Excerpt from "The Perfect Health Diet":
Peroxidizability is zero for saturated fats and almost zero for monounsaturated fats, but high among polyunsaturated fats.
Lipid peroxidation is extremely dangerous, for two reasons:
• It is a cascading process; as in an avalanche, peroxidation of one PUFA leads to peroxidation of many more.
• Peroxidation of PUFA generates highly toxic compounds, such as aldehydes, which mutate DNA, oxidize LDL, and turn proteins into advanced lipoxidation end products (ALEs).
Due to the abundance of PUFA in the body, their extreme fragility, and the highly toxic nature of their peroxidation products, PUFA peroxidation is a central factor affecting health and longevity. Peroxidative damage to mitochondria causes serious health problems:
• Damage to mitochondria in skeletal muscle—the chief disposal organ for excess omega-6 fats—leads to rapid fatigue and decreased physical endurance. These in turn lead to reduced physical activity and contribute to obesity.
• Damage to liver mitochondria leads to liver disease.
Peroxidative damage to LDL particles creates oxidized LDL, a major factor in atherosclerosis. The rate of lipid peroxidation appears to be a dominant factor controlling longevity in animals. The more PUFA animals have in their membranes, the shorter their life span. Here is how the “peroxidation index” of membranes relates to life span across a number of animal species:
[[ graph ]]
The lower the peroxidation index, the longer the maximum life span. If PUFA are so dangerous, why do our bodies keep them around? There are two main reasons:
• Some biological processes function best in flexible PUFA-rich membranes. Saturated fats, which lack carbon double bonds, are rigid, which is why beef fat (which is full of saturated fat) is white and solid at room temperature. PUFA bend and twist at their double bonds and are liquid, flexible, and slippery. (Next time you have fresh salmon, get some of the oil on your hands and feel how slippery it is.) Neurons and retinal cells, in particular, need PUFA-rich membranes. Cold-water fish such as salmon and arctic char have a lot of PUFA in order to maintain flexible membranes at cold body temperatures.
• The body uses the fragility of highly unsaturated fatty acids (HUFA)—PUFA with four or more double bonds—to sense when something is awry. For instance, infections and immune activity generate oxidative stress, and the body uses oxidated HUFA to sense and regulate the local level of oxidative stress. Oxidation of omega-6 HUFA detects infections and stimulates an inflammatory immune response; oxidation of omega-3 HUFA detects excessive inflammation and tamps it down. The body carefully regulates the amount of HUFA in membranes to preserve the integrity of this signaling.
SCIENCE OF THE PHD (Perfect Health Diet)
Life Span Extension with a PUFA-Restricted Diet
No other factor accounts for variations in life span as well as the rate of lipid peroxidation. A study of the reasons why rats live at most five years, while pigeons live up to thirty-five years, concluded:
The only substantial and consistent difference that we have observed
between rats and pigeons is their membrane fatty acid composition,
with rats having membranes that are more susceptible to damage.
Diet can modify the peroxidation index. In mice, calorie restriction extends life span and lowers the peroxidation index. The reduction in peroxidation index and the increase in life span exactly track the interspecies relationship. This is exciting, because it suggests that dietary interventions that reduce polyunsaturated fat content of membranes can
extend human life span.
The Peak Health Range for Omega-6 Fats
As we did with carbs, we’ll let biology guide us to the optimal intake. You’ll recall that when carb intake is too low, the body manufactures glucose from protein; when carb intake is too high, the body converts carbs to fat. The neutral carb intake, where the body neither manufactures nor destroys glucose, is the optimal carb intake.
Something similar happens with PUFA. Omega-6 and omega-3 fats cannot be manufactured, but the body can regulate PUFA abundance in tissue by controlling whether they are burned for energy and can regulate HUFA levels in membranes by controlling whether PUFA are lengthened and desaturated into HUFA.
