Saturday, December 29, 2012

Antidepressants dont work

Depression is a debilitating condition and a major public health problem. It is the top-ranking cause of non-fatal disease burden in Australia, accounting for eight percent of the total years lost due to disability in 1996 1. It is predicted to be the second largest cause of disability in Australia by the year 2020 2. Depression is a mental disorder that has the potential to greatly impact one’s everyday activities. The experience of depressed mood, insomnia, loss of energy, irritability and other symptoms are commonly linked with depression. Further, recent research demonstrates its association with inflammation.
Unfortunately, although we continue to diagnose and medicate people for depression, there is little science and certainly no evidence to continue to prescribe antidepressants to most individuals. There are more myths in this area than there are facts and, as a result, many people are led astray by an industry that makes huge amounts of money from people’s suffering.
Depression theory
It is important to understand that most of what we know about the biochemistry and physiology of depression is theory and not fact. It is an hypothesis but is often presented by professionals as truth, with the connotation that these professionals know the full truth about depression. No, in fact, they do not. What we do know is that serotonin is located in the pineal gland, blood platelets, the digestive tract and the brain. Serotonin acts as a chemical messenger that transmits nerve signals between nerve cells and also causes blood vessels to narrow 3. We know that there are many other chemical messengers in the body that can have an impact on our mood and state of wellbeing.
Traditionally it has been thought that drugs most commonly used to treat depression—the selective serotonin reuptake inhibitors (SSRIs) such as Prozac® and Zoloft®—act according to the serotonin hypothesis. This hypothesis purports that levels of serotonin in the brain determine how we feel: high levels of serotonin cause heightened happiness, while decreased levels lead to sadness. Clinical depression has been attributed to low levels of serotonin transmission in the brain 4. The serotonin transporter 5-HT is a reuptake molecule that removes serotonin, so it is thought that the SSRIs act to interfere with the action of 5-HT and therefore allow serotonin to accumulate and levels to increase 4. This theory is still strongly supported by the pharmaceutical industry 5, which even uses it to encourage people to “correct” their serotonin levels in advertising for the drugs 6.
More recently, this theory has received much criticism as neuroscience research has failed to confirm “any serotonergic lesion in any mental disorder” 6. That is, the theory is just not supported by evidence. A growing body of research disagrees with the serotonin hypothesis 6,7,8. In support of this, a Cochrane review found that tricyclic antidepressants are of the same efficacy as SSRIs 8. Since tricyclics do not impact serotonin levels, this would suggest that the serotonin hypothesis has been disproved. But someone forgot to tell the drug companies and professionals who continue to aggressively dish out these drugs.
Despite the blind acceptance of the serotonin theory, the GlaxoSmithKline website has posted: “There is no clear cut reason for depression, and a number of factors may be at play, including altered levels of chemical messengers (neurotransmitters) in the brain, such as serotonin and noradrenaline” 9. If antidepressants were a cure for depression, there would be a definite illness, with definitive symptoms and causes that the drugs are targeting. GlaxoSmithKline’s statement does not support this case.
Antidepressants describe the broad range of medications prescribed to alleviate the symptoms of certain depression- and anxiety-related mood disorders and include a number of different groups of medications. These include monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), tetracyclic antidepressants (TeCAs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and the current standard treatment group: selective serotonin reuptake inhibitors (SSRIs), which became immensely popular in the 1990s 10.
The first antidepressant that came along with a huge fanfare was Prozac®. Prozac® appeared on the market in 1988 and is still being prescribed today. It has become one of the most prescribed drugs to date 11. Prozac® is part of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs).
The prescription of antidepressants has skyrocketed over recent decades 10. From 1996 to 2005, individuals treated with antidepressants became more likely to also receive treatment with antipsychotic medications and less likely to undergo psychotherapy—the net result is more drugs and less treatment. The percentage of the U.S. population using at least one psychotropic medication increased from 5.9% in 1996 to 8.1% in 2001 12. Among the psychotropic drugs, antidepressants are the most frequently prescribed medications. The U.S. CDC found that antidepressant use in the United States jumped nearly 400% by the 2005-2008 survey period, compared with the 1988-1994 period, with 11% of those over age 12 taking the drugs (U.S. CDC and Prevention’s National Center for Health Statistics) up from six percent in 1996 13.
