Dr Peter Dingle

A Catalyst for fat myths. The Heart of the Matter. Catalyst ABC TV

2013-10-28T23:22:00.000-07:00

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Last Thursday (October 24) the ABC Catalyst program aired part one of the Fat Myths and how saturated fat and cholesterol are not actually the ogres the some would have us believe. http://www.abc.net.au/pm/content/2013/s3876403.htm
I was amazed to see it actually as Catalyst is normally very conservative but this was good and there'll be a follow up this week looking at statins (my pet topic after my book “The Great Cholesterol Deception”. I was also amazed that it was the number one watched program that night and next Thursday it will be even bigger.

The Catalyst program highlighted that despite decades of organizations like The Heart Foundation and Nutrition Australia telling the public there really is no credible scientific evidence that saturated fat causes heart disease or, more generally, cardiovascular disease. It was embarrassing to say the least to see the Heart Foundation squirm on TV. Although we are constantly told that saturated fats are “bad” and that margarine is better than butter (which it is not), there is no evidence to support this “bad fat” myth.

Unfortunately there are many myths perpetuated by certain members of the health industry as well as so-called reputable groups who have strong vested interests in margarine and other foods. For example the position paper by the Heart Foundation 3 states that:

Saturated fatty acids (SFA) intake is associated with coronary heart disease (CHD); and

Replacing SFA with omega-6 PUFA (vegetable oils) to achieve a ratio of PUFA to SFA of greater than 1 will reduce the risk of CHD.

While a quote from Nutrition Australia states “Butter is high in saturated fats and when consumed in excess amounts it can increase LDL (BAD) cholesterol levels, thus increasing the risk of cardiovascular disease.”

During the past 40 years the dietary instructions from governments and other authoritative bodies have told us to avoid all animal fats. Average fat consumption decreased, average blood cholesterol levels decreased and vegetable oils increased but the rate of heart disease and the cost of its treatment continued to rise.

The Catalyst program highlighted that poor studies and vested interests have led us astray and date back over 100 years to studies feeding rabbits animal fat, although rabbits normally do not eat meat or animal fat. The evidence against saturated fat has at best always been circumstantial. That is, saturated fat was said to elevate blood cholesterol and elevated blood cholesterol was said to cause heart disease therefore saturated fat would cause heart disease. There never has been any direct evidence that cholesterol or saturated fat cause heart disease or even of a mechanism whereby heart disease would occur.

Even the famous Framingham study, which originally hinted at a problem with saturated fats, now shows there is no association between dietary fat and heart disease and indeed the association of elevated cholesterol and heart disease is limited to a small segment of the study population. In the Framingham Heart Study, researchers working with a population-based cohort study, a total of 832 men, aged 45 through 65 years, found the risk of ischemic stroke declined with total fat, saturated fat and monounsaturated fat (e.g., olive oil) but not polyunsaturated fat such as margarine and vegetable oils. In effect, increased intakes of fat, saturated fat, and monounsaturated fat (olive oil) were associated with reduced risk of ischemic stroke in men. The exact opposite of what we have been told.

This is all summed up in a major independent, international review by The Expert Consultation held jointly by the World Health Organization (WHO) and Food and Agriculture Organization (FAO) in late 2008 which found no evidence that saturated fat causes heart disease. The WHO/FAO report states: “Intake of SFA [saturated fatty acids] was not significantly associated with CHD mortality…. SFA intake was not significantly associated CHD events [e.g., heart attacks]…. fatal CHD was not reduced by… low-fat diets.”

For the sake of our health, and the health of our parents and children, it’s time to change our thinking and start questioning what we are told about saturated fats and for that matter a lot of the information we are spoon fed.

Interestingly and as expected Catalyst was approached by a medical professor who called on the ABC to drop the second program - totally predictable comment - but the AMA head is more supportive and says the profession needs to examine the evidence. About time!

I say BRING it on and watch Catalyst next Thursday.

Statins reduce the effectiveness of exercise.

2013-10-28T19:11:00.000-07:00

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Statins are the most widely prescribed drugs worldwide and have serous side effects but the latest study shows they reduce the benefits of any exercise you do. The study found the statin previously sold under the brand name "Zocor," hindered the positive effects of exercise for obese and overweight adults. That means if you’re taking stains then you are not going to get the full benefits (85% less) of the exercise. A lot of research, including this study also found that taking the stain decreased the mitochondria (power house) in the muscles. This has also lead to a number of studies showing increased risks of diabetes type 2 with increasing statin use.

"Fitness has proven to be the most significant predictor of longevity and health because it protects people from a variety of chronic diseases," said John Thyfault, an associate professor of nutrition and exercise physiology at MU. "if patients start exercising and taking statins at the same time, it seems that statins block the ability of exercise to improve their fitness levels."

Participants in the exercise-only group increased their cardiorespiratory fitness by an average of 10 percent compared to a 1.5 percent increase among participants also prescribed statins. Additionally, skeletal muscle mitochondrial content, the site where muscle cells turn oxygen into energy, decreased by 4.5 percent in the group taking statins while the exercise-only group had a 13 percent increase, a normal response following exercise training.

Statins have only been used for about 15-20 years, so we don't know what the long-term effects of statins will be on aerobic fitness and overall health. We are now only just beginning to see some of the long term side effects of statins including increasing the breast cancer rate.

Journal of the American College of Cardiology, Volume 62, Issue 8, 20 August 2013, Pages 709–714

Statins (used to lower cholesterol) use does not reduce the risk of heart attacks

2013-10-08T18:40:00.000-07:00

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In a recent study no connection was found between the level of exposition to statins in the population and the incidence or mortality from heart attack (Nilsson et al 2011). The use rate of statins increased almost three times for both men and women between 1998 and 2002. However, the change in statin use from 1998 to 2000 showed no correlation to the change in heart attack mortality. They concluded, “despite a widespread and increasing utilisation of statins, no correlation to the incidence or mortality of AMI (heart attack) could be detected.” It should be highlighted that all these researchers are medical doctors or working in a medical establishment.

The drugs don’t work but have serious side effects including recent studies showing increases in diabetes and breast cancer. Although there are many more serous side effects.

In one study Atorvastatin (a statin drug used to lower cholesterol) increases the risk for new-onset type 2 diabetes, according to an analysis of three large trials published in the Journal of the American College of Cardiology. (The trials, as well as this analysis, were sponsored by atorvastatin's manufacturer). Researchers were responding to a 2010 Lancet meta-analysis, which found an increased risk for new-onset diabetes after all statin use and were trying to show their drug was not so bad. In the meta analysis released in the Lancet, using data from 13 randomized trials comprising some 90,000 subjects, found a 9% increase in diabetes risk among those receiving statins compared with controls. The statin-diabetes association was stronger with increasing age and given these drugs are give to older people this is of even more concern. The authors calculate that 255 patients would have to be treated with statins for 4 years to produce an additional case of diabetes. This compares to the need to treat around 300 people with statin drugs to reduce the risk of heart attack (not death) by one or according to the research above no reduction at all. However, the medical profession continue to use relative statistics and say they benefit by 30 or more percent. Obviously these doctors failed stats at university or more likely did not do them.

A recent study (McDougall et al September 2013) found current users of statins for 10 years or longer had a 1.83-to 1.97-fold increased respectively for Ductal and Lobular Breast Cancer. In their conclusion they reported that long-term use of statins was associated with increased risks of both IDC and ILC.

In support of t is here is a comment from one of my readers that might interest you.

“I recently stopped my statin drugs as I was experiencing bad muscle pains. My GP actually said that "statins don't really help women anyway". Hello, why has he then prescribed this and wasted all my money? “ GD, Brisbane

Statin and cholesterol update

2013-10-08T16:01:00.000-07:00

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In summing up more than 500 articles around cholesterol and the statin drugs used to treat cholesterol all I can conclude is that it is The Great Cholesterol Deception. To sum it up, however, the medical industry fudges the figures to fool the doctors that cholesterol is Public Enemy Number One. In fact, cholesterol is one of the most important bio-chemicals in the body and not a single life has ever been saved by lowering cholesterol. Many people suffer serious side effects as a result of taking statin drugs like Lipitor®, Zocor®, Crestor®, Pravachor and others.

Cholesterol is a normal part of our biochemistry and high levels—above six or seven—may be a symptom of an underlying health condition. But it is not the health condition itself. Elevated cholesterol predicts less than 35% of cardiovascular disease. In fact, most heart attack and stroke events occur in individuals without elevated cholesterol, at least half of all cardiac arrests occur in people with normal cholesterol levels and 20% occur in people without any traditional risk factors. But now the drug industry wants to lower the normal level of cholesterol even further so that almost everyone will have “high cholesterol.” At worst cholesterol is simply a messenger telling us there is stress on the liver, and it is not the killer it is made out to be. Cholesterol is a part of our immune, nervous and endocrine system and if high is only doing its job to protect us.

A significantly better predictor of the risk of heart attack or stroke is the concentration of Omega 3 oils in the blood: the higher the concentrations, the lower the risk ^{1,2,3,4,5,6,7,8}, which predict up to 90% of CVD compared to 35% prediction from cholesterol readings. But there is no money to be made in prescribing Omega 3 oils. Omega 3 oils also reduce triglycerides and other risk factors for CVD, as well as reducing the risk of many other forms of chronic illness, from Alzheimer’s to arthritis and cancer. This is due to the anti-inflammatory effect of fish oils. Imagine if the specialists prescribed a few fish oils to patients. No one would require a specialist.

Millions of people are prescribed cholesterol-lowering drugs, statins like Pravachol®, Zocor® and Lipitor® each year, with no measurable benefit. Despite the media hype from poor and lazy journalism at best these drugs lower the actual risk of heart attack by around 0.3 percent and at the same time have side effects in 15% to 40% of people given statins ^9,10,11,12 and serious side effects in as many as five percent of the population of users. And the studies of the side effects have only been short term. Most doctors will simply tell you that statins are safe and hand you a prescription. However if your GP reads the fine print there are two and a half pages of side effects. In some cases up to 65% of people started on statins stop taking them ^13,14. Unfortunately, far too many people take statins and far too many prescriptions are dished out by GPs and specialists whom they trust but who do not read or understand the scientific literature and who have become the retail arm of the pharmaceutical industry.

