Missed my morning FaceBook post due to a 90+ mile bike ride, but it served as motivation for what to write about today.
One of the amino acids which even the most nutritionally ignorant among us has heard of is tryptophan. After all, that's what makes you sleepy after that turkey dinner on Thanksgiving, right? Well, not exactly. But that's not my point.
Tryptophan is the precursor for the neurotransmitter 5-hydroxytryptamine (5-HT), which is involved in fatigue. It's also one of the primary amino acids released when muscle is catabolized during times when fuel is inadequate to meet the demands placed on an organism's physiology. In the case of my group ride this morning, there were many examples of people getting tired. Some of those cyclists could blame their training, of course. Others, however, need to consider how their fueling strategy--both on AND
off the bike--might be contributing to their fatigue at a given intensity/duration. When glucose levels/glycogen stores are not sufficient to keep muscle (along with free fatty acids, primarily in the form of PUFAs) from being catabolized to fuel the activity, performance of the activity will suffer or stop altogether.
And if you think about it, it's simply another ingenious example of the body trying to survive. The body believes that fuel is scarce. It has no idea you could simply stop at the next convenience store and buy a coke or, better yet, some o.j. But since you won't stop, you body stops you. Or slows you down--anything it can do to spare the body's limited resources. And it has a lot of built in safeguards at play in these conditions just in case. From the production of serotonin (not the happy hormone you've been led to believe) to the inhibition of glucose utilization via the Randle Cycle, the body's gonna win this one. So you can live to ride another day.
And this time, maybe you'll fuel yourself appropriately.
Original Source: http://www.nzherald.co.nz/lifestyle/news/article.cfm?c_id=6&objectid=11613993
Vegetarianism can lead to heart disease and cancer
By Sarah Knapton 2:38 PM Wednesday Mar 30, 2016
Long term vegetarianism can lead to genetic mutations that raise the risk of heart disease and cancer, scientists have found.
Populations who have had a primarily vegetarian diet for generations were found to be far more likely to carry DNA that makes them susceptible to inflammation.
Scientists in the US believe that the mutation occurred to make it easier for vegetarians to absorb essential fatty acids from plants.
But it has the knock-on effect of boosting the production of arachidonic acid, which is known to increase inflammatory disease and cancer. When coupled with a diet high in vegetable oils - such as sunflower oil - the mutated gene quickly turns fatty acids into dangerous arachidonic acid.
The finding may help explain previous research which found vegetarian populations are nearly 40 per cent more likely to suffer colorectal cancer than meat eaters, a finding that has puzzled doctors because eating red meat is known to raise the risk.
Researchers from CornellUniversity in the US compared hundreds of genomes from a primarily vegetarian population in Pune, India to traditional meat-eating people in Kansas and found there was a significant genetic difference.
"Those whose ancestry derives from vegetarians are more likely to carry genetics that more rapidly metabolise plant fatty acids," said Tom Brenna, Professor of Human Nutrition at Cornell.
"In such individuals, vegetable oils will be converted to the more pro-inflammatory arachidonic acid, increasing the risk for chronic inflammation that is implicated in the development of heart disease, and exacerbates cancer. The mutation appeared in the human genome long ago, and has been passed down through the human family."
To make the problem worse, the mutation also hinders the production of beneficial Omega 3 fatty acid which is protective against heart disease. Although it may not have mattered when the mutation first developed, since the industrial revolution there has been a major shift in diets away from Omega 3 - found in fish and nuts - to less healthy Omega 6 fats - found in vegetable oils.
"Changes in the dietary Omega 6 to Omega 3 balance may contribute to the increase in chronic disease seen in some developing countries," added Dr Brenna. "The message for vegetarians is simple. Use vegetable oils that are low in omega-6 linoleic acid such as olive oil." (I would add that avoidance of PUFAs in general is a good strategy, replacing them in the diet with saturated fat from quality sources).
The mutation is called rs66698963 and is found in the FADS2 gene which controls the production of fatty acids in the body.
Previous studies have shown that vegetarianism and veganism can lead to problems with fertility by lowering sperm counts. (Nature doesn’t want to perpetuate weakness. Thus, anytime one’s vitality sinks below the level where one can positively contribute to the gene pool, the ability to procreate is compromised or lost entirely).
Separate research from Harvard University also found that a diet high in fruit and vegetables may impact fertility because men are consuming high quantities of pesticides.
Many vegetarians also struggle to get enough protein, iron, vitamin D, vitamin B12 and calcium which are essential for health. One study found that vegetarians had approximately five percent lower bone-mineral density (BMD) than non-vegetarians.
However other research suggests vegetarianism lowers the risk of diabetes, stroke and obesity.
The new research was published in the journal Molecular Biology and Evolution
Original Study can be accessed here: http://mbe.oxfordjournals.org/content/early/2016/03/09/molbev.msw049.full.pdf+html
Positive selection on a regulatory insertion-deletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid
Long chain polyunsaturated fatty acids (LCPUFA) are bioactive components of membrane phospholipids and serve as substrates for signaling molecules. LCPUFA can be obtained directly from animal foods or synthesized endogenously from 18 carbon precursors via the FADS2 coded enzyme. Vegans rely almost exclusively on endogenous synthesis to generate LCPUFA and we hypothesized that an adaptive genetic polymorphism would confer advantage. The rs66698963 polymorphism, a 22 bp insertion-deletion within FADS2, is associated with basal FADS1 expression, and coordinated induction of FADS1 and FADS2 in vitro. Here we determined rs66698963 genotype frequencies from 234 individuals of a primarily vegetarian Indian population and 311 individuals from the U.S. A much higher I/I genotype frequency was found in Indians (68%) than in the U.S. (18%). Analysis using 1000 Genomes Project data confirmed our observation, revealing a global I/I genotype of 70% in South Asians, 53% in Africans, 29% in East Asians, and 17% in Europeans. Tests based on population divergence, site frequency spectrum and long-range haplotype consistently point to positive selection encompassing rs66698963 in South Asian, African and some East Asian populations. Basal plasma phospholipid arachidonic acid status was 8% greater in I/I compared to D/D individuals. The biochemical pathway product-precursor difference, arachidonic acid minus linoleic acid, was 31% and 13% greater for I/I and I/D compared to D/D, respectively. Our study is consistent with previous in vitro data suggesting that the insertion allele enhances n-6 LCPUFA synthesis and may confer an adaptive advantage in South Asians because of the traditional plant-based diet practice.
In 1957, a fledgling nutrition scientist at the University of Illinois persuaded a hospital to give him samples of arteries from patients who had died of heart attacks.
When he analyzed them, he made a startling discovery. Not surprisingly, the diseased arteries were filled with fat — but it was a specific kind of fat. The artificial fatty acids called trans fats, which come from the hydrogen-treated oils used in processed foods like margarine, had crowded out other types of fatty acids.
The scientist, Fred Kummerow, followed up with a study that found troubling amounts of artery-clogging plaque in pigs given a diet heavy in artificial fats. He became a pioneer of trans-fat research, one of the first scientists to assert a link between heart disease and processed foods.
It would be more than three decades before those findings were widely accepted — and five decades before the Food and Drug Administration decided that trans fats should be eliminated from the food supply, as it proposed in a rule issued last month.
Now, Dr. Kummerow (KOO-mer-ow) is still active at age 99, living a few blocks from the university, where he runs a small laboratory. And he continues to come to contrarian conclusions about fat and heart disease.
In the past two years, he has published four papers in peer-reviewed scientific journals, two of them devoted to another major culprit he has singled out as responsible for atherosclerosis, or the hardening of the arteries: an excess of polyunsaturated vegetable oils like soybean, corn and sunflower — exactly the types of fats Americans have been urged to consume for the past several decades.
The problem, he says, is not LDL, the “bad cholesterol” widely considered to be the major cause of heart disease. What matters is whether the cholesterol and fat residing in those LDL particles have been oxidized. (Technically, LDL is not cholesterol, but particles containing cholesterol, along with fatty acids and protein.)
“Cholesterol has nothing to do with heart disease, except if it’s oxidized,” Dr. Kummerow said. Oxidation is a chemical process that happens widely in the body, contributing to aging and the development of degenerative and chronic diseases. Dr. Kummerow contends that the high temperatures used in commercial frying cause inherently unstable polyunsaturated oils to oxidize, and that these oxidized fatty acids become a destructive part of LDL particles. Even when not oxidized by frying, soybean and corn oils can oxidize inside the body.
If true, the hypothesis might explain why studies have found that half of all heart disease patients have normal or low levels of LDL.
“You can have fine levels of LDL and still be in trouble if a lot of that LDL is oxidized,” Dr. Kummerow said.
This leads him to a controversial conclusion: that the saturated fat in butter, cheese and meats does not contribute to the clogging of arteries — and in fact is beneficial in moderate amounts in the context of a healthy diet (lots of fruits, vegetables, whole grains and other fresh, unprocessed foods).
His own diet attests to that. Along with fruits, vegetables and whole grains, he eats red meat several times a week and drinks whole milk daily.
He cannot remember the last time he ate anything deep-fried. He has never used margarine, and instead scrambles eggs in butter every morning. He calls eggs one of nature’s most perfect foods, something he has been preaching since the 1970s, when the consumption of cholesterol-laden eggs was thought to be a one-way ticket to heart disease.
“Eggs have all of the nine amino acids you need to build cells, plus important vitamins and minerals,” he said. “It’s crazy to just eat egg whites. Not a good practice at all.”
Dr. Robert H. Eckel, an endocrinologist and former president of the American Heart Association, agreed that oxidized LDL was far worse than nonoxidized LDL in terms of creating plaque.
But he disputed Dr. Kummerow’s contention that saturated fats are benign and that polyunsaturated vegetable oils promote heart disease. “There are studies that clearly show a substitution of saturated fats with polyunsaturated fats leads to a reduction in cardiovascular disease,” said Dr. Eckel, a professor at the University of Colorado.
Robert L. Collette, the president of the Institute of Shortening and Edible Oils, a trade association, says oil manufacturers work with their customers to take precautions against oxidation.
“Oxidation is something that consumers can detect,” he said. “Therefore, it is in everyone’s best interest to control it.”
The long arc of Fred Kummerow’s life and career illustrates the frustratingly slow pace of science and the ways in which scientific conformity can hinder the search for answers. Born in Germany just after World War I broke out, he moved to Milwaukee with his family when he was 9. His father, who worked at a cement block factory, did not have the money to send him to college, so Dr. Kummerow worked full time at a drug distribution company while attending the University of Wisconsin in the evenings. After he earned a Ph.D. in biochemistry, his first job was at Clemson University in South Carolina, where he helped prevent thousands of deaths in the South from pellagra, a disease resulting from a deficiency of vitamin B3.
His early research on trans fats was “resoundingly criticized and dismissed,” said Dr. Walter Willett, the chairman of the nutrition department at the Harvard School of Public Health, who credited Dr. Kummerow with prompting his desire to include trans fats in the Nurses’ Health Study. A 1993 finding from that study, which showed a direct link between the consumption of foods containing trans fats and heart disease in women, was a turning point in scientific and medical thinking about trans fats.
“He had great difficulty getting funding because the heart disease prevention world strongly resisted the idea that trans fats were the problem,” Dr. Willett continued. “In their view, saturated fats were the big culprit in heart disease. Anything else was a distraction from that.”
At an age when life itself is an accomplishment, Dr. Kummerow said he had no intention of stepping away from the work that has consumed him for six decades. He continues to work from home and talks daily to the two scientists who work in his lab, which receives funding from the Weston A. Price Foundation.
His wife of 70 years, Amy, died last year at age 94 from Parkinson’s disease; he has three children, three grandchildren and a great-grandchild.
He takes no medications, and his mind shows no sign of aging: He has an encyclopedic recall for names, dates and, more impressive, complex scientific concepts. After his muscles became inflamed from a blood pressure drug that he has since stopped taking, he started using a wheelchair combined with a walker.
His most significant health problem, appropriately enough, was an artery blockage at age 89 — probably a result of the inevitable effects of aging, not diet.
Bypass surgery took care of the blockage, and the fact that he now has an artery from his arm running into his heart has made him even more determined to keep working. Heart disease remains the leading cause of death for Americans, and he would like to stick around to continue funding research that will help change that.
“What I really want is to see trans fats gone finally,” he said, “and for people to eat better and have a more accurate understanding of what really causes heart disease.”
Need some advice, 3rd week in a row since changing from chemicals on ride to organic snacks and water/honey/salt that I've had difficult cycle rides. Started out great today and burnt up with leg and hip cramps at mile 40, by mile 50 very little leg power.
My Response With His Answers:
Where were the cramps exactly? Started in Thighs then hamstrings and worked it’s way to hips
We could really look at the whole week, but those are the most important meals.
What was breakfast? Freshly made organic fruit smoothie with gelatin and milk, half a bagel with peanut butter
What was dinner the night before? Lasagna
What was dinner 2 nights before? Steak, baked potato, zucchini
Are you pre-ex stretching? Not for a long period but focused on legs, arms, back, stomach
Have you been fit on the bike? Matt Cole fit me when I bought my Parlee from him in early 2014
How much time before your pre-ride meal and the start of the ride? 45 minutes
How soon do you eat once you start? Drank a bottle ever hour with water, salt, honey, started eating buffalo bites, organic blocks within 45 minutes of ride
Is VW suffering, too, or is it just you? Just me, thank God, VW is rocking it on this nutrition and on the bike/run
--I'd nix the bagel or at least the PB--the PUFA content in it inhibits the body's ability to utilize glucose (stored and brought in at dinner and bfast) as well O2 and it's also pro-inflammatory.
--noodles are gluten, I assume, and sub-optimal for those with opposable thumbs.
--beautiful--more/less what I'd do with some fruit or quality dessert at the end!
--good--just use reps before.
--most folks (especially triathletes) are quad dominant. Learning to utilize the hammies will help so the quads don't overwork, then get tight, then force the hammies to overwork, the the whole kinetic chain falls apart.
--you may find that you do better with a longer time period between the end of the last feeding and the start of training. As soon as exercise begins, blood flow to the digestive system is compromised and any calories/nutrition you could have derived from the food in the stomach becomes unavailable (or less so, depending on intensity and several other factors).
--looks pretty good. If the organic blocks are homemade, you should be fine. If commercial, look out for sunflower oil or another PUFA which would inhibit glucose utilization.
--good to know, and I'm glad (but not surprised). Now we just need to dial you in. And I hope my responses help.
Adele Hite January 13, 2015 Original source found here: http://www.westonaprice.org/health-topics/abcs-of-nutrition/the-baneful-consequences-of-the-u-s-dietary-guidelines/
The next set of Dietary Guidelines for Americans (DGA), the public health nutrition policy that directs all federal nutrition activities “including research, education, nutrition assistance, labeling, and nutrition promotion,”1 are due out in 2015. The DGA are meant to address a simple question: What should Americans eat to be healthy?2 As the 2015 Dietary Guidelines Advisory Committee (DGAC) begins to create the report that will advise any possible changes to the DGA, they appear poised to provide the same answer to that question that has proven largely ineffective for the past thirty-five years.
Although the DGAC has retreated from the recommendation that Americans reduce their intake of total fat, limits on saturated fat and cholesterol from animal products remain firmly in place and these levels may be restricted further. Thus despite the superficial movement away from reduced-fat guidance, in terms of which foods are permitted and which are restricted or forbidden, nothing has changed.
According to the 2015 DGAC, eggs, meat, butter and full-fat dairy are still to be limited or eliminated from the diet altogether. Consumption of whole grains, fruits and vegetables, lowfat or no-fat dairy, fish, and lean cuts of poultry are encouraged, and, with restrictions on fat intake relaxed, Americans will now be allowed to consume even more vegetable oil than before.
While the 2015 DGAC has acknowledged that when Americans replaced dietary fat with starches and sugars obesity rates climbed, there has been no recognition of the relationship between this phenomenon and DGA guidance. Rather, the implication remains that high rates of being overweight and obese in America are due to the fact that Americans have simply failed to comply with what the U.S. Departments of Agriculture (USDA) and Health and Human Services (DHHS)―the two government agencies in charge of the DGA―have determined is best for the public. “Poor diet and physical inactivity are the most important factors contributing to an epidemic of overweight,”3 not poor dietary recommendations based on inadequate science.
A PRIMARY MISCONCEPTION
In fact, a primary misconception in public health nutrition is that current national nutrition polices are based on scientific agreement about what constitutes a healthy diet. However from the beginning, federal dietary guidance has been based more on ideology, including romantic notions of returning to a “natural” way of eating, than science. Although nutrition science has changed dramatically in the thirty-five years since the first national dietary recommendations were issued, the recommendations themselves have remained virtually unchanged. The historical and cultural influences behind federal dietary recommendations, their controversies and their consequences, warrant a close critical examination. They demonstrate that although science and policy perform very different functions, they can be mutually reinforcing. Though this does serve to make science more political, it does not make policy more scientific.
A cascade of unintended consequences has resulted from those original dietary recommendations, guidance that remains entrenched, held in place by politics, ideology, institutional agendas, and the influence of interested industries.4,5 This entrenchment has resulted in millions of U.S. taxpayer dollars spent on nutrition policies, programs and practices that do not result in good health, while the very same taxpayers are expected to shoulder the blame for these negative outcomes.
HISTORY OF THE DGA
When the first national nutrition recommendations for the prevention of chronic disease, the 1977 Dietary Goals for Americans, were originally proposed, not only was the content of the recommendations hotly debated, the very concept of one-size-fits-all, population-wide dietary advice was itself highly controversial. The 1977 Dietary Goals introduced a diet―high in grains and cereals and low in fat, with few animal products, and vegetable oils substituting for animal fats―that was an extreme departure from what Americans were then eating. Not only was the diet recommended by the 1977 Goals a radical change for many Americans, the very idea that the federal government could know what foods were best for any given individual was a dramatic shift in how public health nutrition was understood and administered.
Before the 1977 Goals were created, the determination of which foods were “good” for you and which were “bad” was located within the family and community, rather than with the government. Packaged food did not carry a nutrition label, and government dietary guidance focused on acquisition of adequate essential nutrition, rather than the avoidance of foods that might cause chronic disease. Despite the lack of government guidance on how to prevent chronic disease through nutrition, heart disease rates had been decreasing in America since 1968,6 and in 1975, less than 15 percent of the population was considered obese.7
In many regards, the health of Americans in the 1970s had never been better. However, concerns about “lifestyle-related” diseases permeated the consciousness of much of middle class America, and food manufacturers responded accordingly. The American Heart Association (AHA) had created a national platform for a theory proposed by a physiologist named Ancel Keys, which asserted that dietary fat—especially saturated fat and cholesterol from animal products—led to heart disease. Responding to these interests, manufacturers of “heart-healthy” margarines and meat substitutes began claiming their products could reduce the risk of heart disease, although the federal government remained unconvinced.