Antidepressants are now used by more than 27 million Americans, most of whom are women 14. Women are twice as likely as men to be diagnosed with major depressive disorder and up to three times more likely to be diagnosed with dysthymic disorder 15. However, despite the absence of any scientific evidence, antidepressants are increasingly being prescribed for other conditions such as hot flashes, headache, back pain, neuropathy, sleep-related conditions, anxiety spectrum disorders, eating disorders and fibromyalgia 16. Once prescribed, many people continue taking antidepressants, with more than 60% of Americans who use the drugs reporting being on them for two years or more. And about 14% of Americans taking antidepressant medication have done so for 10 years or longer. Patients who take the drugs often get them from their regular doctor rather than a so-called mental health professional.
Last year in Australia, there were 29 million prescriptions written for medications related to mental health issues. Antidepressant medications accounted for nearly 60% of these scripts, followed by anti-anxiety and anti-psychotic drugs 17. This suggests that around 2.4 million Australians are using medication to deal with mental health issues.
In the United States, “The number of visits by patients for depression was 24.5 million in 2001, a 70% increase since 1987” 18. The ambiguous nature of depression has provided leeway for significant misdiagnosis. The difficulty in identifying valid cases of depressive disorder lies within its tendency to share unclear boundaries with other mental disorders and normality 19. The distinction between major depression and sadness, for instance, has become completely obscure. Previously, depression was classed as either endogenous or reactive 19. Endogenous depression was regarded as a rare biological condition, whereas reactive depression was exogenous and triggered by stressful events outside our control, such as the loss of a loved one 19.
Under the Diagnostic and Statistical Manual (DSM-III), the diagnosis of clinical depression requires the presence of at least five of the possible nine symptoms for at least two weeks. Some of these symptoms include loss of interest in usual activities, depressed mood, fatigue, insomnia and lowered appetite. Yet many of these symptoms can be seen in natural responses to stress, loss 19, illness, fatigue and poor sleep. Unfortunately this weak criterion translates into a “low threshold for diagnosing clinical depression” 20. This suggests that there are huge risks in misdiagnosing normal emotional states as clinical illnesses. As an example, chronic fatigue is also commonly mistaken for depression due to the large overlap in symptoms. In one study involving 3,200 individuals, patients who were depressed in the beginning of the study were found to be four times more likely to be fatigued, rather than “depressed” 21. Alas, due to the reinforcing nature of depression and fatigue, diagnosis becomes difficult.
Considering the major ambiguities surrounding the concept of depression, it is not surprising that the quantity of prescriptions for antidepressant medication is so high. What is of most concern is the number of people who are taking antidepressants and exposing themselves to unnecessary risk and, in too many cases, are not taking action to resolve underlying issues.
In a later analysis of additional data, Kirsch supported his earlier findings and reported antidepressants may be more effective than a placebo only in severe depression 23. Now with more than a dozen major meta analyses, the research continues to show there is little supporting evidence that antidepressants work when placebos appear to be just as—and in some case more—effective. The research also shows the long-term effects tend to be severe 22,23,24,25,26,27. In the majority of studies, antidepressants performed the same as inactive placebo pills.
A recent study found that a minority of antidepressant users actually fared worse than placebo users. In this study, researchers randomly assigned 156 depression patients to either take the antidepressant sertraline (Zoloft® and other brands) daily for 16 weeks or be in a placebo group given inactive pills. After 16 weeks, there were no overall differences in how the groups fared 28. Of the antidepressant patients, 31% were treatment “responders,” meaning they had fallen below a certain score on a standard measure of depression symptoms, or had seen their score drop at least 50%. The same was true of about 28% of patients in the talk-therapy group, and 24% in the placebo group. The differences among the three groups were so small as to likely be due to chance 28.