One of the side effects of statin drugs is that they lower the levels of CoenzymeQ10 ¹⁵. Coenzyme Q10 is not only required for energy production in cells, but also protects against free radicals by acting as an essential fat-soluble antioxidant. Clinical evidence also shows a beneficial effect of Coenzyme Q10 in cardiac arrhythmias, irregular heartbeats, and lowering the risk of heart attack ¹⁶. A recent study found Coenzyme Q10 (CoQ10) for treating people with severe heart failure reduced the mortality and morbidity by around 50%. In essence CoQ10 is essential for our health and is important in lowering the risks of heart attack or stroke and statin drugs lower levels of this essential nutrient.

Major side effects associated with statin drugs include muscle wastage including a form of muscle disease, rhabdomyolysis, that is fatal, memory loss and amnesia. Not only is cholesterol not the enemy but also it is essential to good health and wellbeing. Every cell in the body needs cholesterol in its membrane where it plays a critical role in cell communication. Without cholesterol, cell membranes are incomplete and as a result their functional role deteriorates.

Cholesterol is also used in the mitochondria, the powerhouse of the cell, and plays a vital role in cell energy production not to mention its essential role in the brain structure and function. Cholesterol is the starting material of many essential chemicals including vitamin D, steroid hormones and bile acids for digestion. Cholesterol is metabolised into vital body steroids such as the steroid hormones, these include: sex hormones, oestrogen, progesterone, testosterone and DHEA, as well as the adrenal hormones aldosterone and cortisol. When you lower cholesterol levels you reduce your production of your hormones. As a result statin use can induce gynecomastia, an abnormal enlargement of one or both breasts in men and the proliferation of the glandular component of the breast tissue ¹⁷.

Numerous studies have shown that cholesterol is an important part of your immune system. Low cholesterol levels have also been shown in studies to increase a person’s susceptibility to infections ¹⁸ This is due to cholesterol’s functional role in preventing infections in the body. The lipoproteins that carry cholesterol through our bloodstream aid in our protection against the harmful effects of bacterial endotoxins that are released during infection. Studies have also found cholesterol may have protective properties against some cancers ¹⁹.

Cholesterol is the most abundant organic molecule in the brain and is a vital component required for synapse function ^20,21,22. In fact the person who discovered this essential role in the brain won a Nobel Prize in biochemistry. Cholesterol is also required for the function of serotonin receptors in the brain. Serotonin is the chemical in our brain that makes us feel happy. Cholesterol is a significant component of the cell membrane that influences its fluidity. It therefore indirectly affects neurotransmitters by interfering with their membrane bound receptors ²³. It also forms part of the myelin that surrounds our nerves aiding in the fast transmission of nerve signals. Lower cholesterol levels in the blood are correlated with slower visuomotor speed ²⁴ and has potential implications for some diseases like multiple sclerosis and motor neurone disease.

Statin statistics: lies and deception

Various independent studies in prestigious, peer-reviewed journals have shown that statin use in primary prevention—that is to prevent heart attacks—have minimal or no value in reducing mortality. It does not matter how one processes the statistics, the results just aren’t there. In data gathered in 2009 from six trials, a review of their ability to lower the risk of death with statins found virtually no difference between the treatment group who received the drug and the control group ²⁵. And there are many more of these studies.

The problem really comes down to vested interests and the abuse of statistics. As readers of the scientific journals we should not get confused between statistical significance and clinical significance. Statistically significant means that the outcome was likely (95% chance) a result of the treatment whether it was 100% effective or less than 0.1% effective. That is, if you treat 1,000 people to save one life (0.1%) it may be statistically significant but it is not clinically significant. Clinical significance refers to the expectations doctors and patients have for the success of the treatment and is usually 30% or more. That is, if ten people get the drug at least three will benefit. The best studies on statins by the drug companies report statistical significance, mostly less than half of one percent usually around 0.3%, around 100 times less than our expectations of clinical significance and none at all have so far found any clinical significance. GPs just do not understand the difference between statistical and clinical significance. So if the professionals don’t understand how do we expect the media or public to understand?

Interestingly, the use of other cholesterol lowering drugs (non statins) that reduce cholesterol just as effectively as the statins don’t even reach clinical significance, that is they don’t even reach 0.1 percent. So we know the effect of the statins is not the effect of lowering cholesterol that gives the drugs their incredibly small but statistically significant 0.3% effect. Otherwise the other cholesterol lowering drugs would work at the same rate. As the statin drugs are a synthetic mimic of a natural cholesterol treatment, “red rice yeast,” which had been used successfully for decades before the drug companies patented the statins. Red rice yeast works just as effectively as the statins but with many fewer side effects. Red rice yeast also has small anti-inflammatory and anti oxidative properties. It seems the small benefit the statins have (0.3%) is because they act like nutrition. Not because they lower cholesterol.

The studies on statins also report relative risk not absolute or real risk. This really fools the GPs. The relative risk reduction is highly misleading and deceptive. An example of relative risk is if you have four people out of 1,000 in a study who die in the placebo group (no drug) compared to three people out of 1,000 who die in the drug treatment group, that is four were likely to die but only three did, then for most of us it is a change of 0.1% (1 in 1,000, not much) but when you use relative risks it shoots up to 25%. They compare three to four and say four is 25% higher than three so the relative risk is 25%. It is still only one person in 1,000 a reduction of 0.1% but the doctors who believe the drug companies obviously never mastered statistics. Relative risk is like adding 1+1 to get 11 or 2+5 to get 25 or more.

The well known JUPITER Study (which I like calling the STUPITOR study if you believe the sales hype) found that treatment with statins went from 68 heart attacks in the placebo group (no drug) to 31 heart attacks in the drug treatment group a 58% relative risk reduction and 64 strokes in the placebo group to 33 strokes in the treatment group a relative risk reduction of 48% ²⁶. Sounds good doesn’t it? However, the drug treatment group had 8,901 participants in it. In real terms the heart attack risk went from a very low 0.76% to 0.35% and the risk of stroke went from 0.72% to 0.37%. That is, they had about a 0.35% reduction. Effectively if you treat 300 people with expensive and dangerous drugs you might save one life. Under the best possible scenario the real risk reduction was well under one half of one percent. Interestingly while the heart attack risk was reduced by around 0.35% the number of deaths increased with the drug use. Oops… no one reported this.

References

1. Kris-Etherton et al. 2002;

2. Wang et al. 2006;

3. Schacky and Harris 2006;

4. Psota et al. 2006;

5. Harris et al. 2006;

6. Robinson J.G. and Stone 2006;

7. Reiffel J.A. and McDonald 2006;

8. Jacobson 2006

9. Wierzbicki et al. 1999;

10. Nawrocki et al. 1995;

11. Bertolini et al. 1997;

12. Marz et al. 1999

13. Jackerviciua et al. 2002;

14. Benner et al. 2002

15. Folkers et al. 1990

16. Rosenfeldt et al. 2005

17. Romao 2007

18. Leardi S. et al. 2000

19. Goldstein et al. 2009

20. Mauch et al. 2001;

21. Koudinov and Koudinova 2001

22. Göritz et al. 2002

23. Heron et al. 1980

24. Zhang J. et al. 2004

25. Bartolucci et al. 2009

26. Ridker et al. 2008

Mediterranean diet lowers Alzheimer’s and depression.

2013-10-07T22:43:00.000-07:00

The Mediterranean diet has been associated with lower risk of various age-related diseases including CVD, some cancers and Alzhiemer’s. A recent review of twelve studies found that following a Mediterranean diet is associated with slower cognitive decline and a significantly lower risk of developing Alzheimer disease. In an older study of 2258 elderly New Yorkers with no dementia they found a higher adherence to the Mediterranean diet was associated with significantly lower risk of developing Alzheimer's disease. More importantly the more they followed the Mediterranean diet the lower the risk. They found that each increasing point on the Mediterranean diet score was linked with a 10 per cent drop in Alzheimer's risk and individuals whose diet closely resembled the Mediterranean diet had a 40 per cent lower risk of Alzheimer's than those who adhered the least to the diet (Scarmeas et al, 2006). In support of this a number of studies have also reported the benefits of eating fruit, vegetables and oily fish for reducing your risk of Alzheimer's disease.

In other research following a Mediterranean-style diet is also associated with lower risk for developing depression. After a 4 year follow-up, people who followed the Mediterranean diet had lower hazard ratios for incident self-reported depression. High consumption of fruits and nuts, legumes, monounsaturated- to saturated-fatty-acids ratio and fish were each separately associated with lower depression risk (Sánchez-Villegas et al 2009).

However, the Mediterranean diet is not pasta, pizza and lots of cheese. The Mediterranean dietary is high in fruits, vegetables, fish, nuts and legumes; low in dairy, meat, junk food, trans fatty acids; moderate alcohol intake; and high ratio of monounsaturated-to-saturated fatty acids. Moreover, a particular feature of the diet is the abundant use of virgin olive oil in everything from cooking to spreading on bread and salads. Not vegetable oils or margarine. In fact, the exact opposite. The diet's is rich in many nutrients including beta-carotene, vitamin C, tocopherols, polyphenols, and essential minerals.

Dingle Speaking Dates and Locations

2013-04-12T16:19:00.000-07:00

-Due to some personal reasons I have removed the dates and locations of my upcoming talks. Sorry

Mandurah Presentation

2013-04-09T22:28:00.000-07:00

WAKE UP TO WELLNESS !

IF YOU WANT TO IMPROVE YOUR HEALTH OR JUST STAY WELL THIS SEMINAR IS A MUST !
Chronic illness such as cancer, heart attack, stroke, diabetes and Alzheimer’s are skyrocketing. We now see illness in our children that never existed before including infant tumours, cancers and diabetes while allergies and ADHD continue to increase. It is not a result of our genetics but due to our poor lifestyle and diet. It is our everyday choices which cause these health problems and it is our everyday choices that can keep us healthy or even overcome these illnesses.
We have been overloaded with toxins from our personal care products, chemicals in our home and poisons hidden in our food and water. At the same time we eat over-processed food empty of nutrients and laden with sugar and toxic oils.

IT’S TIME TO TAKE CONTROL OF YOUR OWN HEALTH !
Dr Peter Dingle (B Ed, B Sc, PhD) has spent the last 25 years as a researcher, educator and author. He spent many years as an Associate Professor in Health and the Environment at Murdoch University. He is one of Australia’s leading motivational and entertaining speakers and a top public health advocate.
Tickets $10 each - Book early as seats are limited. Some tickets sold at the door. Date Saturday 13th April 2013
Time 1.15 pm for 1.30 pm start concluding at 3.30 pm
Venue Bendigo Bank Stadium, Platinum Room, Dower St, Mandurah
Contact Marilyn Morley 0403 680 694 or Christin Smith 0432 941 004
Take a chance to win in the raffle for some door prizes / Refreshments included
Part proceeds to Women ’ s Refuge

Margarine is toxic

2013-03-21T03:39:00.000-07:00

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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.