Omega-6 Benefits End: The Bottom of the Peak Health Range
On omega-6-deficient diets, omega-6 fats are conserved and rarely oxidized for energy. Reduced oxidation of omega-6 fats indicates that dietary omega-6 intake is too low. Another sign of PUFA deficiency is a failure of the body to achieve optimal levels of HUFA in membranes. This failure to achieve optimal HUFA levels causes dysregulation of immune function and generates the clinical symptoms of omega-6 or omega-3 deficiency. When dietary PUFA intake increases from zero, PUFA are rapidly converted to membrane HUFA until the membrane HUFA levels reach their
optimum. From that point, membrane HUFA levels plateau; cells resist adding more HUFA to their membranes. Additional dietary PUFA are burned for energy.
Only a small amount of dietary PUFA is necessary to prevent a deficiency:
• Judged by the dietary omega-6 intake at which tissue levels of arachidonic acid (an omega-6 HUFA) plateau, omega-6 deficiencies are eliminated by 1 to 2 percent of calories as omega-6 fats if the diet has no omega-3 fats and by just 0.3 percent of calories as omega-6 fats if the diet has over 1 percent omega-3 fats. Thus, a little omega-3 fat in the diet reduces the requirement for omega-6 fat.
• Omega-3 fat deficiency can be relieved, bringing DHA in the liver to normal levels, by eating as little as 0.2 percent of calories as omega-3 fats. Thus, the peak health range for PUFA can be entered by consuming as little as 1 percent of energy as PUFA (0.5 percent each of omega-6 and omega-3). Even on unbalanced diets, 2 percent of energy as PUFA will achieve optimal membrane HUFA levels.
Omega-6 fats constitute 2 percent or more of most natural foods, so on plant-and-animal-food diets it is impossible to become deficient in omega-6 fats, unless some medical condition such as cystic fibrosis prevents fat digestion. Absolute omega-3 deficiencies are also rare.
Although deficiency of omega-6 fats in general is almost impossible, it is possible to achieve a deficiency of omega-6 HUFA, such as arachidonic acid, under oxidative stress. High levels of immune activity generate oxidative stress, and if the diet is deficient in antioxidants, depletion of AA may follow, generating classic omega-6 deficiency symptoms such as eczema.
Omega-6 Toxicity: The Upper End of the Peak Health Range
As omega-6 intake increases above optimal levels, the body begins to preferentially oxidize omega-6 fats ahead of other fats. This is an effort to dispose of excess omega-6.
On nearly all modern diets, omega-6 fats are preferentially oxidized. An ingested omega-6 fatty acid is three times more likely to be burned for energy than an ingested saturated fatty acid. Moreover, omega-6 fats are not completely oxidized to carbon dioxide and water; rather, most omega-6 fats are partially oxidized and then reassembled into cholesterol and saturated fat. This increases the number of omega-6 fats that can be disposed within the limits to mitochondrial energy production and transforms the dangerous and useless omega-6 fatty acids into safer and more useful cholesterol and saturated fatty acids.
The crossover point—the “natural intake” level at which omega-6 fats are equally likely as saturated and monounsaturated fats to be burned for energy—is not known, but it probably occurs with not more than 3 percent of energy as PUFA.
Looking instead at HUFA levels in tissue, intake of 1 to 4 percent of calories as omega-6 fats enables the body to optimize HUFA ratios. However, when omega-6 intake exceeds 4 percent of energy, tissue levels of omega-6 DGLA and omega-3 EPA are suppressed. DGLA is a long-chain omega-6 fat, but one that moderates the inflammatory effects of AA. Due to this effect, omega-6 consumption above 4 percent of energy increases AA-to-DGLA and AA-to-EPA ratios with inflammatory effects.
A number of toxicity effects appear with omega-6 intake above 4 percent of calories. This omega-6 intake has been shown to reduce EPA and DHA levels in pregnant mothers. In piglets, 1.2 percent omega-6 consumption with adequate omega-3 leads to healthy brain development, but increasing omega-6 intake to 10.7 percent of calories deprives brains of DHA and compromises neurodevelopment.
Four percent of calories as omega-6 fats is the threshold of health impairment.Further problems appear when omega-6 fat intake reaches 6 percent of calories. At this intake level, oxidation can’t remove the omega-6 fats fast enough, and they start to build up in the body, especially in adipose tissue.