Two even bigger reviews in 2010 came to the same conclusions. A review of four meta analyses of efficacy trials submitted to the U.S. Food and Drug Administration (FDA) suggests that antidepressants are only “marginally efficacious” compared with placebo and “document profound publication bias that inflates their apparent efficacy.” In addition, when the researchers analysed the largest antidepressant effectiveness trial ever conducted, they found that “the effectiveness of antidepressant therapies was probably even lower than the modest one reported... with an apparent progressively increasing dropout rate across each study phase” due to side effects 29. A review of nine studies involving 751 participants found that, from the results presented, antidepressants had only a small positive effect when compared to an active placebo 30. Other studies have also shown St John’s Wort to be more effective than an SSRI 31 and exercise to be at least as effective in older patients 32.
Other irregularities were seen in the data. It was noted that published data consisted entirely of positive outcomes and that many of the negative trials’ reports were not published or that negative data were displayed in a positive manner 25,26.  Publication bias, where only the positive results are reported and published, is well known in the drug industry and just a part of the drug companies’ everyday lies and deception.
Despite the findings of researchers, the FDA in the U.S. reports that 94% of its studies have shown positive results, with antidepressants found to be effective in treating depression 33. However, publication of antidepressant studies by the FDA is highly selective: “The studies that the FDA judged as positive were approximately 12 times as likely to be published in a way that agreed with the FDA analysis as were studies with non-positive results according to the FDA” (Turner et al. 2008). Why have the FDA in the U.S. and Australian regulatory authorities continued to go against the scientific evidence?
The likely benefit of antidepressants is the placebo effect 23,25. In trials, the patients on placebos would see the doctor on a weekly basis for check-ups and to update the analysts for the report. In addition, the patients were within easy access to help 24 hours a day 26,34. Thus, the amount of human contact, attention and care skews the results 26. This could possibly reveal the reason the placebo had such a strong effect. Imagine the positive feeling from being closely cared for by your medical practitioner, including having his or her phone number, rather than just in and out of the office in 12 minutes. The amount of attention and care influenced the strength of the placebo. Under real-world conditions, the patient sees the doctor less frequently and is less likely to seek help 26,34.
The actual efficacy of SSRIs, therefore, remains in question and often subject to the merits and interests of those conducting a particular study. Many people drop out of drug trials because of the seriousness of side effects. The serotonin receptors are responsible for a variety of functions unrelated to mood, such as sleep, appetite and sexual function, as well as symptoms such as pain, nausea, depression, and anxiety 35. Common side effects of taking an SSRI include nausea, dizziness, gastrointestinal disturbances, anxiety, agitation, insomnia, sexual dysfunction and weight gain 35. Significant literature exists documenting the symptoms of SSRI discontinuation syndrome, which range from moderate to severe 36. There can also be more serious consequences: SSRI use has been linked to serotonin syndrome, birth defects and high risk of suicide. The link between antidepressants and suicide has been recognised for at least 20 years and the United States FDA requires that antidepressants carry a label warning of this increased risk on each box 37. In such cases it would seem antidepressants are not effective at all and, in fact, can have serious and even deadly side effects.

Despite these findings that have now been repeated many times, “professionals” working in the field still state that antidepressants work and continue to prescribe them to more and more people.
It is also worth pointing out that in the United States, until 1990 tryptophan dietary supplements were being taken by approximately 15 million Americans. On March 22, 1990, the Food and Drug Administration (FDA) banned the sale of L‑tryptophan in response to several deaths during the previous year from a deadly flu‑like condition called EMS 38. This is despite L-tryptophan having been used as a supplement for decades prior to this, by a large number of people, without any adverse side effects. The problem was caused by a contaminated batch of tryptophan, not the tryptophan itself. One wonders why it was banned, as most drugs including antidepressants would be removed from the marketplace if this principle were applied across the board, including drugs that have been linked with hundreds of thousands of deaths.