More research shows that omega 6 fatty acids (vegetable oils-margarine) have no health benefit and in fact might be worse for you than saturated fats. This study showed people on the ‘heart-healthy’ diet were at increased risk of dying from cardiovascular disease and heart disease (increases of 70 and 74 per cent respectively).

"Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit."

The Heart Foundation continues to educate people to swap to margarine. Why do they continue to do this?
this information is so widespread it is dangerous. I recently spoke to and AFL footballer who was told not to have butter and to use margarine by the club dietician.

The study also found that lower cholesterol as a result of the omega 6 heart healthy diet was also associated with more deaths not fewer. Cholesterol is not the killer. It is just a symptom of an illness.

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.

References

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

Statin drugs lower omega 3 oils

2013-03-21T03:31:00.001-07:00

A recent review suggests that the benefits of taking omega 3 fatty acids (vegetable oils) is cancelled out by taking statin drugs to lower cholesterol.

Omega 3(fish, krill) oils have multiple benefits beyond heart health. Omega 3 oils have been shown to reduce inflammation in various tissues and organs which is associated with almost every form of chronic illness (if not all) including diabetes, cancers, cardiovascular disease, auto immune diseases (including asthma and arthritis) osteoporosis, multiple scelosis, dementia and even depression, obesity and premature aging.

Although inflammation is natural it can be seriously problematic if it is reoccurring as a result of our body being out of balance. Numerous studies have also shown the real problem related to heart attacks is inflammation in the arteries not cholesterol.

In this review they reported

"Recent RCTs (random controlled trials) testing n-3 against arrhythmias suggest that n-3 reduce the risk only in patients not taking a statin. Other recent RCTs in secondary prevention were negative although, in a post-hoc analysis separating statin users and non-users, non-significant protection of n-3 was observed among statin non-users whereas statin users had no effect. Recent RCTs testing statins - after the implementation of the New Clinical Trial Regulation in 2007 - are negative (or flawed) suggesting that the lack of effect of n-3 cannot be attributed to a parallel protection by statins. Finally, statins favor the metabolism of omega-6 fatty acids (n-6), which in turn inhibits n-3 and, contrary to n-3, they increase insulin resistance and the risk of diabetes. Thus, n-3 and statins are counteractive at several levels and statins appear to inhibit n-3.

It seems that we have a choice. Omega 3 oils which make up a natural part of a healthy diet and have multiple positive side effects or statin drugs that have questionable benefits at best and serious side effects.

Acidosis and chronic illness

2013-03-21T03:30:00.000-07:00

Although inflammation, oxidation and acidosis are natural they can be seriously problematic if they are reoccurring as a result of our body being out of balance. Recent studies have established that all three conditions, the triad, are a leading pathogenic force in the development, of chronic diseases, including diabetes, cancers, cardiovascular disease, auto immune diseases (including asthma and arthritis) osteoporosis, multiple sclerosis, dementia and even depression, obesity and premature aging can all be attributed to this triad of conditions. A cancer or CVD does not just happen it is because these conditions prevail in the body over a long period of time and create the preconditions for these disease states. On the other hand if you want to reduce the risk of these disease states you reduce the levels of the disease triad, inflammation, oxidation and acidosis

Acid refers to one of the fundamental principals of science. All chemical reactions require numerous conditions to be present for the process to occur. For example if you warm up the temperature reactions usually go faster. Fever is a classic example of this, whereby the body’s metabolism is running faster as a result of the fever. The same occurs with acid levels. The level of acid, known as the pH (potential Hydrogen) determines the speed at which chemical reactions occur. Some reactions need higher acid levels (lower pH) while most chemical reactions in our body require neutral to alkaline (the opposite to acid) to occur. An example of this is in the stomach which requires a pH as low as 1 or 2 for certain digestive enzymes to work (pepsin the main protein digestive enzyme in the stomach works at a pH of 1-2.4 that is why the consumption of antacids only reduce digestion and create more digestive problems) but in the small intestine the pH has to be alkaline for the other digestive enzymes to work so the body injects in bicarbonate (H C O3) into the small intestine.

The pH scale ranges from 1 to 14. 1 being highly acidic and 14 being highly alkaline. So the lower the number the higher the acidity. A pH of 7 is neutral. A pH less than 7 is acidic. A pH greater than 7 is basic/alkaline. The pH scale is also logarithmic which means, each whole pH value below 7 is ten times more acidic than the next higher value. Not just one. For example, pH 6 (acidic) is ten times more acidic than pH 7 (neutral) and 100 times (10 times 10) more acidic than pH 8. Similarly a pH 8 is ten times more alkaline than pH 7.

When we refer to acidosis we are freeing to the pH level in the internal body fluids. When the body fluids such as the blood and the fluid between the cells and in the cells becomes slightly acidic it is so smart it sets up a triage system to rebalance the pH (acid/alkali levels) to maintain homeostasis. The pH of the blood is between 7.35-7.45. When the blood pH falls below 7.35, this is called “acidosis,” (too much acid) and our death can occur at a blood pH of 7.0. So we want to avoid this. If the pH varies slightly from this level it dramatically affects many of the 90 or so enzyme functions in the blood. These enzymes literally do all the work, repair, cleaning up, immune function, transport etc in the blood. If they slow down too much we get very sick and die quickly. To make sure this doesn’t happen the body has a few mechanisms to keep the pH in perfect balance. These include buffers, respiratory regulation and renal regulation of pH.

Unfortunately, many of the body’s natural process produce acid waste by products so we have a constant requirement to balance out the pH. Each cell, in the presence of Oxygen performs its task of respiration (the chemical and physical process in which oxygen is delivered to tissues or cells in an organism), it also creates acidic end products that are used for energy and function. The residue of these products and functions is known as metabolic wastes, and these are acidic in nature. This acidic waste must not be allowed to build up as it becomes increasingly toxic to the body. One example of the short term waste build-up is the often painful lactic acid which is created through extreme exercise.

The importance of acid-base homeostasis (balance) in the maintenance of normal cellular responses and physiological integrity has long been recognized. Many cellular responses are diminished at lowered extracellular pH, including intracellular fluid and membrane-associated enzyme activities, ion transport activity, protein and DNA synthesis, metabolism and calcium levels. Even at low levels of acidosis it decreases the body’s ability to absorb minerals and other nutrients, lowers energy production in the cells and the body’s ability to repair damaged cells. Essentially, it stops all the normal functioning, growth and repair in the cells so we slowly start to decay. Acidosis also increases the body’s ability to grow abnormal cells, increases fatigue and susceptibility to infections and also contributes to cardiovascular disease, weight gain, diabetes, kidney and gall bladder stones, hormonal problems, premature ageing and much more. An acid environment is also required for cancer cells to survive and increases the inflammation in the body, which feeds cancers. Dr. Otto Warburg was awarded the Nobel Peace Prize in 1931 and 1946 for his studies on how cancer can not thrive in an alkaline medium and the interstitial fluid of tumors has shown pH values of less than 6.0, 0.2–0.6 units lower than mean pH of normal tissues. In fact a major by product of cancers due to their incomplete metabolism is high levels of acid.

In the case of chronic acidosis the main mechanism is to allocate or triage alkali minerals like magnesium and calcium from where they should be working in optimal conditions, such as in the muscle cells and in bones, to balance the pH in the blood. Acidosis literally causes physicochemical dissolution of bone and cell-mediated bone resorption (inhibition of osteoblast – which cause bone to be laid down- and stimulation of osteoclast function – which breaks down the bone). While this protects our urgent health requirements and keeps us alive today it increases our long risk of chronic health conditions such as osteoporosis heart attack and cancer as a result of the shortage of these minerals. The body allocates the nutrients for short-term survival, the “essential,” functions are protected from nutrient deficiency over other “nonessential, non immediate” functions needed only for long-term health. As a result acidosis does not refer to the body becoming full of acid but the conditions that are created around the body by chronic low-grade metabolic acidosis.

What causes acidosis

Under normal conditions the body produces acid as a byproduct of metabolism and breakdown of other molecules. In a healthy body with a nutritious diet and well-balanced healthy lifestyle our body eliminates the wastes. Unfortunately, a nutritious diet and well-balanced healthy lifestyle are relatively rare now.

When food is altered from its natural state, the way it interacts with the body also changes. It is not the organic matter of foods (whether the food itself is acidic or alkaline such as in the case of lemon juice being acidic), but their inorganic matter, how they break down in our bodies into minerals, that determines either the acidity or alkalinity of our internal body. Following digestion, absorption and metabolism, nearly all foods release either acid or base into the systemic circulation. The pH of the body is determined and measured by the mineral residues in the blood and tissue. Acid and alkaline minerals bind to each other to neutralise the pH and bring about balance. If there is not enough alkaline minerals it will draw on minerals from the bone and other organs as described earlier.

Alkalising elements include

Calcium

Magnesium

Sodium

Potassium

Manganese

Zinc

Iodine

Borax

Acidic elements include

Phosphorus

Sulphur

Chlorine

Bromide

Fluoride

Copper

Silica

Hydrogen

There is significant differences between modern diets and those typical of our Homo sapiens ancestors. Studies in hunter – gatherer tribes suggest a relatively high intake of plant foods compared with modern-day humans. In a recent study estimating the net acid load 87% of 159 pre-agricultural diets were found to be alkaline compared with the average American diet was acid producing. This represents a major switch from the alkaline producing diet we ate for the majority of our evolutionary history to the acid producing diet we now eat.

The adoption of a diet which is high in alkaline foods has been shown to reduce the occurrence of diseases such as osteoporosis, age- related muscle degeneration, kidney stones, hypertension, asthma and kidney degeneration. The adoption of a predominantly acidic diet can lead to a condition called pathogenic metabolic acidosis which causes degeneration of the kidneys.

