fact, the researchers did not even study the inflammation occurring in the blood vessels of the people eating the meals. Instead, they performed an interesting experiment on isolated cells in which they found high-density lipoprotein (HDL) isolated from people eating safflower oil to have greater anti-inflammatory power than HDL isolated from people eating coconut oil. They attributed this observation to the saturation of fat that the study subjects consumed without a shred of evidence, and overlooked the more plausible explanation that these effects were due to the large difference in vitamin E contents of the two diets.
Study Design
The researchers fed fourteen adults a meal of carrot cake and a milk shake on two separate occasions one month apart, once made with highly saturated coconut oil and once made with highly polyunsaturated safflower oil. Both oils were non-hydrogenated, organic, unrefined and virgin.3
The researchers, who were blinded to which meals the subjects were receiving, took each of three types of measurements at three different time points: first, after an overnight fast and before the meal was administered; second, three hours after the meal was administered; third, six hours after the meal was administered.
The first type of measurement they took was the levels of various constituents in the subjects' blood: total cholesterol, LDL, HDL, triglycerides, insulin and free fatty acids.
The second type of measurement they took was of various parameters of blood flow, including the total amount of blood flow through the subjects' forearms and the degree of "flow-mediated dilation" in their brachial arteries. Flow-mediated dilation is the ability of a blood vessel to dilate to rush blood to an area that has been deprived of oxygen. To measure it, researchers use pressure to stop blood flow through an artery and then test to what extent the artery reacts once the pressure is released by dilating to increase the return of blood to the blood-deprived area. With this type of test, the more the blood vessel dilates when pressure is released, the better shape it is believed to be in.
Finally, the researchers extracted HDL from the subjects' blood at each time point. They incubated isolated endothelial cells from human umbilical veins with the HDL at various concentrations. After the incubation period, they added an inflammatory chemical called tumor necrosis factor-alpha (TNF-a) to the cells, which stimulates the production of adhesion molecules with long-winded names like intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), which are believed to play a role in the adhesion of immune cells to arterial plaque. HDL has been shown to inhibit the expression of these inflammatory molecules, and the researchers conducted this part of the study to see whether how you eat can affect how much potential HDL has to inhibit the expression of these presumably harmful adhesion molecules.
The researchers claimed to generate two findings:
Flow-mediated dilation decreased more strongly after the coconut oil meal than after the safflower oil meal. From this, they concluded that "consumption of saturated fat impairs . . . endothelial function."
When cells were incubated with HDL taken from subjects after they ate the coconut oil meal, the expression of the inflammatory adhesion molecules in response to TNF-a stimulation was increased compared to cells incubated with HDL taken from fasting subjects. By contrast, when cells were incubated with HDL taken from subjects after they ate the safflower oil meal, the expression of inflammatory molecules in response to TNF-a stimulation was decreased compared to cells incubated with HDL taken from fasting subjects. From this, the authors concluded that "consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins."
Although both of these conclusions are more conservative than the statements written in the Associated Press article, neither of them is justified by the study.
Let's take a closer look at each.
Flow Mediated Dilation
The researchers claim that consumption of the saturated fat meal impaired flow-mediated dilation (FMD). They did indeed show that at the three-hour mark the decline in FMD was almost twice as great in the coconut oil group as it was in the safflower oil group. Yet the FMD was actually higher in the coconut oil group than in the safflower oil group at every point along the way! The reason? When the subjects were fasting, those who were about to eat the coconut oil meal had 33 percent better FMD than those who were about to eat the safflower oil meal. Even at the three-hour point, when FMD had declined the most, it was still 9 percent higher in the coconut oil group than in the safflower oil group.
There are two ways we could look at this paradoxical situation. Figure 1 shows the changes that took place in FMD three and six hours after the meals, relative to the FMD before the meals (called "baseline"). You can see that for both the coconut oil meal and the safflower oil meal, FMD declined substantially at the three-hour mark, although the rate at which it declined was nearly double after the coconut oil meal.
Figure 1. Percent change in the degree of flow-mediated dilation (FMD) compared to baseline values.
Group Baseline Three Hours Six Hours
Saffllower Oil No Change 17 percent lower 8 percent lower
Coconut Oil No Change 32 percent lower 10 percent lower
Now let's look at these findings another way. Figure 2 compares the relative degree of FMD of the coconut oil group with that of the safflower oil group. Here you can see that the FMD is higher (a good thing) in the coconut oil group at every single time point during the study.
Figure 2. Comparison of the degree of flow-mediated dilation (FMD) in the coconut oil group to that in the safflower oil group at three time points.
Baseline 3 hours 6 hours
33 percent higher in coconut oil group 9 percent higher in coconut oil group 29 percent higher in coconut oil group
Thus, we have to ask: is consumption of coconut oil rather than safflower oil the reason for the greater decline of FMD in the coconut oil group? Or, is the reason for this decline the simple fact that the people who ate the coconut oil meal started out with a higher value of FMD in the first place, and therefore, so to speak, had more to lose?
There are two reasons that the latter scenario might be true: first, the decline in FMD after a meal might not even be a function of the FMD; second, a randomly high sampling error for the FMD before the meal could result in what is called "regression to the mean."
In the first case, it could be that eating carrot cake and drinking a milkshake, whether made with safflower oil or coconut oil, depresses FMD to a certain point regardless of fasting levels. For example, eating the meal might depress FMD to about 5 percent, regardless of whether the person's fasting level was 6 percent or 9 percent.
In such a scenario, a person whose fasting level is 9 percent would experience a 44 percent decline in FMD, while a person whose fasting level is 6 percent would experience only a 17 percent decline in FMD.
Thus, if the effect of a meal on FMD is not a function of fasting FMD, the coconut oil group, which by random chance had a 33 percent higher fasting FMD, would exhibit a greater relative decline than the safflower oil group for no other reason than that they started off with substantially better FMD in the first place!
Regression to the Mean
The authors themselves admitted a very similar explanation in the journal article, writing that "it is possible that 'regression to the mean' may have contributed to some of the FMD reduction observed after consumption of the saturated fat." The concept of "regression to the mean" is essentially this: if by random sampling error an initial value tends to be higher than the mean, a second value will tend to be closer to the mean. Thus, a decline in values could result simply from the first value being randomly high.
Yet was this caveat noted in the press? Of course not. Instead, we were told that when we eat saturated fat, "damage to the vessels happens immediately afterward," and thus we must "aggressively reduce the amount of saturated fat consumed in the diet."
No one warned us that if when fasting, by random sampling error we happen to have a higher-than-average value of FMD, rapid but unmeaningful FMD reduction will occur after we eat due to "regression to the mean." No one warned us that we must "aggressively reduce the amount of random sampling error" lest we suffer statistically indicated arterial dysfunction with one, single meal.
Inflammation in the Test Tube
Contrary to the Associated Press report's claim that "fewer inflammatory agents were found in the arteries" after the safflower oil meal than before it, the researchers did not measure any type of inflammation in the arteries of the test subjects. Instead, they incubated isolated umbilical vein endothelial cells with HDL taken from these subjects at various time points before and after the meals, and then stimulated these isolated cells to produce inflammatory adhesion molecules by adding a compound called TNF-a to them. Finally, they measured whether HDL isolated after the different meals had a different ability to lower the amount of adhesion molecules released after stimulation with TNF-a.
The researchers found that cells incubated with the HDL isolated from subjects after they had eaten the coconut oil meal produced more adhesion molecules (ICAM-1 and VCAM-1) after stimulation with TNF-a than did cells incubated with HDL isolated from fasting subjects, and that cells incubated with HDL isolated from subjects after they had eaten the safflower oil meal produced fewer adhesion molecules after stimulation than did cells incubated with HDL isolated from fasting subjects. In other words, eating safflower oil seemed to make the HDL a more powerful anti-inflammatory agent, while eating coconut oil seemed to make the HDL a less powerful anti-inflammatory agent.
There are a number of problems with the large leap of logic it takes to conclude from this finding that a meal rich in saturated fat causes inflammation. First, we are neither test tubes nor petri dishes, but complex organisms with many different chemical and electrical feedback systems that do not exist in laboratory dishes. The researchers could have directly measured the levels of ICAM-1 and VCAM-1 in the subjects' blood, but that is not what they chose to study.
Second, the researchers only studied the anti-inflammatory potential of HDL. They could have incubated the cells with whole plasma to measure the total anti-inflammatory capacity of the blood, but they chose not to, for the simple reason that they were only trying to answer one small question about HDL and not look at the bigger picture.4
Virgin coconut oil is rich in very powerful polyphenols,5 some types of which have been shown to decrease expression of TNF-a and adhesion molecules,6, 7 and which are carried by water-soluble proteins in the blood and not by HDL.8 Thus, virgin coconut oil's contribution to the anti-inflammatory capacity of the blood could be primarily in the non-HDL fraction, whereas safflower oil's contribution to the anti-inflammatory capacity of the blood might be primarily in the HDL fraction. We simply do not have enough knowledge at this point to say for sure.
The only way to determine the effect of safflower oil and coconut oil on the total anti-inflammatory capacity of the blood is to perform the experiment by incubating the cells with whole blood. The only way to determine the effect of safflower oil and coconut oil on the actual level of inflammation in the people consuming the oils is to measure the inflammatory compounds being directly produced in their blood. This study did neither.
Finally, and most importantly, the researchers provided no evidence whatsoever that the effects they observed were due to the type of fat in the two meals. They simply assumed that the difference they observed between safflower oil and coconut oil was due to the fact that coconut oil is high in saturated fat and safflower oil is high in unsaturated fat. In doing so, they overlooked a very interesting hypothesis that could explain their results and that has substantial support in the scientific literature.
An Alternative Hypothesis: Vitamin E
The difference between safflower oil and coconut oil does not stop at the relative degree of fatty acid saturation. Figure 3 shows the difference in vitamin E content between the two oils. Safflower oil is 77 times higher in alpha-tocopherol and 47 times higher in total tocopherols.9
Figure 3. Typical tocopherol (vitamin E) content of coconut oil and safflower oil.
Tocopherol Coconut Oil Safflower Oil
Alpha-tocopherol 5 mg/kg 387 mg/kg
Beta-tocopherol -- --
Gamma-tocopherol -- 174 mg/kg
Delta-tocopherol 6 mg/kg 240 mg/kg
TOTAL tocopherol 11 mg/kg 801 mg/kg
Source: (Enig, 2000).
Is it plausible that the difference in vitamin E content of the oils could account for the difference in the expression of adhesion molecules in the isolated cells? Absolutely.
A recent review of alpha-tocopherol's role in regulating gene expression listed the suppression of the gene that codes for ICAM-1 as one of its functions.10 In fact, Chinese researchers performed a very similar experiment to the one we have been discussing, wherein they incubated endothelial cells taken from human umbilical veins with vitamin E instead of HDL. They found that incubating the cells with alpha-tocopherol, gamma-tocopherol and mixed tocopherols all inhibited the ability of oxidized LDL to induce ICAM-1 expression in the cells in a dose-dependent manner.10 Another group found vitamin E to reduce both ICAM-1 and VCAM-1 in the heart cells of rats.11
Vitamin E suppressed ICAM-1 and VCAM-1 levels in vivo in rabbits, although the effect on VCAM-1 was not statistically significant.13 In humans, the combination of vitamins E and C, but not vitamin C alone, decreased blood levels of ICAM-1 after six months. When the supplementation was stopped, blood levels of ICAM-1 returned to their initial levels. A similar effect was seen on VCAM-1, but it was not statistically significant. Unfortunately the researchers did not study the effect of vitamin E alone.14
Vitamin E travels in the blood associated with lipoproteins, including HDL.15 When endothelial cells are incubated with vitamin E-enriched HDL, they selectively take up vitamin E from the HDL at ten times the rate at which they take up the HDL particles themselves.16
It is therefore reasonable to suggest that the high vitamin E content of safflower oil led to an enrichment of the subjects' HDL particles with vitamin E, which was then taken up by the endothelial cells where it suppressed the expression of adhesion molecules.
Yet one question remains: why would the HDL taken from subjects after they ate the coconut oil meal be less effective at suppressing the expression of adhesion molecules than HDL taken from subjects when they were fasting? The one study I've found on the effect of a meal on the distribution of vitamin E in the blood15 suggests that the fraction of vitamin E in HDL actually declines temporarily after a meal when the meal is relatively low in vitamin E, but rises if the meal is high in vitamin E. It may be, then, that the vitamin E content of HDL declined after the coconut oil meal not because of the coconut oil itself but because any low-vitamin E meal reduces the amount of vitamin E in circulating HDL. On the other hand, the safflower oil meal may have been high enough in vitamin E to make the vitamin E content of HDL rise.
The only way to actually know would be to directly measure the vitamin E content of the HDL particles after the meal. Although the researchers who conducted the study we have been discussing measured the amount of protein, phospholipid, triglyceride and cholesterol in the HDL particles that they extracted, they unfortunately did not measure the amount of vitamin E in these particles.
The foregoing is, of course, a hypothesis. I have not shown conclusively that the effects observed in the study must have been due to vitamin E; I have simply shown that this is a plausible explanation. Further research would be needed to confirm or refute the hypothesis.
Likewise, it is an unconfirmed hypothesis that the effect observed was a result of the consumption of saturated fat. This unfortunately did not stop the researchers from titling their paper "Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function" as if they had actually shown this to be the case.
So Which Oils Should We Eat?
If it turns out to be true that the difference in the protective effect of HDL in the test tube was in fact due to the high vitamin E content of safflower oil and the low vitamin E content of coconut oil, that does not mean we should avoid coconut oil. It does not even mean we should eat safflower oil.
These findings simply reflect the fact that coconut oil is not a good source of vitamin E. Coconut oil is still the best source of medium-chain fatty acids, which boost metabolism and support the immune system, and virgin coconut oil is rich in powerful antioxidant polyphenols.