However, on March 26, 1990, only four days after the banning of L-tryptophan, Prozac®, the wonder drug in the treatment of depression, was introduced with great fanfare after more than 10 years of development. What a coincidence. As mentioned earlier, Prozac® is an SSRI, whilst tryptophan actually increases the serotonin levels in the body.
Other interesting facts about this controversy:
L‑tryptophan was banned as a dietary supplement in the United States and Australia until 2005. It could, however, be imported from Japan and became available as a prescription-only drug. One hundred 500 mg capsules cost approximately $75.00. This is about five times more expensive than its previous cost as a dietary supplement.
L‑tryptophan is still used in baby food produced and sold in the United States.
Farmers are still allowed to use it in stock feed for animals. I wonder if this is because happy animals are more likely to gain weight?
1.     Mathers et al. 2000
2.     Minas et al. 2007
3.     MedicineNet 2003
4.     Schafer 1999
5.     Cowen 2008
6.     Lacasse and Leo 2005
7.     Murphy 1998
8.     Geddes et al. 2005
9.     GlaxoSmithKline 2008
10.  Olfsen et al. 1998
11.  Wrobel 2007
13.  Olfson et al. 2009
14.  Cosgrove et al.
15.  American Psychiatric Association 2000
16.  Roberts 2007
17.  Australian Institute of Health and Welfare
18.  Fergusson et al. 2006
19.  Parker 2007
20.  Lucassen et al. 2007
21.  Skapinakis 2004
22.  Kirsch 2002
23.  Johnson and Kirsch 2008
24.  Kirsch and Moncrieff 2005
25.  Ioannidis et al 2008
26.  Posternak and Zimmerman 2007
27.  Crawford and Parker 2007
28.  Barber 2011
29.  Pigott et al. 2010
30.  Moncrieff et al. 2010
31.  Szegedi et al. 2005
32.  Blumenthal et al. 1999
33.  Turner et al. 2008
34.  Blier 2008;
35.  Ferguson 2001
36.  Haddad 1998
37.  Reeves and Ladner 2010
38.  Manders 1995

Shannon Fitzgerald , Ben Gundry, Kahlia Belli, Noratiah Larry, Grant Swan and Jan van der Walt, Geraldine Treloar

Thursday, December 13, 2012

Margarine is much worse than butter

In the 1970s, I was instructed to swap from butter to margarine. Fortunately, I did not like the taste of margarine and, over the years, the more research I conducted on the topic the more I realised that we were being lead astray and even lied to about this. Today, when I ask any of my audiences, sometimes in the hundreds, “Who thinks margarine is better for you than butter?” I rarely get a positive response. It seems most people already know that margarine is a dangerous substitute.
It appears that there is no scientific evidence that margarine is healthier than butter. In fact, evidence suggests the exact opposite is true. This is summed up first of all in one of my earlier articles that showed saturated fat is not the demon it is made out to be and may even be associated with reduced heart attack (another myth shattered). At least that is what the biggest and best studies show. Furthermore, we consume many more Omega 6 (vegetable) oils today than our ancestors did and this is having a negative impact on our health. These oils are not just in our margarine but also hidden in most of our food. We ate margarine for 50 years thinking it was made up of so-called “good fats” only to find out it was laden with the deadliest form of fat: trans fats. Finally, there is emerging evidence that margarine may not be good for our health, with or without trans fats, and is nowhere near a natural food; the push to sell more margarine has come from organisations like the Heart Foundations around the world and branches of margarine companies with strong vested interests in promoting margarine sales.