Acidic foods include:

Meats and seafood

Dairy products

Drinks: coffee, tea, alcohol, processed fruit juice

Fats and Oils

Sugar

Pasta, bread,

Artificial sweeteners

Acidity within the body can also occur as a result of dehydration and/or the quality of liquids we drink. While liquids are needed to flush out the wastes, including the acid wastes the different drinks we consume can have a big impact on our internal pH. Acid forming drinks include coffee, alcohol and soft drinks. The worst of these is without doubt is soft drinks. Not just because of the pH of the drinks but the sheer amount some people use and the fact they are consumed mainly by young people, even infants.

When soft drinks are consumed, pH regulatory mechanisms come into force to reduce the acidity of the soft drink. Soft drinks have a high buffering capacity, which means that more pressure is placed on the body to neutralise the pH, as the soft drink is resistant to small changes in the pH. The lower the pH (more acidic), the more alkaline needed to make the soft drink return to a neutral pH. Therefore not only is the initial pH of the soft drink bad, but also the corresponding buffering capacity results in greater stress on the body. Soft drinks are associated with many adverse health effects as well as osteoporosis and tooth decay. If the minerals are drawn out of the bone they are also removed from the teeth with acidosis, leading to an increased risk of tooth decay. Literally from the inside out.

It is not just our diet. Stress and anxiety are acid generators aside outside of our diet. An over active adrenal gland caused by high levels of stress can release a hormone called aldosterone into the blood stream causing large quantities of potassium and magnesium, alkaline minerals, to be excreted into the urine.

Diet, Not Drugs

2013-01-29T19:13:00.000-08:00

As a society we spend so much money that is absolutely wasted on medication. The disease is not high cholesterol or even obesity. The disease is our diet and our lifestyle. When we address these issues then all the symptoms, yes - all, disappear and we can lead a healthy long life.

A recent randomized controlled study (NORDIET) on 88 mildly people with elevated cholesterol showed how simple the solution is. 1One group had a diet rich in high-fibre plant foods: fruits, berries, vegetables, whole grains, grapeseed oil, nuts, fish and low-fat milk products, but low in salt, added sugars and saturated fats. The other group had the average western processed diet. Compared with controls, those on the healthy Nordic diet (ND. similar to the Mediterranean diet) had a decrease in plasma cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol, LDL/HDL and apolipoprotein (apo)B/apoA1. The ND also had reduced insulin and systolic BP by compared with the control diet. Body weight decreased after 6 weeks in the ND compared with the control group. The conclusions after 6 weeks in the study was that a healthy ND improves blood lipid profile and insulin sensitivity and lowers blood pressure at clinically relevant levels in people with elevated cholesterol without any medication.

While cholesterol is not a health problem it is an indicator of poor health, primarily stress on the liver and growing research is also showing that cholesterol may actually be protective.

A study of 6984 patients aged 65 years or older found mortality was inversely related to cholesterol levels. That is low cholesterol levels were associated with in-hospital mortality 2. The study concluded that among older hospitalized adults, low serum cholesterol levels appear to be an independent predictor of short-term mortality.

In another study of more than 52,000 Norwegians over a 10-year period the overall risk of death was the same in men with cholesterol levels of 7.0 mmol/l or higher than in individuals with levels of less than 5.0 mmol 3. In the individuals with cholesterol levels in the 5.0 – 5.9 mmol/l the risk of death was 23 per cent lower than in men with the lowest cholesterol levels. In women, the higher the cholesterol level the lower the overall risk of death. The third study of 82,000 adults in the UK over 8 years again found that higher total cholesterol levels were actually associated with a reduced risk of death due to stroke and that higher cholesterol levels are not a risk factor for heart disease 4.

There is no valid reason to focus on lowering cholesterol and especially no valid reason to take statin medication which has serious side effects, when the solution really is so simple.

References:

Adamsson, et al 2011. Effects of a healthy Nordic diet on cardiovascular risk factors in hypercholesterolaemic subjects: a randomized controlled trial (NORDIET).

DOI: 10.1111/j.1365-2796.2010.02290.Journal of Internal Medicine

Volume 269, Issue 2, pages 150–159, February 2011

Onder G, Landi F, Volpato S, Fellin R, Carbonin P, Gambassi G, Bernabei R

The American Journal of Medicine [2003, 115(4):265-271]

DOI: 10.1016/S0002-9343(03)00354-1

Petursson H, et al. Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study. J Eval Clin Pract. 25 Sept 2011 [Epub ahead of print]

Hamer M, et al. Comparison of risk factors for fatal stroke and ischemic heart disease: A prospective follow up of the health survey for England. Atherosclerosis epub 22 August 2011.

Complimentary and Sustainable Medicine

2013-01-29T18:28:00.002-08:00

Complimentary and Sustainable Medicine

A recent study of 14,329 employed adults in the US found that doctors and nurses use complimentary medicine more than the general population 1. They found 76 percent of healthcare workers use complementary and alternative medicine (CAM) compared to 63 percent of the general population.

On the one hand this is positive, but on the other this is concerning given not only the lack of encouragement from the medical establishments to use CAM, but also their willingness to dish out drugs which could otherwise be treated by CAM. However, this is understandable given that the doctors know more about the toxic, even deadly side effects of drugs. There are more than 400 000 adverse reactions to pharmaceutical drugs in Australia each year and probably more than 10 000 people die as a result of these drugs (although true numbers are not available). Government information from the US shows that there were 3,764,698,318 prescription drugs filled in the US in 2011. The average American aged between 19 and 64 used 12 prescriptions a year and those over 65 used 28 prescriptions each year. Males used 9.7 prescriptions on average while females used 14.3.

The study shows that most doctors and nurses who operate in mainstream medicine actually have more knowledge and appreciation for alternative medicine than most people suspect.

Another study in the UK in 2010 2 showed growing numbers of people are turning to alternative medicines and that sales of alternative medicines are booming 2. The market has reportedly grown by 18 per cent in two years and they predict sales will increase by 33 per cent over the next four years as more patients reject prescription drugs in favour of natural remedies. This growth can be explained by the acceptance of many treatments such as acupuncture, which is available on the NHS as well as a move away from potentially dangerous prescription drugs.

There are many other additional benefits of using CAM in Australia, including financial ones. The study found herbal preparations and omega-3s are effective treatments against an array of illnesses including osteoarthritis, heart disease and depression and could save the country more than $220m every year. However, the real benefit is that these supplements have no negative side effects and can help with multiple conditions. Omega 3 oils can assist in more than 50 different health conditions from asthma, cancer, CVD to depression and Alzheimer’s.

The researchers found omega-3s were effective against heart disease and that St John’s Wort could save $50m annually in anti-depression pharmaceutical spending.

The clinical evidence showing complementary medicine can play a vital role in improving an individual's health has been clear for some time and needs to be considered as a serious part of the health care system in Western nations.

References

1) Johnson, Pamela Jo, Andrew Ward, Lori Knutson, Sue Sendelbach4

Personal Use of Complementary and Alternative Medicine (CAM) by U.S. Health Care Workers. Health Services Research. Volume 47, Issue 1pt1, pages 211–227, February 2012

Article first published online: 22 AUG 2011

DOI: 10.1111/j.1475-6773.2011.01304.x

2) Alternative medicine sales soar as consumers shake off cynicism By Daily Mail Reporter. 26th January 2010

Stress: The Silent Killer. Chronic Stress and CVD

2013-01-10T03:14:00.000-08:00

“Not everything that matters can be measured, and not everything that is measured matters.” – Elliot Eisner

Cardiovascular diseases (CVDs) are the number one cause of death globally. In 2008, more than 17 million people died from them. On a national level, based on the 2004-2005 National Health Survey, 3.7 million Australians are estimated to have existing cardiovascular problems; CVDs were the direct cause of 35% of total mortality in 2005, again the number one cause of death ^1,2. This is despite the billions of dollars spent on medications to reduce the risk and intensity of cardiovascular diseases ³. CVD is no longer considered a disorder of lipid (fat) accumulation, but rather a disease process characterized by low-grade inflammation of the vascular (artery) lining and an inappropriate wound healing of the blood vessels. The answer is to treat the cause of inflammation not cholesterol.

A study in 2004 known as the INTERHEART study found that 90% of all myocardial infarctions (heart attacks) could be attributed to nine potentially modifiable risk factors ^4,5. These factors include tobacco use, atherosclerosis, hypertension, diabetes, abdominal obesity, psychosocial factors, alcohol consumption, physical inactivity and poor diets ^4,6.

Despite convincing evidence linking psychosocial factors such as chronic and acute stress to the risks of cardiovascular disease ^7,8,9, there remains a lack of focus on stress reduction for the prevention and treatment of cardiovascular disease. Risk reduction for stress is low-cost, simple to administer, and “non-pharmaceutical” ¹⁰.

Stress is the failure of an individual to cope with an emotional or physical threat. It results in both psychological and physical effects on individuals by means of two main stress groups: acute stress and chronic stress. Chronic stress occurs from exposure to stressors such as family, society (traffic, population, etc.) and, almost all the time, the workplace. When the body is stressed, a large number of biological and chemical processes can occur that put the body at increased risk of CVD. Chemical mediators are released, which cause the prolonged activation of the sympathetic nervous system ⁷ and increase heart rate and blood pressure, which puts a lot of strain on the heart and cardiovascular system ¹¹. Over time, the strain on the system leads to deterioration of the heart muscle, arteries and vessels ¹¹. Chemical mediators can also result in sleep deprivation, elevated cortisol levels, elevated insulin and blood glucose levels and increases in ghrelin, the hormone that increases appetite ¹¹.

Chronic stress, which is what we are often confronted with in our daily busy lives, plays a huge role in these increases, as it can cause the prolonged activation of the sympathetic nervous system ⁷. This results in an increase in blood pressure and heart rate, which remain elevated, leading to an increased risk of cardiovascular disease. In extreme circumstances this is also linked with endothelial dysfunction (inability of arteries to dilate) and possible necrosis of artery walls ⁷.