Evidence that dietary fat and cholesterol had significant effects on heart disease was elusive, and the Federal Trade Commission repeatedly warned manufacturers not to make false and misleading claims linking food products to the prevention of heart disease.8 Although the AHA primarily aimed its fear-of-fat message at businessmen who might be lucrative donors,8 the counter-culture thinking that emerged from the social upheavals of the 1960s picked up the refrain, marrying concerns about chronic disease to anxiety about the environment and world hunger.
Earlier in the decade, a popular vegetarian cookbook by Frances Moore Lappé, Diet for a Small Planet, suggested that a meat-free diet would be low in saturated fat and cholesterol, thus reducing risk of obesity, heart disease and cancer; furthermore, Lappé asserted, a vegetarian way of life would reduce world hunger, energy costs, and environmental impacts of agriculture.9
While Frances Moore Lappé’s Diet for a Small Planet popularized vegetarian ideology, then-Secretary of Agriculture Earl Butz, an economist with many ties to large agricultural corporations, was enacting policies that encouraged the planting of large-scale, monoculture crops on all arable land.10
The “fencerow to fencerow” policies Butz initiated helped to shift farm animals from pasture land to feed lots. Making room for government-subsidized corn and soybeans would increase efficiency of food production; what didn’t go into cows could go into humans, including the oils that were a by-product of turning crops into animal feed.
The agenda of vegetarians and health reformers who urged Americans to consume fewer animal products, eat more grain and cereal products, and to substitute polyunsaturated oils found in corn and soybean oil for saturated animal fats like butter and lard, fit neatly into large agribusiness efforts to increase the market for processed foods that have a wider profit margin than eggs and meat.11
These cultural forces coalesced around Senator George McGovern’s Senate Select Committee on Nutrition and Human Needs, which was first created in order to address malnutrition in America. The work of the Select Committee had been so successful that it shifted its attention from malnutrition to “overnutrition” and focused on the creation of a report that was meant to do for diet and chronic disease what the 1964 Surgeon General’s Report had done for cigarettes and cancer.12 This work took on renewed urgency and significance as the committee’s tenure seemed about to come to an end.13 Such a report would address the public’s growing fears about obesity and chronic disease and policymakers’ concerns about rising health care costs―and perhaps extend the lifespan of the committee itself.14
During the summer of 1976, the committee conducted a series of hearings, entitled “Diet Related to Killer Diseases,” from doctors and scientists specifically chosen for their willingness “to talk about eating less fat, eating less sugar, eating less meat.”15 The title of the hearings and the experts chosen to testify set the direction for their findings. In early 1977, the committee released the Dietary Goals for Americans, blaming what they saw as an “epidemic” of killer diseases—obesity, diabetes, heart disease and cancer—on changes in the American diet that had occurred in the previous fifty years, specifically the increase in “fatty and cholesterol-rich foods.”16
The report claimed that in order to reduce their risk of chronic disease, Americans should reduce their intake of food that contained fat, particularly saturated fat and cholesterol from animal products like meat, whole milk, eggs and butter, and instead consume more grains, cereals, vegetable oils, fruits, and vegetables. These particular recommendations reflected not only concerns related to health, but the “back-to-nature” ideology that was becoming increasingly popular with regard to food and diet. The committee used material from Diet for a Small Planet, along with research on vegetarian diets, to argue that a shift to plant-based protein could reduce intake of calories, cholesterol and saturated fat, as well as reduce blood pressure, risk of cancer, use of natural resources, and food costs.16 This message gave official sanction to the romantic notion that a plant-based diet could not only prevent chronic disease, but feed the hungry and save the planet.
These recommendations were met with vehement objections from scientists, doctors, and public health professionals, who argued that the recommendations were scientifically unsound and potentially harmful.17 Those who supported the Dietary Goals felt the proposed radical change in the American diet presented no risk to the health of the American people.16 In contrast, the American Medical Association said, “The evidence for assuming that benefits to be derived from the adoption of such universal dietary goals . . . is not conclusive and there is potential for harmful effects from a radical long-term dietary change as would occur through adoption of the proposed national goals.”18 Yet this warning went unheeded, and the controversy over the Dietary Goals had little effect on future USDA/ DHHS recommendations. With few changes, the 1977 Goals became the first Dietary Guidelines for Americans in 1980. The DGA have since become a powerful policy document, although the limitations that have afflicted them since the beginning have resulted in several unintended negative consequences.
The controversy surrounding the original 1977 Dietary Goals took shape along several lines. Critics raised doubts regarding the appropriateness of a single, population-wide dietary prescription, applied to all individuals regardless of level of risk, to prevent diseases that were not established as nutritional in nature.19 In addition, they made strenuous objections to the fact that these recommendations had not been tested for safety or efficacy and would be the equivalent of conducting a population-wide dietary experiment.20
Critics of the report pointed to the report’s “new age, neo-naturalist” stance, noting that the nutrition scientists at the Department of Health, Education, and Welfare (now the DHHS), who urged caution in the face of the limited science on nutrition and chronic disease, could not compete with this popular ideology either for public support or for government funds for additional research.21
That the creators of the 1977 Goals had used a thin veneer of science to support their preconceived notions of what diet was best for Americans was evident in the contradictory nature of the report’s own data. For example, the 1977 Goals suggested consumers should increase vegetable oil consumption. However, dissenting scientists pointed out that increased consumption of vegetable oils and decreased consumption of saturated fats were, according to data supplied by the 1977 Goals themselves, associated with increased levels of heart disease.17 As a result of this shaky scientific foundation, significant scientific controversy continues about some of the original and current assertions upon which the DGA recommendations are built. These can be seen generally as an on going inability to firmly establish the connections between dietary patterns and chronic disease with available methodology. More specifically, controversy continues to surround the theories that 1) dietary fat, saturated fat, and cholesterol cause heart disease, obesity, diabetes and cancer and should be replaced in the diet with polyunsaturated vegetable oils; 2) a diet high in carbohydrates will reduce the risk of chronic disease; and 3) excessive sodium intake is the primary variable in the etiology of hypertension, a risk factor for heart disease.
The case against saturated fat and cholesterol has been particularly difficult to maintain in the face of evidence to the contrary that has accumulated in the past three decades. When the first DGA were created, there was no agreement regarding the relationship of diet to blood lipids and atherosclerosis. The reasons given then for the difficulty in clarifying the relationship were “the complicated nature of this disease, as well as the multitude of contributing factors and their relationships.”22 Large observational and intervention studies conducted early in the history of the DGA, such as the Framingham study, Multiple Risk Factor Intervention Trial, and the National Diet-Heart Study, are frequently cited as proving that a lowfat, low-cholesterol diet reduces risk of heart disease, yet the results from these studies are weak or inconclusive with regard to the relationship between diet and the development of heart disease.23-26 The science since that time remains inconsistent, limited, and open to question.
In 1997, Ancel Keys, the scientist whose theories about dietary cholesterol and heart disease first warned Americans away from meat and eggs, acknowledged, “There’s no connection whatsoever between cholesterol in food and cholesterol in the blood. None. And we’ve known that all along.”27 Studies cited by the 2010 DGAC Report demonstrate varied metabolic responses to lowered dietary saturated fat, with certain subpopulations exhibiting adverse rather than improved health outcomes.3 Two recent comprehensive meta-analyses indicate that saturated fat is not linked to heart disease.28,29 In fact, in a definitive review of forty-eight clinical trials, with over sixty-five thousand participants, the reduction or modification of dietary fat had no effect on mortality, cardiovascular mortality, heart attacks, stroke, cancer, or diabetes.30 Yet, avoiding saturated fat remains a cornerstone of national dietary guidance. Surveys show that the vast majority of Americans have come to believe that consuming animal fats increases one’s risk of heart disease, and many try to limit their intake of foods that contain these fats.31
UNDERMINING INDEPENDENT FARMERS
The 1977 Dietary Goals did more than change the health beliefs of Americans. They affected all aspects of the food environment. That the 1977 Goals would have a powerful effect on the food industry was apparent even before they were finalized, but it is unlikely that the result was the intended one. While the initial hearings were being held, members of McGovern’s committee were warned that the food industry would respond with an explosion of products designed to meet whatever new dietary standards were established.32 With the creation of the 1977 Goals, the federal government had unmistakably designated who the “winners” and “losers” in the food sector would be. The “winners” would be manufacturers of breads, cereals, margarine, cooking oils, and soy products; “losers” would be producers of meats, butter, eggs and cheese.
Experts recognized at the time that many processed food manufacturers could “reformulate existing products to remove their allegedly deleterious nutritional effects,” something that would be very difficult for farmers who produced eggs and meat.33 To compound the advantage, for “food producers and processors whose product categories are favored by the goals, greater promotional emphasis on the nutrition value of these products may be expected. In effect products can be promoted using the national dietary goals as a ‘stamp of approval’ to gain greater acceptance in an increasingly nutrition-conscious marketplace.”33 The group most likely to be hurt by the new paradigm was not food processors but farmers: “The farmers feel especially threatened . . . because their livelihood could be most directly affected by the recommended changes. As the primary element in the food chain, farmers tend to be the most specialized and do not enjoy the flexibility and insulation of a multi-product line food processor.”33
Indeed, since the advent of the first DGA, the amount of money farmers receive for food produced has fallen by half.34 As consumers adopted eating patterns recommended in the DGA, a much larger share of their food dollar went to increased processing and marketing and the labor costs associated with these activities. Since the DGA encourages Americans to consume fewer of the products that generate a higher farm value―in other words, what the farmer is paid for the product that leaves the farm―and more of the products that generate a lower farm value, farmers overall receive less of each dollar spent on food in America. For example, the farm value of eggs, a food the DGA tells Americans to limit, is worth 54 percent of the consumer’s dollar. Instead, the DGA recognizes cereal as a preferred “healthy” breakfast; its farm value is worth only 8 percent of the consumer’s dollar.
Conventional arguments that promote plant-based diets as the most beneficial for health, the environment, and feeding the world neglect to address the way in which those diets are compatible with the agricultural policies that benefit large agricultural corporations and undermine the interests of farmers. Creating a more “democratic, socially and economically just, and environmentally sustainable” food system that supports farmers may need to begin with a reassessment of what foods may be considered nourishing.35
INCREASING CHRONIC DISEASES
With federal nutrition directives to avoid saturated fat and cholesterol driving food manufacturing and consumer demand, eating patterns in America have changed dramatically since the first DGA were created. Consumers, whether they were interested in reducing the saturated fat content of their diet or not, were faced with food choices that had changed according to the DGA. As a result, despite accusations that they have ignored federal dietary advice, Americans have increased their intake of flour and cereal products and the vegetable oils that could be added to them, changes that are in line with DGA recommendations. Consumption data gathered from national health surveys indicate that virtually all of the increase in calories in the past 30 years has come from carbohydrate foods (starches and sugars such as would be found in flour and cereal products), while calories from saturated (animal) fats have decreased.36 While these changes are in line with recommendations from the DGA, they may have transformed the American diet in ways incompatible with good health.
In 1988, a vegetarian-oriented food activist group, Center for Science in the Public Interest (CSPI), warned the American public against the dangers of saturated fat and campaigned for the food industry to switch from beef tallow and lard to partially hydrogenated vegetable oil—specifically soybean oil. This is the kind of oil that is now associated with harmful trans fats. But in 1988, CSPI insisted trans fats were an improvement over saturated fat from animals.37 Oil seed companies were prepared with the technology to make this switch; Earl Butz’s agricultural policies provided plenty of the soybeans needed to create the oils that would be partially hydrogenated. Thus, far from resisting this change, “nearly all targeted firms responded by replacing saturated fats with trans fats.”37 For consumers, CSPI’s successful campaign meant that natural animal fats that cause no danger to health were replaced with highly-processed and harmful trans fats―whether t he public w anted t hose changes or not.
Surplus corn provided another substitute for saturated fats in the form of high-fructose corn syrup (HFCS). As Dr. Robert Lustig, an endocrinologist specializing in obesity has noted, “When you take the fat out of a recipe, food tastes like cardboard, and you need to replace it with something— that something being sugar.”38 HFCS offered a cheap, plentiful, sugary replacement for the animal fats that Americans were now told to avoid. For example, “fat-free” yogurt, sweetened with HFCS, appeared on grocery store shelves, as a “healthy” alternative to full-fat yogurt.
In time, scientists on the 2000 DGAC realized that the emphasis on reducing fat in the diet could lead to “adverse metabolic consequences” resulting from a high intake of sugars and starches.39 They went on to note that “an increasing prevalence in obesity in the United States has corresponded roughly with an absolute increase in carbohydrate consumption.”32 At least some of that increase in carbohydrate consumption came from the HFCS that replaced saturated fats in food.
Obesity was not the only thing that increased in prevalence since the creation of the first DGA. In fact, trends indicate that, since 1980, the rates of many chronic diseases have increased dramatically. Prevalence of heart failure and stroke has increased significantly.6 Rates of new cases of all cancers have gone up.40 Rates of diabetes have tripled.41 In addition, although body weight is not in itself a measure of health, as the 2000 DGAC noted, rates of overweight and obesity have increased as Americans have adopted the eating patterns recommend by the DGA.7
In all of these categories, the health divide between black and white Americans has persisted or worsened, with black Americans especially negatively affected by the increase in diabetes. When following DGA recommendations, African-American adults gain more weight than their Caucasian counterparts, and low-income individuals have increased rates of diabetes, hypertension, and high cholesterol.42,43 Despite adherence to healthy eating patterns as determined by the DGA, studies have shown that African-American children remain at higher risk for development of diabetes and prediabetic conditions.44 African-Americans are almost twice as likely to have diabetes as non- Hispanic white Americans, and these differences in health outcomes have not been adequately explained by social and economic disparities in these populations.45 Long-standing differences in environmental, genetic and metabolic characteristics may mean recommendations that are merely ineffective in preventing chronic disease in white, middle-class Americans and are in fact detrimental to the long-term health of black and low-income Americans.
ADEQUATE ESSENTIAL NUTRITION
While on the one hand the DGA have failed to prevent chronic disease, on the other hand they have also failed to provide Americans with guidance in accordance with obtaining adequate essential nutrition. Before the 1977 Dietary Goals were created, federal dietary recommendations focused on foods Americans were encouraged to eat in order to acquire adequate nutrition, not on food components to limit or avoid in order to prevent chronic disease.46 Meat, eggs, butter and whole milk were considered important sources of essential nutrients, and avoiding saturated fat in food was considered a “questionable dietary practice” adopted by “food faddists.”47 During World War II, meat and fats were considered such valuable sources of nutrition that Americans back home were asked to save them for the troops and eat fish and vegetables instead. In fact, prior to the creation of the DGA, Americans got about 36 percent of their calories from grains, fruits, and vegetables and over 50 percent of their calories from meat, eggs, cream, cheese, and fat.48
From the beginning, scientists were concerned that recommendations warning people to limit their intake of foods that were traditionally considered to be highly nutritious would adversely affect intake of essential nutrients. In response to the 1977 Dietary Goals, one scientist argued that “there are serious nutritional problems that affect many Americans that are clearly related to dietary inadequacies, particularly of high-quality protein . . . implementation of your recommendations could have a negative effect on these problems.”17
In fact, research has found that following DGA recommendations can have a detrimental impact on intake of essential nutrition. A 2013 study demonstrated that sodium restrictions in the 2010 DGA are “incompatible with potassium guidelines and with nutritionally adequate diets, even after reducing the sodium content of all foods by 10 percent.”49 The reduced-fat diet recommended by the DGA has also been linked to lower intakes of several important essential nutrients. In one study, lower fat intake was associated with lower intake of nine out of fourteen important micronutrients, independent of calorie intake.50
Choline, which was not recognized as an essential nutrient until after the first DGA were created, plays an important role in brain development in fetuses, and adequate amounts are important for the prevention of liver disease, atherosclerosis, and neurological disorders.51 Current average intakes of choline are far below established adequate levels.40 Scientists have suggested that, “Given the importance of choline in a wide range of critical functions in the human body, coupled with the less than optimal intakes among the population, dietary guidance should be developed to encourage the intake of choline-rich foods.”40 However, consumption of eggs and meat, two foods that are rich in choline, is restricted by current DGA recommendations that limit intake of cholesterol and saturated fat.
NARROW APPROACH TO NUTRITION AND HEALTH
In 1977, the Dietary Goals acknowledged that “genetic and other individual differences mean that these guidelines may not be applicable to all.”16 However, this qualification has been muted in subsequent DGA. Although it is clear that good nutrition plays an important role in long-term health, when the first DGA were created the particular dietary pattern that would be optimal for achieving lifelong health was unclear; that is still the case today. Early critics of the Guidelines felt that the scientific model used to address nutrient deficiencies did not apply to chronic diseases such as heart disease and cancer.52 Scientists thirty years later express similar concerns, adding that “nutrient-based metrics [of current recommendations] are hampered by imprecise definitions and inconsistent usage,” and “few individuals can accurately gauge daily consumption of calories, fats, cholesterol, fiber or salt.”53 However, current Guideline recommendations urge Americans to track food and calorie intake as means of achieving a healthy diet.3
Furthermore, the DGA have institutionalized the idea that overweight and obese people are different from “normal”—establishing, as part of national dietary policy, the notion that they are less likely to accurately or honestly report on their own eating habits. The 2010 DGA indicate that, on the basis of national survey data, Americans do not seem to be consuming excessive amounts of calories. Thus the inexplicably high rates of obesity in America must be due to the fact that people who are overweight or obese lie about how much they eat: “[T]he numbers are difficult to interpret because survey respondents, especially individuals who are overweight or obese, often underreport dietary intake.”3
This moralistic approach to obesity and weight loss has contributed to extensive and unrecognized “collateral damage” in the form of fat-shaming, eating disorders, weight discrimination, and poor health from restrictive food habits. At the same time, researchers at the Centers for Disease Control have shown that overweight and obese people are often as healthy as their “normal” weight counterparts.54
Finally, the emphasis on plant-based nutrition and the demonization of animal-based foods is a culturally biased perspective. Although the 2010 DGA claim that the recommendations they contain “accommodate the varied food preferences, cultural traditions and customs of the many and diverse groups who live in the United States,”27 this is most certainly not the case. Animal products containing saturated fat are an important part of many food cultures: sausages of Eastern European and Chinese cuisine; ghee, the clarified butter of Indian cuisine; chorizo and eggs from Latin America; liver patés eaten by Jewish Americans; greens and fatback of Southern and soul food traditions.