I think one of the best things to have happened to the Australian cuisine is Master Chef. It has inspired a whole generation to go back to the kitchen and start cooking again. It has also encouraged the increased use of butter over vegetable oils, something the Heart Foundation and the margarine manufacturers did not like so they had to come up with campaigns to sway people back to margarine. Interestingly one of the foundation’s ploys was to create, through a public relations company, a group called “Mums United” which pretends to be a grassroots mothers campaign against evil butter. According to David Gillespe (Sweet Poison) and the “duck test” of inductive reasoning, “It walks like a margarine advertisement and quacks like a margarine advertisement, so guess what it I think it is?” And the margarine companies fund it! Some of the group’s tactics have included offering financial support to people who pledged not to eat butter. So much for it being a grassroots organisation. It seems that margarine interests have taken some of the old tactics taught to us by the tobacco industry and big drug companies.
I want to make it very clear that I have no vested interests in anything other than people’s health and the truth.
Various heart associations around the world recommend increasing Omega 6 (vegetable) oil consumption and reducing saturated fats, based on flawed studies that have been seriously questioned due to data manipulation. This includes the omission of relevant trials with unfavourable outcomes—that is, leaving out any negative studies 1,2,3 and including studies that combine both Omega 3 (fish oils, which are good for you) and Omega 6 consumption together under the title of “polyunsaturated fats.” The associations even included poorly done studies as long as the studies showed the desired results. This type of publication bias is well known in the research literature particularly with big drug companies trying to show that their drugs work better than they really do.
Margarine is far from being a natural product—well, as much as you can claim that plastic is natural. The major components of margarine are “vegetable” oils, obtained from foods such as sunflower seeds, rapeseed, or potentially genetically modified canola and soya beans. These oils are usually extracted using the application of pressure, heat and possibly solvents and then treated with sodium hydroxide to “neutralise” certain fats in the oil. It is then bleached, filtered and steam-treated to produce what is essentially a colourless, flavourless murky looking liquid. The liquid is converted into a solid at room temperature through esterifcation, which uses high temperature and pressure, along with enzymes or acids, to harden the oil—this is also called hydrogenation. Hydrogenation produces trans fats that are strongly linked with heart disease, cancer and other chronic illnesses. The final product is coloured and flavoured with various agents to make it feel and look like butter. Then finally ingredients like plant sterols and stanols and alpha linolenic acid is added to make it appear healthy. The finished product is not natural or healthy.
Plant stanols and sterols are added to reduce cholesterol. However, overwhelming evidence now shows cholesterol is just a poor indicator of heart attack, not the cause 4. It is just the warning sign or, if I can use an analogy, like a fire alarm in your home, it is not the problem itself, but a warning about the problem. You can get plenty of stanol and sterols in nuts, beans and seeds, which are not only natural but also full of other healthful benefits including vitamins, antioxidants, minerals and so much more and reduce all forms chronic illness. Margarine manufacturers can trumpet the presence of “heart-healthy” Omega 3 fats on the label, however they are putting plant-based Omega 3 fats (alpha linolenic acid) that do not act like Omega 3 from fish sources. They still have to be converted in our body to fish-like Omega 3s. It is also questionable whether they will be oxidised or not and therefore of any value. Adding a nutrient to toxic food does not make it healthy. Do you really believe the advertising?
Margarine is a major source of trans fatty acids, the intake of which has risen since the early 20th century. Trans fatty acids are synthetic fats produced as a byproduct of the hydrogenation of liquid vegetable oils, making them into solid margarine. An abundance of data indicates that consumption of trans fatty acids increases the risk of coronary heart disease (CHD), cancer, diabetes and other chronic illnesses. Margarine companies are now obliged to list the amount of trans fats on the side of the packet. Until recently however, margarine has been the single biggest source of these very toxic fats.
In a study of women, long-term margarine and trans fat consumption was associated with a 67% increased risk of heart disease 5. The decrease in intake of trans fatty acids in Denmark saw a 50% reduction in the number of deaths from ischemic heart disease 6. A recent study found that trans fatty acids promote cardiovascular disease by triggering inflammatory processes in the cells lining blood vessels 7. Increased intake of trans fatty acids has also been linked with an increase in the risk of colorectal tumours by about 86% 8. The potentially damaging effects of trans fats may also be passed from a mother to her child during breast feeding and can lead to an increase in cardiac insulin resistance when the kids become adults 9.