Polyunsaturated fatty acids such as those found in safflower oil actually deplete the body of vitamin E and thereby increase the body's need for vitamin E--this is basic textbook biochemistry.17 Safflower oil may raise the amount of vitamin E in lipoproteins immediately after a vitamin E-rich meal, but what is the long-term effect on vitamin E status of an excessive intake of polyunsaturated fats?
It makes sense then that the best way to obtain vitamin E would be from sources that are high in vitamin E but low in polyunsaturated fat. Unrefined palm oil is an excellent example of such a source.
Palm oil is only 9 percent polyunsaturated, compared to safflower, which is 75 percent polyunsaturated. In terms of the absolute amount of vitamin E, compared to safflower oil, palm oil has a somewhat lower level of alpha-tocopherol, more than double the gamma-tocopherol, and large amounts of tocotrienols, which are another important part of the vitamin E complex that are completely absent in safflower oil. The combined absolute value of tocopherol and tocotrienol forms of vitamin E is 46 percent higher in palm oil than safflower oil.9
When one takes into account the high polyunsaturated fat content of safflower oil, which increases the need for vitamin E, the advantage of more saturated palm oil becomes obvious: the ratio of vitamin E to polyunsaturated fatty acids in palm oil is 12 times greater than the same ratio in safflower oil!
Yet newspapers the world over carrying the Associated Press article told us to reduce our intake of palm oil and other saturated fats "aggressively."
Dire Warnings
We've been told that this study shows that when "you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward." We've been told that it shows we must "aggressively reduce the amount of saturated fat consumed in the diet." We've been further told to throw out the beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, replacing all these fats with safflower oil, sesame oil, sunflower seeds, corn and soybeans.
These dire warnings are based on a study that couldn't differentiate the effect of coconut oil from the effect of random sampling error on flow-mediated dilation and that showed people consuming coconut oil to have better flow-mediated dilation at all time points than people consuming safflower oil; they are based on a study that could not differentiate between the effect of saturated fat and the effect of vitamin E on the capacity of HDL to prevent inflammation in isolated, laboratory-cultured cells; and they are based on a study that tells us nothing about the amount of inflammation going on within the people consuming the meals, who are much more complex than globs of isolated laboratory-cultured cells.
Further research should uncover whether the effects seen in the test tube are due to vitamin E, to saturated or unsaturated fats, or to other causes entirely, and what relevance these observations in the test tube have for real, living people.
In the meantime, traditional animal fats, tropical oils and olive oil remain our best bet for avoiding the modern diseases that suspiciously ascended to prominence soon after researchers began heralding seed oils like safflower oil as a healthy alternative to traditional, saturated fats.
We can, however, draw two conclusions from the present study to make life safer for all of us and to advance the public health. First, always avoid random sampling error before you eat; otherwise, it would take only a single meal for "regression to the mean" to result in statistically induced markers of arterial dysfunction immediately afterward. Second, if you do eat a meal high in saturated fats, resist the urge to extract your HDL and throw it into the nearest petri dish. Chances are there's a researcher just waiting for your defenseless lipoproteins with a pipette full of inflammatory chemicals, and at that point, all hope of preventing cell-to-cell adhesion is lost.
A Better Experiment
A major drawback of the current study is that it could not distinguish between the effect of the saturation of the fats that the study subjects consumed and the amount of vitamin E in their diets. One way to conduct an experiment while avoiding this pitfall would be to use palm oil, which is very rich in vitamin E despite being a highly saturated fat.
A better experiment would use three groups: one fed palm oil alone, a second fed a mixture of coconut oil and olive oil, and a third fed olive oil alone. This experiment would be able to differentiate between the effects of saturated fat and those of vitamin E because the dietary fat of the first and second groups would be similarly and highly saturated but the first group would receive 15 times as much vitamin E as the second group. Conversely, the second and third groups would receive similar amounts of vitamin E, but the dietary fat of the third group would be much lower in saturated fat.18
If HDL isolated from the first group was much more effective at inhibiting the expression of adhesion molecules by stimulated endothelial cells than HDL isolated from the second and third groups, this would support the hypothesis that it is the vitamin E content of the diet rather than the saturation of the dietary fat that is operative. If, on the other hand, HDL isolated from the first group was no more or less effective than HDL isolated from the second group but considerably less effective than HDL isolated from the third group, this would support the hypothesis that the saturation of the dietary fat rather than the amount of vitamin E is operative.
But even these findings would be tenuous. HDL is only one constituent of many in the blood, and the functioning of an artery within a living human is much more complex than the functioning of a mass of cells in a petri dish upon which a researcher has dropped solutions of isolated chemicals with a pipette. The ultimate test to teach us which oils to eat is which oils are consumed by the people who live the longest, are the healthiest, and have the best quality of life.
Anthony Colpo Comments on the Carrot Cake & Milkshake Study
The study discussed in this article was supported by a Pfizer Cardiovascular Lipid award. Pfizer makes over ten billion dollars per year from sales of Lipitor, the world's best-selling cholesterol-lowering drug.
Dr. Nicholls is supported by a postgraduate research scholarship from the National Heart Foundation of Australia. Co-author Dr. Rye is a National Heart Foundation of Australia Principal Research Fellow. The National Heart Foundation of Australia operates a program in which it charges a fee so that food manufacturers can display the "Heart Foundation Tick." Polyunsaturated vegetable oils and margarines contribute a significant portion of ingredients in these certified products.
Another co-author of the study, Dr. Lundman, is supported by postdoctoral scholarships from the Swedish Heart and Lung Foundation, which counts among its sponsors Unilever, the food giant that manufactures numerous vegetable oil and margarine products.
There have been numerous randomized controlled CHD prevention trials conducted since the 1960s, in which people have been given either high-polyunsaturate diets or high-saturate diets as the sole intervention. In these trials, extending up to eight years, no cardiovascular or overall mortality advantage has ever been observed that can be attributed to saturated fat restriction. In fact, a number of these trials observed poorer mortality outcomes in the high-polyunsaturate group.
Healthy subjects placed on high polyunsaturated diets for four-week periods have exhibited higher levels of free radical activity and blood clotting markers than those on high-saturated diets. In animal studies, polyunsaturated vegetable oils consistently promote cancer growth; an eight-year trial with real live humans that observed significantly higher cancer incidence in the polyunsaturated group suggests this phenomenon is not merely confined to lab rats.1 This same study, by the way, showed little difference in extent of atherosclerosis among autopsied subjects from the high-saturate and high-polyunsaturate diets. If anything, the aortas of those eating the polyunsaturated-enhanced diet tended to show more plaque build-up.
So when clueless health "experts" tell you to opt for polyunsaturated fat instead of saturated fat, ignore the living daylights out of them. Doing so could well save your life.
Anthony Colpo is the author of The Great Cholesterol Con, a no-holds-barred exposé of the farcical cholesterol theory of heart disease. Unlike the authors of the above study, Colpo has absolutely no ties to any food, drug, medical, or supplement industry groups, nor health organizations that receive money from these groups.
1. Dayton S, et al. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation, 1969; XL: II-1-63.
References and Notes
Milicia, Joe, "One High-Saturated Fat Meal Can Be Bad," Associated Press. Carried by the Washington Post. http://www.washingtonpost.com/wp-yn/content/article/2006/08/07/AR2006080700905.html. Published August 7, 2006. Accessed August 19, 2006.
Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer, DS. Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function. Journal of the American College of Cardiology, 2006; 48(4): 715-720.
David Celermajer and Jason Harmer, personal communication.
David Celermajer, personal communication.
Nevin KJ, Rajamohan T. Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem. 2004 Sep; 37(9): 830-5.
Ukil A, Maity S, Das PK. Protection from experimental colitis by theaflavin-3,3'-digallate correlates with inhibition of IKK and NF-kappaB activation. Br J Pharmacol. 2006 Jul 31; [Epub ahead of print].
Mazzon E, Muia C, Paola RD, Genovese T, Menegazzi M, De Sarro A, Suzuki H, Cuzzocrea S. Green tea polyphenol extract attenuates colon injury induced by experimental colitis. Free Radic Res., 2005 Sep; 39(9): 1017-25.
Manach C, Scalbert A, Morand C, Remesy C, Jimenez L. Polyphenols: food sources and bioavailability. Am J Clin Nutr. 2004 May; 79(5): 727-47.
Enig, Mary G, PhD, Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol, Silver Spring, MD: Bethseda Press (2000) 115; 118; 122.
Azzi A, Gysin R, Kempna P, Munteanu A, Negis Y, Villacorta L, Visarius T, Zingg JM. Vitamin E mediates cell signaling and regulation of gene expression. Ann NY Acad Sci, 2004 Dec; 1031:86-95.
Fan Y, Liu ML, Qi YY, Ren ZW. [Effect of different isofoms of tocopherols on expression of intercellular adhesion molecule-1 in human umbilical vein endothelial cells]. Beijing Da Xue Xue Bao, 2004 Feb; 36(1):70-4.
Schulte I, Bektas H, Klempnauer J, Borlak J. Vitamin E in heart transplantation: effects on cardiac gene expression. Transplantation, 2006 Mar 15; 81(5):736-45.
Koga T, Kwan P, Zubik L, Ameho C, Smith D, and Meydani M. Vitamin E supplementation suppresses macrophage accumulation and endothelial cell expression of adhesion molecules in the aorta of hypercholesterolemic rabbits. Atherosclerosis, 2004 Oct; 176(2): 265-272.
Tahir M, Foley B, Pate G, Crean P, Moore D, McCarroll N, Walsh M. Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial. Am Heart J, 2005 Aug; 150(2): 302-6.
Meydani M, Cohn JS, Macauley JB, McNamara JR, Blumberg JB, Schaefer, EJ. Postprandial Changes in the Plasma Concentration of [alpha]- and [gamma]-Tocopherol in Human Subjects Fed a Fat-Rich Meal Supplemented with Fat-Soluble Vitamins. Journal of Nutrition, 1989; 119:1252-1258.
Balazs Z, Panzenboeck U, Hammer A, Sovic A, Quehenberger O, Malle E, Sattler W. Uptake and transport of high-density lipoprotein (HDL) and HDL-associated alpha-tocopherol by an in vitro blood-brain barrier model. J Neurochem, 2004 May; 89(4): 939-50.
Harvey and Champe, eds., Biochemistry: 3rd Edition, Baltimore: Lippincott Williams and Wilkins (2005) 389.
If each meal contained 100 grams of fat, the first and second groups would receive identical amounts of monounsaturated fat (39 g), similar amounts of saturated fat (54 g and 52 g), and similar amounts of polyunsaturated fat (7 g and 9 g), while the third group would receive more monounsaturated fat (72 g), much less saturated fat (16 g), and more polyunsaturated fat (12 g). The first group would receive 117 mg of vitamin E, while the second would receive 8 mg and the third would receive 13 mg. If the second group received a supplement of 5 mg of natural vitamin E, the second and third groups would receive equivalent amounts of this vitamin. See reference 9.
About the Author
Chris Masterjohn is the author of several Wise Traditions articles and the creator and maintainer of Cholesterol-And-Health.Com, a website dedicated to extolling the virtues of cholesterol and cholesterol-rich foods. He has authored two items accepted for publication in peer-reviewed journals: a letter in an upcoming issue of the Journal of the American College of Cardiology criticizing the conclusions of a recent study on saturated fat and a full-length feature in an upcoming issue of Medical Hypotheses proposing a molecular mechanism of vitamin D toxicity. Masterjohn holds a Bachelor's degree in History and is preparing to pursue a PhD in Molecular and Cellular Biology. He is also a Weston A. Price Foundation Local Chapter Leader in West Brookfield, Massachusetts
The Benefits of High Cholesterol
By Uffe Ravnskov, MD, PhD
People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.
But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2 Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.
Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.
But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.
High Cholesterol Protects Against Infection
Many studies have found that low cholesterol is in certain respects worse than high cholesterol. For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.3
Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection? To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.4,5 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered? Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.
Low Cholesterol and HIV/AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. The Minnesota researchers, now led by Dr. Ami Claxton, followed such individuals for 7-8 years. After having excluded those who became HIV-positive during the first four years, they ended up with a group of 2446 men. At the end of the study, 140 of these people tested positive for HIV; those who had low cholesterol at the beginning of the study were twice as likely to test postitive for HIV compared with those with the highest cholesterol.6
Similar results come from a study of the MRFIT screenees, including more than 300,000 young and middle-aged men, which found that 16 years after the first cholesterol analysis the number of men whose cholesterol was lower than 160 and who had died from AIDS was four times higher than the number of men who had died from AIDS with a cholesterol above 240.7
Cholesterol and Chronic Heart Failure
Heart disease may lead to a weakening of the heart muscle. A weak heart means that less blood and therefore less oxygen is delivered to the arteries. To compensate for the decreased power, the heart beat goes up, but in severe heart failure this is not sufficient. Patients with severe heart failure become short of breath because too little oxygen is delivered to the tissues, the pressure in their veins increases because the heart cannot deliver the blood away from the heart with sufficient power, and they become edematous, meaning that fluid accumulates in the legs and in serious cases also in the lungs and other parts of the body. This condition is called congestive or chronic heart failure.
There are many indications that bacteria or other microorganisms play an important role in chronic heart failure. For instance, patients with severe chronic heart failure have high levels of endotoxin and various types of cytokines in their blood. Endotoxin, also named lipopolysaccharide, is the most toxic substance produced by Gram-negative bacteria such as Escherichia coli, Klebsiella, Salmonella, Serratia and Pseudomonas. Cytokines are hormones secreted by white blood cells in their battle with microorganisms; high levels of cytokines in the blood indicate that inflammatory processes are going on somewhere in the body.