As a dietitian, I was taught to respect the preferences of those who choose vegetarian or vegan diets. However, when it comes to animal products, dietitians, in accordance with the DGA, are encouraged to engage in “pork-shaming,” counseling people on how to eliminate, limit, or modify traditional foods in order to avoid saturated fat and cholesterol. As a dietitian, I found that people who were told to give up their traditional dishes, or to change them in ways that reduced saturated fat and cholesterol, were very likely to give up those dishes altogether; substitutions were not as good as the “real thing” and for a reason. For example, in Southern U.S. cooking, salt pork cuts the bitter taste of greens and fatback provides a vehicle for flavor as well as for fat-soluble vitamins. Greens made with little or no fat may actually be less nutritious; certainly they are if people don’t eat them.
FAILURE TO FULFILL THE ORIGINAL MANDATE
The first DGA, created in 1980 without a specific legislative mandate, began as a very simple twenty-page, one-column booklet directed at consumers. However, it became apparent in the decade following the release of the first DGA that obesity rates in America had increased, despite the fact that Americans were making alterations to their diets in line with their recommendations.55,56 In light of these circumstances, the DGA needed not only to explain the noted discrepancies between behavior and outcome, but should attempt to prevent further negative changes in the health of Americans. In 1990, Congress passed a law indicating that DGA should be reviewed and reissued every five years, emphasizing that: “Each such report shall contain nutritional and dietary information and guidelines for the general public,. . . and shall be based on the preponderance of the scientific and medical knowledge which is current at the time the report is prepared [emphasis mine].”57
However, the DGA have never been able to overcome their original shaky scientific foundations. They have grown in size, right along with the waistlines of Americans, but have failed to improve health outcomes. Over the years, the seven recommendations from the 1980 DGA became twenty-three complicated instructions to micromanage food components in the 2010 DGA. As a result, the DGA are considered too complex for consumers to use and are instead meant for policymakers and healthcare professionals, who “translate” the DGA for consumers.
Both the lack of science and the lack of simplicity that current DGA exhibit are violations of their legislative mandate. At the same time, the DGA have become a powerful and influential document that goes far beyond providing information to consumers. These recommendations shape all government dietary guidance, dictate nationwide nutrition standards, influence agricultural policies and nutrition research protocols, direct how food manufacturers target consumer demand, guide healthcare practices, and affect how the American public thinks about diet, weight, and health. They can be considered the most influential health-related pronouncements in the world.
The 2015 DGAC has made sustainability and environmental concerns part of its agenda, indicating that one of their goals is to “develop dietary guidance that supports human health and the health of the planet.”58 There is no mistaking the fact that protecting the environment and ensuring a sustainable food supply are important issues. In fact, they are far too important to be entrusted to a committee of nutrition scientists with little knowledge or expertise in the vast and complex interactions that make up the American agriculture and food production system. The American public has already been subject to the unintended effects of policy established by the USDA and DHHS without the support of sufficient evidence. The world simply cannot withstand the consequences if the DGA’s impact on the environment is similar to its impact on obesity and chronic disease.
WHAT CAN BE DONE INSTEAD?
In 1977, the Dietary Goals presented a single perspective on food and health to the public as if it were a commonsense approach to nutrition grounded firmly in science and applicable to all Americans. This was not the case. However, there is such an approach available to the leadership at USDA and DHHS. Dietary recommendations that focus on a food-based guidance that assists Americans in acquiring adequate essential nutrition is based in solid, non-controversial science and is equally applicable to all Americans. Although scientific understanding of essential nutrition is not complete by any means, it is nevertheless supported by evidence that has stood the test of time with little controversy. All Americans require essential nutrition; without exception, inadequate intake results in diseases of deficiency. It is not necessary to eliminate, restrict or modify culturally traditional foods under the essential nutrition paradigm.
Focusing on essential nutrition is an approach that includes and celebrates a wide variety of food traditions. Such guidance would shift the focus of public health nutrition towards general health and wellness, and away from weight and other surrogate markers like cholesterol levels and blood pressure, leaving those areas of concern for the healthcare setting. Importantly, guidance that emphasizes adequate essential nutrition would be clear, concise, and useful to the general public. Contradictory messages about nutrition―unavoidable when most dietary guidance lacks a strong scientific basis because it simply echoes the DGA―have led to widespread general confusion and a lack of confidence in the science of nutrition.59 The proliferation of “food rules” that stem from DGA guidance have left many consumers frustrated by the feeling that the standards for “healthy eating” are unreachable, even as they strive to meet those standards.60 DGA recommendations based on adequate essential nutrition from wholesome, nourishing foods would not only provide the foundation for good health, they would finally provide what has been missing from the past thirty-five years of federal nutrition policy: dietary guidance that works―for all Americans.
1. U.S. Department of Agriculture, Center for Nutrition Policy and Promotion. 2010 Dietary Guidelines for Americans Backgrounder: History and Process [Internet]. 2011 [cited 2011 Jan 31]. Available from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/ Backgrounder.pdf
3. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2010 [Internet]. 7th ed. Washington, DC: U.S. Government Printing Office; 2011 [cited 2010 Jan 31]. Available from: http://www.cnpp.usda.gov/DGAs2010-Policy-Document.htm
4. Taubes G. Good calories, bad calories: challenging the conventional wisdom on diet, weight control, and disease. New York: Knopf; 2007.
5. Teicholz N. The Big Fat Surprise: Why meat, butter, and cheese belong in a healthy diet. New York: Simon & Schuster; 2014.
6. National Heart, Lung, and Blood Institute. Morbidity and Mortality: 2007 Chart Book on Cardiovascular, Lung, and Blood Diseases [Internet]. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; 2007 [cited 2011 Sep 24]. Available from: http:// www.nhlbi.nih.gov/resources/docs/07-chtbk.pdf
7. Ogden CL, Carroll MD. Prevalence of overweight, obesity, and extreme obesity among adults: United States, trends 1976-1980 through 2007-2008. [Internet]. Hyattsville, MD: National Center for Health Statistics; 2010 Jun [cited 2011 Sep 1]. Available from: http://www.cdc.gov/nchs/data/ hestat/obesity_adult_07_08/obesity_adult_07_08.pdf
8. Levenstein H. Fear of Food: A history of why we worry about what we eat. Chicago: Univ Of Chicago Press; 2013.
9. Lappé FM. Diet for a Small Planet. 10th anniversary ed., completely rev. & updated. New York: Ballantine Books; 1982. 496 p.
10. Butz EL. An Emerging, Market-Oriented Food and Agricultural Policy. Public Adm Rev. 1976 Mar;36(2):137.
11. Pyle G. Raising less corn, more hell: the case for the independent farm and against industrial food.1st ed. New York: Public Affairs; 2005. 229 p.
12. Oppenheimer GM, Benrubi ID. McGovern’s Senate Select Committee on Nutrition and Human Needs Versus the: Meat Industry on the Diet-Heart Question (1976–1977). Am J Public Health. 2013 Nov 14;104(1):59–69.
13. Austin JE, Hitt C. Nutrition intervention in the United States: cases and concepts. Cambridge, Mass: Ballinger Pub. Co; 1979. 387 p.
15. Peretti J, Sahota M. The Men Who Made Us Fat. BBC Two; 2012.
16. Select Committee on Nutrition and Human Needs of the United States Senate. Dietary goals for the United States [Internet]. 2nd ed. Washington: U.S. Government Printing Office; 1977 [cited 2013 Aug 1]. Available from: http://catalog.hathitrust.org/Record/000325810
17. Select Committee on Nutrition and Human Needs, United States Senate. Dietary Goals for the United States: Supplemental Views. Washington, D.C.: U.S. Government Printing Office; 1977.
18. American Medical Association. Dietary goals for the United States: statement of The American Medical Association to the Select Committee on Nutrition and Human Needs, United States Senate. R I Med J. 1977 Dec;60(12):576–81.
19. Harper AE. Dietary goals-a skeptical view. Am J Clin Nutr. 1978 Feb;31(2):310–21.
20. Weil WB Jr. National dietary goals. Are they justified at this time? Am J Dis Child 1960. 1979 Apr;133(4):368–70.
21. Broad W. Jump in funding feeds research on nutrition. Science. 1979 Jun 8;204(4397):1060–1.
22. Jacobson NL. The Controversy over the Relationship of Animal Fats to Heart Disease. BioScience. 1974 Mar;24(3):141–8.
23. Smil V. Coronary Heart Disease, Diet, and Western Mortality. Popul Dev Rev. 1989 Sep;15(3):399. 24. Truswell AS. Some problems with Cochrane reviews of diet and chronic disease. Eur J Clin Nutr. 2005 Aug;59 Suppl 1:S150–4; discussion S195–6.
25. Multiple risk factor intervention trial. Risk factor changes and mortality results. Multiple Risk Factor Intervention Trial Research Group. JAMA 1982 Sep 24;248(12):1465–77.
26. The National Diet-Heart Study Final Report. Circulation. 1968 Mar;37(3 Suppl):I1–428.
27. Rosch PJ. Cholesterol does not cause coronary heart disease in contrast to stress. Scand Cardiovasc J. 2008 Jan 1;42(4):244–9.
28. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk. Ann Intern Med. 2014 Mar 18;160(6):398–407.
29. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr. 2010 Mar 1;91(3):502–9.
30. Hooper L, Summerbell CD, Thompson R, Sills D, Roberts FG, Moore H, et al. Reduced or modified dietary fat for preventing cardiovascular disease. In: The Cochrane Collaboration, Hooper L, editors. Cochrane Database of Systematic Reviews [Internet]. Chichester, UK: John Wiley & Sons, Ltd; 2011 [cited 2013 May 29]. Available from: http://doi.wiley.com/10.1002/14651858.CD002137.pub2
31. Eckel RH, Kris-Etherton P, Lichtenstein AH, Wylie-Rosett J, Groom A, Stitzel KF, et al. Americans’ Awareness, Knowledge, and Behaviors Regarding Fats: 2006-2007. J Am Diet Assoc. 2009 Feb;109(2):288–96.
33. Austin JE, Quelch JA. US national dietary goals: Food industry threat or opportunity? Food Policy. 1979 May;4(2):115–28.
34. Sexton R. Market Consolidation Poses Challenges for Food Industry. Calif Agric. 2002 Oct;56(5):146.
35. Wilkins JL. Eating Right Here: Moving from Consumer to Food Citizen. Agric Hum Values. 2005 Sep 1;22(3):269–73.
36. Wright J, Kennedy-Stephenson J, Wang C, McDowell M, Johnson C. Trends in Intake of Energy and Macronutrients —- United States, 1971—2000. Morb Mortal Wkly Rep. 2004 Feb 6;53(4):80–2.
37. Schleifer D. The perfect solution. How trans fats became the healthy replacement for saturated fats. Technol Cult. 2012 Jan;53(1):94–119.
39. Dietary Guidelines Advisory Committee. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2000 [Internet]. Washington, D.C.: U.S. Department of Agriculture and U.S. Department of Health and Human Services; 2000 Feb [cited 2012 Apr 12]. Available from: http://www.health.gov/dietaryguidelines/dgac/pdf/dgac_ful.pdf
40. Jemal A, Murray T, Ward E, Samuels A, Tiwari RC, Ghafoor A, et al. Cancer Statistics, 2005. CA Cancer J Clin. 2005;55(1):10–30.
41. Centers for Disease Control and Prevention. Number (In Millions) of Civilian, Noninstitutionalized Persons with Diagnosed Diabetes, United States, 1980-2011 [Internet]. National Center for Chronic Disease Prevention and Health Promotion, Division of Diabetes Translation; [cited 2013 Apr 12]. Available from: http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm
42. Zamora D, Gordon-Larsen P, Jacobs DR Jr, Popkin BM. Diet quality and weight gain among black and white young adults: the Coronary Artery Risk Development in Young Adults (CARDIA) Study (1985-2005). Am J Clin Nutr. 2010 Oct;92(4):784–93.
43. Ben-Shalom Y, Fox MK, Newby PK. Characteristics and Dietary Patterns of Healthy and Less- Healthy Eaters in the Low-Income Population. U.S. Department of Agriculture, Food and Nutrition Service, Office of Research and Analysis; 2012 Feb.
44. Lindquist CH, Gower BA, Goran MI. Role of dietary factors in ethnic differences in early risk of cardiovascular disease and type 2 diabetes. Am J Clin Nutr. 2000 Mar;71(3):725–32.
45. Kurian AK, Cardarelli KM. Racial and ethnic differences in cardiovascular disease risk factors: a systematic review. Ethn Dis. 2007;17(1):143–52.
46. McNutt K. Dietary Advice to the Public: 1957 to 1980. Nutr Rev. 1980 Oct;38(10):353–60. 47. Jalso SB, Burns MM, Rivers JM. Nutritional beliefs and practices. J Am Diet Assoc. 1965 Oct;47(4):263–8.
48. LeBovit C, Cofer E, Murray J, Clark F. Dietary Evaluation of Food Used in Households in the United States. Household Economic Research Division, Agricultural Research Service, U.S. Department of Agriculture; 1961. Report No.: 16.
49. Maillot M, Monsivais P, Drewnowski A. Food pattern modeling shows that the 2010 Dietary Guidelines for sodium and potassium cannot be met simultaneously. Nutr Res N Y N. 2013 Mar;33(3):188–94.
50. Obarzanek E, Hunsberger SA, Van Horn L, Hartmuller VV, Barton BA, Stevens VJ, et al. Safety of a fat-reduced diet: the Dietary Intervention Study in Children (DISC). Pediatrics. 1997 Jul;100(1):51–9.
51. Zeisel SH, da Costa K-A. Choline: An Essential Nutrient for Public Health. Nutr Rev. 2009 Nov;67(11):615–23.
52. Harper A. Killer French Fries. Sciences. 1988;28:21–7. 53. Mozaffarian D, Ludwig DS. Dietary guidelines in the 21st century—a time for food. JAMA. 2010 Aug 11;304(6):681–2.
54. Flegal KM, Kit BK, Orpana H, Graubard BI. Association of all-cause mortality with overweight and obesity using standard body mass index categories: A systematic review and meta-analysis. JAMA. 2013 Jan 2;309(1):71–82.
55. Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL. Increasing prevalence of overweight among us adults: The national health and nutrition examination surveys, 1960 to 1991. JAMA. 1994 Jul 20;272(3):205–11.
56. Nestle M, Porter DV. Evolution of federal dietary guidance policy: from food adequacy to chronic disease prevention. Caduceus Spring. 1990;6(2):43–67.
57. 101st Congress. National Nutrition Monitoring and Related Research Act of 1990. Sect. 301, 101- 445 Oct 22, 1990.
58. Nelson M, Abrams S, Brenna T, Hu F, Millen B. Subcommittee 5: Food Sustainability and Food Safety. 2015 Dietary Guidelines Advisory Committee; 2014 Jan.
59. Nagler RH. Steady diet of confusion: Contradictory nutrition messages in the public information environment. Diss Available ProQuest. 2010 Jan 1;1–301.
60. Brenton J. In Pursuit of Health: Mothers, Children, and the Negotiation of an Elusive Ideal [Internet]. [Raleigh, North Caroline]: North Carolina State University; 2014. Available from: http://www.lib.ncsu.edu/resolver/1840.16/9541
Facebook and PUFAs Posted on September 10, 2014, 0 Comments
So a buddy of mine posted a clip from the movie Fed Up. I haven't seen the movie, but I'm sure I agree with the majority of it. However, the bit my friend put on his page showed the effects of sugar on the brain and compared it to the effects of cocaine on the brain. Coming to the defense of this poor maligned substance, I posted:
Another sensationalist (and, thus, interesting to watch) demonizing of sugar. Glucose is the body's preferred source of fuel and, in the presence of quality nutrition, is therapeutic. I agree that most of the processed crap can be a problem. But if your caloric needs warrant it, and your overall diet is supported by appropriate levels of nutrition, even some of these "foods" can be well tolerated. Also, your brain's pleasure centers activate/light up when exposed to other stimuli like sex or exercise, so I'd take that clip with a grain of salt. But that's probably another nutrient that's being bashed by filmmakers who understand more about what makes good entertainment than what makes for good nutrition.
Somebody else, let's call him--well, let's call him Josh, because that's his name--Josh chimed in with "those are a lot of if's [sic], Andrew. Processed sugar (what doesn't appear naturally in food) is a key ingredient in obesity, cancer, and heart disease in in the world."
Known for my brevity, I replied with: Think PUFAs primarily. Sugar is a red herring.
To which Josh with his knack for exhaustive research responded: "Polyunsaturated fats exists in all kinds of natural foods and there's zero evidence they cause anything. http://www.hsph.harvard.edu/news/magazine/sugar-and-salt/. Processed sugar (and all its refined carbohydrate relatives) on the other hand, cause the body to go into starvation mode, despite the presence of food and fat in the body. And salt causes people to eat more than they otherwise would."
and then added: "coincidentally, herring also contains polyunsaturated fats"
I hadn't written a blog post in a bit, so I thought this particular subject might make for an enlightening discussion. So here's what I wrote:
You’re right, Josh. There’s nothing in Nature which occurs in isolation. For example, coconut oil is 92.1% saturated fat. The remainder is made up of a monounsaturated fat called oleic acid (6.2%) and a polyunsaturated fat called linoleic (1.6%). Thus, I find it funny that you support such a reductionist approach to health/disease. Since the body is an integrated system of systems, don’t you think it’s a bit of a (precarious) leap to blame health/disease on any one factor?
I know you probably don’t study nutrition. You likely have a much more exciting job like practicing law—one which keeps you so busy you cannot do your own research. So I don’t blame you for regurgitating the misinformation you’ve been fed by the diet demigods. I’m actually quite impressed that you didn’t quote Wikipedia during your rebuttal. However, lipid science is quite clear on the subject of PUFAs.