During the past 150 years, the Industrial Revolution and the emergence of agribusiness with processed foods, grain-fattened livestock, and hydrogenation of vegetable fats have considerably reduced the available content of Omega 3 fatty acids and increased that of Omega 6 fatty acids. While Omega 6 and 3 oils are considered essential fatty acids, the research is now showing that it is important to get the correct balance of the fats. An imbalance leads to various metabolic diseases. Western diets are now deficient in Omega 3 fatty acids and are laden with excessive amounts of Omega 6 fatty acids compared with the diet on which human beings evolved and their genetic patterns were established. Our diets now have 14 to 20 times more Omega 6 (vegetable oil) than Omega 3 fatty acids. This imbalance is now linked with diseases such as heart attack, stroke, cancer, obesity, insulin resistance, asthma, arthritis, depression, ADHD, Alzheimer’s disease and even premature ageing. The ideal balance is less than 4:1 or even 1:1 Omega 6 and 3, respectively.
Omega 6 oils such as corn, safflower, cottonseed, sunflower, and soya are now in nearly all our foods. Apart from the obvious consumption of vegetable oils and margarine you buy in the supermarket—which I hope you are now not going to buy—Omega 6 oils are hidden in most foods. You will find vegetable oils in just about every processed and semi-processed food including bread, cakes, and breakfast cereals and in lots of the plant-based drinks like almond or soya milk the main ingredient is often vegetable oil. All the takeaway foods, frozen and packaged dinners have Omega 6 oils. Even the “new” Mediterranean diet is laden with Omega 6 oils. When you buy olives, pesto sauce, sundried tomatoes or anything soaking in oil it is now vegetable oil in which it is soaked, not olive oil because vegetable oil is cheaper, unless you go to Italy where most foods are still soaked in olive oil. It is almost impossible to get away from the excess of Omega 6 oils. Time to read the labels! Factory produced eggs have 20 times more Omega 6 than Omega 3 compared to free-range eggs, which have a ratio of 1:1. Similarly, grain-fed beef (which I do not recommend you eat) has around 20:1 Omega 6 to Omega 3 oils because the cows are fed grains rich in Omega 6 oils. Alpha linolenic acid is found in the grass and is converted into the important Omega 3 oils by the animals. It is found only in grass-fed animals. Grass-fed cows are also a lot less stressed and have as a result lower levels of inflammation.
On the topic of animals fats, I have highlighted in earlier articles that despite claims by the Heart Foundation there is no scientific evidence to suggest that saturated fat through dairy consumption is associated with increased heart attack. By contrast, in a 16-year prospective study of 1,529 adult Australians, researchers found a possible beneficial association between intake of full-fat dairy and cardiovascular mortality 10. Whoops… the Heart Foundation got it wrong again.
By contrast, the Framingham study, which followed people for 20 years (a very long and comprehensive study) and recorded heart attack incidence, found margarine intake increased coronary heart disease in men 11. The scientists in their very conservative language wrote, “These data offer modest support to the hypothesis that margarine intake increases the risk of coronary heart disease.” Not the opposite. In the second ten-year period of the study, the group eating the most margarine had 77% more heart attacks than the group eating none.
Studies that investigated increasing the amount of Omega 6 without a subsequent increase in animal-based Omega 3 (fish oil) consistently found an increase in coronary heart disease (CHD) and all-cause mortality. In an early study, published in 1965, researchers found that people consuming corn oil, a rich source of Omega 6, had a 4.64 times (over 400%) increased risk for both chronic heart disease and death from all causes 12. In the conservative language of scientists, the authors of the study concluded that corn oil is “possibly harmful.” In another study, in which participants consumed more safflower oil and a safflower oil polyunsaturated margarine, participants had a 49% increased risk of death from all causes including a 91% increase from chronic heart disease and 96% from CVD 13.