The role of infections in chronic heart failure has been studied by Dr. Mathias Rauchhaus and his team at the Medical Department, Martin-Luther-University in Halle, Germany (Universitätsklinik und Poliklinik für Innere Medizin III, Martin-Luther-Universität, Halle). They found that the strongest predictor of death for patients with chronic heart failure was the concentration of cytokines in the blood, in particular in patients with heart failure due to coronary heart disease.8 To explain their finding they suggested that bacteria from the gut may more easily penetrate into the tissues when the pressure in the abdominal veins is increased because of heart failure. In accordance with this theory, they found more endotoxin in the blood of patients with congestive heart failure and edema than in patients with non-congestive heart failure without edema, and endotoxin concentrations decreased significantly when the heart’s function was improved by medical treatment.9
A simple way to test the functional state of the immune system is to inject antigens from microorganisms that most people have been exposed to, under the skin. If the immune system is normal, an induration (hard spot) will appear about 48 hours later at the place of the injection. If the induration is very small, with a diameter of less than a few millimeters, this indicates the presence of "anergy," a reduction in or failure of response to recognize antigens. In accordance, anergy has been found associated with an increased risk of infection and mortality in healthy elderly individuals, in surgical patients and in heart transplant patients.10
Dr. Donna Vredevoe and her group from the School of Nursery and the School of Medicine, University of California at Los Angeles tested more than 200 patients with severe heart failure with five different antigens and followed them for twelve months. The cause of heart failure was coronary heart disease in half of them and other types of heart disease (such as congenital or infectious valvular heart disease, various cardiomyopathies and endocarditis) in the rest. Almost half of all the patients were anergic, and those who were anergic and had coronary heart disease had a much higher mortality than the rest.10
Now to the salient point: to their surprise the researchers found that mortality was higher, not only in the patients with anergy, but also in the patients with the lowest lipid values, including total cholesterol, LDL-cholesterol and HDL-cholesterol as well as triglycerides.
The latter finding was confirmed by Dr. Rauchhaus, this time in co-operation with researchers at several German and British university hospitals. They found that the risk of dying for patients with chronic heart failure was strongly and inversely associated with total cholesterol, LDL-cholesterol and also triglycerides; those with high lipid values lived much longer than those with low values.11,12
Other researchers have made similar observations. The largest study has been performed by Professor Gregg C. Fonorow and his team at the UCLA Department of Medicine and Cardiomyopathy Center in Los Angeles.13 The study, led by Dr. Tamara Horwich, included more than a thousand patients with severe heart failure. After five years 62 percent of the patients with cholesterol below 129 mg/l had died, but only half as many of the patients with cholesterol above 223 mg/l.
When proponents of the cholesterol hypothesis are confronted with findings showing a bad outcome associated with low cholesterol--and there are many such observations--they usually argue that severely ill patients are often malnourished, and malnourishment is therefore said to cause low cholesterol. However, the mortality of the patients in this study was independent of their degree of nourishment; low cholesterol predicted early mortality whether the patients were malnourished or not.
Smith-Lemli-Opitz Syndrome
As discussed in The Cholesterol Myths (see sidebar), much evidence supports the theory that people born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true.
Children with the Smith-Lemli-Opitz syndrome have very low cholesterol because the enzyme that is necessary for the last step in the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the central nervous system. Those who survive are imbecile, they have extremely low cholesterol and suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent.14
Laboratory Evidence
Laboratory studies are crucial for learning more about the mechanisms by which the lipids exert their protective function. One of the first to study this phenomenon was Dr Sucharit Bhakdi from the Institute of Medical Microbiology, University of Giessen (Institut für Medizinsche Mikrobiologie, Justus-Liebig-Universität Gießen), Germany along with his team of researchers from various institutions in Germany and Denmark.15
Staphylococcus aureus ?-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy a wide variety of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in 0.9 percent saline, the blood is hemolyzed, that is the membranes of the red blood cells burst and hemoglobin from the interior of the red blood cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified ?-toxin with human serum (the fluid in which the blood cells reside) and saw that 90 percent of its hemolyzing effect disappeared. By various complicated methods they identified the protective substance as LDL, the carrier of the so-called bad cholesterol. In accordance, no hemolysis occurred when they mixed ?-toxin with purified human LDL, whereas HDL or other plasma constituents were ineffective in this respect.
Dr. Willy Flegel and his co-workers at the Department of Transfusion Medicine, University of Ulm, and the Institute of Immunology and Genetics at the German Cancer Research Center in Heidelberg, Germany (DRK-Blutspendezentrale und Abteilung für Transfusionsmedizin, Universität Ulm, und Deutsches Krebsforschungszentrum, Heidelberg) studied endotoxin in another way.16 As mentioned, one of the effects of endotoxin is that white blood cells are stimulated to produce cytokines. The German researchers found that the cytokine-stimulating effect of endotoxin on the white blood cells disappeared almost completely if the endotoxin was mixed with human serum for 24 hours before they added the white blood cells to the test tubes. In a subsequent study17 they found that purified LDL from patients with familial hypercholesterolemia had the same inhibitory effect as the serum.
LDL may not only bind and inactivate dangerous bacterial toxins; it seems to have a direct beneficial influence on the immune system also, possibly explaining the observed relationship between low cholesterol and various chronic diseases. This was the starting point for a study by Professor Matthew Muldoon and his team at the University of Pittsburgh, Pennsylvania. They studied healthy young and middle-aged men and found that the total number of white blood cells and the number of various types of white blood cells were significantly lower in the men with LDL-cholesterol below 160 mg/dl (mean 88.3 mg/l),than in men with LDL-cholesterol above 160 mg/l (mean 185.5 mg/l).18 The researchers cautiously concluded that there were immune system differences between men with low and high cholesterol, but that it was too early to state whether these differences had any importance for human health. Now, seven years later with many of the results discussed here, we are allowed to state that the immune-supporting properties of LDL-cholesterol do indeed play an important role in human health.
Animal Experiments
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold at the Department of Medicine, University of California, San Francisco, and his group have published several interesting results from such research. In one of them they lowered LDL-cholesterol in rats by giving them either a drug that prevents the liver from secreting lipoproteins, or a drug that increases their disappearance. In both models, injection of endotoxin was followed by a much higher mortality in the low-cholesterol rats compared with normal rats. The high mortality was not due to the drugs because, if the drug-treated animals were injected with lipoproteins just before the injection of endotoxin, their mortality was reduced to normal.19
Dr. Mihai Netea and his team from the Departments of Internal and Nuclear Medicine at the University Hospital in Nijmegen, The Netherlands, injected purified endotoxin into normal mice, and into mice with familial hypercholesterolemia that had LDL-cholesterol four times higher than normal. Whereas all normal mice died, they had to inject eight times as much endotoxin to kill the mice with familial hypercholesterolemia. In another experiment they injected live bacteria and found that twice as many mice with familial hypercholesterolemia survived compared with normal mice.20
Other Protecting Lipids
As seen from the above, many of the roles played by LDL-cholesterol are shared by HDL. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more.
Triglycerides, molecules consisting of three fatty acids linked to glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by a lipoprotein named VLDL (very low-density lipoprotein) and by chylomicrons, a mixture of emulsified triglycerides appearing in large amounts after a fat-rich meal, particularly in the blood that flows from the gut to the liver.
For many years it has been known that sepsis, a life-threatening condition caused by bacterial growth in the blood, is associated with a high level of triglycerides. The serious symptoms of sepsis are due to endotoxin, most often produced by gut bacteria. In a number of studies, Professor Hobart W. Harris at the Surgical Research Laboratory at San Francisco General Hospital and his team found that solutions rich in triglycerides but with practically no cholesterol were able to protect experimental animals from the toxic effects of endotoxin and they concluded that the high level of triglycerides seen in sepsis is a normal immune response to infection.21 Usually the bacteria responsible for sepsis come from the gut. It is therefore fortunate that the blood draining the gut is especially rich in triglycerides.
Exceptions
So far, animal experiments have confirmed the hypothesis that high cholesterol protects against infection, at least against infections caused by bacteria. In a similar experiment using injections of Candida albicans, a common fungus, Dr. Netea and his team found that mice with familial hypercholesterolemia died more easily than normal mice.22 Serious infections caused by Candida albicans are rare in normal human beings; however, they are mainly seen in patients treated with immunosuppressive drugs, but the finding shows that we need more knowledge in this area. However, the many findings mentioned above indicate that the protective effects of the blood lipids against infections in human beings seem to be greater than any possible adverse effects.
Cholesterol as a Risk Factor
Most studies of young and middle-aged men have found high cholesterol to be a risk factor for coronary heart disease, seemingly a contradiction to the idea that high cholesterol is protective. Why is high cholesterol a risk factor in young and middle-aged men? A likely explanation is that men of that age are often in the midst of their professional career. High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body’s need for more cholesterol because cholesterol is the building material of many stress hormones. Any possible protective effect of high cholesterol may therefore be counteracted by the negative influence of a stressful life on the vascular system.
Response to Injury
In 1976 one of the most promising theories about the cause of atherosclerosis was the Response-to-Injury Hypothesis, presented by Russell Ross, a professor of pathology, and John Glomset, a professor of biochemistry and medicine at the Medical School, University of Washington in Seattle.23,24 They suggested that atherosclerosis is the consequence of an inflammatory process, where the first step is a localized injury to the thin layer of cells lining the inside of the arteries, the intima. The injury causes inflammation and the raised plaques that form are simply healing lesions.
Their idea is not new. In 1911, two American pathologists from the Pathological Laboratories, University of Pittsburgh, Pennsylvania, Oskar Klotz and M.F. Manning, published a summary of their studies of the human arteries and concluded that "there is every indication that the production of tissue in the intima is the result of a direct irritation of that tissue by the presence of infection or toxins or the stimulation by the products of a primary degeneration in that layer."25 Other researchers have presented similar theories.26
Researchers have proposed many potential causes of vascular injury, including mechanical stress, exposure to tobacco fumes, high LDL-cholesterol, oxidized cholesterol, homocysteine, the metabolic consequences of diabetes, iron overload, copper deficiency, deficiencies of vitamins A and D, consumption of trans fatty acids, microorganisms and many more. With one exception, there is evidence to support roles for all of these factors, but the degree to which each of them participates remains uncertain. The exception is of course LDL-cholesterol. Much research allows us to exclude high LDL-cholesterol from the list. Whether we look directly with the naked eye at the inside of the arteries at autopsy, or we do it indirectly in living people using x-rays, ultrasound or electron beams, no association worth mentioning has ever been found between the amount of lipid in the blood and the degree of atherosclerosis in the arteries. Also, whether cholesterol goes up or down, by itself or due to medical intervention, the changes of cholesterol have never been followed by parallel changes in the atherosclerotic plaques; there is no dose-response. Proponents of the cholesterol campaign often claim that the trials indeed have found dose-response, but here they refer to calculations between the mean changes of the different trials with the outcome of the whole treatment group. However, true dose-response demands that the individual changes of the putative causal factor are followed by parallel, individual changes of the disease outcome, and this has never occurred in the trials where researchers have calculated true dose-response.
A detailed discussion of the many factors accused of harming the arterial endothelium is beyond the scope of this article. However, the protective role of the blood lipids against infections obviously demands a closer look at the alleged role of one of the alleged causes, the microorganisms.
Is Atherosclerosis an Infectious Disease?
For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Chlamydia pneumonia (also named TWAR bacteria) participate in the development of atherosclerosis. Research within this area has exploded during the last decade and by January 2004, at least 200 reviews of the issue have been published in medical journals. Due to the widespread preoccupation with cholesterol and other lipids, there has been little general interest in the subject, however, and few doctors know much about it. Here I shall mention some of the most interesting findings.26
Electron microscopy, immunofluorescence microscopy and other advanced techniques have allowed us to detect microorganisms and their DNA in the atherosclerotic lesions in a large proportion of patients. Bacterial toxins and cytokines, hormones secreted by the white blood cells during infections, are seen more often in the blood from patients with recent heart disease and stroke, in particular during and after an acute cardiovascular event, and some of them are strong predictors of cardiovascular disease. The same is valid for bacterial and viral antibodies, and a protein secreted by the liver during infections, named C-reactive protein (CRP), is a much stronger risk factor for coronary heart disease than cholesterol.
Clinical evidence also supports this theory. During the weeks preceding an acute cardiovascular attack many patients have had a bacterial or viral infection. For instance, Dr. Armin J. Grau from the Department of Neurology at the University of Heidelberg and his team asked 166 patients with acute stroke, 166 patients hospitalized for other neurological diseases and 166 healthy individuals matched individually for age and sex about recent infectious disease. Within the first week before the stroke, 37 of the stroke patients, but only 14 of the control individuals had had an infectious disease. In half of the patients the infection was of bacterial origin, in the other half of viral origin.27
Similar observations have been made by many others, for patients with acute myocardial infarction (heart attack). For instance, Dr. Kimmo J. Mattila at the Department of Medicine, Helsinki University Hospital, Finland, found that 11 of 40 male patients with an acute heart attack before age 50 had an influenza-like infection with fever within 36 hours prior to admittance to hospital, but only 4 out of 41 patients with chronic coronary disease (such as recurrent angina or pervious myocardial infarction) and 4 out of 40 control individuals without chronic disease randomly selected from the general population.28
Attempts have been made to prevent cardiovascular disease by treatment with antibiotics. In five trials treatment of patients with coronary heart disease using azithromyzin or roxithromyzin, antibiotics that are effective against Chlamydia pneumonia,yielded successful results; a total of 104 cardiovascular events occurred among the 412 non-treated patients, but only 61 events among the 410 patients in the treatment groups.28a-e In one further trial a significant decreased progression of atherosclerosis in the carotid arteries occurred with antibiotic treatment.28f However, in four other trials,30a-d one of which included more than 7000 patients,28d antibiotic treatment had no significant effect.
The reason for these inconsistent results may be that the treatment was too short (in one of the trials treatment lasted only five days). Also, Chlamydia pneumonia, the TWAR bacteria, can only propagate inside human cells and when located in white blood cells they are resistant to antibiotics.31 Treatment may also have been ineffective because the antibiotics used have no effect on viruses. In this connection it is interesting to mention a controlled trial performed by Dr. Enrique Gurfinkel and his team from Fundación Favaloro in Buenos Aires, Argentina.32 They vaccinated half of 301 patients with coronary heart disease against influenza, a viral disease. After six months 8 percent of the control patients had died, but only 2 percent of the vaccinated patients. It is worth mentioning that this effect was much better than that achieved by any statin trial, and in a much shorter time.