They oxidize quite readily and are very heat sensitive due to the incomplete saturation of the carbon bonds with a hydrogen atom. Specifically, they are immunosuppressive, pro-inflammatory, and down regulate the thyroid. In the body they are known to kill off lymphocytes and block thymic cells (immunity). Prostaglandins are made from linoleic acid and arachidonic acid—both types of PUFAs—and are involved in inflammation. PUFAs decrease Vit E in the body. They also increase the development of alpha cells (which produce glucagon) while preventing the development of beta cells (which produce insulin). Oh, and they inhibit the body’s ability to use glucose for fuel. Can you say diabetes? I knew you could. Additionally, PUFAs interfere with the production of proteolytic enzymes—that’s a problem if you want to digest your food or dissolve any clots in the blood. PUFAs liberate estrogen from serum proteins (SHBG), too. This emancipation, however, is one you’d probably want to avoid. Increased availability/activity of estrogen is a precursor to many types of cancer (as well as PMS, endometriosis, etc). And in the form of vegetable oils or nut/seed oils, they are highly processed and VERY unnatural/unhealthy. In fact, since you love to quote somebody else’s research, here are a few studies you can check out:
Cancer can't occur, unless there are unsaturated oils in the diet. [C. Ip, et al., Cancer Res. 45, 1985.] Alcoholic cirrhosis of the liver cannot occur unless there are unsaturated oils in the diet. [Nanji and French, Life Sciences. 44, 1989.] Heart disease can be produced by unsaturated oils, and prevented by adding saturated oils to the diet. [J. K. G. Kramer, et al., Lipids 17, 372, 1983].
And here’s a very detailed bit of research you can find on my website: http://triumphtraining.com/blogs/blog/14885549-the-fallacy-of-fish-oil-part-1
And here’s a bunch of others:
Cancer Res. 1998 Aug 1;58(15):3312-9.
Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver.
Griffini P, Fehres O, Klieverik L, Vogels IM, Tigchelaar W, Smorenburg SM, Van Noorden CJ.
Nutr Cancer. 1998;30(2):137-43.
Effects of dietary n-3-to-n-6 polyunsaturated fatty acid ratio on mammary carcinogenesis in rats.
Sasaki T, Kobayashi Y, Shimizu J, Wada M, In’nami S, Kanke Y, Takita T.
J Lipid Res. 2005 Jun;46(6):1278-84. Epub 2005 Mar 16.
Role of omega-3 polyunsaturated fatty acids on cyclooxygenase-2 metabolism in brain-metastatic melanoma.
Denkins Y, Kempf D, Ferniz M, Nileshwar S, Marchetti D.
Clin Exp Metastasis. 2000;18(5):371-7.
Promotion of colon cancer metastases in rat liver by fish oil diet is not due to reduced stroma formation.
Klieveri L, Fehres O, Griffini P, Van Noorden CJ, Frederiks WM.
Am. J. Epidemiol. (2011) doi: 10.1093/aje/kwr027
Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial
Theodore M. Brasky, Cathee Till, Emily White, Marian L. Neuhouser, Xiaoling Song, Phyllis Goodman, Ian M. Thompson, Irena B. King, Demetrius Albanes and Alan R. Kristal
I have probably a couple hundred more if you’d like me to give them to you as I think your "zero evidence" statement was a bit over the top. It’ll take some time to read. But maybe by then you’ll be able to answer a question I’ve been wondering about since you threw sugar and salt under the bus with the link you posted. If sugar/salt are so bad for you, why is it the first thing physicians give you when you’re rushed into the emergency room? Since the brain’s only source of fuel is glucose, we may both might want to lay off the PUFAs while we ponder that last one.
Do I believe sugar is abused? Most definitely. But I'd encourage everyone, including those with books or diets to sell, research to publish, or agendas to push, to consider a more holistic view when it comes to nutrition. After all, like the chaos found at the edges of a hurricane, extreme views are often more destructive than they are helpful. Somewhere in the calm of the center is where the truth is often found.
Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis by B. S. Peskin
Original Article Found Here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3914521/#sec18title
14. Failure of LDL Cholesterol to Prevent CVD
It is now well known that LDL-C level, in and of itself, is not predictive of a cardiovascular event. This should not be a surprise, as the body has no plasma LDL-C sensor. This is not a “genetic defect” or oversight since the body has numerous sensors, such as for plasma blood glucose levels in nondiabetics, ranging from 70 to 90 mg/dL. This extremely tight tolerance of plasma glucose levels is 1 part in 1,000—approximately 0.1%. Since there is no hormonal-limiting metabolic factor for LDL-C, it must be viewed as a “dependent” variable, determined as a function of many other biological factors—not independent of them—as previously thought.
Studies confirm this fact. A review of a cholesterol/CVD causal effect categorically failed: among 12 populations with similar cholesterol levels clustered around “normal” levels—5.70 to 6.20 mmol per liter (220 to 240 mg per dL), the blood pressure readings and the serum cholesterol levels were not predictive of ischemic heart disease mortality . If there were a causal correlation, then a 10% reduction should have had significant positive effects; it did not. Nothing has changed today regarding LDL-C's dismal success rate in both predicting and lowering patient CVD.
15. Lipids Are Variable in Tissue Composition
The significant variable in tissue is its lipid structure. Although the genetics of a particular species precisely specify cellular structure, its lipid composition can vary significantly—in particular, when suprapharmacologic amounts of long-chain metabolites are consumed, such as the case with fish oil supplements. A pharmacologic overdose cannot completely be oxidized away for energy or otherwise. Consequently, much of “the overdose” is forced into tissue composition, causing an improper structure—often in maintaining a linear relationship as does plasma and liver and as do RBCs [44, 46, 47]. Cellular bilipid membrane structure and its LDL-C structure warrant intense investigation.
Each of the approximately 100 trillion cells in the human body consists of a bilipid membrane. Importantly, PEOs comprise 25–33% of their polyunsaturated lipids . Additionally, every mitochondrion, typically a hundred to thousands per cell, contains them, too [49, 50]. PEOs can be considered the “brick and mortar” of every cell, tissue, and organ, including mitochondria. In contrast, aside from the brain, eyes, and nervous system, most tissue and organs contain few derivatives like EPA/DHA.
16. Variability in LDL-C
The structure of LDL-C is complex. Its cholesteryl ester is key. The structure of cholesterol itself never changes, merely its esterified moiety—the acyl side chain. That is a big difference that many in the medical community may not appreciate. This is a simple condensation reaction, removing the water, catalyzed by the enzyme ACAT (acyl CoA: cholesterol acyl transferase) between a fatty acid and cholesterol. “R” symbolizes the hydrocarbon portion of the fatty acid. For example, if oleic acid were esterified with cholesterol, then R would be –C8H17=CH–C7H14 with the double bond in cis configuration.
Lipoproteins transport cholesterol and its esterified PEOs to the tissues via apoprotein B-100 (ApoB100).
Although the molecule itself may become oxidized, including its highly significant protein component (on a weight basis), that likelihood is extremely low. What is primarily oxidized are the fatty acids esterified to LDL-C comprising the majority of the lipoprotein's center. Parent omega-6 quantities of esterified LA are approximately 85% of its overall 50% fatty acid content .
16.1. Esterified Cholesterol
The cholesteryl part or cholesteryl moiety is tied to a structure that does change—particularly, its EFA-based variable “R” component (Figure 1). It is well understood that the PEO LA dominates the esterified portion of cholesterol. The majority of the cholesteryl ester component is LA (Parent omega-6) .
The cholesterol ester portion is highly significant compared to free cholesterol or phospholipids (Figure 2). Approximately 70% of the cholesterol in the lipoproteins of the plasma is in the form of cholesterol esters attached to apolipoprotein B . Of dietary cholesterol absorbed, 80%–90% is esterified with long-chain fatty acids in the intestinal mucosa .
16.2. LDL-C Is Highly Resistant to Oxidation in the Bloodstream
The fact that cholesterol itself is extremely resistant to oxidization is highly underpublicized, whereas its main esterified component, Parent omega-6 (LA), is more easily oxidized, especially ex vivo by food processing. Dietary LA that has already become oxidized prior to ingestion ex vivo is ubiquitous through processing of foods or overheating, since heating in the presence of air enhances peroxidation of PUFA glycerol esters [55, 56]. This insight suggests that looking in a new direction other than merely lowering LDL-C for the prevention of heart disease is warranted.
17. Human Antioxidant Levels Are Naturally Low
Normal antioxidant levels are lower than would be presumed to be adequate and normal if analysis were not performed in healthy patient populations as a control. The results are startling. Experiments show that the sum molar ratio of all antioxidants to PUFA is a mere 1 : 165 (0.61%), with one antioxidant molecule having to protect the large number of 165 PUFA molecules .
The total number of fatty acids bound in the different lipid classes of an LDL particle with a molecular mass of 2.5 million is on average 2,700, of which about one-half (1/2) are polyunsaturated fatty acids (PUFAs), mainly linoleic acid (Parent omega-6), with small amounts of arachidonic acid and docosahexaenoic acid (DHA). Furthermore, only minimal physical and chemical changes related to oxidation are produced by even a prolonged storage of LDL with oxygen or by incubation with low concentrations of copper ions.
Clearly, the quantity of naturally occurring antioxidants is too small for oxidation in vivo to be a significant physiologic issue [14, 51]. The sole logical conclusion is that the PUFA, in particular, LA, is being consumed and is entering the body in an already oxidized state caused by ubiquitous food processing.
18. New Insight: LDL-C Transports an Ingested “Poison”
18.1. CVD Explained: Processed Food Is the Culprit
Heating produces toxic products such as cholesterol oxides. If they are consumed—not produced in the body—they cause deleterious effects. Professor Gerhard Spiteller, who is Chairholder of Biochemistry, Institute of Organic Chemistry at the University of Bayreuth, Germany, has investigated EFAs and their degradation products—specifically, the influence of these substances on the physiology of mammals. He, too, concluded that consumption of oxidized PUFA-cholesterol esters is responsible for the initial damage to endothelial cells and that cholesterol oxidation products are incorporated into LDL cholesterol in the liver .
Given that both the cholesterol molecule itself is highly resistant to oxidation and Parent omega-6 is relatively resistant, the only acceptable conclusion is that the majority of the oxidized cholesterol damage is from its esterified component, that is, adulterated (oxidized) LA, patients unknowingly consume.
LDL then carries these toxic compounds into the endothelial walls where they cause cell damage. Injury is not caused by an increase in free cholesterol but by an increase in cholesterol esters of processed LA . In atherosclerotic patients, LDL cholesterol is altered ex vivo by oxidation, and this altered LDL is taken up in unlimited amounts by macrophages. Dead macrophages filled with cholesterol's damaged, functionally impaired esters are then deposited in arteries. LDL-C is effectively transmitting a poison, that is, nonfunctional, adulterated, and harmful LA. We can now explain why statins fail.
18.2. Statin's Failure Explained
From the pharmaceutical company's own admission, the number needed to treat (NNT) for statins is no better than 60 over a 5-year period. This means that 60 patients would need to be treated for 5 years to see 1 positive outcome—a 98.3% (59/60) failure rate. Researchers often say that the NNT is much higher (worse). For example, JUPITER had an NNT of 95, meaning a 99% failure rate .
By statin's lowering of LDL-C, its esterified PEO component is also lowered, both adulterated (good outcome) and fully functional (bad outcome). This is problematic and precisely explains why statins do not work. By focusing on the ex vivo LA that has already become oxidized prior to ingestion through processing of foods, cooking, or overheating, a solution can be found to mitigate this damage.
19. Investigating Oils with respect to Arterial Health: IOWA Screening Experiment
A seminal screening experiment was conducted in 2010 comparing the effectiveness of PEO in increasing arterial compliance (flexibility) against fish oil . This is a broad-based population screening—the most realistic population to see effectiveness, if any.
Arterial compliance is the most accurate physiologic assessment of a subject's cardiovascular health. Photoplethysmography is utilized with computer analysis of the (volumetric) curve's second derivative obtaining an acceleration curve. This output is compared to the database consisting of prior population scans grouped by age. The highly statistically significant results and excellent NNTs of IOWA confirm the theoretical predictions of both the failure of fish oil to increase arterial compliance and the significant (predictable) success of PEOs to improve arterial compliance across all populations.
19.1. Marine Oils Decrease Arterial Compliance: A Bad Outcome
The most remarkable finding was that subjects taking fish oil prior to PEOs obtained the most improvement. This was anticipated since those subjects started at a greater vascular deficit caused by the fish oil consumption.
Compared to PEOs, fish oil users had an “11-year-older” cardiovascular system as measured by arterial compliance population scans—more than a decade's additional “hardening of the arteries” compared to their physical age.
Ceasing fish oil use allowed the arterial system to revert to “normal” . Once the vascular system was back to “normal,” the expected improvement from PEOs, as shown by the other groups, was also achieved, which translated to an even greater decrease in biological age based on where they had started. Clearly, fish oil accelerates vascular aging . Marine oils are an anti-antiaging substance.
20. PEOs in Plasma, Lipids, and Esterified Cholesterol
It is necessary to analyze the Parent and derivative content of plasma lipids (lipoproteins, triglycerides, and esterified cholesterol) to determine the specific “bad actor” in CVD and cancer—every country's number 1 and number 2 killers—and confirm LA's prime importance. LDL's esterified linoleic acid is the major source for lipid peroxidation products, yet linoleic acid is highly resistant in LDL against oxidation . This is critically important to understand.
With all the focus on omega-3 series fatty acids, both Parent and derivative, it is significant to note that the free Parent fatty acids (nonesterified) in human plasma, although minute in quantity, are ordinarily composed of about 15% LA (linoleic acid, Parent omega-6) and just 1% ALA (alpha-linolenic acid, Parent omega-3) .
Derivatives such as EPA/DHA are naturally much less significant in quantity than LA. In sharp contrast to the high amounts of n-6 series PUFAs, n-3 series PUFAs account for only 1.8% of the fatty acids in triglycerides, 3.5% in the phospholipids, and only 1.7% (ALA is 0.5%) in cholesterol esters. This high preponderance of LA is pervasive throughout: the LA/ALA ratio in triglycerides is 23 : 1; n-3 PUFA makes up only 1-2% of fatty acids in plasma . Even in the brain, LA/ALA uptake is 100 times greater in favor of that of LA . In the brain, AA, an omega-6 long-chain metabolite, comprises a significant 10% of the brain's long-chain fatty acids. Of particular importance is that the triglyceride stores concentrate the important Parent omega-6 fatty acid.
20.1. Importance of Parent Omega-6 and Prostaglandin Metabolites
In human lipid physiology, Parent omega-6 and its long-chain metabolites dominate over Parent omega-3 and its long-chain metabolites. The majority of the plasma fatty acids are LA (Parent omega-6) as are the triglyceride stores (adipose tissue). The metabolites of LA—in particular, prostaglandins PGE1 and PGI2 (prostacyclin)—are significant vasodilators. PGE1 is also the body's most potent anti-inflammatory. If functional LA bioavailability is lowered, the potential for inflammation will rise, leading to atherosclerosis. Weiss, for example, has noted that PGE1 (produced from functional Parent omega-6) reduces the fibrin deposition associated with the pathogenesis of atherosclerosis . Membrane fluidity increases when more functional (undamaged) polyunsaturated fatty acids—in particular, linoleic acid—are available to incorporate into the membrane lipid bilayer.
Because LDL cholesterol is the transport vehicle for PEO delivery into the cell, LDL cholesterol will transport any LA into cells—defective or not—such as oxidized or trans entities. Mitigating the damage caused by extensive ex vivo intake of already oxidized LA is possible by supplemental ingestion of fully functional, unadulterated, nonoxidized LA.
21. Physiologic Excess of Omega-3 Series Fatty Acids Is Harmful, Decreasing Critical Omega-6 Series: Increases in CVD, Diabetes, and Cancer Are Expected
It was understood decades ago that consumed physiologic excess of omega-3 series PUFA is detrimental. Burns and Spector showed that the capacity of endothelial cells—relevant to carcinomas—and macrophages to release prostaglandins is reduced when they accumulate n-3 polyunsaturated fatty acids . This is important because prostaglandins produced from PUFAs—in particular, Parent omega-6 (LA)—reduce the adhesion of tumor cells to microvascular endothelium. Most importantly, fish oil is known to decrease critical anti-inflammatory PGE1 output in proportion to the amount of EPA/DHA consumed .
21.1. Marine Oils Raise Resting Blood Glucose Levels and Blunt the Insulin Response Causing Insulin Resistance
Diabetes has become the world's number 1 epidemic. China has recently surpassed the USA in percentages of diabetics. Spontaneous autooxidation of blood glucose is a significant cause of diabetic patients' elevated increased risk of CVD. China has recently surpassed the USA in percentages of diabetics, and their consumption of marine oils keeps rising . The negative impact marine oils have on diabetes, both Type I and Type II, is staggering.
Spontaneous autooxidation of blood glucose is a significant cause of diabetic patients' elevated increased risk of CVD, and marine oils increase plasma glucose levels. Both fish oil supplements and even “oily fish” itself are highly problematic for diabetics. In 2011, researchers looked at the effects on Type II diabetic patients consuming more fish. Only from nonfatty fish, containing more Parent omega-6 and much less EPA/DHA, did the experiment show significantly decreased blood sugar (good outcome). Further, those who ate “fatty” fish saw a decreased insulin output of 21% (bad outcome) compared to those not eating “fatty” fish .
“Fatty” fish (containing more EPA/DHA), not a supplement, caused the elevated blood glucose. EPA/DHA fish oil supplements cause elevated blood glucose and blunt the insulin response in diabetics. This deleterious finding was known years ago [68, 69]. Since “fatty/oily” fish caused the same deleterious effects as those of the supplement, the only logical conclusion is that fish oil—in any form—is harmful to any diabetic. Diabetes is America's number 1 epidemic and both oily fish and fish oil supplements exacerbate the condition. Furthermore, marine oils negatively impact the cellular membrane causing elevated insulin resistance. Because marine oils are known to displace critical Parent omega-6 in the cell membrane, this harmful effect is predictable. This issue impacts all tissue as shown below. Furthermore, it is well known cancer cells utilize glucose as their prime metabolic substrate (fuel). Oily fish and marine oil supplements—by allowing much greater blood glucose levels—both exacerbate patients' existing cancer metabolism and metastatic potential . This effect is the opposite of any treatment's desired outcome.
21.2. Potential Brain Developmental Issue: Fish Oil Displaces Critical Omega-6 Metabolites Harming Tissue Structure
Importantly, fish oil potentially damages the brains of both infants and adults because critical omega-6 series metabolites are displaced . This is another reason why fish oil failed to help Alzheimer's victims in a monumentally disappointing 2010 study . The medical journal's authors specifically warned against feeding fish oil to human infants. This experiment was performed in rodents, but the results are applicable to humans because EFA metabolism is similar and applicable to both mammals and rodents . Systemic rises in fish oil's EPA are largely compensated by decreased Parent omega-6 .