Stress increases the release of hormones like cortisol, adrenaline and noradrenaline, which act to increase the heart rate and contractile volume, as well as constricting arteries in the gastrointestinal tract, whilst dilating those in the periphery. Aldosterone and vasopressin, two lesser hormones in the stress response, are also released and act to increase blood volume through increased water retention. One of the functions of cortisol is to increase the concentration of fatty acids carried by lipoproteins and sugars in the bloodstream, leading to more damage to the arterial wall, producing excessive levels of cholesterol that may then bond to the artery walls (and lead to high cholesterol readings by your doctor), a process called atherosclerosis ¹². Atherosclerosis is the process in which a blood vessel wall thickens due to a build-up of fatty substances. The combined effect of these hormones is a marked increase in blood pressure, which may over time result in damage to the vascular tissue in the form of small micro-tears in the vessel walls. These minute tears heal by bonding with molecules floating in the blood (that is, cholesterol acts as a Bandaid). This cholesterol then forms a hard fibrous plaque with calcium, which may build up over time, constricting blood flow in the artery. Stress also causes the blood to become stickier in preparation of potential injury, increasing the likelihood of an artery‑clogging blood clot ¹³. One study found that those who expressed feeling high levels of stress and despair had a 20% greater chance of developing atherosclerosis over a four-year period. This was the same magnitude of increased risk as seen in a pack-a-day smoker. Studies on animals have shown similar results. A study on hypertensive rats and normal rats found that the hypertensive rats suffering from stress had a higher rate of these events ¹⁴.

There is a large body of evidence demonstrating the relationship between increased stress and increased CVD. A study commenced before the terrorist attacks in the U.S. on September 11, 2001 examined the degree to which acute stress reactions as a result of the terrorist attacks could predict future cardiovascular outcomes through follow-up surveys over three years ¹⁵. In a sample of 2,592 adults, researchers found that the acute stress response was associated with a 53% increased incidence of cardiovascular ailments ¹⁵. Those individuals who had high levels of acute stress following the attacks also reported a two-fold increase in physician-diagnosed hypertension and a three-fold increase in other heart-related problems over the three-year period.

In a study of 11,119 patients found that those patients who had experienced a myocardial infarction reported a higher prevalence of all four stress factors: stress at home, stress at work, financial stress and major life events in the prior year ¹⁶. The study also found that the four stress factors worsened coronary atherosclerosis and endothelial dysfunction and increased inflammation ¹⁶.

The Whitehall II study found a 2.15-fold (215%) increased risk for cardiovascular disease in men who experienced a disparity between effort and reward at work ¹⁷. The study also concluded that high-risk individuals included those who were overcommitted at work, had poor promotion prospects, blocked or stalled careers as well as competitive and hostile work environments. Similarly, in a study of nearly two thousand male workers over a six-year period, researchers found that those who experienced chronic work-related stress were four times more likely to experience cardiovascular ailments ¹⁶. A study at the Beth Israel Deaconess Medical Centre in Boston found evidence that managers who fire someone run twice the usual risk of heart attack in the week following the dismissal; the greatest danger occurred to those who had conducted the firing while working under a high-pressure deadline. Another study found that chronic work stress and divorce increased the risk of cardiovascular mortality ¹⁷.

In a study of 791 patients, researchers reported that high-pressure deadlines increased the risk of heart attacks by 2.3 times within the seven days after the stress of the deadlines. Specific time pressures dramatically increase the risk of heart attack and early death. In a study of 60 women ages 30 to 45, researchers found that those under stress who secreted the highest levels of cortisol were also the ones who turned to high-fat foods in attempts to cope with their stress.

The results are similar for younger populations. In a study of 158 healthy adolescents who undertook self-report measures of chronic stress over 3.3 years, adolescents exposed to chronic, negative stressors that worsened over time demonstrated heightened cardiovascular risk ¹⁸. In a study investigating the responses of university students to stressful situations, researchers found that students exposed to stressful laboratory tasks displayed high levels of cardiovascular responses, which extended into a continued increase in blood pressure during instances of perceived stress in everyday life situations ¹⁹.

Being angry more than doubles the risk of cardiac arrest. In a study of 1,500 people who had suffered heart attacks who were surveyed and asked what their feelings were a few hours prior to the heart attack, it was found that the heightened risk appears to last for about two hours after the episode of anger.

Psychosocial stress also results in changes in physiological behaviours ^5,7,11, which can put a person at increased risk of CVD. These behaviours include increased smoking and drinking, unhealthy eating and reductions in physical activity ^20,21,22. In addition, chronic stress can lead to constrained appetites or overeating, leading to problems of anorexia or obesity ²³. In extreme cases, anorexia or extreme weight loss can have an effect on heart rhythms and even lead to heart failure ²⁰¹⁰, while overeating may lead to obesity that has significant health risks associated with coronary heart disease, hypertension and type 2 diabetes ²⁵.

Stress is our great silent killer. Despite the growing body of evidence of this, we continue to focus on pharmaceutical treatments to reduce CVD and we continue to fail. The mechanisms behind stress being such a large contributing factor are now understood and numerous major studies have shown that the effects of chronic stress increase the risk from two to nine times. By contrast, medication to reduce cholesterol reduces the risk by 1% or 0.001 times (that is more than 2,000 times less important than stress). The next stage then is to invest in stress management practices. It’s that simple. Or is it?

1. NHMRC 2009

2. Bonthuis et al. 2010

3. Ademi et al. 2009

4. Yusef et al. 2004

5. Dimsdale 2008

6. Begg et al. 2008).

7. Rozanski et al. 1999

8. Black and Gabutt 2002

9. Siegrist 1995

10. Cade et al. 2010).

11. McEwen 2008

12. Brotman et al. 2007

13. Newton et al. 1990

14. Hallbäck and Folkow 2008

15. Holam et al. 2008

16. Rosengren et al. 2004

17. Dimsdale 2007

18. Low et al. 2009

19. Loft et al. 2007

20. Sturmer et al. 2006

21. Logan and Barksdale 2008

22. Hamer, Bates and Mishra 2011

23. Rutledge and Linden 1997

24. Bell 2010

25. Rapoport, Clark and Wardle 2000

Acknowledgements. Brigitta Curley, Amy Williams

Antidepressants dont work

2012-12-29T20:09:00.003-08:00

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 2002, a group of researchers studying the “placebo effect” compared studies on those taking sugar pills (placebo) and those taking antidepressants—a group of drugs the researchers expected to be effective—and found the opposite of what they expected. The meta analysis, written by Professor Irving Kirsch, was titled “The Emperor’s New Drugs: An Analysis of Antidepressant Medication Data Submitted to the U.S. Food and Drug Administration.” Kirsch obtained data from the FDA and reported that antidepressants were no more effective than a placebo. However, he did state that antidepressants might have a small effect and that in severe depression the placebo did not function as well as normal while the drug did show some efficacy ²². Professor Kirsch has also published a book of the same title (The Emperor’s New Drugs) that is well worth reading.

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

12. Zuvekas 2005

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

Acknowledgements

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

Margarine is much worse than butter

2012-12-13T17:50:00.000-08:00

I want to make it very clear that I have no vested interests in anything other than people’s health and the truth.

References

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

Diet drinks cause cancer in animals and humans

2012-11-16T12:58:00.000-08:00

Aspartame has come under scrutiny numerous times, with claims of health effects ranging from cancer to seizures. A new study has supported earlier animal studies that artificial sweeteners in soft drinks are associated with an increased risk of lymphoma and leukemia ¹

As a part of the Nurses' Health Study (NHS) and Health Professionals Follow-Up Study (HPFS they found men, drinking one or more serving of diet drink per day was associated with a 31 per cent increased risk of non-Hodgkin lymphoma, a more than doubling of risk of multiple myeloma. While in men and women combined, drinking one or more serving of diet soda each day was associated with a 42 per cent increased risk of leukaemia. They also found positive associations also existed between intakes of aspartame specifically and non-Hodgkin lymphoma and multiple myeloma.

There are also significant animal studies to support this. A series of independently funded experiments showed a link between Aspartame and cancer in rat eperiments when tested with life-time use of Aspartame, starting while still in the womb ^2,3. These experiment were impressive because they monitored rats until their natural death (up to 144 weeks), rather than ceasing tests at the usual 110 weeks. This gives a better idea of the potential for Aspartame to cause cancer, because 80% of cancer diagnoses are typically made in the last 1/3 of life, a critical point which other experiments miss.

Not unlike the recent human study reported above, the Mega life span study identified multiple tumours located at different sites of the body and being of numerous types. Dose related increases occurred in both male and females. That is the more aspartame consumed the higher the rates of cancer. This is a very powerful indicator of the problem. The most occurring tumours where lymphomas/leukaemia, preneoplastic and neoplastic lesions of the renal pelvis and ureter, malignant schwannomas of peripheral nerves, preneoplastic and neoplastic lesions of the olfactory epithelium, malignant brain tumours as well as other malignant tumours including tumours of the bladder ². The study identified aspartame to be a "multi-potential carcinogenic compound".

In a follow up study which consisted of over 4000 male and female sprague- drawley rats which were administered prenatally till natural death 100 or 20mg/ per kg of body weight of aspartame ³. As with the first mega study multiple types and locations of tumors were identified in rats which were significantly lower than the ADI and comparing the postnatal and prenatal studies prenatal exposure further increased the occurrence of lymphomas/leukaemia in females ³.

Of greatest concern was that these carcinogenic effects where identified at doses which were that of at least half of the accepted daily intake and could easily be consumed in a day. However, Food Standards Australia New Zealand regulatory body advises Australian and New Zealand consumers that aspartame is safe and advocates that aspartame has no cancer causing properties

1 Schernhammer ES, Bertrand KA, Birmann BM, Sampson L, Willett WW, Feskanich D. Experimental Demonstration of the Multipotential Carcinogenic Effects of Aspartame Administered in the Feed to Sprague‑Dawley Rats. Environmental Health Perspectives 114 (3). 2012

2 Soifritti, M., F. Belpoggi, D. D. Esposti, L. Lambertini, E. Tibaldi, and Anna Rigano. 2006. First Am J Clin Nutr. 2012 Oct 24. [Epub ahead of print]. Consumption of artificial sweetener- and sugar-containing soda and risk of lymphoma and leukemia in men and women.

3 Soffritti, M., F. Belpoggi, E. Tibaldi, D. D. Esposti, and M. Lauriola. 2007. Life‑span exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats. Environmental Health Perspective. 115 (1293‑7).

Saturated Fats are not so bad for us: Truth and Lies

2012-11-14T13:42:00.000-08:00

We are, without a doubt, facing a nutritional crisis in Australia and the U.S. One manifestation is confusion as to what constitutes sound nutritional principles ^1,2. Recent scientific advances have not led to consensus, but rather to substantial disagreement among experts and further uncertainty for the public. The public are confused. One such area of uncertainty is that there really is no credible scientific evidence that saturated fat causes heart disease or, more generally, cardiovascular disease. Although we are constantly told that saturated fats are “bad” and that margarine is better than butter (which it is not), there is no evidence to support this “bad fat” myth.