Does High Cholesterol Protect Against Cardiovascular Disease?
Apparently, microorganisms play a role in cardiovascular disease. They may be one of the factors that start the process by injuring the arterial endothelium. A secondary role may be inferred from the association between acute cardiovascular disease and infection. The infectious agent may preferably become located in parts of the arterial walls that have been previously damaged by other agents, initiating local coagulation and the creation of a thrombus (clot) and in this way cause obstruction of the blood flow. But if so, high cholesterol may protect against cardiovascular disease instead of being the cause!
In any case, the diet-heart idea, with its demonizing of high cholesterol, is obviously in conflict with the idea that high cholesterol protects against infections. Both ideas cannot be true. Let me summarize the many facts that conflict with the idea that high cholesterol is bad.
If high cholesterol were the most important cause of atherosclerosis, people with high cholesterol should be more atherosclerotic than people with low cholesterol. But as you know by now this is very far from the truth.
If high cholesterol were the most important cause of atherosclerosis, lowering of cholesterol should influence the atherosclerotic process in proportion to the degree of its lowering.
But as you know by now, this does not happen.
If high cholesterol were the most important cause of cardiovascular disease, it should be a risk factor in all populations, in both sexes, at all ages, in all disease categories, and for both heart disease and stroke. But as you know by now, this is not the case
I have only two arguments for the idea that high cholesterol is good for the blood vessels, but in contrast to the arguments claiming the opposite they are very strong. The first one stems from the statin trials. If high cholesterol were the most important cause of cardiovascular disease, the greatest effect of statin treatment should have been seen in patients with the highest cholesterol, and in patients whose cholesterol was lowered the most. Lack of dose-response cannot be attributed to the knowledge that the statins have other effects on plaque stabilization, as this would not have masked the effect of cholesterol-lowering considering the pronounced lowering that was achieved. On the contrary, if a drug that effectively lowers the concentration of a molecule assumed to be harmful to the cardiovascular system and at the same time exerts several beneficial effects on the same system, a pronounced dose-response should be seen.
On the other hand, if high cholesterol has a protective function, as suggested, its lowering would counterbalance the beneficial effects of the statins and thus work against a dose-response, which would be more in accord with the results from the various trials.
I have already mentioned my second argument, but it can’t be said too often: High cholesterol is associated with longevity in old people. It is difficult to explain away the fact that during the period of life in which most cardiovascular disease occurs and from which most people die (and most of us die from cardiovascular disease), high cholesterol occurs most often in people with the lowest mortality. How is it possible that high cholesterol is harmful to the artery walls and causes fatal coronary heart disease, the commonest cause of death, if those whose cholesterol is the highest, live longer than those whose cholesterol is low?
To the public and the scientific community I say, "Wake up!"
References
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2. Ravnskov U. High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine 96, 927-934, 2003.
3. Jacobs D and others. Report of the conference on low blood cholesterol: Mortality associations. Circulation 86, 1046–1060, 1992.
4. Iribarren C and others. Serum total cholesterol and risk of hospitalization, and death from respiratory disease. International Journal of Epidemiology 26, 1191–1202, 1997.
5. Iribarren C and others. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiology and Infection 121, 335–347, 1998.
6. Claxton AJ and others. Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. Journal of acquired immune deficiency syndromes and human retrovirology 17, 51–57, 1998.
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14. Elias ER and others. Clinical effects of cholesterol supplementation in six patients with the Smith-Lemli-Opitz syndrome (SLOS). American Journal of Medical Genetics 68, 305–310, 1997.
15. Bhakdi S and others. Binding and partial inactivation of Staphylococcus aureus a-toxin by human plasma low density lipoprotein. Journal of Biological Chemistry 258, 5899-5904, 1983.
16. Flegel WA and others. Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins. Infection and Immunity 57, 2237-2245, 1989.
17. Weinstock CW and others. Low density lipoproteins inhibit endotoxin activation of monocytes. Arteriosclerosis and Thrombosis 12, 341-347, 1992.
18. Muldoon MF and others. Immune system differences in men with hypo- or hypercholesterolemia. Clinical Immunology and Immunopathology 84, 145-149, 1997.
19. Feingold KR and others. Role for circulating lipoproteins in protection from endotoxin toxicity. Infection and Immunity 63, 2041-2046, 1995.
20. Netea MG and others. Low-density lipoprotein receptor-deficient mice are protected against lethal endotoxemia and severe gram-negative infections. Journal of Clinical Investigation 97, 1366-1372, 1996.
21. Harris HW, Gosnell JE, Kumwenda ZL. The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity. Journal of Endotoxin Research 6, 421-430, 2001.
22. Netea MG and others. Hyperlipoproteinemia enhances susceptibility to acute disseminated Candida albicans infection in low-density-lipoprotein-receptor-deficient mice. Infection and Immunity 65, 2663-2667, 1997.
23. Ross R, Glomset JA. The pathogenesis of atherosclerosis. New England Journal of Medicine 295, 369-377, 1976.
24. Ross R. The pathogenesis of atherosclerosis and update. New England Journal of Medicine 314, 488-500, 1986.
25. Klotz O, Manning MF. Fatty streaks in the intima of arteries. Journal of Pathology and Bacteriology. 16, 211-220, 1911.
26. At least 200 reviews about the role of infections in atherosclerosis and cardiovascular disease have been published; here are a few of them: a) Grayston JT, Kuo CC, Campbell LA, Benditt EP. Chlamydia pneumoniae strain TWAR and atherosclerosis. European Heart Journal Suppl K, 66-71, 1993. b) Melnick JL, Adam E, Debakey ME. Cytomegalovirus and atherosclerosis. European Heart Journal Suppl K, 30-38, 1993. c) Nicholson AC, Hajjar DP. Herpesviruses in atherosclerosis and thrombosis. Etiologic agents or ubiquitous bystanders? Arteriosclerosis Thrombosis and Vascular Biology 18, 339-348, 1998. d) Ismail A, Khosravi H, Olson H. The role of infection in atherosclerosis and coronary artery disease. A new therapeutic target. Heart Disease 1, 233-240, 1999. e) Kuvin JT, Kimmelstiel MD. Infectious causes of atherosclerosis. f.) Kalayoglu MV, Libby P, Byrne GI. Chlamydia pneumonia as an emerging risk factor in cardiovascular disease. Journal of the American Medical Association 288, 2724-2731, 2002.
27. Grau AJ and others. Recent bacterial and viral infection is a risk factor for cerebrovascular ischemia. Neurology 50, 196-203, 1998.
28. Mattila KJ. Viral and bacterial infections in patients with acute myocardial infarction. Journal of Internal Medicine 225, 293-296, 1989.
29. The successful trials: a) Gurfinkel E. Lancet 350, 404-407, 1997. b) Gupta S and others. Circulation 96, 404-407, 1997. c) Muhlestein JB and others. Circulation 102, 1755-1760, 2000. d) Stone AFM and others. Circulation 106, 1219-1223, 2002. e) Wiesli P and others. Circulation 105, 2646-2652, 2002. f) Sander D and others. Circulation 106, 2428-2433, 2002.
30. The unsuccessful trials: a) Anderson JL and others. Circulation 99, 1540-1547, 1999. b) Leowattana W and others. Journal of the Medical Association of Thailand 84 (Suppl 3), S669-S675, 2001. c) Cercek B and others. Lancet 361, 809-813, 2003. d) O’Connor CM and others. Journal of the American Medical Association. 290, 1459-1466, 2003.
31. Gieffers J and others. Chlamydia pneumoniae infection in circulating human monocytes is refractory to antibiotic treatment. Circulation 104, 351-356, 2001
32. Gurfinkel EP and others. Circulation 105, 2143-2147, 2002.
About the Author
Dr. Ravnskov is the author of The Cholesterol Myths and chairman of The International Network of Cholesterol Skeptics (thincs.org).
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Risk Factor
There is one risk factor that is known to be certain to cause death. It is such a strong risk factor that it has a 100 percent mortality rate. Thus I can guarantee that if we stop this risk factor, which would take no great research and cost nothing in monetary terms, within a century human deaths would be completely eliminated. This risk factor is called "Life."
Barry Groves, www.second-opinions.co.uk.
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Familial Hypercholesterolemia -
Not as Risky as You May Think
Many doctors believe that most patients with familial hypercholesterolemia (FH) die from CHD at a young age. Obviously, they do not know the surprising finding of the Scientific Steering Committee at the Department of Public Health and Primary Care at Radcliffe Infirmary in Oxford, England. For several years, these researchers followed more than 500 FH patients between the ages of 20 and 74 and compared patient mortality during this period with that of the general population.
During a three- to four-year period, six of 214 FH patients below age 40 died from CHD. This may not seem particularly frightening but as it is rare to die from CHD before the age of 40, the risk for these FH patients was almost 100 times that of the general population.
During a four- to five-year period, eight of 237 FH patients between ages 40 and 59 died, which was five times more than the general population. But during a similar period of time, only one of 75 FH patients between the ages of 60 and 74 died from CHD, when the expected number was two.
If these results are typical for FH, you could say that between ages 20 and 59, about 3 percent of the patients die from CHD, and between ages 60 and 74, less than 2 percent die, in both cases during a period of 3-4 years. The authors stressed that the patients had been referred because of a personal or family history of premature vascular disease and therefore were at a particularly high risk for CHD. Most patients with FH in the general population are unrecognized and untreated. Had the patients studied been representative for all FH patients, their prognosis would probably have been even better.
This view was recently confirmed by Dr. Eric Sijbrands and his coworkers from various medical departments in Amsterdam and Leiden, Netherlands. Out of a large group they found three individuals with very high cholesterol. A genetic analysis confirmed the diagnosis of FH and by tracing their family members backward in time, they came up with a total of 412 individuals. The coronary and total mortality of these members were compared with the mortality of the general Dutch population.
The striking finding was that those who lived during the 19th and early 20th century had normal mortality and lived a normal life span. In fact, those living in the 19th century had a lower mortality than the general population. After 1915 the mortality rose to a maximum between 1935 and 1964, but even at the peak, mortality was less than twice as high as in the general population.
Again, very high cholesterol levels alone do not lead to a heart attack. In fact, high cholesterol may even be protective against other diseases. This was the conclusion of Dr. Sijbrands and his colleagues. As support they cited the fact that genetically modified mice with high cholesterol are protected against severe bacterial infections.
"Doctor, don’t be afraid because of my high cholesterol." These were the words of a 36-year-old lawyer who visited me for the first time for a health examination. And indeed, his cholesterol was high, over 400 mg/dl.
"My father’s cholesterol was even higher," he added. "But he lived happily until he died at age 79 from cancer. And his brother, who also had FH, died at age 83. None of them ever complained of any heart problems." My "patient" is now 53, his brother is 56 and his cousin 61. All of them have extremely high cholesterol values, but none of them has any heart troubles, and none of them has ever taken cholesterol-lowering drugs.
So, if you happen to have FH, don’t be too anxious. Your chances of surviving are pretty good, even surviving to old age.
Scientific Steering Committee on behalf of the Simon Broome Register Group. Risk of fatal coronary heart disease in familial hypercholesterolaemia. British Medical Journal 303, 893-896, 1991; Sijbrands EJG and others. Mortality over two centuries in large pedigree with familial hypercholesterolaemia: family tree mortality study. British Medical Journal 322, 1019-1023, 2001.
From The Cholesterol Myths by Uffe Ravnvskov, MD, PhD, NewTrends Publishing, pp 64-65.
People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.
But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2 Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.
Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.
But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.
High Cholesterol Protects Against Infection
Many studies have found that low cholesterol is in certain respects worse than high cholesterol. For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.3
Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection? To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.4,5 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered? Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.
Low Cholesterol and HIV/AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. The Minnesota researchers, now led by Dr. Ami Claxton, followed such individuals for 7-8 years. After having excluded those who became HIV-positive during the first four years, they ended up with a group of 2446 men. At the end of the study, 140 of these people tested positive for HIV; those who had low cholesterol at the beginning of the study were twice as likely to test postitive for HIV compared with those with the highest cholesterol.6
Similar results come from a study of the MRFIT screenees, including more than 300,000 young and middle-aged men, which found that 16 years after the first cholesterol analysis the number of men whose cholesterol was lower than 160 and who had died from AIDS was four times higher than the number of men who had died from AIDS with a cholesterol above 240.7
Cholesterol and Chronic Heart Failure
Heart disease may lead to a weakening of the heart muscle. A weak heart means that less blood and therefore less oxygen is delivered to the arteries. To compensate for the decreased power, the heart beat goes up, but in severe heart failure this is not sufficient. Patients with severe heart failure become short of breath because too little oxygen is delivered to the tissues, the pressure in their veins increases because the heart cannot deliver the blood away from the heart with sufficient power, and they become edematous, meaning that fluid accumulates in the legs and in serious cases also in the lungs and other parts of the body. This condition is called congestive or chronic heart failure.
There are many indications that bacteria or other microorganisms play an important role in chronic heart failure. For instance, patients with severe chronic heart failure have high levels of endotoxin and various types of cytokines in their blood. Endotoxin, also named lipopolysaccharide, is the most toxic substance produced by Gram-negative bacteria such as Escherichia coli, Klebsiella, Salmonella, Serratia and Pseudomonas. Cytokines are hormones secreted by white blood cells in their battle with microorganisms; high levels of cytokines in the blood indicate that inflammatory processes are going on somewhere in the body.