Accumulation of omega-6 fats in adipose tissue is observed in clinical trials. In the Finnish Mental Hospital Study, over four years on a diet rich in soybean oil, participants’ omega-6 fats rose from 10.2 percent of adipose tissue fats to 32.4 percent. In the Los Angeles Veterans Administration Study, on a diet that was 15 percent omega-6 by calories, participants’ adipose tissue omega-6 levels rose from 10 percent at the start of the study to 33.7 percent over a five-year period.
A similar accumulation of omega-6 in adipose tissue has occurred in Americans over the last fifty years, according to data assembled by Stephan Guyenet of the University of Washington. Here’s how it looks:
[[ graph ]]
The circles mark the percentage of body fat that is linoleic acid (the major omega-6 fat); the crosses mark the fraction of 18- to 29-year-olds who are obese. The obesity epidemic began at the same time, or a few years after, omega-6 fats began accumulating in Americans’ bodies. Americans currently obtain 9 percent of calories as omega-6 fats, their adipose fats are 23.4 percent omega-6, and fully a quarter of 18- to 29-year-olds are obese. Back in 1961, omega-6 fats made up 5.8 percent of the diet, adipose fats were about 9 percent omega-6, and obesity was rare.
It appears that when dietary omega-6 intake exceeds 6 percent of energy, omega-6 fats start to accumulate in adipose tissue, and obesity often follows.
It’s a safe bet that 6 percent of energy as omega-6 fats is far above the peak health range.
Health Effects of Omega-6 Toxicity
Americans are now getting 9 percent of their energy as omega-6 fats, and toxicity begins at 4 percent of energy; so we ought to be able to see negative effects from this excess. And we do. As a result of their excessive intake of omega-6 fats, Americans are experiencing elevated rates of liver disease, atherosclerosis, obesity, allergies and asthma, mental illness, bowel disorders, and cancer, not to mention elevated mortality rates. Let’s look at some of the evidence.
Liver Disease Caused by High-PUFA Diets
Polyunsaturated fats—both omega-6 and omega-3—readily produce liver disease when eaten in conjunction with fructose or alcohol, which increase oxidative stress in the liver. High PUFA intake (say, from soybean oil or corn oil) is a prerequisite for liver disease, while low-PUFA diets (say, with coconut oil or butter) prevent liver disease.
Here is a sampling of studies in which PUFA destroyed and SaFA rescued the health of lab animals’ livers:
• Researchers induced fatty liver disease in mice by feeding diets deficient in key nutrients. One diet provided 34 percent of calories as corn oil, the other as coconut oil. (Corn oil is 57 percent omega-6 PUFA, while coconut oil is 2 percent omega-6 PUFA and 92 percent SaFA.) The mice fed corn oil had severe liver damage, but “histological scores demonstrated significantly less steatosis, inflammation and necrosis in SaFA-fed mice of all mouse strains.”
• Researchers induced liver disease by feeding mice a combination of alcohol and omega-3-rich fish oil. They then stopped the alcohol and split the mice into two groups, one fed fish oil plus glucose, the other SaFA-rich palm oil plus glucose. Livers of the fish oil group failed to recover, but the palm oil group “showed near normalization.” The researchers hailed SaFA as “a novel treatment for liver disease.”
• A study compared a high-carb corn oil diet (62 percent of calories as carbs, 21 percent as corn oil, 17 percent as protein) with low-carb coconut oil or butter diets (17 percent of calories as carbs, 71 percent as coconut oil or butter, 12 percent as protein). Mice eating the coconut oil and butter diets maintained healthy livers despite nutrient deficiencies that normally induce liver disease, while mice on the high-carb corn oil diet developed severe disease.
• Scientists induced liver disease in mice by feeding alcohol plus corn oil. They then substituted a saturated fat–rich mix based on beef tallow and coconut oil for 20 percent, 45 percent, and 67 percent of the corn oil. The more saturated fat, the healthier the liver.
• Mice fed 27.5 percent of calories as alcohol developed severe liver disease and metabolic syndrome when given a corn oil diet, but no disease at all when given a SaFA-rich cocoa butter diet. (the first line of this paper reads, “the protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known”—yet somehow this knowledge has eluded many nutritionists.)
It goes on..... But I'm getting bored of copying this in. You could probably find a PDF of this somewhere online if you searched...