21.3. Fish Oil Causes Decreased Prostacyclin Production, Increasing CVD
Prostaglandins (hormone-like substances with extremely short half-lives not entering the bloodstream) are capable of both limiting thrombosis and reversing thrombosis in atherosclerotic patients .
Prostaglandin PGE1 is the body's most powerful anti-inflammatory and vasodilator and prostacyclin (PGI2) is a vasodilator and prevents both platelet adhesion and aggregation. These are both omega-6 metabolites.
Fish oil increases endothelial platelet aggregation in heart patients . In patients with atherosclerosis, prostacyclin (produced in endothelial tissue) biosynthesis fell by a mean of 42% during the fish-oil period (extremely bad outcome). Synthesis of the platelet agonist thromboxane A2 (produced in the platelets) declined by 58% (good outcome). This may first appear to be a reasonably successful intervention, but that analysis would be incorrect for the following reason: atherosclerotic patients require increased intimal PGI2 output, as vessel wall thrombogenicity, and not reduced platelet adhesion, is a much more significant factor for minimizing thrombosis . Furthermore, template-bleeding times were significantly prolonged in all fish-oil-consuming patients (bad outcome).
22. Association of Increased Marine Oils and Multiple Pathophysiologic Diseases
22.1. Skin Cancer Has Become Epidemic as Fish Oil Supplement Consumption Increases and Results in Epidemics of Pathophysiologic Incorporation of DHA into Epithelial Tissue
The following associative speculation about marine oil's deleterious effects in the development of epithelial-based skin cancers requires confirmation. However, the physiologic/biochemical metabolic pathways detailing this conclusion are strong. Fish oil produces a pathophysiology in epithelial tissue, potentially leading to skin cancer. Likewise, adenocarcinoma of the prostate develops from aberrant epithelial cells. Are these conditions related? Logic tells us they are. We know there are no Parent omega-3 or omega-3 derivatives like EPA/DHA naturally occurring in epithelial tissue [12, 13]; therefore, any incorporation is supraphysiologic. Epithelial tissue's long-chain fatty acid composition is exclusive to Parent omega-6 (LA).
22.2. Increased Carcinoma with Increased Marine Oil Consumption: A Causal Relationship
A very strong melanoma/fish oil consumption association warrants attention. Skin cancer rates and fish oil consumption are both increasing. This is a very troubling (worldwide) association that must be addressed. Based on established physiology, it is predictable that the countries consuming the most fish-oil supplementation will contract skin cancer and prostate cancer the most—and they do, as will be shown later in this section. There are three quantitative EFA physiologic facts that must be understood in determining the definitive cause-effect relationship with fish oil use and cancer contraction. (A) There is neither Parent omega-3 (ALA) nor omega-3 long-chain metabolites (EPA/DHA) in epithelial tissue [12, 13]. (B) Each of the body's 100 trillion cells is comprised of a lipid bilayer with very little EPA/DHA, but significant LA and ALA (25–33%)—excepting those in epithelial tissue which is exclusively comprised of Parent omega-6 only (LA) [48, 49, 74, 75]. The same is true for the mitochondrion, except containing less ALA. Again, there is a physiologically negligible amount of EPA/DHA [49, 50]. We know excess EPA/DHA displaces the main fatty acid in the membrane, Parent omega-6 (LA) . Is the (forced) incorporation of the derivatives EPA/DHA—by consumed supraphysiologic amounts—into epithelial tissue a direct cause of the increased skin cancer and therefore all epithelial-related cancers? The logical answer is yes.
Dermatologists are at a loss to explain the increase in skin cancer regardless of recommendations to their patients that they have less exposure to the sun. Human physiology strongly suggests that fish oil is a significant culprit. A seminal study in Norway revealed that fish oil significantly increased the risk of skin cancer. This is highly underpublicized, but reported in the International Journal of Cancer in 1997. Meticulous study (confirmed by pathology and cancer registry) of over 50,000 Norwegian men and women showed approximately a 3-fold increase in melanoma in women using cod liver oil (considered a superb fish oil supplement). The study was particularly strong, based on its unbiased approach, high participation and response rate, the fact that dietary data was collected prior to the onset of cancer, and the fact that each participant had a complete followup regarding occurrences of cancer, death, and emigration. In fact, all physicians and medical professionals in Norway are required to report malignant diseases to the Cancer Registry, and 98% of these cases are confirmed with microscopic tissue analysis . In Norway, where fishing is a principal industry, they did not want to see a negative finding and it was not publicized. This study shows fish oil causing or associated with an increase in cancer—not prevention of cancer.
22.3. Epithelial (Skin) Cancers
The countries with the greatest skin cancer contraction rates, after Australia, are Scandinavia, Canada, and the United States . Why is this? Marine/fish oil sales have constantly increased over the past 15 years and it has become America's number 1 supplement, and the rest of the world quickly follows America's dietary recommendations. Are these correlations mere coincidence? No. Based on the above science, they are predictable. Given that people are in the sun less and use sunscreen more, there are few valid reasons why skin cancer rates should be increasing worldwide and, in particular, these countries.
In 2010, Cancer Research published a historic article linking fish oil and increased colon cancer risk, as well as increased colitis [77, 78]. The researchers had hypothesized that “feeding fish oil enriched with DHA to mice would decrease the cancer risk,” but they found the opposite to be true. Instead, they discovered that the mice developed deadly, late-stage colon cancer when given high doses of fish oil. They observed increased inflammation and that, as a result, it only took just four weeks for the tumors to develop. This was true for mice that received the highest doses of DHA as well as those receiving lower doses. The researchers stated, “Our findings support a growing body of literature implicating harmful effects of high doses of fish oil consumption in relation to certain diseases.”
The researchers were shocked because they had relied on prior “studies,” not lipid (medical) science, to anticipate the effects of fish oil. Of particular importance was that these researchers even found low doses of fish oil to be harmful. In 2009, another significant journal article uncovered more problems with fish oil use, ultimately forcing the researchers to clearly state, “The particularly high pro-metastatic effect of dietary n-3 PUFA on S11 cells rules out the generalisation that dietary n-3 PUFA inhibit tumour growth and progression” .
22.4. Fish Oil Destroys Critical Mitochondrial Physiologic Functionality
Oncologists understand that mitochondrial functionality is a prime factor in the prevention of cancer. Yet, fish oil negatively impacts mitochondrial functionality. A seminal experiment appearing in Cancer Cell in 2006 is critical to the understanding of how fish oil causes such alarming mitochondrial damage, emphasizing that the connection is between fish oil consumption and cancer . This test was conducted on live animals, not in a petri dish. Rats were fed fish oil or beef tallow. The scientists then examined the activity of critical mitochondrial enzymes from their kidney cells. The fish-oil-fed animals suffered an incredible 85% enzyme loss, while the beef-tallow-fed animals suffered only a 45% enzyme loss.
Fish oil caused a 40% net additional reduction in critical mitochondrial enzyme production; that is, cellular respiration in the mitochondria is highly diminished. Why would this be expected with supraphysiologic amounts of marine oils? Cardiolipin structure is highly compromised, as described next.
22.5. A Key Finding: All Tumors Suffer (Often Irreversible) Respiratory Damage
In remarkable research sponsored by the National Cancer Institute and published in 2008 and 2009, researchers found major abnormalities in content or composition of a complex lipid called cardiolipin (CL), stating these abnormalities are “found in all tumors, linking abnormal CL to irreversible respiratory injury” . Cardiolipin is a fat-based complex phospholipid found in all mitochondrial membranes, almost exclusively in the inner membrane, and is intimately involved in maintaining mitochondrial functionality and membrane integrity. It is used for ATP (energy) synthesis and consists roughly of 20% lipids . Nobel Prize-winner Otto Warburg, MD, PhD, first discovered the mitochondrial impairment/cancer causation link [40, 83–85].
With dietary marine/fish oil supplementation and its EPA/DHA modification of membrane fatty acid composition, which accelerates unnatural lipid peroxidation, significant effects of oxidative damage to many and varied cellular macromolecules occur. For example, peroxidized cardiolipin in the mitochondrial membrane can inactivate cytochrome oxidase by mechanisms similar to those of hydrogen peroxide as well as mechanisms unique to organic hydroperoxides. Dr. Hulbert warns, “Lipid peroxidation should not be perceived solely as ‘damage to lipids,' but should also be considered as a significant endogenous source of damage to other cellular macromolecules, such as proteins and DNA (including mutations)” .
Furthermore, the noncharged structure of aldehydes allows their migration with relative ease through hydrophobic membranes and hydrophilic cytosolic media, thereby extending the migration distance far from the production site. On the basis of these features alone, these carbonyl compounds can be more destructive than free radicals and may have far-reaching damaging effects on target sites both within and outside membranes.
Dr. Hulbert makes the importance of mitochondrial functionality clear with his statement, “The insight that the exceptionally long-living species, Homo sapiens, potentially provides for understanding the mechanisms determining animal longevity, is that the fatty acid composition of mitochondrial membranes may be much more important than the composition of other cellular membranes” . A pharmacologic overdose of ALA metabolites exacerbates a shorter lifespan by altering the lipid (mitochondrial) membranes .
Mitochondrial cardiolipin molecules are targets of oxygen free radical attack, due to their high content of fatty acids—normally containing negligible long-chain omega-3 metabolites like DHA—unless pharmacologically overdosed as with marine/fish oil. Mitochondrial mediated ROS generation affects the activity of complex I, as well as complexes III and IV, via peroxidation of cardiolipin following oxyradical attack to its fatty acid constituents .
Most importantly, there is neither Parent omega-3 nor its metabolites in cardiolipin. Its main substrate is Parent omega-6 . Alteration of mitochondrial structure by fish oil was known in 1990 and published at that time in an article in the Proceedings of the National Academy of Science, as follows: “Phospholipase A2 activity and mitochondrial damage are enhanced when mitochondrial membranes are enriched with n-3 fatty acids [from marine/fish oil]” .
Any cancer therapy not taking into account mitochondria efficiency and physiologic structural integrity is deficient and will fail in the long term, as Nobel Prize-winner Otto Warburg, MD, PhD, clearly demonstrated [83–85]. Others have expanded on his seminal discovery with a focus on cellular oxygenation [10, 40]. As confirmation of this fact, it is well supported that hypoxia in the prostate tumor causes greater tumor aggressiveness .
23. Furan Fatty Acids: Are Furan Fatty Acids Cardioprotective and Responsible for Any Positive Effects of Fish Consumption?
In addition to abundant n-3 long-chain fatty acids, marine oil/fish oil contains furan fatty acids. Furan fatty acids (F-acids) are heterocyclic lipid components with a furan moiety in the center of the molecule, the predominate acid being F6 (C22H38O3). They are a large group of fatty acids characterized by a furan ring, which carries at one α-position an unbranched fatty acid chain with 9, 11, or 13 carbon atoms and at the other α-position a short straight-chain alkyl group with 3 or 5 carbon atoms. In most cases, two β-positions of the furan ring are substituted by either one or two methyl residues or other group. However, F-acid without any substitutions in both β-positions of the furan ring has also been found (in certain seed oils). They are labeled F1 to F8 with F3 and F4 being isomers. Algae, plants, and other microorganisms which produce furan fatty acids. There are only small amounts of these and they are often quite difficult to separate from other long-chain fatty acids.
Both marine and land animals consume F-acids, thereby incorporating these fatty acids into their phospholipids and cholesterol esters. These particular fatty acids are radical scavenging and may contribute to possible beneficial properties of fish consumption .
Recently, it was shown that this class of fatty acids efficiently rescues brain cell death induced by oxidative stress . While the protective effect was strong, it was limited to an effective range only within the cell membrane. Regardless, this is still a significant effect and furan fatty acids should help reduce the risk of Alzheimer's disease.
Although promising, furan acids' effectiveness has been confirmed only in limited human controlled studies . The significant issue to address is whether their effectiveness is countered by the inherent ability of supraphysiologic amounts of marine oil to spontaneously oxidize—per radical induced oxidation—as discussed in prior sections. We think so. Furthermore, furan fatty acids do not negate fatty fish's deleterious effects of elevating blood glucose and blunting the insulin response [67–69]. That is why, overall, the effectiveness of fish/marine oil in the amounts typically recommended is harmful; in particular, by elevating blood glucose levels in cancer victims. However, if the amount of marine/fish oil consumption is reduced significantly to normal physiologic levels as detailed per this review, there may be a positive role for marine oil.
As demonstrated in cultures that consume fish, its consumption is fine. However, there are many cultures with excellent health and longevity that do not consume fish—the Hunza in Pakistan, the Vicambamba high in the Andes in Ecuador, the Abhasia of the Caucasus Mountains, and—in the United States—fully vegetarian 7th Day Adventists. This review speaks solely of marine oil/fish oil supplements and the concentrated pharmaceuticals of concentrated DHA or EPA like Lovaza and Vascepa. The medical profession is unaware or is not acknowledging the lipid science that unequivocally shows the great harm that marine/fish oil's recommended yet supraphysiologic amounts of EPA/DHA cause. This review gives the medical community many underpublicized physiologic facts that must be known and understood as the healthcare community revisits the practice of prescribing prophylactic marine oil to patients.
Fish oil cannot work, based on human physiology and biochemistry. Humans do not live in frigid waters where an “anti-freeze” is required, that is, EPA/DHA. These so-called active components spontaneously oxidize (radical induced oxidation) at room temperature and are even more problematic at physiologic body temperatures, causing numerous deleterious aldehyde secondary/end products regardless of antioxidant levels.
It has been clearly shown that the general population does not suffer impairment of delta-6/-5 desaturation enzyme impairments, as previously thought in the 20th century.
Prostate and other cancers along with CVD are predicted to increase in patients consuming fish oil on purely theoretical grounds, utilizing known physiology and biochemistry—and they do—in particular, epithelial cancers and impaired arterial intima.
Fully functional, Parent omega-6, LA, has been shown to be critical to both cellular oxygenation and mitochondrial function. Not distinguishing an adulterated (processed) EFA against a fully functional unprocessed EFA—in particular, LA—is the prime cause of confusion leading to inconsistent clinical trials on cardiovascular disease and cancer. The criticality of distinguishing between the effects of adulterated versus unadulterated forms of LA is obvious. Failure to do so has led to the incorrect and misleading conclusion that dietary intake of LA increases CVD risk, when it is only the adulterated LA that does . The Parent EFAs are key; food processing is the root cause of EFA-related issues. Fish-oil supplementation has nothing to do with solving this issue. Although furan fatty acids found in fish oil are strongly radical scavenging, their quantities are too limited to counter the deleterious effects of supplemental marine/fish oils.
Marine/fish oil, in the supraphysiologic, prophylactic amounts often consumed, is harmful, possibly even more harmful than trans fats . If proper physiologic amounts were utilized (<20 mg EPA/DHA), perhaps their furan acid content would be a significant positive factor; the concern of rampant oxidation is alleviated. Otherwise, given today's high quantities of fish oil recommendation, we see that their furan acid component is rendered ineffective. The medical profession needs to thoroughly review highly quantitative 21st century lipid physiology and biochemistry and offer the appropriate patient warnings. It is sincerely hoped that future researchers will approach the fish oil controversy with a more comprehensive grasp of the lipid biochemistry and physiology involved. Science must take precedence over “studies” which are often open to (mis)interpretation, leading to continual reversals and inconsistent results in clinical trials.
Using the most direct and effective physiologic measure, fish oil in the doses suggested is unequivocally shown to be an anti-antiaging substance, increasing vascular “biologic aging” by over a decade—causing “hardening of the arteries”—compared to PEO consumption. Compared to taking nothing, fish oil decreased subjects' arterial compliance (a bad outcome), by nearly four years .
Prophylactic marine oil consumption given its supraphysiologic EPA/DHA amounts—both theoretically and in clinical use—leads to increased inflammation, increased CVD, and increased cancer risk.
Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis by B. S. Peskin
Original Article Found Here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3914521/#sec18title
The medical community suffered three significant fish oil failures/setbacks in 2013. Claims that fish oil's EPA/DHA would stop the progression of heart disease were crushed when The Risk and Prevention Study Collaborative Group (Italy) released a conclusive negative finding regarding fish oil for those patients with high risk factors but no previous myocardial infarction. Fish oil failed in all measures of CVD prevention—both primary and secondary. Another major 2013 setback occurred when fish oil's DHA was shown to significantly increase prostate cancer in men, in particular, high-grade prostate cancer, in the Selenium and Vitamin E Cancer Prevention Trial (SELECT) analysis by Brasky et al. Another monumental failure occurred in 2013 whereby fish oil's EPA/DHA failed to improve macular degeneration. In 2010, fish oil's EPA/DHA failed to help Alzheimer's victims, even those with low DHA levels. These are by no means isolated failures. The promise of fish oil and its so-called active ingredients EPA / DHA fails time and time again in clinical trials. This lipids-based physiologic review will explain precisely why there should have never been expectation for success. This review will focus on underpublicized lipid science with a focus on physiology.
The object of this review is to show how there could be no possible expectation of general patient benefit with prophylactic fish oil use. It will be shown that the amount of EPA/DHA from routine fish oil recommendations is 20Xs–500Xs more than the body would naturally produce on its own from alpha-linolenic acid (ALA)—Parent omega-3.
Advances in quantitative analysis have been made in the 21st century which are not yet disseminated in the medical community; that is, the delta-6/-5 enzymes are not impaired in the general patient population, and the amount of EPA/DHA required on a daily basis by the brain is now known to be less than 7.2 mg/day. Neither extremely important fact was known in the 20th century.
Lipid physiology makes the following clear: (a) Marine oil's EPA/DHA spontaneously oxidizes at room temperature and more rapidly at normal body temperature—no level of antioxidants can stop this deleterious effect. (b) Fish oil blunts the insulin response and raises resting blood glucose levels. (c) Fish oil decreases critical prostacyclin (PGI2) in patients with atherosclerosis—a very bad outcome. (d) Fish oil rapidly decreases arterial compliance—increasing “hardening of the arteries.” (e) In contrast to researcher's expectations, fish oil accelerates metastases in animals. (g) Fish oil's EPA/DHA do nothing to increase cellular and tissue oxygenation; to the contrary, marine oils increase inflammation. (h) Marine oil consumption impairs mitochondrial functionality, making it an anti-antiaging substance.