The role of infections in chronic heart failure has been studied by Dr. Mathias Rauchhaus and his team at the Medical Department, Martin-Luther-University in Halle, Germany (Universitätsklinik und Poliklinik für Innere Medizin III, Martin-Luther-Universität, Halle). They found that the strongest predictor of death for patients with chronic heart failure was the concentration of cytokines in the blood, in particular in patients with heart failure due to coronary heart disease.8 To explain their finding they suggested that bacteria from the gut may more easily penetrate into the tissues when the pressure in the abdominal veins is increased because of heart failure. In accordance with this theory, they found more endotoxin in the blood of patients with congestive heart failure and edema than in patients with non-congestive heart failure without edema, and endotoxin concentrations decreased significantly when the heart’s function was improved by medical treatment.9
A simple way to test the functional state of the immune system is to inject antigens from microorganisms that most people have been exposed to, under the skin. If the immune system is normal, an induration (hard spot) will appear about 48 hours later at the place of the injection. If the induration is very small, with a diameter of less than a few millimeters, this indicates the presence of "anergy," a reduction in or failure of response to recognize antigens. In accordance, anergy has been found associated with an increased risk of infection and mortality in healthy elderly individuals, in surgical patients and in heart transplant patients.10
Dr. Donna Vredevoe and her group from the School of Nursery and the School of Medicine, University of California at Los Angeles tested more than 200 patients with severe heart failure with five different antigens and followed them for twelve months. The cause of heart failure was coronary heart disease in half of them and other types of heart disease (such as congenital or infectious valvular heart disease, various cardiomyopathies and endocarditis) in the rest. Almost half of all the patients were anergic, and those who were anergic and had coronary heart disease had a much higher mortality than the rest.10
Now to the salient point: to their surprise the researchers found that mortality was higher, not only in the patients with anergy, but also in the patients with the lowest lipid values, including total cholesterol, LDL-cholesterol and HDL-cholesterol as well as triglycerides.
The latter finding was confirmed by Dr. Rauchhaus, this time in co-operation with researchers at several German and British university hospitals. They found that the risk of dying for patients with chronic heart failure was strongly and inversely associated with total cholesterol, LDL-cholesterol and also triglycerides; those with high lipid values lived much longer than those with low values.11,12
Other researchers have made similar observations. The largest study has been performed by Professor Gregg C. Fonorow and his team at the UCLA Department of Medicine and Cardiomyopathy Center in Los Angeles.13 The study, led by Dr. Tamara Horwich, included more than a thousand patients with severe heart failure. After five years 62 percent of the patients with cholesterol below 129 mg/l had died, but only half as many of the patients with cholesterol above 223 mg/l.
When proponents of the cholesterol hypothesis are confronted with findings showing a bad outcome associated with low cholesterol--and there are many such observations--they usually argue that severely ill patients are often malnourished, and malnourishment is therefore said to cause low cholesterol. However, the mortality of the patients in this study was independent of their degree of nourishment; low cholesterol predicted early mortality whether the patients were malnourished or not.
Smith-Lemli-Opitz Syndrome
As discussed in The Cholesterol Myths (see sidebar), much evidence supports the theory that people born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true.
Children with the Smith-Lemli-Opitz syndrome have very low cholesterol because the enzyme that is necessary for the last step in the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the central nervous system. Those who survive are imbecile, they have extremely low cholesterol and suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent.14
Laboratory Evidence
Laboratory studies are crucial for learning more about the mechanisms by which the lipids exert their protective function. One of the first to study this phenomenon was Dr Sucharit Bhakdi from the Institute of Medical Microbiology, University of Giessen (Institut für Medizinsche Mikrobiologie, Justus-Liebig-Universität Gießen), Germany along with his team of researchers from various institutions in Germany and Denmark.15
Staphylococcus aureus ?-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy a wide variety of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in 0.9 percent saline, the blood is hemolyzed, that is the membranes of the red blood cells burst and hemoglobin from the interior of the red blood cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified ?-toxin with human serum (the fluid in which the blood cells reside) and saw that 90 percent of its hemolyzing effect disappeared. By various complicated methods they identified the protective substance as LDL, the carrier of the so-called bad cholesterol. In accordance, no hemolysis occurred when they mixed ?-toxin with purified human LDL, whereas HDL or other plasma constituents were ineffective in this respect.
Dr. Willy Flegel and his co-workers at the Department of Transfusion Medicine, University of Ulm, and the Institute of Immunology and Genetics at the German Cancer Research Center in Heidelberg, Germany (DRK-Blutspendezentrale und Abteilung für Transfusionsmedizin, Universität Ulm, und Deutsches Krebsforschungszentrum, Heidelberg) studied endotoxin in another way.16 As mentioned, one of the effects of endotoxin is that white blood cells are stimulated to produce cytokines. The German researchers found that the cytokine-stimulating effect of endotoxin on the white blood cells disappeared almost completely if the endotoxin was mixed with human serum for 24 hours before they added the white blood cells to the test tubes. In a subsequent study17 they found that purified LDL from patients with familial hypercholesterolemia had the same inhibitory effect as the serum.
LDL may not only bind and inactivate dangerous bacterial toxins; it seems to have a direct beneficial influence on the immune system also, possibly explaining the observed relationship between low cholesterol and various chronic diseases. This was the starting point for a study by Professor Matthew Muldoon and his team at the University of Pittsburgh, Pennsylvania. They studied healthy young and middle-aged men and found that the total number of white blood cells and the number of various types of white blood cells were significantly lower in the men with LDL-cholesterol below 160 mg/dl (mean 88.3 mg/l),than in men with LDL-cholesterol above 160 mg/l (mean 185.5 mg/l).18 The researchers cautiously concluded that there were immune system differences between men with low and high cholesterol, but that it was too early to state whether these differences had any importance for human health. Now, seven years later with many of the results discussed here, we are allowed to state that the immune-supporting properties of LDL-cholesterol do indeed play an important role in human health.
Animal Experiments
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold at the Department of Medicine, University of California, San Francisco, and his group have published several interesting results from such research. In one of them they lowered LDL-cholesterol in rats by giving them either a drug that prevents the liver from secreting lipoproteins, or a drug that increases their disappearance. In both models, injection of endotoxin was followed by a much higher mortality in the low-cholesterol rats compared with normal rats. The high mortality was not due to the drugs because, if the drug-treated animals were injected with lipoproteins just before the injection of endotoxin, their mortality was reduced to normal.19
Dr. Mihai Netea and his team from the Departments of Internal and Nuclear Medicine at the University Hospital in Nijmegen, The Netherlands, injected purified endotoxin into normal mice, and into mice with familial hypercholesterolemia that had LDL-cholesterol four times higher than normal. Whereas all normal mice died, they had to inject eight times as much endotoxin to kill the mice with familial hypercholesterolemia. In another experiment they injected live bacteria and found that twice as many mice with familial hypercholesterolemia survived compared with normal mice.20
Other Protecting Lipids
As seen from the above, many of the roles played by LDL-cholesterol are shared by HDL. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more.
Triglycerides, molecules consisting of three fatty acids linked to glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by a lipoprotein named VLDL (very low-density lipoprotein) and by chylomicrons, a mixture of emulsified triglycerides appearing in large amounts after a fat-rich meal, particularly in the blood that flows from the gut to the liver.
For many years it has been known that sepsis, a life-threatening condition caused by bacterial growth in the blood, is associated with a high level of triglycerides. The serious symptoms of sepsis are due to endotoxin, most often produced by gut bacteria. In a number of studies, Professor Hobart W. Harris at the Surgical Research Laboratory at San Francisco General Hospital and his team found that solutions rich in triglycerides but with practically no cholesterol were able to protect experimental animals from the toxic effects of endotoxin and they concluded that the high level of triglycerides seen in sepsis is a normal immune response to infection.21 Usually the bacteria responsible for sepsis come from the gut. It is therefore fortunate that the blood draining the gut is especially rich in triglycerides.
Exceptions
So far, animal experiments have confirmed the hypothesis that high cholesterol protects against infection, at least against infections caused by bacteria. In a similar experiment using injections of Candida albicans, a common fungus, Dr. Netea and his team found that mice with familial hypercholesterolemia died more easily than normal mice.22 Serious infections caused by Candida albicans are rare in normal human beings; however, they are mainly seen in patients treated with immunosuppressive drugs, but the finding shows that we need more knowledge in this area. However, the many findings mentioned above indicate that the protective effects of the blood lipids against infections in human beings seem to be greater than any possible adverse effects.
Cholesterol as a Risk Factor
Most studies of young and middle-aged men have found high cholesterol to be a risk factor for coronary heart disease, seemingly a contradiction to the idea that high cholesterol is protective. Why is high cholesterol a risk factor in young and middle-aged men? A likely explanation is that men of that age are often in the midst of their professional career. High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body’s need for more cholesterol because cholesterol is the building material of many stress hormones. Any possible protective effect of high cholesterol may therefore be counteracted by the negative influence of a stressful life on the vascular system.
Response to Injury
In 1976 one of the most promising theories about the cause of atherosclerosis was the Response-to-Injury Hypothesis, presented by Russell Ross, a professor of pathology, and John Glomset, a professor of biochemistry and medicine at the Medical School, University of Washington in Seattle.23,24 They suggested that atherosclerosis is the consequence of an inflammatory process, where the first step is a localized injury to the thin layer of cells lining the inside of the arteries, the intima. The injury causes inflammation and the raised plaques that form are simply healing lesions.
Their idea is not new. In 1911, two American pathologists from the Pathological Laboratories, University of Pittsburgh, Pennsylvania, Oskar Klotz and M.F. Manning, published a summary of their studies of the human arteries and concluded that "there is every indication that the production of tissue in the intima is the result of a direct irritation of that tissue by the presence of infection or toxins or the stimulation by the products of a primary degeneration in that layer."25 Other researchers have presented similar theories.26
Researchers have proposed many potential causes of vascular injury, including mechanical stress, exposure to tobacco fumes, high LDL-cholesterol, oxidized cholesterol, homocysteine, the metabolic consequences of diabetes, iron overload, copper deficiency, deficiencies of vitamins A and D, consumption of trans fatty acids, microorganisms and many more. With one exception, there is evidence to support roles for all of these factors, but the degree to which each of them participates remains uncertain. The exception is of course LDL-cholesterol. Much research allows us to exclude high LDL-cholesterol from the list. Whether we look directly with the naked eye at the inside of the arteries at autopsy, or we do it indirectly in living people using x-rays, ultrasound or electron beams, no association worth mentioning has ever been found between the amount of lipid in the blood and the degree of atherosclerosis in the arteries. Also, whether cholesterol goes up or down, by itself or due to medical intervention, the changes of cholesterol have never been followed by parallel changes in the atherosclerotic plaques; there is no dose-response. Proponents of the cholesterol campaign often claim that the trials indeed have found dose-response, but here they refer to calculations between the mean changes of the different trials with the outcome of the whole treatment group. However, true dose-response demands that the individual changes of the putative causal factor are followed by parallel, individual changes of the disease outcome, and this has never occurred in the trials where researchers have calculated true dose-response.
A detailed discussion of the many factors accused of harming the arterial endothelium is beyond the scope of this article. However, the protective role of the blood lipids against infections obviously demands a closer look at the alleged role of one of the alleged causes, the microorganisms.
Is Atherosclerosis an Infectious Disease?
For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Chlamydia pneumonia (also named TWAR bacteria) participate in the development of atherosclerosis. Research within this area has exploded during the last decade and by January 2004, at least 200 reviews of the issue have been published in medical journals. Due to the widespread preoccupation with cholesterol and other lipids, there has been little general interest in the subject, however, and few doctors know much about it. Here I shall mention some of the most interesting findings.26
Electron microscopy, immunofluorescence microscopy and other advanced techniques have allowed us to detect microorganisms and their DNA in the atherosclerotic lesions in a large proportion of patients. Bacterial toxins and cytokines, hormones secreted by the white blood cells during infections, are seen more often in the blood from patients with recent heart disease and stroke, in particular during and after an acute cardiovascular event, and some of them are strong predictors of cardiovascular disease. The same is valid for bacterial and viral antibodies, and a protein secreted by the liver during infections, named C-reactive protein (CRP), is a much stronger risk factor for coronary heart disease than cholesterol.
Clinical evidence also supports this theory. During the weeks preceding an acute cardiovascular attack many patients have had a bacterial or viral infection. For instance, Dr. Armin J. Grau from the Department of Neurology at the University of Heidelberg and his team asked 166 patients with acute stroke, 166 patients hospitalized for other neurological diseases and 166 healthy individuals matched individually for age and sex about recent infectious disease. Within the first week before the stroke, 37 of the stroke patients, but only 14 of the control individuals had had an infectious disease. In half of the patients the infection was of bacterial origin, in the other half of viral origin.27
Similar observations have been made by many others, for patients with acute myocardial infarction (heart attack). For instance, Dr. Kimmo J. Mattila at the Department of Medicine, Helsinki University Hospital, Finland, found that 11 of 40 male patients with an acute heart attack before age 50 had an influenza-like infection with fever within 36 hours prior to admittance to hospital, but only 4 out of 41 patients with chronic coronary disease (such as recurrent angina or pervious myocardial infarction) and 4 out of 40 control individuals without chronic disease randomly selected from the general population.28
Attempts have been made to prevent cardiovascular disease by treatment with antibiotics. In five trials treatment of patients with coronary heart disease using azithromyzin or roxithromyzin, antibiotics that are effective against Chlamydia pneumonia,yielded successful results; a total of 104 cardiovascular events occurred among the 412 non-treated patients, but only 61 events among the 410 patients in the treatment groups.28a-e In one further trial a significant decreased progression of atherosclerosis in the carotid arteries occurred with antibiotic treatment.28f However, in four other trials,30a-d one of which included more than 7000 patients,28d antibiotic treatment had no significant effect.