In one study specifically on Omega 6 consumption in more than 9,000 people, the risk of non-fatal heart attack and death from coronary heart disease was significantly increased among women consuming the n-6 specific polyunsaturated fatty acid (PUFA) diet for one year or less 14. Women consuming this n-6 specific PUFA diet for any duration had non-significant trends to increased risk of non-fatal heart attack and coronary heart disease and any cardiovascular event including death and stroke 14. In fact the Lyon Diet Heart Study found that after follow up of 27 months, non-fatal heart attack and coronary heart disease death and overall mortality were 73% and 70% lower in the experimental group who consumed lower Omega 6 oils and replaced vegetable oils with olive oil. This study also demonstrated that lowering linoleic acid (Omega 6 vegetable oil) below 50% is not harmful and may even be beneficial, producing a profound risk reduction in coronary heart disease.
A recent meta-analysis of randomised controlled trials investigating polyunsaturated Omega 6 oil consumption (vegetable oils and margarine) found that there is absolutely no scientific justification for recommending the increased consumption of Omega 6 oils 2. Or, to quote their conclusion, “Advice to specifically increase n-6 PUFA intake … is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.” The study found for non-fatal myocardial infarction (heart attack) and death from coronary heart disease there was an increased risk of 13% for diets with increased Omega 6. The studies that substituted Omega 6 for saturated fatty acids without simultaneously increasing Omega 3 oils also produced an increase in risk of death. It seems the vegetable oils are just as bad as the trans fats and what we are really lacking are the Omega 3 fish oils.
Arachidonic acid is produced in the body from too much Omega 6 and produces chemical messengers that lead to inflammation in the body called eicosanoids and cytokines. The increase in linoleic acid (Omega 6) has been shown to increase the oxidation of low-density lipoprotein (LDL cholesterol) 15. There is nothing wrong with cholesterol until it is oxidised. The evidence from animal studies also shows that a high linoleic acid diet can promote certain cancers 16 and other inflammatory diseases. In a study of 203,193 men and women, increased intakes of Omega 6 fatty acid (linoleic acid) doubled the risk of ulcerative colitis, an inflammatory bowel disease, which has seen a rapid increase during recent decades. By contrast the highest intakes of Omega 3 were associated with 77% reduction in the risk of the disease 17. Omega 6 fatty acids are present in the cell membrane of colon cells in the form of arachidonic acid. This can be metabolised to chemical messengers in the body called prostaglandin E2, leukotriene B4 and thromboxane A2, all of which are associated with inflammation. On the other hand, Omega 3 fatty acids, including docosahexaenoic acid (DHA) may prevent colonic inflammation.
There is also research showing that too much Omega 6 oil is contributing to premature ageing. Telomeres, which are in all our cells, are thought to be markers of our ageing because they reflect cumulative oxidative stress and inflammation. The shorter they are, the more we have aged. Because the metabolites of Omega 6 promote inflammation, it is believed that an increase in Omega 6 fatty acid content in our diet decreases the leukocyte telomere length 18,19 and hence speeds up the ageing process.
It is time to rethink our fat consumption. The research shows that fat in itself is not bad—in fact, it is essential and the move away from fat has lead to a more obese and sicker population. What we need to do however is decrease our consumption of processed oils like margarine and vegetable oils and increase our Omega 3 fish oils along with Omega 9 oils, including olive oil.
1.     Ramsden 2009;
2.     Ramsden et al. 2010,
3.     Ramsden et al. 2011
4.     Dingle 2011 The Great Cholesterol Deception
5.     Willett et al. 1993
6.     Stender and Dyerberg 2004
7.     Harvey et al 2008
8.     Vinikoor et al. 2010
9.     Osso et al. 2008
10. Bonthuis et al. 2010
11. Gillman 1997
12. Rose et al. 1965
13. Woodhill et al. 1978
14. Frantz et al. 1989
15. Tsimikas et al. 1999
16. Welsh 1992
17. Hart 2008
18. Kang 2010;
19. Kiecolt-Glaser 2012