The medical profession is unaware of or is not acknowledging the lipid science unequivocally showing the great harm that marine/fish oil's supraphysiologic amounts of EPA/DHA cause. As will be shown, the claim that prophylactic use of marine oil produces positive patient results is completely counter to 21st century lipid science.
2. Fish Oil Fails Extensively in Clinical Trials, but These Failures Are Often Underpublicized: Three Significant 2013 Fish Oil Failures
Since many medical professionals are under the wrong impression that fish oil incontrovertibly works, it is instructive to make clear there are numerous recent and not so recent marine oil/fish oil failures occurring across all clinical areas. There are more (underpublicized) failures than (supposed) successes. These failures should cause great pause.
Three highly significant fish oil failures occurred in 2013. In May 2013, The Risk and Prevention Study Collaborative Group (Italy) released a conclusive negative finding regarding fish oil for those patients with high risk factors but no previous myocardial infarction. Fish oil failed in all measures of cardiovascular disease (CVD) prevention—both primary and secondary . This study was so conclusive that Eric Topol, MD, Editor-in-Chief of Medscape and Medscape's Heartwire for cardiologists, issued a new directive to patients to stop taking fish oil, that is, long-chain EFA metabolites of EPA/DHA . The July 2013 landmark article published in the Journal of the National Cancer Institute entitled “Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial”  confirmed prior post-2007 findings of increased prostate cancer risk among men with high blood concentrations of long-chain metabolites of ω-3 fatty acids from fish oil studies [4, 5]. The authors warned, “The consistency of these findings suggests that these fatty acids are involved in prostate tumorigenesis. Recommendations to increase LCω-3PUFA (marine oil's EPA/DHA) intake should consider its potential risks.” The May 2013 trial  showed that macular degeneration victims were not helped by fish oil's significant DHA content. The year 2013 was very bad for fish oil findings. Why the failures?
3. Pre-2007 Studies Were Poorly Conducted and Inconsistent with the Science
In a 2012 meta-analysis regarding cardiovascular disease, reviewing 1,007 articles, only 14 studies met the criteria of randomization, double blindness, and placebo control . Clearly, an enormous number of poorly conducted studies in the journals have conclusions that cannot be relied on and are misleading physicians and researchers worldwide. Studies should be used to confirm the physiologic, lipid science, not to be counter to it as many pre-2007 studies were.
In researchers' haste to offer patients a new, effective treatment, fish oil “successes” were highlighted and its failures downplayed. However, post-2007 “studies” of fish oil show significant accumulated failure . When well-controlled studies and experiments are performed, as was done in Harvard Medical School's 1995 experiment giving one group of patients fish oil and a control group olive oil, CVD progression did not lessen with fish oil . Fish oil fails; it has to as the science below confirms.
4. EFAs: Parent Essential Oils (PEOs) and Derivatives
There are only two true 18-chain carbon essential fatty acids (EFAs): linoleic acid (LA) with two double bonds and alpha-linolenic acid (ALA) with three double bonds. Neither can be manufactured in the body; both must come from food.
Longer-chain metabolites are synthesized from LA and ALA. These long-chain metabolites—not essential and often incorrectly termed “EFAs”—are correctly termed “derivatives.” For example, common derivatives of the omega-3 series are EPA (eicosapentaenoic acid) with five double bonds and DHA (docosahexaenoic acid) with six double bonds. To clarify the issue, I term LA and ALA “Parent Essential Oils” (PEOs) or “Parents.” I properly term all of their long-chain metabolites “derivatives.” The body makes these important derivatives from Parents “as needed” in naturally minute amounts. The literature often fails to clearly distinguish these two vastly different substances.
4.1. Most Parents Stay as Parents
A major mistake was made in the 20th century, which misdirected researchers. It was wrongly assumed that the vast majority of “Parents” would be converted into “derivatives.” This did not occur, causing the medical research community to proclaim that there were ubiquitous metabolic deficiencies impacting the delta-6 and delta-5 desaturase enzymes in the general population. This has been shown to be categorically false by advanced 21st century quantitative methods (described later). In humans, no more than one percent (1%) of Parents are naturally converted into derivatives. Fish oil mania wrongly (and hazardously) assumes the converse.
5. Fish Oil Impairs Normal Cellular Physiology: Pathophysiologic Disorders Are Expected
Theoretically (and in clinical experiments) fish oil supplements, in their “normal” although supraphysiologic amounts (calculated below), cause changes in membrane properties that impair oxygen transmission into and through the cell . Physicians and other health professionals often prescribe these supraphysiologic amounts, deleteriously altering phospholipids of cell and mitochondrial membranes.
As will be detailed later, nonfunctional LA-based trans fats, oxidized LA entities, and inappropriate omega-6/omega-3 ratios (caused in part from normally recommended, yet supraphysiologic, marine oil supplementation) are all potential sources of unsaturated fatty acids—in particular, LA (Parent omega-6)—that can disrupt the normal membrane structure, significantly increasing the potential for cancer . All of the supraphysiologic, excess EPA/DHA cannot be beta-oxidized away. Thus a significant amount of the excess will be physiologically incorporated into all cell membranes, detrimentally.
6. Arterial Intima: Endothelial Tissue Comprised of Epithelial Cells—CVD Explained
The innermost lining of arterial intima is endothelial tissue, comprised of epithelial cells containing significant LA, but no alpha-linolenic acid (ALA) [12, 13]. A significant biologic effect of oxidized LDL is its cytotoxic effect on cultured endothelial cells directly lining the arterial wall . Dietary LA becomes adulterated (peroxidized) from food processing (described later) and deposited in arterial intimal cell membranes and leads to abnormal oxidation at the vascular injury site, thus causing injurious inflammation.
In this case, abnormal oxidation, caused by ex vivo radical induced lipid peroxidation (adulteration) of LA, involves formation of a hydroperoxide from LA by abstraction of a hydrogen atom as a radical from the doubly allylic methylene group between the two double bonds, followed by the addition of oxygen, a diradical, to make a hydroperoxide radical, which can then pick up another reactive hydrogen atom, perhaps from another LA molecule, to form the hydroperoxide. This, in turn, may break the O–O bond to form an alkoxide and a hydroxyl radical, which can continue to make more undesirable oxidized products . Therefore, atherosclerosis can be prevented/arrested if endothelial cells remain fully functional .
Although lipid peroxidation can be caused by injury to tissue or aging, it does not have to be initiated in this fashion. Furthermore, a bivalent metal ion can cleave the O–O bond; nonfunctionality can occur from the commercial processing of the linoleic oil (LA).
7. Bis-Allylic Bonds: Fish Oil's Spontaneous Oxidation (Rancidity) at Room Temperature and In Vivo
Polyunsaturated fatty acids including LA contain the system HC=CH–CH2–CH=CH. Long-chain fatty acids contain bis-allylic hydrogens whereby the –C=C– units are separated by a single-bonded –C– (carbon) atom. The hydrogen atoms attached to each of these intermediate –C– atoms are called bis-allylic hydrogens and have the lowest C–H (weakest) bond-energies of the fatty acid chain. The weak bond makes them enormously susceptible to attack by reactive oxygen species (ROS) generated elsewhere in the body . Because of the five double bonds in EPA and six double bonds in DPA, these metabolites are highly sensitive to temperature.
In particular, DHA, with its 6 double bonds, contains 5 bis-allylic bonds and is therefore 320 times more susceptible to oxidative attack, that is, becoming rancid, than monounsaturated oleic acid (18 : 1), which has no bis-allylic hydrogens in its chain. A saturated fat membrane containing just 5% DHA (fish oil) is 16 times more susceptible to peroxidative damage . Fish oil's DHA is 7 times more susceptible to peroxidative damage than LA (Parent omega-6), the most significant fatty acid by both weight and functionality in the cell's bilipid membrane. The shifting of the body's antioxidants required to combat this physiologic insult causes a shortage elsewhere. This fact should cause the medical community great concern. Keeping tissue fluid in frigid waters is not a physiologic concern of humans.
7.1. Marine Oils Keep Membranes of Fish Fluid in Frigid Waters
The following underpublicized medical fact goes a long way toward explaining marine oil's tremendous cancer- causing potential in humans. Fatty, cold-water fish (the type we are told is best) live in temperatures as low as 32°F, but warm-water fish may live in 70°F waters and have 14Xs less EPA/DHA content than their cold-water relatives . At normal human physiologic temperatures, fish oil spontaneously becomes rancid (as the above section detailed).
A human placed in ice-cold, frigid waters would suffer hypothermia, freeze, and likely die. Fish do not freeze because they have significantly higher levels of the EFA derivatives EPA and DHA than those in humans.
Our ambient and physiologic conditions are not similar to that of fish. Marine/fish oil researchers did not consider this important fact. EPA/DHA acts as “biological antifreeze” to fish living in frigid waters. Humans do not require such copious amounts because we have an internal temperature of 98.6°F. The deleterious effects when humans consume supraphysiologic amounts of marine oil's EPA/DHA are described next.
8. Primary and Secondary Lipid Oxidation and Hydroperoxides
There is much to know regarding specific lipid oxidation markers. Oxidative rancidity occurs in 3 distinct stages/phases: initiation, propagation, and ultimately termination. During the initiation stage, molecular oxygen combines with unsaturated fatty acids to produce hydroperoxides and free radicals, both of which are very reactive. Heat and light increase the rate of all phases. Then, the products of this stage react with additional lipids to form other reactive chemical species—often termed “autooxidation.” In the final termination (secondary) phase, relatively unreactive compounds are formed, including hydrocarbons, aldehydes, and ketones. Quantitative measure of all phases is required for a complete picture.
8.1. Malondialdehyde (MDA)/p-Anisidine Increases with Fish Oil/Marine Oil
Supplementation with polyunsaturated fatty acids in particular, EPA/DHA, as opposed to saturated fatty acids, results in a statistically significant increase in lipid peroxidation in the plasma and liver. Fish oil ingestion raises levels of extremely harmful malondialdehyde (MDA) : “Ingestion of CLO [cod liver oil] was associated with an increase in MDA excretion in all six subjects. The mean increase of 37.5%, from 24.5 ± 3.5 μg to 34.7 ± 2.5 μg MDA (mean + SEM), was [statistically] significant and CLO ingestion again was associated with an increase in MDA excretion in all subjects. The mean increase of 54.3%, from 31.7 μg to 49.1 μg MDA/sample was highly significant.” Parent omega-6 (LA) undergoes—like all PUFAs—lipid peroxidation, but the amount of MDA produced is much, much lower than that by oxidation of EPA or DHA because MDA production requires at least 3 or more double bonds in a molecule.
The p-anisidine test measures the aldehyde content generated during decomposition of hydroperoxides. It correlates well with volatile substances. Volatile aldehydes and other later-stage aldehydes leave behind a nonvolatile product that the p-anisidine test measures well (via correlation). “Pristine” fish oil can have an allowable p-anisidine value of 19, clearly showing significant secondary stage oxidation , whereas a PEO formulation without fish oil is closer to a p-anisidine value of 4—confirming fish oil's substantial inherent propensity to become rancid at room temperature.
8.2. Thiobarbituric Acid Reactive Substances (TBARS) Increase with Fish Oil/Marine Oil
A 2000 study reported in the American Journal of Clinical Nutrition found that plasma TBARS (substances which react to the organic compound thiobarbituric acid and which are a result of lipid peroxidation) were >21% higher after fish-oil supplementation than after sunflower-oil supplementation (containing Parent LA, not derivatives) and 23% higher than after safflower-oil supplementation (containing Parent LA, not derivatives). The article explored the limitations of the various assays available for the measurement of lipid peroxidation in vivo, including the F2-isoprostane assay's inability to provide direct information about the peroxidation of 20:5n-3 (EPA) and 22:6n-3 (DHA) . Fish oil oxidizes in plasma, producing numerous deleterious products. This long-term damaging effect is cumulative.
8.3. Clinical Proof and Verification of Fish Oil's Harmful Oxidation
Regardless of antioxidant level added to the fish oil supplement, rancidity/peroxidation upon ingestion (in vivo) becomes a very significant and problematic issue. Oxidation of EPA leads to generation of a mixture of aldehydes, peroxides, and other oxidation products. Highly polyunsaturated, long-chained EPA and more so with DHA, due to its additional double bond, is readily oxidized at room temperature even in the absence of exogenous oxidizing reagents. Importantly, in vivo, a large increase in tissue and plasma accumulation of fatty acid oxidation products is noted in subjects consuming fish oil even after addition of antioxidant supplements to the diet—this effect strongly suggests extensive oxidation of omega-3 fatty acids such as EPA in vivo. This deleterious effect is true as evidenced by the trial in which a 14% decrease in life expectancy occurred in those animals fed fish oil .
In humans and primates such as the monkey, no quantity of in vivo antioxidants will stop EPA/DHA damage as measured by lipofuscin, the peroxidized “age spots.” Lipofuscin was three-fold (3Xs) greater in the livers of monkeys fed fish oil. Furthermore, another measure of oxidative damage, the levels of basal thiobarbituric acid reactive substances (TBARS), was four-fold (4Xs) greater than that of the monkeys fed corn oil with no EPA/DHA. The researchers found that even a ten-fold (10Xs) increase in alpha-tocopherol, a potent antioxidant, was not fully able to prevent the peroxidative damage from fish oil .
9. Inflammation and the Cancer Connection
As per the above details, oxidation of marine oil's EPA/DHA is inherently inflammatory. Inflammation is now seen as causal to cancer as it is to CVD: “The connection between inflammation and cancer has moved to center stage in the research arena” . This rewriting of the textbooks comes from one of the world's most renowned cancer researchers, Robert Weinberg of MIT (originator of the term “oncogene”), causing him to revise his leading textbook, The Biology of Cancer (Garland Science, 2006), to reflect this new understanding.
Prior sections detailed how fish oil causes inflammation in vivo because EPA/DHA spontaneously oxidize at room temperature and much more quickly at body temperature. Their harmful hydroperoxide products become incorporated in esterified cholesterol and it is well known in cardiology that oxidized cholesterol causes the inflammation leading to CVD. Increased cancer is expected with increased consumption of marine oils.
The inflammation/cancer connection is supported with the finding that asbestos causes inflammation, reported in 2010 in Medical News Today. “For the past 40 years researchers have tried to understand why asbestos causes cancer. This research emphasizes the role of inflammation in causing different types of cancer” [26, 27].
Inflammation alone, regardless of initiating conditions, accelerates cancer proliferation. Since 2007, cancer researchers understand and acknowledge that the fundamental, prime cause of cancer is inflammation, not genetics [28–30]. A further inflammation/cancer connection was reported in Cancer Epidemiology, Biomarkers & Prevention in 2005, with the statement that “There is a growing body of evidence supporting the role of chronic inflammation with prostate carcinogenesis and thus the associations of transfatty acids with increased inflammatory response may explain their associations with prostate cancer risk” . The SELECT  showed that marine oil's DHA was more inflammatory than trans fats.
10. Parent-to-Derivative Amounts and Metabolism
What percentage of PEOs does become converted (naturally) to long-chain metabolites such as EPA and DHA? This important question must be addressed and answered before their correct supplemental dosage (if any) can be determined. This fundamental research was neglected concerning marine oils, which tragically led to recommendations of haphazard supraphysiologic overdoses of marine oil's EPA/DHA.
New, twenty-first century quantitative research from both NIH and USDA shows considerably lesser amounts of natural DHA conversion/usage from ALA than the medical community has been led to believe. These findings will be upsetting to those health professionals recommending fish oil prophylactically. The conversion amount is much less than the medical field assumes: it is less than 5%—often less than 1%—with at least 95% of PEOs staying in Parent form. This singular mistake of assuming very high conversion amounts, whereas in actuality their conversion amounts are extremely low, led to the irrational fish oil mania.
Contrary to wrong dogma, the enzymes that produce PEO derivatives (the delta-6 and delta-5 desaturase enzymes) are not impaired in the vast majority of patients . Conversion of ALA (Parent omega-3) to DHA is unlikely to ever normally exceed 1% in humans .
Research at the United States Department of Agriculture's USDA Food Composition Laboratory (2001) reported a natural net conversion rate of a mere 0.046% of ALA to DHA and 0.2% to EPA—not the highly misleading 15% conversion rate that is often quoted . This is a mistake of nearly 2 orders of magnitude (100-fold). In 2009 NIH researchers determined the amount of DHA utilized in human brain tissue to be a mere 3.8 mg ± 1.7 mg/day. Therefore, based on the variance, brain tissue in 95% of all subjects, allowing for variation in brain size, would consume no more than 0.4 mg–7.2 mg of DHA per day .
10.1. No Delta-6/-5 Desaturase Widespread Impairment in (Average) Patients
Highly accurate, quantitative experiments were performed showing that both animals and the average healthy person are quite capable of metabolizing adequate amounts of DHA from Parent omega-3 (ALA).
As will be clearly demonstrated, there is no widespread impairment in the typical patient whatsoever; the normal conversion amounts are simply very low. These conversion amounts are extremely small and naturally limited. This mistake often leads to suprapharmacologic recommendations and can potentially overdose patients by factors of 20-fold to 500-fold, depending on specific supplement and amounts prescribed.
Because the body cannot oxidize away these tremendous overdoses of EPA/DHA, they become incorporated into tissue and organs with deleterious effects as confirmed by the skyrocketing increase in all epithelial-based cancers (described later). Supraphysiologic amounts are forced into tissue, causing gross physiologic imbalance and great potential for harm.
An important experiment measuring plasma fatty acids in 62 fire fighters concluded that the consumption of ALA-enriched (Parent omega-3) supplements over a 12-week period elevated levels of long-chain metabolites EPA and DHA. This experiment unequivocally showed the unimpaired effectiveness of ALA conversion from Parent omega-3. The researchers further stated that the general population could achieve the amounts of ALA required to obtain these effects by modifying their diet, ensuring adequate ALA (Parent omega-3) .
10.2. Vegans—Consuming No Fish—Produce Sufficient DHA
Even vegetarians consuming little or no fish had acceptable EPA/DHA levels . This is a group that absolutely would be expected to manifest gross neurological abnormalities, including both visual impairment and cognitive impairment, yet there is no clinical evidence of such neurologic and cognitive abnormalities in vegetarians [36, 37].
Confirmation in 2010 showed that vegetarians with an intake of 0.3% DHA compared to fish eaters produced 85% of the EPA levels and 83% of the DHA levels that consumers of fish did. These amounts are within the “normal” ranges .