The reason for these inconsistent results may be that the treatment was too short (in one of the trials treatment lasted only five days). Also, Chlamydia pneumonia, the TWAR bacteria, can only propagate inside human cells and when located in white blood cells they are resistant to antibiotics.31 Treatment may also have been ineffective because the antibiotics used have no effect on viruses. In this connection it is interesting to mention a controlled trial performed by Dr. Enrique Gurfinkel and his team from Fundación Favaloro in Buenos Aires, Argentina.32 They vaccinated half of 301 patients with coronary heart disease against influenza, a viral disease. After six months 8 percent of the control patients had died, but only 2 percent of the vaccinated patients. It is worth mentioning that this effect was much better than that achieved by any statin trial, and in a much shorter time.
Does High Cholesterol Protect Against Cardiovascular Disease?
Apparently, microorganisms play a role in cardiovascular disease. They may be one of the factors that start the process by injuring the arterial endothelium. A secondary role may be inferred from the association between acute cardiovascular disease and infection. The infectious agent may preferably become located in parts of the arterial walls that have been previously damaged by other agents, initiating local coagulation and the creation of a thrombus (clot) and in this way cause obstruction of the blood flow. But if so, high cholesterol may protect against cardiovascular disease instead of being the cause!
In any case, the diet-heart idea, with its demonizing of high cholesterol, is obviously in conflict with the idea that high cholesterol protects against infections. Both ideas cannot be true. Let me summarize the many facts that conflict with the idea that high cholesterol is bad.
If high cholesterol were the most important cause of atherosclerosis, people with high cholesterol should be more atherosclerotic than people with low cholesterol. But as you know by now this is very far from the truth.
If high cholesterol were the most important cause of atherosclerosis, lowering of cholesterol should influence the atherosclerotic process in proportion to the degree of its lowering.
But as you know by now, this does not happen.
If high cholesterol were the most important cause of cardiovascular disease, it should be a risk factor in all populations, in both sexes, at all ages, in all disease categories, and for both heart disease and stroke. But as you know by now, this is not the case
I have only two arguments for the idea that high cholesterol is good for the blood vessels, but in contrast to the arguments claiming the opposite they are very strong. The first one stems from the statin trials. If high cholesterol were the most important cause of cardiovascular disease, the greatest effect of statin treatment should have been seen in patients with the highest cholesterol, and in patients whose cholesterol was lowered the most. Lack of dose-response cannot be attributed to the knowledge that the statins have other effects on plaque stabilization, as this would not have masked the effect of cholesterol-lowering considering the pronounced lowering that was achieved. On the contrary, if a drug that effectively lowers the concentration of a molecule assumed to be harmful to the cardiovascular system and at the same time exerts several beneficial effects on the same system, a pronounced dose-response should be seen.
On the other hand, if high cholesterol has a protective function, as suggested, its lowering would counterbalance the beneficial effects of the statins and thus work against a dose-response, which would be more in accord with the results from the various trials.
I have already mentioned my second argument, but it can’t be said too often: High cholesterol is associated with longevity in old people. It is difficult to explain away the fact that during the period of life in which most cardiovascular disease occurs and from which most people die (and most of us die from cardiovascular disease), high cholesterol occurs most often in people with the lowest mortality. How is it possible that high cholesterol is harmful to the artery walls and causes fatal coronary heart disease, the commonest cause of death, if those whose cholesterol is the highest, live longer than those whose cholesterol is low?
To the public and the scientific community I say, "Wake up!"
References
1. Krumholz HM and others. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. Journal of the American Medical Association 272, 1335-1340, 1990.
2. Ravnskov U. High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine 96, 927-934, 2003.
3. Jacobs D and others. Report of the conference on low blood cholesterol: Mortality associations. Circulation 86, 1046–1060, 1992.
4. Iribarren C and others. Serum total cholesterol and risk of hospitalization, and death from respiratory disease. International Journal of Epidemiology 26, 1191–1202, 1997.
5. Iribarren C and others. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiology and Infection 121, 335–347, 1998.
6. Claxton AJ and others. Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. Journal of acquired immune deficiency syndromes and human retrovirology 17, 51–57, 1998.
7. Neaton JD, Wentworth DN. Low serum cholesterol and risk of death from AIDS. AIDS 11, 929–930, 1997.
8. Rauchhaus M and others. Plasma cytokine parameters and mortality in patients with chronic heart failure. Circulation 102, 3060-3067, 2000.
9. Niebauer J and others. Endotoxin and immune activation in chronic heart failure. Lancet 353, 1838-1842, 1999.
10. Vredevoe DL and others. Skin test anergy in advanced heart failure secondary to either ischemic or idiopathic dilated cardiomyopathy. American Journal of Cardiology 82, 323-328, 1998.
11. Rauchhaus M, Coats AJ, Anker SD. The endotoxin-lipoprotein hypothesis. Lancet 356, 930–933, 2000.
12. Rauchhaus M and others. The relationship between cholesterol and survival in patients with chronic heart failure. Journal of the American College of Cardiology 42, 1933-1940, 2003.
13. Horwich TB and others. Low serum total cholesterol is associated with marked increase in mortality in advanced heart failure. Journal of Cardiac Failure 8, 216-224, 2002.
14. Elias ER and others. Clinical effects of cholesterol supplementation in six patients with the Smith-Lemli-Opitz syndrome (SLOS). American Journal of Medical Genetics 68, 305–310, 1997.
15. Bhakdi S and others. Binding and partial inactivation of Staphylococcus aureus a-toxin by human plasma low density lipoprotein. Journal of Biological Chemistry 258, 5899-5904, 1983.
16. Flegel WA and others. Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins. Infection and Immunity 57, 2237-2245, 1989.
17. Weinstock CW and others. Low density lipoproteins inhibit endotoxin activation of monocytes. Arteriosclerosis and Thrombosis 12, 341-347, 1992.
18. Muldoon MF and others. Immune system differences in men with hypo- or hypercholesterolemia. Clinical Immunology and Immunopathology 84, 145-149, 1997.
19. Feingold KR and others. Role for circulating lipoproteins in protection from endotoxin toxicity. Infection and Immunity 63, 2041-2046, 1995.
20. Netea MG and others. Low-density lipoprotein receptor-deficient mice are protected against lethal endotoxemia and severe gram-negative infections. Journal of Clinical Investigation 97, 1366-1372, 1996.
21. Harris HW, Gosnell JE, Kumwenda ZL. The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity. Journal of Endotoxin Research 6, 421-430, 2001.
22. Netea MG and others. Hyperlipoproteinemia enhances susceptibility to acute disseminated Candida albicans infection in low-density-lipoprotein-receptor-deficient mice. Infection and Immunity 65, 2663-2667, 1997.
23. Ross R, Glomset JA. The pathogenesis of atherosclerosis. New England Journal of Medicine 295, 369-377, 1976.
24. Ross R. The pathogenesis of atherosclerosis and update. New England Journal of Medicine 314, 488-500, 1986.
25. Klotz O, Manning MF. Fatty streaks in the intima of arteries. Journal of Pathology and Bacteriology. 16, 211-220, 1911.
26. At least 200 reviews about the role of infections in atherosclerosis and cardiovascular disease have been published; here are a few of them: a) Grayston JT, Kuo CC, Campbell LA, Benditt EP. Chlamydia pneumoniae strain TWAR and atherosclerosis. European Heart Journal Suppl K, 66-71, 1993. b) Melnick JL, Adam E, Debakey ME. Cytomegalovirus and atherosclerosis. European Heart Journal Suppl K, 30-38, 1993. c) Nicholson AC, Hajjar DP. Herpesviruses in atherosclerosis and thrombosis. Etiologic agents or ubiquitous bystanders? Arteriosclerosis Thrombosis and Vascular Biology 18, 339-348, 1998. d) Ismail A, Khosravi H, Olson H. The role of infection in atherosclerosis and coronary artery disease. A new therapeutic target. Heart Disease 1, 233-240, 1999. e) Kuvin JT, Kimmelstiel MD. Infectious causes of atherosclerosis. f.) Kalayoglu MV, Libby P, Byrne GI. Chlamydia pneumonia as an emerging risk factor in cardiovascular disease. Journal of the American Medical Association 288, 2724-2731, 2002.
27. Grau AJ and others. Recent bacterial and viral infection is a risk factor for cerebrovascular ischemia. Neurology 50, 196-203, 1998.
28. Mattila KJ. Viral and bacterial infections in patients with acute myocardial infarction. Journal of Internal Medicine 225, 293-296, 1989.
29. The successful trials: a) Gurfinkel E. Lancet 350, 404-407, 1997. b) Gupta S and others. Circulation 96, 404-407, 1997. c) Muhlestein JB and others. Circulation 102, 1755-1760, 2000. d) Stone AFM and others. Circulation 106, 1219-1223, 2002. e) Wiesli P and others. Circulation 105, 2646-2652, 2002. f) Sander D and others. Circulation 106, 2428-2433, 2002.
30. The unsuccessful trials: a) Anderson JL and others. Circulation 99, 1540-1547, 1999. b) Leowattana W and others. Journal of the Medical Association of Thailand 84 (Suppl 3), S669-S675, 2001. c) Cercek B and others. Lancet 361, 809-813, 2003. d) O’Connor CM and others. Journal of the American Medical Association. 290, 1459-1466, 2003.
31. Gieffers J and others. Chlamydia pneumoniae infection in circulating human monocytes is refractory to antibiotic treatment. Circulation 104, 351-356, 2001
32. Gurfinkel EP and others. Circulation 105, 2143-2147, 2002.
About the Author
Dr. Ravnskov is the author of The Cholesterol Myths and chairman of The International Network of Cholesterol Skeptics (thincs.org).
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Risk Factor
There is one risk factor that is known to be certain to cause death. It is such a strong risk factor that it has a 100 percent mortality rate. Thus I can guarantee that if we stop this risk factor, which would take no great research and cost nothing in monetary terms, within a century human deaths would be completely eliminated. This risk factor is called "Life."
Barry Groves, www.second-opinions.co.uk.
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Familial Hypercholesterolemia -
Not as Risky as You May Think
Many doctors believe that most patients with familial hypercholesterolemia (FH) die from CHD at a young age. Obviously, they do not know the surprising finding of the Scientific Steering Committee at the Department of Public Health and Primary Care at Radcliffe Infirmary in Oxford, England. For several years, these researchers followed more than 500 FH patients between the ages of 20 and 74 and compared patient mortality during this period with that of the general population.
During a three- to four-year period, six of 214 FH patients below age 40 died from CHD. This may not seem particularly frightening but as it is rare to die from CHD before the age of 40, the risk for these FH patients was almost 100 times that of the general population.
During a four- to five-year period, eight of 237 FH patients between ages 40 and 59 died, which was five times more than the general population. But during a similar period of time, only one of 75 FH patients between the ages of 60 and 74 died from CHD, when the expected number was two.
If these results are typical for FH, you could say that between ages 20 and 59, about 3 percent of the patients die from CHD, and between ages 60 and 74, less than 2 percent die, in both cases during a period of 3-4 years. The authors stressed that the patients had been referred because of a personal or family history of premature vascular disease and therefore were at a particularly high risk for CHD. Most patients with FH in the general population are unrecognized and untreated. Had the patients studied been representative for all FH patients, their prognosis would probably have been even better.
This view was recently confirmed by Dr. Eric Sijbrands and his coworkers from various medical departments in Amsterdam and Leiden, Netherlands. Out of a large group they found three individuals with very high cholesterol. A genetic analysis confirmed the diagnosis of FH and by tracing their family members backward in time, they came up with a total of 412 individuals. The coronary and total mortality of these members were compared with the mortality of the general Dutch population.
The striking finding was that those who lived during the 19th and early 20th century had normal mortality and lived a normal life span. In fact, those living in the 19th century had a lower mortality than the general population. After 1915 the mortality rose to a maximum between 1935 and 1964, but even at the peak, mortality was less than twice as high as in the general population.
Again, very high cholesterol levels alone do not lead to a heart attack. In fact, high cholesterol may even be protective against other diseases. This was the conclusion of Dr. Sijbrands and his colleagues. As support they cited the fact that genetically modified mice with high cholesterol are protected against severe bacterial infections.
"Doctor, don’t be afraid because of my high cholesterol." These were the words of a 36-year-old lawyer who visited me for the first time for a health examination. And indeed, his cholesterol was high, over 400 mg/dl.
"My father’s cholesterol was even higher," he added. "But he lived happily until he died at age 79 from cancer. And his brother, who also had FH, died at age 83. None of them ever complained of any heart problems." My "patient" is now 53, his brother is 56 and his cousin 61. All of them have extremely high cholesterol values, but none of them has any heart troubles, and none of them has ever taken cholesterol-lowering drugs.
So, if you happen to have FH, don’t be too anxious. Your chances of surviving are pretty good, even surviving to old age.
Scientific Steering Committee on behalf of the Simon Broome Register Group. Risk of fatal coronary heart disease in familial hypercholesterolaemia. British Medical Journal 303, 893-896, 1991; Sijbrands EJG and others. Mortality over two centuries in large pedigree with familial hypercholesterolaemia: family tree mortality study. British Medical Journal 322, 1019-1023, 2001.
From The Cholesterol Myths by Uffe Ravnvskov, MD, PhD, NewTrends Publishing, pp 64-65.
Abstracts on the Effect of Pasteurization on the Nutritional Value of Milk
Abstracts on the Effect of Pasteurization on the Nutritional Value of Milk
Pasteurization was also found to affect the hematogenic and growth-promoting properties of the special milk (raw milk from specially fed cows, whose milk did not produce nutritional anemia—whereas commercially pasteurized milk did). . .
—Krauss, W. E., Erb, J.H. and Washburn, R. G., Studies on the nutritive value of milk II. "The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 11, January, 1933.
Resistance to tuberculosis increased in children fed raw milk instead of pasteurized, to the point that in five years only one case of pulmonary TB had developed, whereas in the previous five years, when children had been given pasteurized milk, 14 cases of pulmonary TB had developed.