Unfortunately there are many myths perpetuated by certain members of the food and drug industry as well as so-called reputable groups who have strong vested interests in margarine. For example the position paper by the Heart Foundation ³ states that:

· Saturated fatty acids (SFA) intake is associated with coronary heart disease (CHD); and

· Replacing SFA with omega-6 PUFA (vegetable oils) to achieve a ratio of PUFA to SFA of greater than 1 will reduce the risk of CHD.

The foundation also states, “Our position on dietary fats and dietary cholesterol was developed from a review of the latest scientific evidence and incorporates recommendations from our previous papers.” In truth, though, all of this is out of date and absolutely wrong. The first thing to note is that this evidence is based on research from1999 that has never been updated. All the research over the past decade and even more recent findings, including our own research below, has shown exactly the opposite of these claims. Most importantly if you look at our evolution it just does not make sense.

Despite half a century of rigorous research, dietary advice from governments and doctors alike, and public campaigns urging the reduction of dietary fat, cardiovascular disease is still the leading cause of death in developed countries ⁴. We have consistently heard that saturated fat increases the risk of cardiovascular disease while polyunsaturated fats like vegetable oils and margarine have a protective effect in reducing fat overall (in particular saturated fat) and, as such, are supposed to be good for our health. During the past 40 years the dietary instructions from governments and other authoritative bodies have told us to avoid all animal fats. Average fat consumption decreased, average blood cholesterol levels decreased but the rate of heart disease and the cost of its treatment continued to rise. Replacement of saturated fat by polyunsaturated or monounsaturated fat lowers both LDL and HDL cholesterol. However, overwhelming research shows that cholesterol is not the public enemy it has been made out to be, it is just a warning that you liver (and body) are under stress and you need to take some action to reduce that stress, not the warning signs.

By contrast, replacement of cholesterol with a higher carbohydrate intake, particularly refined carbohydrates, can exacerbate the build-up of plaque in the arteries (atherosclerosis) associated with insulin resistance and obesity that includes increased triglycerides, small LDL particles, and reduced HDL cholesterol. Dietary efforts to improve the increasing burden of CVD risk associated with atherosclerosis should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.

Unfortunately, poor studies and vested interests have led us astray. For example, some older broad based (ecological) studies found, through cross-examining per capita intake of saturated fatty acids and other dietary fat items, a correlation with the death rate from coronary heart disease ⁴. However, in some studies, equally as strong coefficients were found in the number of radio and TV licences, and almost equally as strong as the number of registered motor vehicles, suggesting the implausibility of ecological-based study conclusions ⁴. The evidence against saturated fat has at best always been circumstantial. That is, saturated fat was said to elevate blood cholesterol and elevated blood cholesterol was said to cause heart disease therefore saturated fat would cause heart disease. There never has been any direct evidence that cholesterol or saturated fat cause heart disease or even of a mechanism whereby heart disease would occur.

Bias very likely exists in the findings of the studies, with researchers choosing particular countries or data sets to indicate a preferred result ⁴. An example of this is the early work of Dr Ancel Keys, which launched this attack on saturated fat and, at the same time, introduced the cholesterol myth back in the 1960s. In the Seven Countries Study, Keys looked at Italy, Greece, Yugoslavia, Netherlands, Finland, the United States and Japan reporting a strong straight-line relationship between saturated fat intake, heart disease and cholesterol levels ⁵. He chose to ignore 14 countries that had good data available. Choosing another seven countries—Finland, Israel, Netherlands, Germany, Switzerland, France and Sweden—shows the exact opposite results and thus reveals the bias in the early studies ⁵.

When we review theses studies, we find no relationship with saturated fat and heart disease of any type. When we review updated data, this lack of relationship clear. The top seven consumers of saturated fats (France, Switzerland, Netherlands, Iceland, Finland, Austria and Germany), with saturated fat energy percentage ranging from 15.5% to 13.7 %, all have a lower death rate from CHD than the seven bottom consumers of saturated fats (Georgia, Tajikistan, Azerbaijan, Moldova, Croatia, Armenia and Macedonia)—with saturated fat energy percentage ranging from 7.5% to 5.2%. Similarly, countries with the top five highest cardiovascular death rates (Belarus, Kazakhstan, Russian Federation, Ukraine and Azerbaijan) are in the lowest 50% of saturated fat consumers. These facts appear to be the exact opposite of what we are told by governments and doctors.

The lowest death rate in the bottom seven consumers of saturated fats (Croatia) of 17 per 100, 000 is same as the highest death rate in the top seven consumers (United Kingdom and Ireland). This may also be confounded by socioeconomic differences with the more developed countries being closer to the top with better health care facilities and less poverty. As in the men, the highest consumer of saturated fat (France) also has the lowest death rate from cardiovascular disease with 4 per 100, 000 for women and 22 per 100,000 for men. For years this was called the French paradox and was an excuse to make up another myth that alcohol is good for you. The bottom five death rates (France, Switzerland, Iceland, Italy and Spain ) are all in the top 50% consumers of saturated fat. The top five highest death rates (Turkmenistan, Uzbekistan, Azerbaijan, Kazakhstan and Moldova) are in the bottom 50% consumers of saturated fat. The death rates for coronary heart disease in women are also significantly less than for men in comparison of the two graphs, indicating a possible gender difference. This is not reflected in Australian data with both a higher prevalence (20% of women and 17% of males) and death percentage (37% for women 32% for men) of CVD existing in women ⁶.

Even the famous Framingham study, which originally hinted at a problem with saturated fats, now shows there is no association between dietary fat and heart disease and indeed the association of elevated cholesterol and heart disease is limited to a small segment of the study population ⁹. In the Framingham Heart Study, researchers working with a population-based cohort study, a total of 832 men, aged 45 through 65 years, found the risk of ischemic stroke declined with total fat, saturated fat and monounsaturated fat (e.g., olive oil) but not polyunsaturated fat such as margarine and vegetable oils ¹⁰. In effect, increased intakes of fat, saturated fat, and monounsaturated fat (olive oil) were associated with reduced risk of ischemic stroke in men. The exact opposite of what we have been told.

The evidence continues to mount that there’s no benefit and, in fact, probable harm from a low-fat diet. I cringe when I hear people talking about a low fat diet and laugh at all the marketing around low fat foods which are usually both full of sugars and low nutrient density carbohydrates. Two recent studies underscoring this finding are the Women’s Health Initiative and the Nurses’ Health Study. The Women’s Health Initiative studied 48,835 women and demonstrated no benefit from a low-fat diet in terms of heart disease or breast cancer ¹¹. The Nurses’ Health Study, which has followed 90,000 female health professionals, demonstrated no reduction in heart disease or cancer as a result of a low-fat diet ¹².

A meta-analysis of the research of 27 separate studies found that modification of dietary fat did not lead to a significant reduction in either deaths due to cardiovascular disease or overall risk of death ¹³. Ten years later, the same researchers examined another 21 studies and found exactly the same results ¹⁴. The researchers reported that pooled results of all the studies showed low-fat eating or replacing saturated fat with polyunsaturated fats had no benefit whatsoever and may even be harmful. Similarly, examination of the 33 data sets from prospective cohort studies in a meta-analysis found no plausible evidence for a consistent association between saturated fatty acid intake and risk of coronary heart disease (CHD) ⁴. A separate analysis which examined 16 studies with CHD as the focus and eight studies with stroke as the focus, showed no association between dietary saturated fat intake and prevalence of disease ¹⁵.

The most recent definitive examination of all the competent studies on saturated fats and heart disease shows that over a five- to 23-year follow-up of 347,747 subjects, there is no association between the intake of saturated fat and heart disease or stroke. The meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or cardio vascular disease (CVD) ¹⁶.

Even in animal trials, evidence shows positive effects of saturated fat. One study published in the American Journal of Physiology-Heart and Circulatory Physiology investigated heart functioning by evaluating gene expression profiles of rats fed high dietary fat after a heart attack ¹⁷. The research demonstrated that a high-fat diet improved overall cardiac mechanical function (the heart’s ability to pump)—that is, heart functioning was seen to improve on the high-fat diet.

The links between dietary fat, saturated fatty acids, serum cholesterol and cardiovascular disease are all part of the same “diet-heart hypothesis” with milk and dairy products—especially those with high fat content (butter, whole milk, cheese)—being publicly demonised due to saturated fats’ association with increased serum cholesterol ^4,15,19-21. This, despite the fact that numerous studies found that overall consumption of dairy products (typically high saturated fat content) was not associated with mortality ^21,22.

The cholesterol hypothesis separates cholesterol into two types for the sake of simplicity, low-density lipoproteins (LDL) or “bad cholesterol” and high-density lipoproteins (HDL) or “good cholesterol” ²³. Cholesterol has been so successfully publicly demonised that lowering cholesterol is earning pharmaceutical companies more than 20 billion dollars annually in the US with the sale of the top two statin drugs, Zocor (simvastatin) and Lipitor (atorvastatin), alone ²³. Despite this, supporters of the diet-heart hypothesis seem to have forgotten cholesterol’s essential and natural role in human biochemistry, with 80% of total body cholesterol being manufactured by the liver ²⁴. They also ignore the basic science studies demonstrating that blood fat profiles, the presumed cause for concern, is largely determined by consumption of carbohydrates, not fat consumption ^25,26.

In a recent review of dietary guidelines, researchers were scathing of the guidelines for critical weaknesses, including use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science. This is a mild way of saying scientific lying. The researchers also said that it “does not provide sufficient evidence to conclude that increases in whole grain and fibre and decreases in dietary saturated fat, salt and animal protein will lead to positive health outcomes” ²⁷. It seems that dietary guidelines around the world are lead by the money not the science.

References

1. Boyle et al. 2008;

2. Nestle 2007

3. Heart Foundation (October 2012

4. Parodi 2009

5. Kendrick 2007

6. Australian Institute of Health and Welfare, 2010

7. Luzzi (1998

8. European Heart Network (2008).

9. http://www.framinghamheartstudy.org

10. Gillman et al. 1997

11. Howard et al. 2006

12. http://www.channing.harvard.edu/nhs).