10.3. Rodents Have a 50-Fold Safety Margin: Would Not Humans?
Rats fed a DHA-free but α-LNA (n-3 PUFA) (Parent omega-3) adequate diet naturally produced from Parent omega-3 (ALA) fifty times (50Xs) more DHA than their brains required —an enormous “safety factor.” Certainly, nature would ensure humans the same margin of safety shown to a rodent. This result in an animal species clearly supports highly quantitative 21st century research from the National Institutes of Health (NIH) finding extremely low—yet adequate—natural conversion rates in humans .
11. Amounts of EPA/DHA in Fish Oil Supplements: Pharmacological Plasma Overdoses
Given the above analyses, how much EPA/DHA does the typical marine oil/fish oil supplement provide? An average 1,000 mg health-food-grade fish oil capsule contains approximately 180 mg EPA and 120 mg DHA. Pharmaceutical-grade versions contain higher doses. Furthermore EPA [left and right double arrow ] DHA. This is not the case with PEOs. They are unidirectional. The American Heart Association states that those with documented CHD are advised to consume about 1 gm (1,000 mg) of EPA + DHA per day. Is this advice rational? No.
As an example, using the USDA food composition research formulas covered earlier, if patients consumed a supplement of 600 mg of Parent ALA, they would naturally convert it to EPA by no more than the (generous) factor of 0.25% = 1.5 mg EPA and 1.5 mg × 0.63 × 0.37 = 0.35 mg to DHA in patient plasma. Therefore, just one capsule provides the amounts shown in the analysis below, and many people are overdosing even more by taking 2 to 4 fish oil capsules each day, likely in part because the cardiology and heart recommendations are often “EPA + DHA ranging from 0.5 to 1.8 grams per day.” What overdose does this translate to?
11.1. Potential EPA/DHA Overdoses Are Frequent
Potential Overdose equates to the following plasma overdoses: EPA = 180 mg/1.5 mg = 120 times overdose and DHA = 120 mg/0.35 mg = 340 times overdose. These facts should cause great pause and concern. (Technically, a bit more is required for additional metabolic pathways aside from direct tissue incorporation like prostaglandin production, but it is not a significant amount by weight on a daily basis.) The medical community and most physicians and other health professionals may unknowingly be overdosing patients prophylactically with supraphysiologic supplemental amounts of omega-3 derivatives.
12. The Significant Problem: Radical Induced Lipid Peroxidation—Food Processors Require Long Shelf Life
Radical induced lipid peroxidation (adulteration) of omega-6 fats—in particular, LA—is created by food processors' need for long oil life during frying and baking, especially because their use of saturated fats is avoided. Omega-3 fats are never used in cooking; they are far too reactive.
Abnormal peroxidation of the Parent omega-6 oil (LA), therefore, is the core of the EFA-based deficiency. It has nothing to do with marine oils and everything to do with the adulteration of the plant-based Parent essential oil, LA. For example, trans fats—to some extent—are found in all commercial restaurants, supermarkets' prepared food and frozen food sections, and even in fine-dining restaurants' frying oils. The substrate for trans fats is Parent omega-6 (LA). Just 0.5 grams of a 1% trans fat containing adulterated oil (a conservative amount) is very harmful to humans. Even with the FDA's 2014 ban on trans fats, the FDA allows <0.5 grams/serving to be labeled as zero (0). Yet, this apparently negligible amount contains enough trans fats to overpower each cell in the body by a factor of approximately 3,600 .
12.1. Cellular Oxygenation Maximized with Unadulterated LA—Parent Omega-6
Marine/fish oils do nothing to promote cellular oxygenation in the mitochondria—this is a key role exclusive to Parent omega-6 (LA) [10, 40]. Marine oils, due to their inherent inflammatory property in vivo, cause the opposite of the desired effect and are therefore deleterious.
12.2. Pathophysiology Effects from Damaged Cell Membranes Caused by Radical Induced Lipid Peroxidation
With functional LA deficiency there is an enormous increase in permeability of epithelial tissue and an increase in capillary fragility, further explaining the pathophysiology of CVD and how it may be prevented . Oxidation of LDL-C causes significant depletion of LA (Parent omega-6) . Because LDL cholesterol is the transport vehicle for PEO delivery into the cell (described below), LDL cholesterol will transport LA into cells, whether the LA is defective or not (such as oxidized or trans entities).
Of great importance is the fact that with ingestion of marine/fish oil (EPA/DHA) there was a corresponding decrease in tissue's LA, causing pathophysiologic deficiency .
13. Tissue Incorporation of Dietary Fats is Proportional to Consumption
The concentration in adipose tissue triacylglycerols is roughly proportional to dietary concentration and is now frequently used as a measure of relative dietary intake. It has been long known that the fatty acid composition of the diet can influence membrane fatty acid composition [43, 44].
Fortunately, tissue alteration caused by supraphysiologic amounts of marine oil consumption can be remedied. Once removed, it takes 18 weeks to fully rid patients of the negative effects of fish oil .
Thanks for writing.
Constipation can have several etiologies, but here's what I'd consider the most helpful in restoring your health in full:
1) Thyroid function.
Thyroid health has an impact on all of the body's systems including elimination and detoxification. Nutrition is a key factor in thyroid function, and many politically correct diet recommendations are adversely impacting the health of this critical organ. Specifically
--PUFAs (Polyunsaturated Fatty Acids): vegetable oils are the prime culprits here. They are pro-inflammatory, down regulate the thyroid, and actually inhibit immunity.
--most processed foods will use PUFAs as they are cheap alternatives to better quality ingredients.
--Cruciferous veggies when eaten raw (i.e. broccoli, cauliflower, cabbage, etc). They work as goitrogens and actually down regulate the thyroid. Cook them well and eat them with a saturated fat (animal product or even coconut oil--the latter of which is pro-thryoid and has anti-bacterial and anti-viral properties).
--anything which you may be intolerant of (gluten, for example) can cause inflammation and all the resulting dysfunctions
--many of the foods touted as being high in fiber (i.e. beans, grains, green leafy veggies) are not optimal for human digestion (we're omnivores and not ruminant herbivores--thus, we have a difficult time breaking down these foods and utilizing them effectively). Anytime digestion is impaired, fueling suffers while inflammation is increased.
--Gums (locust bean, xanthum, etc) all are particularly bad and will literally gum up the intestines.
. You need enough but not too much. Good rule of thumb is 1/2 your body weight in lbs in oz of water each day (i.e. 150lbs = 75oz of water). But this can easily dilute electrolyte status, which is really what hydration is predicated upon, so I recommend adding a bit of salt (sea or pickling with no anti-caking agents) to everything I drink. Not only is this pro-thyroid, it also down regulates the production of aldosterone--a stress hormone. And anytime you see stress, think inflammation/dysfunction on some level and extra demand on the body's resources.
. Should be full body. Think of movements which move you into and out of the fetal position. Squats would be a good example. But swimming could work, too. And running or even walking is great to get things moving. At the very least, bouncing up and down (on a mini trampoline, for example) would help with lymphatic drainage and promote peristalsis. A word of caution here: exercise (especially cardio as typically performed) in excess of your current training status can easily down regulate the thyroid, so I might cap duration at 45mins.
Additional strategies would include exposure to sun light or at least bright (250+w) incandescent lighting to stimulate the mitochondria, adequate protein intake (preferably from animal sources with liberal use of gelatin/bone broth which has minimal tryptophan and can be used to balance the amino acid profile such that it doesn't perpetuate inflammation/sluggish thyroid), enough dietary carbohydrate (fruit and below ground veggies being the best choices), minding natural circadian rhythms, proper breathing mechanics, and awareness of your thinking and how each though/idea/belief impacts your physiology secondary to activation of specific parts of the autonomic nervous system. Lots of other possible ideas, but the above should be more than enough to get you moving in the right direction (pun intended). More info can be found in my book (http://triumphtraining.com/pages/holistic-strength-training-for-triathlon
). And I'm working as quickly as my schedule will allow on my next book which will explore these subject in even greater detail.
Good luck and know that health is your birthright.
Go claim it.
1. Am I to try and avoid all PUFA's? (Looks like you had avocados on one of your recipe)
2. Can you give me examples of good protein/carbo/fat snacks? You said I need a good mix, so I am trying to figure that out.
3. You said to include raw items with meals because of their life giving qualities. Can you provide examples? It seemed like you were steering me more towards fruits. Raw veggies not such a great idea?
3. How should I start my venture back into dairy?
4. Can you tell me my beneficial produce and the produce to stay away from one more time? So salads are bad? What about baby greens?
5. If I have my hip/glute/back pain, should I not do my corrective exercises?
6. I need more advice on myofascial work. I think this could be really beneficial to me! All the muscles surrounding my iliac crest, and on the sides around the notch of my femur seem to hold SO much tension. I think from all the skateboarding, snowboarding, and mountain biking I've done, with NO stretching.
7. Could I potentially have parasites in me? Are parasite cleanses a good idea?
8. My Dad has been recommending Aloe water at his clinic. He wants to know your thoughts on it.
9. My girlfriend recently gave herself a coffee enema. She wants to know if those have the health benefits they promise.
1--it's not one of your action items, but it would serve you well. Avocado is high in PUFA's, but it's one I would be o.k. with using as a garnish and not a staple (like most do with nuts/seeds/veggie oils/etc).
--I think you can come up with some on your own (you're a smart guy), but I've attached a list.
--Raw fruit (ripe) though some are better than others, carrots, cucumbers, peppers, tomatoes. Otherwise, I cook most of the others.
--Above ground veggies except for the ones mentioned above are ones which should be limited and/or cooked and/or eaten with saturated fat. Add squash/zucchini to the above.
--stretches always. DAILY core movements always (and shouldn't hurt). Other movements at the threshold specific to your situation (reps/sets/weight/frequency of workout). You should find that the workout makes you feel better. If not, you're not ready for that particular movement and we need to go slower/fill in holes in your development.
--we can work on that next time, but golf ball/tennis ball/foam roller/stick--I have some explanation/examples in my book (http://triumphtraining.com/pages/holistic-strength-training-for-triathlon
). You can download a copy off my website or get one from me directly.
--You probably do. Don't want to go there yet. Besides, some parasites have a symbiotic relationship with us.
--don't do bells/whistles until you get the basics down. And that bell/whistle is one I wouldn't recommend.
--as #8. And if you're eating/living in a way to support health, you don't need to resort to enemas.
Lipids. 1997 Dec;32(12):1265-70.
Analogous, but less extreme effects are seen even in salmon, which showed increased oxidative stress on a high n-3 diet (DHA and EPA), and lower mitochondrial cytochrome oxidase activity (Kjaer, et al., 2008).
Dietary fatty acid profile affects endurance in rats.
Ayre KJ, Hulbert AJ.
Typically athletes are advised to increase their consumption of carbohydrates for energy and, along with the general population, to reduce consumption of saturated fats. It is now recognized that fats are not identical in their influence on metabolism, and we argue that the composition of the polyunsaturated fat component should not be ignored. The aim of this study was to manipulate the dietary fatty acid profile in a high-carbohydrate diet in order to investigate the effect of dietary polyunsaturates on submaximal endurance performance in rats. Rats were fed one of three isoenergetic diets containing 22 energy percentage (E%) fat for 9 wk. The diets comprised an essential fatty acid-deficient diet (containing mainly saturated fatty acids); a diet high in n-6 fatty acids, High n-6; and a diet enriched with n-3 fatty acids, High n-3. Submaximal endurance in rats fed the High n-3 diet was 44% less than in rats fed the High n-6 diet (P < 0.02). All rats were then fed a standard commercial laboratory diet for a 6-wk recovery period, and their performances were reevaluated. Although endurance in all groups was lower then at 9 wk, it was again significantly 50% lower in the High n-3 group than the High n-6 group (P < 0.005). Although n-3 fats are considered beneficial for cardiovascular health, they appear to reduce endurance times, and their side effects need to be further investigated.
Off the top of my head:
is critical to minimize/eliminate. It's in water (unless using a reverse osmosis filter), toothpaste (of course--though you can easily find alternatives), tea (even organic ones), and anything packaged/canned/made with water.
is problematic for bone mass, too, and can be increased by anything which irritates the intestines (where 90% is produced and triggers peristalsis). SSRI's of any sort should be suspect. It stimulates osteoprotegrin (just like prolactin does), reducing bone resorption, along with PTH and cortisol--both of which remove calcium from bone.
--decreasing the production of nocturnal stress hormones (night is when most bone loss occurs) would be a good strategy. Blood sugar maintenance is one component you can easily manipulate which falls under this heading.
--Anything pro-thyroid (coconut oil, sunlight, salt, etc) is beneficial for bone health (and health in general). As such, anything which inhibits thyroid (PUFA;s being at the top of the list, but there are MANY more) should be minimized.
is an important co-factor in the stimulation of bone
building osteoblasts, even helping to stimulate the production of new osteoblasts. On the other hand, zinc suppresses the excessive activity of osteoclasts, cells that are responsible for bone
resorption, demineralization and ultimately bone
loss. Zinc helps to regulate the key inflammatory gene signal in bone
marrow, NF-kappaB, which is required for optimal balancing of osteoblast and osteoclast formation and function. See the link below:
is essential for both formation of bone and maintenance of bone structure
--Also, diets high in garlic and other related vegetables such as onions and leeks have been shown to reduce the risk of developing osteoporosis. Also, K2 (not K1 which comes from green, leafy greens) has been shown to increase bone density in people already diagnosed with osteoporosis. It does so by blocking the removal of calcium from bone caused by parathyroid hormone. Add D3, too, like we talked about.
--The Calcium Lie by Robert Thompson, MD might be an interesting read for you.
--It’s important to realize that these types of drugs do NOT build any new bone. Rather they are metabolic poisons that kill off your osteoclasts, which halts the normal bone repair process since you now lack the cells that break bone down. Your bones will indeed get denser. However, denser bones are NOT stronger, which is the part they don’t tell you. Eventually your bones become weaker and more prone to fracture. In women who have been taking a bisphosphonate-type drug for five or more years, their bones have literally lost the ability to regenerate and this is why many may be faced with more brittle bones and fractures.
LOTS of info, I know, so ask if you have questions or want to dial in a strategy.
But all this should at least get you (and your doc?) thinking.
Question for you... I did a 70.3 yesterday in prep for IMLP. My swim and
bike went according to plan. I got off the bike running according to plan feeling
very energetic! About 2 miles in, my right quad started twinging, then my left
hammstring. I was forced to walk/run the rest of the run leg, mostly walking.
Eventually, someone gave me a couple salt tabs. After about an hour and with
only about a mile left, they seemed to help and I jogged in without cramping.
It was the very first 90 degree day out here. I drank tons, popped Endurolytes
on the bike, drank the Ironman Perfom, ate pretzels, drank coke...Any thoughts??? I really don't want this to happen during Ironman next month!
Thanks in advance for any tips or suggestions.
Could be any number of things. Magnesium status would be high on the list--it's
not readily found in the diet of most people, gets depleted via sweat, and is
readily lost in cases of hypothyroidism (which a lot of endurance athletes are
prone to). Fueling/hydration (the latter of which depends more on electrolyte
status than amount of water--so drinking tons may be an issue), heat
acclimation, effort related to training status, and several other things should all be
considered. But I would suggest to you that race performance is predicated more
on nutrition/lifestyle/training outside of race day. So consistency with sound
principles of everything mentioned above along with proper breathing
(diphragmatic and nasal when possible), movement (stretching--triathletes often
have facilitated quads/hip flexors and tonic musculature is more prone to cramping
as the origin and insertion are brought closer together--along with other forms
of myofascial work), and sleep (10-6) will increase your threshold for the
stress of racing. And since the intensity at which you race IM will be less
than that which you raced the 70.3, fueling should be easier and your effort
will be less--both of these will decrease the likelihood of cramping. If you do
cramp, slow down, re-focus on hydration/nutrition, breathe as mentioned above,
and press on your upper lip right below the nose--it's a pressure point which
can be used to relieve cramping--has saved me a couple of times. Good luck at
IMLP--great race and one which means a lot to me. Let me know how it goes.
Follow Up Question
Thanks for the info...As for the 70.3, I was practicing my
pacing AND nutrition for IMLP. Since I went to the USAT clinic in January, I've
been a convert to what Seebohar preaches. My daily nutrition refects my
I had a banana/avocado/honey/almond-coconut milk smoothie at
4 am. About 45 minutes prior to my swim start, I took 1/4 tsp salt and about
12oz water. I continued sipping water until the start (no carb drinks). My swim
felt perfect! As soon as i got on the bike, I ate a banana and drank some of my
NUUN. On the bike, I finished my bottle of NUUN, popped 2 Endurolytes, 1/2
bottle of HEED (with an Endurolyte), and 1.5 bonkbuster bars, and grabbed 2
waters and a bottle of Perform at the stops. Some of that water went down my
jersey for cooling. I was easily at my IMLP pace, finished in just shy of 3
I felt great for about 2 miles on the the run and those
friggin' cramps started. Ugh! I think those salt tabs finally kicked in.
Is it possible to take too many electrolytes??? If so, how
do you know the fine line between enough and not enough?
Yes, it's possible to take too many electrolytes, but I
don't think that's necessarily the issue. Personally, I don't
recommend consumption of PUFA's which was the majority of your smoothie (and
the almond milk if not the coconut milk likely had carrageenan unless homemade)
and in your bonk breaker bar, as well. And if you look at the macronutrient content of your breakfast, there really wasn't enough fat or protein to balance the carbs, and I don't doubt that your blood sugar handling was already compromised despite feeling great on the swim. Additionally, any artificial
colors/flavors/sucrolose in the Perform can/will cause issues--I'd use it
judiciously and only if in trouble. The NUUN tabs also contain Acesulfame K
which stimulates insulin secretion in a dose dependent fashion thereby possibly
aggravating reactive hypoglycemia. They also have some sesame oil (PUFA) which
inhibits the use of glucose for fuel (another problem with your a.m. smoothie)--not good for endurance athletes or anyone
interested in health. Lastly, it sounds as if you may have been under fueled.
But, as I said before, what you do during the race has much less impact that
how you prepare before--so you could have had no issue with your fueling
strategy if pre-race/consistent nutrition (and lifestyle) was better.
1. Push away the PUFAs
2. Skip exercise that doesn't serve your biochemistry
3. Press the off button on your t.v. remote
4. Drop the Stinkin' Thinkin'
5. Pick foods you can actually digest
6. Balance macronutrients
7. Pass 12 inches or more of fecal matter daily
8. Stabilize blood sugar
9. Play and laugh everyday
10. Climb into bed by 10 p.m.
HONORABLE MENTION: tie between Squat, Lunge, Push, Pull, Bend, and Twist
Polyunsaturated Fatty Acids (PUFA's) inhibit the oxidation of glucose for fuel. Thus, when consuming nuts, seeds, fatty fish, or vegetable oils with sugar or starch (save Fructose), the calories tend to be stored as fat.