—The Lancet, page 1142, May 8, 1937
Human or cow milk added to an equal volume of agar did not support the growth or allowed only slight growth of B. diphtheriae Staph. aureus, B. coli, B. prodigiosus, B. pyocyaneus, B. anthracis, streptococci, and unidentified wild yeast. The factors in human milk inhibiting bacterial growth ('inhibins') were inactivated by heating at 56 degrees C. (pasteurization temperatures of 60-70 degrees C.) for thirty minutes or by standing twelve to twenty-four days at 5 degrees C., but not by repeated freezing and thawing. The 'inhibins' in cow's milk were not inactivated by heating at 80 degrees C. for seven minutes but were destroyed by heating at 85 degrees C. for seven minutes. Attempts have not been made to identify the natural antiseptics.
—Dold, H., Wizaman, E., and Kleiner, C., Z. Hyt. Inf., "Antiseptic in milk," The Drug and Cosmetic Industry, 43,1:109, July, 1938.
"Milk, an animal product, is the essential food of all infant mammals. Mammals are so classified in the scale of living things because of the common characteristic of the female nursing her young. The infant mammal is accordingly carnivorous in his natural habits irrespective of whether the adult of the species is herbivorous or carnivorous.
"If the adults on a carnivorous diet show conditions of deficiency on cooked meat, is it not reasonable to suppose that growing infants on entirely cooked carnivorous diets will do likewise? Many experimenters, such as Catel, Dutcher, Wilson, and others, have shown such to be the case in animals fed on pasteurized milk. . .
"Can human infants be born of mothers who are deficient, and yet attain a fair degree of skeletal development if given a proper raw milk supply? The three infants in figure 4 were born of mothers known to by hypothyroid. Prior to the birth of the infants shown, all three mothers had given birth to children within three years. Each of the previous children was asthmatic, showed infantile rickets, and possessed poor skeletal development. The first child shown in Figure 4 was breast fed from birth, with the mother living under excellent health-promoting conditions. The second child was on powdered milk for four weeks, and on raw certified milk after that without cod-liver oil or orange juice. Both the first and second child began supplemental feedings when they were about five months old and were very healthy babies. The third baby was always sickly and had been on formulae since birth. These formulae included powdered milk, pasteurized milk, boiled milk, boiled certified milk and canned milk. She had suffered from severe gastric distress during her entire infancy and when eight months old she developed asthma. She is very small though her parents are of larger build than the parents of the other two children.
"The strictest bacteriologic standards for milk must always be maintained. The feeding of cattle should receive greater attention. It should be determined experimentally, if possible, whether health and resistance are undermined by pasteurization. If so, in our attempt to protect the child from milk-borne infections, we may be denying his heritage of good health by removing from his milk vitamins, hormones, and enzymes that control mineral assimilation and promote body development and general resistance to disease. Is it also possible that these same elements are as important to the adult invalid who needs milk as to the infant?
"Let us have closer cooperation between raw-milk producers and public-health officials so that the growth-producing factors of raw milk can be studied. We cannot afford to pasteurize milk if it is found that pasteurization diminishes the potency of the growth-promoting factors that determine the skeletal development of our children. We cannot afford to lessen the resistance of our children to respiratory infection, asthma, bronchitis and the common cold when factors preventing them are present in greater amounts in properly clean raw milk than in pasteurized milk."
—Pottenger, F. M. Jr., "Clinical and experimental evidence of growth factors in raw milk," Certified Milk, January, 1937.
"Some have questioned whether pasteurized milk is really involved in the production of scurvy. The fact, however, that when one gives a group of infants this food for a period of about six months, instances of scurvy occur, and that a cure is brought about when raw milk is substituted, taken in conjunction with the fact that if we feed the same number of infants on raw milk, cases of scurvy will not develop--these results seem sufficient to warrant the deduction that pasteurized milk is a causative factor. The experience in Berlin, noted by Newmann (Newmann, H., Deutsch. Klin., 7:341, 1904) and others, is most illuminating and convincing in this connection. In 1901 a large dairy in that city established a pasteurizing plant in which all milk was raised to a temperature of about 60 degrees C. After an interval of some months infantile scurvy, was reported from various sources throughout the city. Neumann writes about the situation as follows:
'Whereas Heubner, Cassel and myself had seen only thirty-two cases of scurvy from 1896 to 1900, the number of cases suddenly rose from the year 1901, so that the same observers—not to mention a great many others—treated eighty-three cases in 1901 and 1902.'
An investigation was made as to the cause, and the pasteurization was discontinued. The result was that the number of cases decreased just as suddenly as they had increased..."
—Hess, A. F., "Infantile Scurvy, V. A study of its pathogenesis," Am. J Dis. Child., November, 1917.
"Although pasteurized milk is to be recommended on account of the security which it affords against infection, we should realize that it is an incomplete food. Unless an antiscorbutic, such as orange juice, ....or potato water is added, infants will develop scurvy on this diet. This form of scurvy takes some months to develop and may be termed subacute. It must be considered not only the most common form of this disorder, but the one which passes most often unrecognized. In order to guard against it, infants fed exclusively on a diet of pasteurized milk should be given antiscorbutics far earlier than is at present the custom, even as early as at the end of the first month of life."
—Hess, A. F., "Infantile Scurvy. III. Its influence on growth (length and weight)," Am. J. Dis. Child., August, 1916.
"One of the most striking clinical phenomenon of infantile scurvy is the marked susceptibility to infection which it entails--the frequent attacks of 'grippe,' the widespread occurrence of nasal diphtheria, the furunculosis of the skin, the danger of pneumonia in advanced cases..."
—Hess, A. F., "Infantile Scurvy. V. A study of its pathogenesis," Am. J. Dis. Child., November, 1917.
"...Recently, Minot and his colleagues came to the conclusion that adult scurvy can be precipitated by infectious processes; in other words, that latent scurvy can by this means be changed to manifest scurvy. In general, therefore, investigations in the laboratory as well as clinical observations are in agreement in stressing the interrelationship of scurvy and bacterial infection."
—Hess, A. F., "Recent advances in knowledge of scurvy and the antiscorbutic vitamin," J.A.M.A., April 23, 1932.
This illustrates the futility of pasteurization of milk to prevent infection from diseases the cows may sometimes have, such as undulant fever. The infant is then made subject to the common infectious diseases, and deaths from these common diseases are not attributed, as they should be, to the defective nature of the milk.
EFFECTS OF PASTEURIZATION OF MILK ON TOOTH HEALTH
The Lancet, page 1142, May 8, 1937 says that in children the teeth are less likely to decay on diet supplemented with raw milk than with pasteurized milk.
"Dr. Evelyn Sprawson of the London Hospital has recently stated that in certain institutions children who were brought up on raw milk (as opposed to pasteurized milk) had perfect teeth and no decay. Whether this was due actually to the milk being unheated, or possibly to some other, quite different and so far unrecognized cause, we cannot yet say; but we may be sure of one thing, that the result is so striking and unusual that it will undoubtedly be made the subject of further inquiry."
—Harris, L.J., Vitamins in Theory and Practice, page 224, Cambridge, University Press, 1935.
EFFECT OF PASTEURIZATION OF MILK ON GROWTH
...Fisher and Bartlett "point out by statistical treatment that the response in height to raw milk was significantly greater than that to pasteurized milk. Their interpretation of the data led to the assertion that the pasteurized milk was only 66 per cent effective as the raw milk in the case of boys and 91.1 per cent as effective in the case of girls in inducing increases in weight, and 50.0 per cent as effective in boys and 70.0 per cent in girls in bringing about height increases."
—Krauss, W. E., Erb, J. H. and Washburn, R.G., "Studies on the nutritive value of milk, II." "The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 8, January 1933.
...Daniels and Loughlin observed that young rats fed long heat-treated milks, evaporated, condensed, and pasteurized by the 'hold' method failed to grow normally, but if the precipitated calcium salts were incorporated into the various milk, growth was normal..."
—Daniels, A.L., and Loughlin, R., Journal of Biological Chemistry, 44.381, 1920, as abstracted by Holmes and Pigott, "Factors that influence the anti-rachitic value of milk in infant feeding," Oil & Soap, 12.9:202-207, September, 1935.
CALCIUM AVAILABILITY IN PASTEURIZED MILK
"Kramer, Latzke and Shaw (Kramer, Martha M., Latzke, F., and Shaw, M.M., A Comparison of Raw, Pasteurized, Evaporated and Dried Milks as Sources of Calcium and Phosphorus for the Human Subject, Journal of Biological Chemistry, 79:283-295, 1928) obtained less favorable calcium balances in adults with pasteurized milk than with 'fresh milk' and made the further observation that milk from cows kept in the barn for five months gave less favorable calcium balances than did 'fresh milk' (herd milk from a college dairy)."
—Krauss, W. E., Erb, J.H., and Washburn, R.G., "Studies on the nutritive value of milk, II. The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 8, January, 1933.
"Guinea pigs fed raw milk with an addition of skim milk powder, copper and iron salts, carotene, and orange juice grew well and showed no abnormalities at autopsy. When pasteurized whole milk was used, deficiency symptoms began to appear, wrist stiffness being the first sign. The substitution of skim milk for whole milk intensified the deficiency which was characterized by great emaciation and weakness before death....At autopsy the muscles were found to be extremely atrophied, and closely packed, fine lines of calcification ran parallel to the fibers. Also calcification occurred in other parts of the body. When cod liver oil replaced carotene in the diet, paralysis developed quickly. The feeding of raw cream cured the wrist stiffness."
—Annual Review of Biochemistry, Vol. 18, Page 435. (1944).
In The Lancet, page 1142, May 8, 1937 it is shown that chilblains are practically eliminated (result of higher calcium values of raw milk or improved assimilation of calcium) when raw milk rather than pasteurized milk is used in the diet of children.
PASTEURIZATION DESTROYS VITAMIN A
"...According to S. Schmidt-Nielsen and Schmidt-Nielson (Kgl. Norske Videnskab. Selsk. Forhandl., 1:126-128, abstracted in Biological Abstracts, 4:94, 1930), when milk pasteurized at 63 degrees C. (145 degrees F.) was fed to mature rats, early death or diminished vitality resulted in the offspring. This was attributed to the destruction of Vitamin A."
—Krauss, W.E., Erb, J.H. and Washburn, R.G. Studies on the nutritive value of milk, II. "The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 9, January, 1933.
PASTEURIZATION DESTROYS VITAMIN B COMPLEX
"Pasteurization of milk destroys about 38% of the B complex according to Dutcher and his associates..."
—Lewis, L.R., The relation of the vitamins to obstetrics, American Journal of Obstetrics and Gynecology, 29.5:759. May, 1935.
"Mattick and Golding, 'Relative value of Raw and Heated Milk in Nutrition,' in The Lancet (220:662-667) reported some preliminary experiments which indicated that pasteurization destroys some of the dietetic value of milk, including partial destruction of Vitamin B1. These same workers found the raw milk to be considerably superior to sterilized milk in nutritive value."
—Krauss, W. E., Erb, J. H. and Washburn, R.G., "Studies on the nutritive value of milk, II. The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 7, January, 1933.
"...On the 7.5 cc. level two rats on raw milk developed mild polyneuritis toward the end of the trial; whereas three rats on pasteurized milk developed polyneuritis early, which became severe as the trial drew to a close. On the 10.0 cc. level none of the rats on raw milk developed polyneuritis, but three on pasteurized milk were severely afflicted."
—Ibid, page 23.
"Using standard methods for determining vitamins A, B, G and D, it was found that pasteurization destroyed at least 25% of the vitamin B in the original raw milk."
—Ibid, page 30.
PASTEURIZATION DESTROYS VITAMIN C
...The pasteurization of milk has been found to destroy 20 to 50 percent (of the Vitamin C), the first month of life. The reasonable procedure, therefore, appears to be to use pasteurized milk to insure protection against disease germs of various kinds and to supply the vitamin deficiency through other foods.The success in infant feeding based on this principle is evinced especially in the amazing reduction in infant mortality in the summer months."
—Jordan, E.O., A Textbook of General Bacteriology, Twelfth Edition, Revised, page 691, W. B. Saunders Co., 1938.
"Within the past few years an increasing number of patients affected with scurvy have been brought to the Oregon Children's Hospital. As the prophylactic amount of Vitamin C (15 mg. daily) is contained in 300 cc. of breast milk, scurvy is rarely found in breast-fed babies. "The vitamin C of cow's milk is largely destroyed by pasteurization or evaporation."
—Overstreet, R.M., Northwest Medicine, June, 1938, as abstracted by Clinical Medicine and Surgery, "The Increase of Scurvy," 42, 12:598, December, 1938.
"Samples of raw, certified , certified Guernsey and certified vitamin D milks were collected at the different dairies throughout the city of Madison. These milks on the average are only a little below the fresh milks as recorded in Table I, indicating that commercial raw and certified milks as delivered to the consumer lose only a small amount of their antiscorbutic potency. Likewise, samples of commercial pasteurized milks were collected and analyzed. On an average they contained only about one-half as much ascorbic acid as fresh raw milks and significantly less ascorbic acid than the commercial unpasteurized milks.
"It was found that commercial raw milks contained an antiscorbutic potency which was only slightly less than fresh raw milks and that pasteurized milks on the average contained only one-half the latter potency. Mineral modification and homogenization apparently have a destructive effect on ascorbic acid."
—Woessner, Warren W., Evehjem, C.A., and Schuette, Henry A., "The determination of ascorbic acid in commercial milks," Journal of Nutrition, 18,6:619-626, December, 1939.
Reprint No. 7, Lee Foundation for Nutritional Research
Milwaukee, Wisconsin
Publication Date: 12/11/39
Pasteurization was also found to affect the hematogenic and growth-promoting properties of the special milk (raw milk from specially fed cows, whose milk did not produce nutritional anemia—whereas commercially pasteurized milk did). . .
—Krauss, W. E., Erb, J.H. and Washburn, R. G., Studies on the nutritive value of milk II. "The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 11, January, 1933.