13. Hooper et al. 2001

14. Hooper et al. 2011

15. Hu et al. 2010

16. Siri-Tarino et al. 2010

17. Berthiaume et al. 2010

18. Hu et al. 2010;

19. Bonthuis et al. 2010;

20. Elwood et al. 2010;

21. Gibson et al. 2009

22. Bonthuis et al. 2010;

23. Bowden 2010

24. The Great Cholesterol Deception, 2011

25. Volek et al. 2008;

26. Forsythe et al. 2008

27. Hite et al. 2010

Acknowledgements Matthew Partridge

Epigenetics and Disease

2012-10-15T20:36:00.000-07:00

Various genetic messages are “turned on” (expressed) or “turned off” (silenced) through epigenetic processes like DNA methylation. When turned off, it is as if a protein glove covers the DNA message so it can no longer be read or acted upon. Although epigenetic modification of our genes is a natural part of our development and well being, these processes can interact with various chemicals in our environment and in foods and drinks we consume, leading to the development of disease. Conversely, epigenetic actions of other compounds in our environment and nutrition are thought to hold the key to providing therapies to fight and prevent disease.

If a genetic mutation for a disease is “turned off” by epigenetic markers, that particular gene—in such an instance—cannot cause disease. For example, an individual may have inherited the genes for a particular disease; if, however, those genes are not expressed, the disease will not develop. However, change to the epigenetic markers (of a mutated gene) could cause the mutated gene to “tune into” and hence develop a specific disease.

Many human diseases have been associated with epigenetic modifications due to environmental exposure. These include cancer, obesity, diabetes, asthma, multiple sclerosis, mental illness and behavioural disorders as well as premature ageing ^1,2,3,4.

Humans are most vulnerable to epigenetic changes during the development of the embryo in the womb, embryogenesis, where epigenetic disruptions can be passed down through multiple generations ⁵. One study on diethylstilbestrol (DES), an environmental oestrogen, found that DES induced a genetic predisposition to a certain cancer and congenital birth defects that was passed down two generations ⁶. Similarly, foetal exposures to plasticizers such as bisphenol A, a chemical found commonly in plastic, contribute to epigenetic changes, which lead to immune abnormalities. Maternal smoking leads to increased pulmonary disease in adulthood including asthma; and certain therapeutic drug exposure leads to vascular defects. These can all be classified as epigenetic changes.

During the past decade, evidence has accumulated showing that apart from genetic alterations (mutations), epigenetic alterations play a major role in the initiation and progression of cancer ⁷. Human cancers arise from a multi- step process characterised by tumour initiation and progression ⁸ but only five percent of cancers can be attributed to heredity. Genetics alone cannot explain all of the properties of cancer. It is now understood that epigenetic abnormalities and the turning off and on of certain genes play a major role in tumour genesis—the development of and proliferation of tumours ^9,10.

Cancer, which is caused by uncontrolled cellular growth, is induced by mutations in the DNA, which can be initiated by errors in the DNA or foreign chemicals called carcinogens. In addition to uncontrolled cellular growth, a characteristic of cancer is inhibition of normal programmed cellular death, called apoptosis. When the body’s DNA makes mistakes in a cell, the mistakes are either fixed by additional DNA repair mechanisms or the cell is destroyed to prevent further damage (apoptosis). Unfortunately, the genes that are responsible for destroying rogue cells can be silenced (turned off) through epigenetics and, as a result, mistakes in the DNA cannot be rectified before they spread. The genes associated with cellular pathways that are prone to cause cancer are called oncogenes. The silencing of tumour‑suppressing genes, activation of oncogenes, and defects in DNA can be caused by epigenetic mechanisms, which can affect several if not many of the steps in a cancer line ¹¹.

We have literally removed the various roadblocks to formation of cancer. Many of the genes that are inactivated by methylation in carcinogenesis have classic tumour‑suppressor functions or play a critical role in cell cycle control (repair of damage to DNA) apoptosis, differentiation, angiogenesis, metastasis, growth factor response, drug resistance and detoxification ¹². An incorrect change in the methylation of the DNA caused by epigenetic carcinogens is the most common activation of cancer cell lines. Although methylation changes occur to different genes depending on the type of cancer, all cancers undergo changes in methylation, suggesting DNA methylation is a major factor in tumour development and can be used as a genetic marker in tumour development ¹³.

To put this in perspective, methylation in some areas of the DNA, called CpG sites, in some tumour suppressor coding regions contributes to as much as 50% of all inactivating mutations in some cancers and 25% of cancers in general.

In contrast to genetic changes in cancer, epigenetic changes are gradual in onset and are progressive. Their effects are dose-dependent and are potentially reversible which increases the scope for the development of epigenetic therapies for disease ¹⁴. These observations present new opportunities in cancer risk modification and prevention using dietary and lifestyle factors as well as treatment as you will see below. In this regard, folate, a water-soluble B vitamin, has been a focus of intense interest because of an inverse association between folate levels and the risk of several malignancies (in particular, colorectal cancer) and because of its potential ability to modulate DNA methylation. Through this process of supplementing with folate, scientists have achieved a certain degree of reprogramming even in adult cell DNA. The use of such inhibitors as folate has been shown to reactivate expression of tumour‑suppressor genes that would otherwise be silenced and a cancer would develop. Treatment for myelodysplastic syndrome, a form of leukaemia, with epigenetic therapies is already approved for use in the U.S. and there are a host of other treatments that continue to show promise ¹⁵.

Even more promising are the roles of diet and lifestyle. In a study of 30 men with low-risk prostate cancer who decided against conventional medical treatment such as surgery, radiation, chemotherapy or hormone therapy, three months of major lifestyle changes significantly lowered the level of prostate cancer. The changes included eating a diet rich in fruits, vegetables, whole grains and legumes and incorporating moderate exercise such as walking each day along with an hour of daily stress management ¹⁶.

Six of the control patients in this study underwent conventional treatment due to an increase in prostate specific antigen (PSA) levels or progression of disease measured by magnetic resonance imaging (MRI) during the 3 months, while none of the lifestyle group did. PSA levels decreased four percent in the experimental lifestyle group but increased by six percent in the control (no change in lifestyle) group. Other markers such as the growth of prostate cancer cells (LNCaP) were inhibited almost eight times more in blood serum from the experimental group than blood serum from the control group (70% versus nine percent). However, even more definitively, the changes in serum PSA and in prostate cancer cell growth (LNCaP) were positively associated with the degree of change in diet and lifestyle. That is, the more lifestyle changes the men made, the greater the reduction in the prostate cancer markers. The lifestyle group were literally reversing their cancer.

The researchers found even more profound changes when they compared DNA from prostate biopsies taken before and after the lifestyle changes. After only three months, the men had changes in expression of about 500 genes, including 48 that were turned on and 453 genes that were turned off. The activity of disease-preventing genes increased while a number of disease-promoting genes, including those involved in prostate cancer and breast cancer, shut down. The lead researcher, Professor Dean Ornish, noted, “The implications of our study are not limited to men with prostate cancer” ¹⁶. In addition to the benefits in prostate diagnosis the men lost weight, lowered their blood pressure and risk of heart attack and stroke and saw other health improvements while reporting no negative side effects.

There is currently a great deal of interest in the promising chemo-preventive actions of polyphenols, large organic molecules, such as curcumin from curry, resveratrol found in grapes and berries and especially Epigallocatechin-3-Gallate (EGCG) the major polyphenol in green tea ¹⁷. EGCG in green tea has the ability to affect DNA epigenetics to fight cancer beyond just its antioxidant potential. For example, treatment of human oesophageal cancer cells with EGCG caused tumour suppressor genes, the genes that stop cancers from growing, to be “turned on.” The activity of EGCG has also been shown to possibly act to reduce cancer activity in prostate cancer cells ¹⁷.

Other studies link obesity and malnutrition (low nutrient-dense foods) in parents to hypertension in offspring and disease risk in offspring later in life ¹⁸, specifically with regard to obesity and the onset of diabetes later in life ¹⁹. Low-weight newborn babies are biologically different than their bigger counterparts. Smaller infants have fewer kidney nephrons, altered metabolism and are more insulin-resistant. These differences show how dietary habits of the mother during pregnancy can alter the expression of the genes of their offspring in such a way that they will respond differently to the environment that follows after birth. Placental and foetal growth is at its most vulnerable to maternal nutrition status in the first trimester of pregnancy. Promotion of a healthy, nutritionally balanced womb environment will not only ensure optimal foetal development but also reduce the risk of chronic disease in adulthood ²⁰. In support of this, it has been found that folate levels in pregnant women affect DNA methylation in a number of different gene promoter areas associated with infant health.

Some of the most well known studies linking epigenetics and obesity have involved “agouti” mice. Over the past twenty years there have been numerous studies indicating that impaired embryonic, foetal or infant nutrition as a result of out processed western diet and environments can lead to greater risk of obesity and metabolic compromise in later years ²¹. For example, a short‑term dietary intervention in pregnant agouti mice, in the form of supplements of folic acid, vitamin B 12, choline and betaine, have shown long‑lasting beneficial influences on the health and appearance of the offspring for multiple generations ²². By contrast, selectively bred diet‑induced obesity dams (mothers) that were made obese during gestation and lactation had more obese, insulin-resistant children who developed abnormalities of brain neurotransmitter metabolism compared with offspring of lean diet‑induced obesity dams or dams that were diet‑resistant ²³. That is why there is so much emphasis now on pregnant mothers supplementing, particularly with B vitamins. In a study of sheep, metabolic and hormonal signals before birth increased the expression of genes that regulate fat and the conversion of simple sugars into fatty acids in the fat around the kidneys of sheep ²⁴.

In one study, two types of rats were bred: one to develop diet‑induced obesity and the other that was prone to be diet‑resistant. Researchers found that the diet‑induced obesity rats would defend their increased body weight when fed a high-fat diet (31%) whereas the diet‑resistant rats would adjust their (high-fat) diet accordingly to maintain their lean physique. The study also found that the diet‑induced obesity rats, even after long periods of calorie restriction, would return to their higher weight once food was available freely, even when on a five percent fat diet ²⁵.

In other studies, researchers found that in a population with a genetic predisposition toward obesity, the effects of maternal obesity accumulated over successive generations to shift the population distribution toward an increased adult body weight. Perhaps this is something we are heading toward now in the human population…?

It is clear that epigenetic mechanisms may also drive psychiatric and mental disorders. In particular what your mother eats during pregnancy and you eat during childhood not only may influence your adult brain function and its eventual decline as you age, but also may influence your children’s cognitive potential and mental health ²⁶. A foetus that endures poor nutrition during gestation spares the growth of vital organs such as the brain at the expense of tissues such as muscle; the pancreas adapts its metabolism to the limited nutrition ²⁷. Following on from this, increasing evidence indicates that a disturbance in early neurodevelopment may lead to a vulnerability to schizophrenia in adolescence or adulthood ²⁸.