Just a Question Posted on August 22, 2012, 0 Comments
Since cholesterol is protective in the body, why would you ingest anything (statins, PUFA's, Cheerios, etc) that decrease its production?
In brief, fish oil lowers activity/oxidation of omega 6 (seed oil) so has temporary anti-inflammatory effects (thus the hype). But long term effects are as bad/worse since it's still a PUFA and, in fact, the longest chain PUFA. It's kinda like radiation. Radiation will shrink a tumor at first but eventually causes cancer.
PUFA’s and Cancer Posted on June 11, 2012, 0 Comments
by Brad Weeks, MD on June 7, 2008
NOTE: While I don't agree with everything the author writes, I believe the article makes some good points--I have highlighted some of the more important ones in BOLD.
Up to the 19th-century, fat was relatively expensive and butter was a luxury. The poor lived mainly on potatoes and bread, which were cheap, supplemented whenever possible with whatever source of protein and fat they could afford. Not surprisingly, mortality was high amongst the poorer classes. To fill the gap in the market cheap substitutes for butter began to be produced in the last quarter of the Victorian era. Made from cheaper fats and coloured yellow to mimic the look, if not the taste of butter, they were called margarine. And this started, quite slowly at first, a radical change in the types of fat we, as a nation, ate.
Originally margarines were made of beef suet, milk and water. Later the recipes changed to include lard, whale oil and the oils of olive, coconut, ground nut and cottonseed. By the middle of the 20th-century an emulsion of soya bean and water was substituted for the milk and margarines could be made entirely of inexpensive oils from vegetable sources. In all these forms, margarine was the poor relation to butter.
In the 1920s a new disease had suddenly ‘taken off’ all over the industrialised world. By the 1940s it had become a leading cause of premature death — and nobody knew why. In 1950, an American scientists hypothesised that cholesterol might be to blame. (1) In 1953, another American, Ancel Keys, compared levels of this disease in seven countries with the amounts of fat in those countries. (2) And so was born the ‘Diet-Heart’ hypothesis, for the new disease was coronary heart disease.
To reduce the risk of a heart attack, Ancel Keys recommended cutting down on the vegetable oils and margarines. However, it was discovered that vegetable oils, which are composed largely of unsaturated fats and oils, tended to lower blood cholesterol levels, while saturated fats tended to raise them. And by that time, it had been decided, largely by majority vote, (3) that raised cholesterol increased the risk of a heart attack. With the advent of the ‘Prudent Diet’ in the USA in 1982, and COMA’s introduction of ‘healthy eating’ in Britain two years later, the fats in our diet changed even more dramatically: we were told to avoid animal fats such as butter and lard, which have a larger proportion of saturated fats, in favour of largely polyunsaturated vegetable margarines and cooking oils. Now margarines could be priced to rival butter. Recently, margarines have been developed specifically to lower cholesterol levels, and prices have risen again. Benecol, made from tree bark is considerably more expensive than butter.
Before going further, it might be as well for you to learn a little chemistry. This will make understanding how the different fats react under different circumstances. This is essential to understanding how cancers start or are promoted.
Margarine — a natural food?
The polyunsaturated fats used to make margarine are generally obtained from vegetable sources: sunflower seed, cottonseed, and soybean. As such they might be thought of as natural foods. Usually, however, they are pressed on the public in the form of highly processed margarines, spreads and oils and, as such, they are anything but natural.
In 1989, the petroleum-based solvent, benzene, that is known to cause cancer, was found in Perrier mineral water at a mean concentration of fourteen parts per billion. This was enough to cause Perrier to be removed from supermarket shelves. The first process in the manufacture of margarine is the extraction of the oils from the seeds, and this is usually done using similar petroleum-based solvents. Although these are then boiled off, this stage of the process still leaves about ten parts per million of the solvents in the product. That is 700 times as much as fourteen parts per billion.
The oils then go through more than ten other processes: degumming, bleaching, hydrogenation, neutralization, fractionation, deodorisation, emulsification, interesterification, . . . that include heat treatment at 140-160C with a solution of caustic soda; the use of nickel, a metal that is known to cause cancer, as a catalyst, with up to fifty parts per million of the nickel left in the product; the addition of antioxidants such as butylated hydroxyanisol (E320). These antioxidants are again usually petroleum based and are widely believed to cause cancer.
The hydrogenation process, that solidifies the oils so that they are spreadable, produces trans -fatty acids that rarely occur in nature.
The heat treatment alone is enough to render these margarines nutritionally inadequate. When the massive chemical treatment and unnatural fats are added, the end product can hardly be called either natural or healthy.
You may be interested in a list of the ingredients that may be present in butter and margarine:
Butter: milk fat (cream), a little salt
Margarine: Edible oils, edible fats, salt or potassium chloride, ascorbyl palmitate, butylated hydroxyanisole, phospholipids, tert-butylhydroquinone, mono- and di-glycerides of fat-forming fatty acids, disodium guanylate, diacetyltartaric and fatty acid esters of glycerol, Propyl, octyl or dodecyl gallate (or mixtures thereof), tocopherols, propylene glycol mono- and di-esters, sucrose esters of fatty acids, curcumin, annatto extracts, tartaric acid, 3,5,trimethylhexanal, ß-apo-carotenoic acid methyl or ethyl ester, skim milk powder, xanthophylls, canthaxanthin, vitamins A and D.
Dietary fat patterns
The total amount of fats in our diet today, according to the MAFF National Food Survey, is almost the same as it was at the beginning of this century. What has changed, to some extent, is the types of fats eaten. At the turn of the century we ate mainly animal fats that are largely saturated and monounsaturated. Now we are tending to eat more polyunsaturated fats — it’s what we are advised to do. In 1991, two studies, from USA (4) and Canada, (5) found that linoleic acid, the major polyunsaturated fatty acid found in vegetable oils, increased the risk of breast tumours. This, it seems, was responsible for the rise in the cancers noted in previous studies. Experiments with a variety of fats showed that saturated fats did not cause tumours but, when small amounts of polyunsaturated vegetable oil or linoleic acid itself was added, this greatly increased the promotion of breast cancer.
Body cell walls are made of cholesterol, protein and fats. The graph below demonstrates that the human body’s fat make-up is largely of saturated and monounsaturated fatty acids. We contain very little polyunsaturated fat. Cell walls have to allow the various nutrients that body cells need from the blood, but stop harmful pathogens. They must be stable. An intake of large quantities of polyunsaturated fatty acids changes the constituency of cholesterol and body fat. Cell walls become softer and more unstable.
Polyunsaturated fats suppress the immune system
Polyunsaturated fats (PUFs) are greatly immunosuppressive, and anything that suppresses the immune system is likely to cause cancer. The first person to suggest that polyunsaturated fats cause cancer was Dr R A Newsholme of Oxford University, England. (6) What Newsholme wrote was that when our bodies get sufficient nutrition, our diet includes immunosuppressive PUFs which make us prone to infection by bacteria and viruses. When we are starved, however, our body stores of PUFs are depleted. This allows our bodies’ immune systems to recover which, in turn, allows us to fight existing infection and prevent other infections. He was making the point that the immunosuppressive effects of PUFs in sunflower seeds are useful in treating autoimmune diseases such as multiple sclerosis, (7) and that the same fatty acids could be used to suppress the immune system to prevent rejection of kidney transplants.
It was during the early days of kidney transplantation that doctors first encountered the problem of tissue rejection as their patients’ bodies destroyed the alien transplanted kidneys. If transplantation were to be a success, they had to find a way to suppress the immune system. Newsholme had said that there was no better way to immunosuppress a renal patient than with sunflower seed oil. So kidney transplant doctors fed their patients linoleic acid. (8) (Linoleic acid is the major polyunsaturated fatty acid in vegetable oils.) But the transplant doctors were then astonished to see how quickly their patients developed cancers: some cancers were up to twenty times as frequent as was expected.
This was in line with heart trials using diets that were high in PUFs which, reported an excess of cancer deaths from as early as 1971. (9)
By the early 1980s, we were being exhorted by doctors and nutritionists to eat more PUFs because they were ‘good for us’ despite the fact that Oncology Times carried a paper in January 1980 from the University of California at Davis that mice fet PUFs were more prone to develop melanoma. In May 1980, the same publication carried a similar report from Oregon State University which said that PUFs fed to cancer-prone mice increased the numbers of cancers formed.
In 1989 there was a report of a ten-year trial at a Veterans’ Administration Hospital in Los Angeles. In this trial half the patients were fed a diet which had double the amount of PUFs as compared to saturated fats. In the half of the patients on the high PUF diet there was a fifteen percent increase in cancer deaths compared to the saturated fat group. (10) The authors of the report said that the PUFs had been the cause of the increase in cancer deaths. The British Medical Journal carried an editorial in its 6 October 1973 issue which asked if PUFs were carcinogenic. It came to the conclusion that they were.
Wayne Martin likes to tell a story which suggests just how cancer-causing are PUFs. In 1930 in the USA, eighty percent of men smoked cigarettes and the tar content of cigarettes was much higher than it is today. The death rate at that time from lung cancer was very low. In 1955 doctors decided that PUFs were good in terms of heart disease protection. After this lung cancer deaths increased so dramatically. By 1980 although the number of American men who smoked had dropped to only thirty percent, three times as much PUF was being eaten — and there were sixty times as many lung cancer deaths. (11)
In 1990, Martin called Newsholme’s Oxford University office but by then Newsholme had retired. Martin spoke to his successor to find that they were still treating autoimmune diseases with PUFs. By then they were using fish oil. The doctor said the reason for the fish oil was that the degree of immunosuppression increased with the degree of unsaturation and fish oil was much more unsaturated than sunflower oil. Martin asked the doctor why they were not talking about PUFs causing cancer. The doctor replied that if he did that he would be run out of Oxford.
Carcinogens — background radiation, ultraviolet radiation from the sun, particles in the air we breathe and the food we eat — continually attack us all. Normally, the immune system deals with any small focus of cancer cells so formed and that is the end of it. But linoleic acid suppresses the immune system. With a high intake of margarine, therefore, a tumour may grow too rapidly for the weakened immune system to cope thus increasing our risk of a cancer.
Polyunsaturated fats cause cancer
Since 1974, the increase of polyunsaturated fats has been blamed for the alarming increase in malignant melanoma (skin cancer) in Australia. (12) We are all told that the sun causes it. Are Australians going out in the sun any more now than they were fifty years ago? They are certainly eating more polyunsaturated oils: in Australia in 1995 I saw that even the cream on milk was removed and replaced with vegetable oil. Victims of the disease have been found to have polyunsaturated oils in their skin cells. Polyunsaturated oils are oxidised readily by ultra-violet radiation from the sun and form harmful ‘free radicals’. These are known to damage the cell’s DNA and this can lead to the deregulation we call cancer. Saturated fats are stable. They do not oxidise and form free radicals.
Malignant melanoma is also said to be increasing in this country. Does the sun cause this? In Britain the number of sufferers is so small as to be relatively insignificant. Even so, it is not likely that the sun is to blame since all the significant increase is in the over-seventy-five-year-olds. People in this age group tend to get very little sun.
That the sun is not to blame is confirmed by other findings:
Melanoma occurs ten times as often in Orkney and Shetland than it does on Mediterranean islands.
It also occurs more frequently on areas that are not exposed to the sun.
In Scotland, for example, there are five times as many melanomas on the feet as on the hands;
and in Japan, forty per cent of pedal melanomas are on the soles of the feet . (13)
Polyunsaturated fats promote cancer
Many laboratories have shown that diets high in polyunsaturated fatty acids promote tumours. Cancer promotion is not the same as cancer causing. The subject is complex; suffice to say here that promoters are substances that help to speed up reproduction of existing cancer cells.
It has been known since the early 1970s that it is linoleic acid that is the major culprit. As Professor Raymond Kearney of Sydney University put it in 1987: ‘Many laboratories have shown that a greater proportion of polyunsaturated fats are superior to diets rich in saturated fats in promoting the yield of experimental mammary tumours. In such studies, omega-6 linoleic acid appeared to be the crucial fatty acid . . .’ and ‘Vegetable oils (eg Corn oil and sunflower oil) which are rich in linoleic acid are potent promoters of tumour growth.’ (14)
Polyunsaturated fats and breast cancer
A study of 61,471 women aged forty to seventy-six, conducted in Sweden, looked into the relation of different fats and breast cancer. The results were published in January 1998. This study found an inverse association with monounsaturated fat and a positive association with polyunsaturated fat. In other words, monounsaturated fats protected against breast cancer and polyunsaturated fats increased the risk. Saturated fats were neutral. (15)
Flora margarine, the brand leader, is thirty-nine percent linoleic acid; Vitalite and other ‘own brand’ polyunsaturated margarines are similar. Of cooking oils, sunflower oil is fifty percent and safflower oil seventy-two percent linoleic acid. Butter, on the other hand, has only a mere two percent and lard is just nine percent linoleic acid. Linoleic acid is one of the essential fatty acids. We must eat some to live, but we do not need much. The amount in animal fats is quite sufficient.
Because of the heart disease risk from trans-fats in margarines, in 1994 the manufacturers of Flora changed its formula to cut out the trans fats and other manufacturers have since followed. But that still leaves the linoleic acid.
The anti-cancer fat
Linoleic acid is one of the essential fatty acids that our bodies need but cannot synthesise. We must eat some to survive. Fortunately there is one form of linoleic acid that is beneficial. Conjugated linoleic acid (CLA) differs from the normal form of linoleic acid only in the position of two of the bonds that join its atoms. But this small difference has been shown to give it powerful anti-cancer properties. Scientists at the Department of Surgical Oncology, Roswell Park Cancer Institute, New York (16) and the Department of Biochemistry and Molecular Biology, New Jersey Medical School, (17) showed that even at concentrations of less than one percent, CLA in the diet is protective against several cancers including breast cancer, colorectal cancer and malignant melanoma.
Conjugated linoleic acid has one other difference from the usual form — it is not found in vegetables but in the fat of ruminant animals. The best sources are dairy products and the fat on red meat, principally beef. (18)
It has been suggested that the consumption of red meat increases the risk of colon cancer, yet in Britain there is no evidence to support this. (19) It is interesting that all the evidence implicating red meat in cancer comes from the USA — where they cut the fat off.
Saturated fats and animal fats are usually blamed for all manner of diseases in Western society. But look at the facts:
In the 19th-century, when animal fats were all that was available, cancers were rare (as was heart disease).
Polyunsaturated fats and oils are used to suppress the immune system, such immunosuppression is known to cause cancers to start and promote cancer.
In this last century there has been a change in favour of polyunsaturated fats and oils — and cancer rates have soared.
Unfortunately, as polyunsaturated fatty acids are also essential to the body; we must have some. So a proper balance must be struck. Whether the dramatic increase in the numbers of cancers in the last century was as a result of a similarly dramatic rise in our intake of polyunsaturated vegetable oils is not known — but the evidence strongly favours such a conclusion.
Under the circumstances, it seems prudent to get what linoleic acid we need from animal sources. Or to restrict polyunsaturated oil consumption so that linoleic acid is no more than three percent of the total fat intake.
1. Gofman, J W, et al. The role of lipids and lipoproteins in atherosclerosis. Science 1950; 111: 166-181, 186
2. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp 1953; 20: 118-139.
3. Mann G V. Diet-heart: End of an Era. New Eng J Med . 1977; 297: 644.
4. Carroll K K. Dietary fats and cancer. Am J Clin Nutr 1991; 53: 1064S.
5. France T, Brown P. Test-tube cancers raise doubts over fats. New Scientist , 7 December 1991, p 12.
6. Newsholme E A. Mechanism for starvation suppression and refeeding activity of infection. Lancet 1977; i: 654.
7. Miller JD, et al. Br Med J 1973; i: 765.
8. Uldall PR, et al . Lancet 1974; ii: 514.
9. Pearce M L, Dayton S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1971; i: 464.
10. American Heart Association Monograph, No 25. 1969.
11. Nauts HC. Cancer Research Institute Monograph No 18. 1984, p 91.
12. Mackie BS. Med J Austr 1974; 1: 810.
13. Karnauchow PN. Melanoma and sun exposure. Lancet 1995; 346: 915.
14. Kearney R. Promotion and prevention of tumour growth — effects of endotoxin, inflammation and dietary lipids. Int Clin Nutr Rev 1987; 7: 157.
15. Wolk A, et al. A Prospective Study of Association of Monounsaturated Fat and Other Types of Fat With Risk of Breast Cancer. Arch Intern Med . 1998; 158: 41-45
16. Ip C, Scimeca J A, Thompson H J. Conjugated linoleic acid. A powerful anticarcinogen from animal fat sources. Cancer 1994; 74(3 Suppl): 1050-4.
17. Shultz T D, Chew B P, Seaman W R, Luedecke L O. Inhibitory effect of conjugated dienoic derivatives of linoleic acid and beta-carotene on the in vitro growth of human cancer cells. Cancer Letters 1992; 63: 125-133.
18. Lin H, Boylston TD, Chang MJ, Luedecke LO, Schultz TD. Survey of the conjugated linoleic acid contents of dairy products. J Dairy Sci . 1995; 78: 2358-65.
19. Cox BD, Whichelow MJ. Frequent consumption of red meat is not a risk factor for cancer. Br Med J 1997; 315: 1018.
Source – http://weeksmd.com/?p=840
2. Radiation (yes, polyunsaturated fatty acids are worse)
4. Over Exercising
5. Lack of Digestible Fuel (i.e. glucose/protein)
And without a healthy metabolism, you cannot be healthy...
In the 1930's, 80% of men in the U.S. smoked cigarettes. And despite the fact that the tar content of cigarettes was much higher then than it is today, the death rate from lung cancer was actually extremely low. Then, in the 1950's, doctors determined that Polyunsaturated Fats (i.e. vegetable oils) were beneficial in the protection against heart disease--this was undoubtedly due more to a strong Vegetable Oil Lobby than actual education since fewer than 6% of MD's receive any form of nutritional education--and deaths from lung cancer saw a dramatic increase. By the 1980's, the number of American men who smoked had dropped down to 30%. Unfortunately, Polyunsaturated Fat Consumption was 400% higher than in the early part of the century.
Lung cancer deaths were 6000% more common.