Resistance to tuberculosis increased in children fed raw milk instead of pasteurized, to the point that in five years only one case of pulmonary TB had developed, whereas in the previous five years, when children had been given pasteurized milk, 14 cases of pulmonary TB had developed.
—The Lancet, page 1142, May 8, 1937
Human or cow milk added to an equal volume of agar did not support the growth or allowed only slight growth of B. diphtheriae Staph. aureus, B. coli, B. prodigiosus, B. pyocyaneus, B. anthracis, streptococci, and unidentified wild yeast. The factors in human milk inhibiting bacterial growth ('inhibins') were inactivated by heating at 56 degrees C. (pasteurization temperatures of 60-70 degrees C.) for thirty minutes or by standing twelve to twenty-four days at 5 degrees C., but not by repeated freezing and thawing. The 'inhibins' in cow's milk were not inactivated by heating at 80 degrees C. for seven minutes but were destroyed by heating at 85 degrees C. for seven minutes. Attempts have not been made to identify the natural antiseptics.
—Dold, H., Wizaman, E., and Kleiner, C., Z. Hyt. Inf., "Antiseptic in milk," The Drug and Cosmetic Industry, 43,1:109, July, 1938.
"Milk, an animal product, is the essential food of all infant mammals. Mammals are so classified in the scale of living things because of the common characteristic of the female nursing her young. The infant mammal is accordingly carnivorous in his natural habits irrespective of whether the adult of the species is herbivorous or carnivorous.
"If the adults on a carnivorous diet show conditions of deficiency on cooked meat, is it not reasonable to suppose that growing infants on entirely cooked carnivorous diets will do likewise? Many experimenters, such as Catel, Dutcher, Wilson, and others, have shown such to be the case in animals fed on pasteurized milk. . .
"Can human infants be born of mothers who are deficient, and yet attain a fair degree of skeletal development if given a proper raw milk supply? The three infants in figure 4 were born of mothers known to by hypothyroid. Prior to the birth of the infants shown, all three mothers had given birth to children within three years. Each of the previous children was asthmatic, showed infantile rickets, and possessed poor skeletal development. The first child shown in Figure 4 was breast fed from birth, with the mother living under excellent health-promoting conditions. The second child was on powdered milk for four weeks, and on raw certified milk after that without cod-liver oil or orange juice. Both the first and second child began supplemental feedings when they were about five months old and were very healthy babies. The third baby was always sickly and had been on formulae since birth. These formulae included powdered milk, pasteurized milk, boiled milk, boiled certified milk and canned milk. She had suffered from severe gastric distress during her entire infancy and when eight months old she developed asthma. She is very small though her parents are of larger build than the parents of the other two children.
"The strictest bacteriologic standards for milk must always be maintained. The feeding of cattle should receive greater attention. It should be determined experimentally, if possible, whether health and resistance are undermined by pasteurization. If so, in our attempt to protect the child from milk-borne infections, we may be denying his heritage of good health by removing from his milk vitamins, hormones, and enzymes that control mineral assimilation and promote body development and general resistance to disease. Is it also possible that these same elements are as important to the adult invalid who needs milk as to the infant?
"Let us have closer cooperation between raw-milk producers and public-health officials so that the growth-producing factors of raw milk can be studied. We cannot afford to pasteurize milk if it is found that pasteurization diminishes the potency of the growth-promoting factors that determine the skeletal development of our children. We cannot afford to lessen the resistance of our children to respiratory infection, asthma, bronchitis and the common cold when factors preventing them are present in greater amounts in properly clean raw milk than in pasteurized milk."
—Pottenger, F. M. Jr., "Clinical and experimental evidence of growth factors in raw milk," Certified Milk, January, 1937.
"Some have questioned whether pasteurized milk is really involved in the production of scurvy. The fact, however, that when one gives a group of infants this food for a period of about six months, instances of scurvy occur, and that a cure is brought about when raw milk is substituted, taken in conjunction with the fact that if we feed the same number of infants on raw milk, cases of scurvy will not develop--these results seem sufficient to warrant the deduction that pasteurized milk is a causative factor. The experience in Berlin, noted by Newmann (Newmann, H., Deutsch. Klin., 7:341, 1904) and others, is most illuminating and convincing in this connection. In 1901 a large dairy in that city established a pasteurizing plant in which all milk was raised to a temperature of about 60 degrees C. After an interval of some months infantile scurvy, was reported from various sources throughout the city. Neumann writes about the situation as follows:
'Whereas Heubner, Cassel and myself had seen only thirty-two cases of scurvy from 1896 to 1900, the number of cases suddenly rose from the year 1901, so that the same observers—not to mention a great many others—treated eighty-three cases in 1901 and 1902.'
An investigation was made as to the cause, and the pasteurization was discontinued. The result was that the number of cases decreased just as suddenly as they had increased..."
—Hess, A. F., "Infantile Scurvy, V. A study of its pathogenesis," Am. J Dis. Child., November, 1917.
"Although pasteurized milk is to be recommended on account of the security which it affords against infection, we should realize that it is an incomplete food. Unless an antiscorbutic, such as orange juice, ....or potato water is added, infants will develop scurvy on this diet. This form of scurvy takes some months to develop and may be termed subacute. It must be considered not only the most common form of this disorder, but the one which passes most often unrecognized. In order to guard against it, infants fed exclusively on a diet of pasteurized milk should be given antiscorbutics far earlier than is at present the custom, even as early as at the end of the first month of life."
—Hess, A. F., "Infantile Scurvy. III. Its influence on growth (length and weight)," Am. J. Dis. Child., August, 1916.
"One of the most striking clinical phenomenon of infantile scurvy is the marked susceptibility to infection which it entails--the frequent attacks of 'grippe,' the widespread occurrence of nasal diphtheria, the furunculosis of the skin, the danger of pneumonia in advanced cases..."
—Hess, A. F., "Infantile Scurvy. V. A study of its pathogenesis," Am. J. Dis. Child., November, 1917.
"...Recently, Minot and his colleagues came to the conclusion that adult scurvy can be precipitated by infectious processes; in other words, that latent scurvy can by this means be changed to manifest scurvy. In general, therefore, investigations in the laboratory as well as clinical observations are in agreement in stressing the interrelationship of scurvy and bacterial infection."
—Hess, A. F., "Recent advances in knowledge of scurvy and the antiscorbutic vitamin," J.A.M.A., April 23, 1932.
This illustrates the futility of pasteurization of milk to prevent infection from diseases the cows may sometimes have, such as undulant fever. The infant is then made subject to the common infectious diseases, and deaths from these common diseases are not attributed, as they should be, to the defective nature of the milk.
EFFECTS OF PASTEURIZATION OF MILK ON TOOTH HEALTH
The Lancet, page 1142, May 8, 1937 says that in children the teeth are less likely to decay on diet supplemented with raw milk than with pasteurized milk.
"Dr. Evelyn Sprawson of the London Hospital has recently stated that in certain institutions children who were brought up on raw milk (as opposed to pasteurized milk) had perfect teeth and no decay. Whether this was due actually to the milk being unheated, or possibly to some other, quite different and so far unrecognized cause, we cannot yet say; but we may be sure of one thing, that the result is so striking and unusual that it will undoubtedly be made the subject of further inquiry."
—Harris, L.J., Vitamins in Theory and Practice, page 224, Cambridge, University Press, 1935.
EFFECT OF PASTEURIZATION OF MILK ON GROWTH
...Fisher and Bartlett "point out by statistical treatment that the response in height to raw milk was significantly greater than that to pasteurized milk. Their interpretation of the data led to the assertion that the pasteurized milk was only 66 per cent effective as the raw milk in the case of boys and 91.1 per cent as effective in the case of girls in inducing increases in weight, and 50.0 per cent as effective in boys and 70.0 per cent in girls in bringing about height increases."
—Krauss, W. E., Erb, J. H. and Washburn, R.G., "Studies on the nutritive value of milk, II." "The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 8, January 1933.
...Daniels and Loughlin observed that young rats fed long heat-treated milks, evaporated, condensed, and pasteurized by the 'hold' method failed to grow normally, but if the precipitated calcium salts were incorporated into the various milk, growth was normal..."
—Daniels, A.L., and Loughlin, R., Journal of Biological Chemistry, 44.381, 1920, as abstracted by Holmes and Pigott, "Factors that influence the anti-rachitic value of milk in infant feeding," Oil & Soap, 12.9:202-207, September, 1935.
CALCIUM AVAILABILITY IN PASTEURIZED MILK
"Kramer, Latzke and Shaw (Kramer, Martha M., Latzke, F., and Shaw, M.M., A Comparison of Raw, Pasteurized, Evaporated and Dried Milks as Sources of Calcium and Phosphorus for the Human Subject, Journal of Biological Chemistry, 79:283-295, 1928) obtained less favorable calcium balances in adults with pasteurized milk than with 'fresh milk' and made the further observation that milk from cows kept in the barn for five months gave less favorable calcium balances than did 'fresh milk' (herd milk from a college dairy)."
—Krauss, W. E., Erb, J.H., and Washburn, R.G., "Studies on the nutritive value of milk, II. The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 8, January, 1933.
"Guinea pigs fed raw milk with an addition of skim milk powder, copper and iron salts, carotene, and orange juice grew well and showed no abnormalities at autopsy. When pasteurized whole milk was used, deficiency symptoms began to appear, wrist stiffness being the first sign. The substitution of skim milk for whole milk intensified the deficiency which was characterized by great emaciation and weakness before death....At autopsy the muscles were found to be extremely atrophied, and closely packed, fine lines of calcification ran parallel to the fibers. Also calcification occurred in other parts of the body. When cod liver oil replaced carotene in the diet, paralysis developed quickly. The feeding of raw cream cured the wrist stiffness."
—Annual Review of Biochemistry, Vol. 18, Page 435. (1944).
In The Lancet, page 1142, May 8, 1937 it is shown that chilblains are practically eliminated (result of higher calcium values of raw milk or improved assimilation of calcium) when raw milk rather than pasteurized milk is used in the diet of children.
PASTEURIZATION DESTROYS VITAMIN A
"...According to S. Schmidt-Nielsen and Schmidt-Nielson (Kgl. Norske Videnskab. Selsk. Forhandl., 1:126-128, abstracted in Biological Abstracts, 4:94, 1930), when milk pasteurized at 63 degrees C. (145 degrees F.) was fed to mature rats, early death or diminished vitality resulted in the offspring. This was attributed to the destruction of Vitamin A."
—Krauss, W.E., Erb, J.H. and Washburn, R.G. Studies on the nutritive value of milk, II. "The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 9, January, 1933.
PASTEURIZATION DESTROYS VITAMIN B COMPLEX
"Pasteurization of milk destroys about 38% of the B complex according to Dutcher and his associates..."
—Lewis, L.R., The relation of the vitamins to obstetrics, American Journal of Obstetrics and Gynecology, 29.5:759. May, 1935.
"Mattick and Golding, 'Relative value of Raw and Heated Milk in Nutrition,' in The Lancet (220:662-667) reported some preliminary experiments which indicated that pasteurization destroys some of the dietetic value of milk, including partial destruction of Vitamin B1. These same workers found the raw milk to be considerably superior to sterilized milk in nutritive value."
—Krauss, W. E., Erb, J. H. and Washburn, R.G., "Studies on the nutritive value of milk, II. The effect of pasteurization on some of the nutritive properties of milk," Ohio Agricultural Experiment Station Bulletin 518, page 7, January, 1933.
"...On the 7.5 cc. level two rats on raw milk developed mild polyneuritis toward the end of the trial; whereas three rats on pasteurized milk developed polyneuritis early, which became severe as the trial drew to a close. On the 10.0 cc. level none of the rats on raw milk developed polyneuritis, but three on pasteurized milk were severely afflicted."
—Ibid, page 23.
"Using standard methods for determining vitamins A, B, G and D, it was found that pasteurization destroyed at least 25% of the vitamin B in the original raw milk."
—Ibid, page 30.
PASTEURIZATION DESTROYS VITAMIN C
...The pasteurization of milk has been found to destroy 20 to 50 percent (of the Vitamin C), the first month of life. The reasonable procedure, therefore, appears to be to use pasteurized milk to insure protection against disease germs of various kinds and to supply the vitamin deficiency through other foods.The success in infant feeding based on this principle is evinced especially in the amazing reduction in infant mortality in the summer months."
—Jordan, E.O., A Textbook of General Bacteriology, Twelfth Edition, Revised, page 691, W. B. Saunders Co., 1938.
"Within the past few years an increasing number of patients affected with scurvy have been brought to the Oregon Children's Hospital. As the prophylactic amount of Vitamin C (15 mg. daily) is contained in 300 cc. of breast milk, scurvy is rarely found in breast-fed babies. "The vitamin C of cow's milk is largely destroyed by pasteurization or evaporation."
—Overstreet, R.M., Northwest Medicine, June, 1938, as abstracted by Clinical Medicine and Surgery, "The Increase of Scurvy," 42, 12:598, December, 1938.
"Samples of raw, certified , certified Guernsey and certified vitamin D milks were collected at the different dairies throughout the city of Madison. These milks on the average are only a little below the fresh milks as recorded in Table I, indicating that commercial raw and certified milks as delivered to the consumer lose only a small amount of their antiscorbutic potency. Likewise, samples of commercial pasteurized milks were collected and analyzed. On an average they contained only about one-half as much ascorbic acid as fresh raw milks and significantly less ascorbic acid than the commercial unpasteurized milks.
"It was found that commercial raw milks contained an antiscorbutic potency which was only slightly less than fresh raw milks and that pasteurized milks on the average contained only one-half the latter potency. Mineral modification and homogenization apparently have a destructive effect on ascorbic acid."
—Woessner, Warren W., Evehjem, C.A., and Schuette, Henry A., "The determination of ascorbic acid in commercial milks," Journal of Nutrition, 18,6:619-626, December, 1939.
Reprint No. 7, Lee Foundation for Nutritional Research
Milwaukee, Wisconsin
Publication Date: 12/11/39
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