Twin studies have shown that people with schizophrenia and bipolar disorder have changes in genetic activity caused by their respective environments. The findings provide the strongest evidence yet that such gene changes might cause these conditions. A study that scanned the genome of 22 pairs of identical twins (one twin in each pair was diagnosed with schizophrenia or bipolar disorder) found, as expected, that the twins had identical DNA. However, they showed significant differences in epigenetic markings and these changes were on genes that have been linked with bipolar disorder and schizophrenia ²⁹.

Regardless of which condition the twin had, the most significant differences, with variations of up to 20% in the amount of methylation, were in the promoter “switch” for a gene called ST6GALNAC1, which has been linked with schizophrenia. The scans also revealed methylation differences in Gpr24, a gene previously linked to bipolar disorder ²⁹. In support of this, other studies have found differences of up to 25% in methylation of the same gene compared with controls.

Growing evidence suggests how we age is very much epigenetic-related. Some of the strongest, decade-old evidence shows progressive changes in DNA methylation in tissues in the ageing colon, stomach, oesophagus, liver, kidney and bladder adding increased importance to the role of diet and lifestyle in how we age.

Despite the role of our parents’ diet and lifestyles on our future and the future of our own offspring, research shows we can change this outcome by nutrition and lifestyle changes. We are largely in control of our own destiny. From epigenetics, we are learning that it is not all in the genes.

References

1. Bollatti and Baccarelli 2010;

2. Dolinoy et al. 2007;

3. Isles and Wilkinson 2008;

4. Weidmann et al. 2007

5. Attig et al. 2010

6. Newbol 2004

7. Nystrom and Mutanen 2009

8. Dworkin, Huang and Toland 2009

9. Esteller 2008;

10. Shikhar, Kelly and Jones 2010

11. Herceg 2007

12. Kim 2006

13. Banerjee 2009

14. Adcock et al. 2006

15. Issa 2006

16. Ornish et al. 2008

17. Link, Balaguer and Goel 2010

18. Friaz et al. 2011

19. Ryan 2011

20. Wu et al. 2004

21. Gluekman and Hanson 2008

22. Freeman 2009

23. Levin et al. 2005

24. Muhlhausler et al. 2007

25. Levin 2008

26. Williams 2008

27. Jones PB, Rantakallio P, Hartikainen AL, Isohanni M, Sipila P

28. Brown and Susser 2008

29. Dempster, Pidsley et al 2011

ADHD and phthalates.

2012-10-15T19:06:00.003-07:00

Prenatal (before birth) exposure to a group of chemicals called phthalates has been linked with ADHD like symptoms in a study published on the Environmental Health Perspectives website on January 28, 2010. Phthalates are a group of chemicals often added to plastics to give them their plastic-flexible like qualities, as well as in paints, lubricants and detergents (yep the ones in your supermarket). They are also found in some personal car products such as nail polish, liquid soap, shampoos, perfume and eye shadow. They are pretty well everywhere in our homes.

The study found that mothers with higher levels of the phtalates in their blood reported poorer behaviour in their children (ages 4-9 years), including typical ADHD symptoms. However, ADHD is not the only problem associated with phthaltes. Phthaltes have been linked in both animal experiments and human research with sexual organ and sexual behaviour dysfunction to name a just a few of the problems they can create.

Phthaltes are considered endocrine disruptors because, at incredibly low levels, they interfere with hormones such as estrogen in the body. The most vulnerable stage of these chemicals to have an impact is on the developing foetus in pregnant mothers.

In another study in the Journal of Paediatrics, February 2010, the use of baby personal care products such as lotions, shampoos and powder was associated with higher levels of phthalates in the babies blood.

The message is to become aware of the chemicals in your home and reduce the exposure to everyone but particularly to mums to-be. You can find a lot more on toxic chemical exposure in my book “Is Your Home Making You Sick”

More Cholesterol lies

2012-10-15T19:05:00.000-07:00

Last month (August 6) in the West Australian newspaper they parroted an article from the age which suggested more people should be taking statins. Of course the Age just parroted the news brief from the drug company PR machine without asking who funded the study (drug companies of course). What they said was people with even a low level of heart attack risk of around 10% had a 15% reduction in the risk of heart attack. Sounds good doesnt it. What they did not tell you is that to get that 15% relative risk reduction or 0.1% absolute risk reduction, one person only, they had to treat around 1000 people with a drug that has serious side effects. That is why the studies are to tens or even hundreds of thousands of people. If the drug worked well, say 10% they would only need to treat 100 or 200 people.

Here is how they do it. On the statin treatment group 7 people out of 1000 have a heart attack over the period of 5 or more years. In the other control group 8 people out of 1000 have a heart attack. Using relative statistics we compare 7 to 8 and there is close to a 15 percent reduction. A bit confusing isn’t it. Using absolute statistics which is what we are all used to using it is a 0.1% reduction from 8 to 7. So we had to treat around 100 people to get a 1% real reduction or 0.1%. That is a lot of drug for a very small benefit. Someone is making a lot of money

University of Sydney researchers had to review 27 studies to come up with enough people whose life may be saved. Again 1 in 1000 who were treated. And someone forgot to tell the drug representatives how to do statistics that don't lie.

The media also just cherry-pick the scientific literature and never report the science that shows they just don’t work or the 75% of people who drop out of trial due to serious adverse side effects

They also forgot to mention that the benefits of statin drugs is only as a result that it acts like a nutrient. It is a molecule synthetically derived from red rice yeast which by the way has next to no negative side effects. Other types of drugs that lower cholesterol just as well as statins don't even have the 0.3% benefit. So it is not lowering cholesterol that has this very small benefit. Rather, statin drugs mimic some nutrient properties of red rice yeast (available at most health food stores until banned). But if that is the case we can use some safe nutrients to derive the same benefit as statins (one or two almonds a day) with no negative side effects and at a cost of a few cents a day. Not $6 billion a year in Australia.

There is a lot more information on this in my earlier blogs and even more in my book “The great cholesterol deception”

It’s Not All in the Genes: The Science of EPIGENETICS

2012-10-15T18:52:00.000-07:00

In 1953, James D. Watson and Francis Crick proposed the concept of the double helix as the structure of DNA. With this finding, the fields of genetics and biology experienced a monumental shift: seemingly, scientists had finally discovered why we are who we are. The quest began to isolate DNA and map the entire human genome. However, after spending billions and maybe even a trillion dollars unravelling the human genome, researchers have come to the realisation that it is not all in the genes. In recent years, a new idea has come to the forefront of genetics and is the focus of thousands of studies: epigenetics.

Genetic determinism—that is, the notion that “it’s all in the genes,” that everything is determined by our DNA and that we are victims of our hereditary—has been programmed into us since our first high school science lessons. This concept is disseminated by the media and even further propagated in medical school. If one gets a disease, it is deemed “genetic.” However, only a very few diseases—such as Huntington’s chorea, beta thalassemia and cystic fibrosis—can be blamed entirely on one faulty gene. These single-gene diseases affect less than two percent of the population ¹. It is estimated that only five percent of diseases are a direct result of gene mutations; the rest are a result of environmental (about which I have written extensively and coined a term, “the DEAL—Diet, Environment, Attitude and Lifestyle”) influences ². It is now theorised that Alzheimer’s disease, cancers, cardiovascular disease, asthma, autoimmune diseases such as lupus and conditions such as schizophrenia are linked to epigenetic triggers ³. The vast majority of diseases that afflict us today are a result of complex interactions between genes and the environment. Classic genetics alone cannot explain the diversity of disease characteristics in society.

It is true that genes may have an association with a disease, but this does not prove causation. The genes may be related to a disease but are not directing or causing it. Long ago, biologist Jean-Baptiste Lamarck was ridiculed because of his evolutionary ideas when he proposed that the environment, including our diet, can influence our genes. Now science has caught up with Lamarck’s hypothesis. Even Darwin recognized environmental factors outside the hereditary material but that has largely been ignored until now.

Perhaps we need to look at our genes differently. In his book, The Greatest Show on Earth, Richard Dawkins (2009) suggests that our DNA is not a blueprint like that used to build a house, but is in fact a broad recipe from which certain outcomes arise. Tissues and bodily structures are not formed according to set plans or blueprints contained in our DNA, but self-assemble responding to environmental [local] conditions and the laws of chemistry.

Epigenetics provides the missing link between the environment and the development of disease. It goes beyond many of the subtle changes in DNA that explain only a fraction of the diseases humans develop. For the first time since DNA was discovered, epigenetics has encouraged scientists to move from genetic determinism to studying how the environment can shape our lives. Previously, it was believed that DNA would determine the makeup of the person—his or her predisposition to disease, hair colour, metabolic rate, etc. However, not only is “nurture” becoming more significant than “nature,” but also there is a transgenerational property to epigenetics: genes can be turned on and off, and those changes can be passed on for generations ⁴.

It appears that genes are not our destiny. It is environmental signals that activate the expression of the gene. Environmental factors are capable of causing epigenetic changes in DNA that can potentially alter gene expression and result in genetic diseases, including cancer and behavioural disorders. Environmental influences including nutrition, behaviour, stress, chemicals, radiation and emotions can change how the genes are expressed and can silence or activate a gene without altering the genetic code in any way. These are changes in gene expression that occur without a change in DNA sequence.

Known or suspected culprits behind negative epigenetic changes include agents such as heavy metals, pesticides, plastic compounds including BPA, diesel exhaust, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria and deficiencies in basic nutrients. Each nutrient, each interaction, each experience can therefore manifest itself through biochemical changes, which may have effects at birth or 40 years down the track. These epigenetic changes often occur at foetal or embryonic levels, but they set the stage for an adult’s susceptibility to a host of diseases and behavioural responses. There are certain periods of an organism’s life during which it is more susceptible to methylation and epigenetic changes—including gestation, neonatal growth, puberty and old age—but the period in which an organism is most likely affected by methylation is during the formation of the embryo ⁵.

Detractors have largely ignored epigenetics, and in fact harshly criticised early studies, including one in which researchers used supplements to offset the results of a particular gene in mice. Researchers fed pregnant mice, all of which had an abnormal “agouti” gene, methyl-rich supplements, folic acid, B12, betaine and choline and, as a result, changed the binding characteristics of the regulatory chromosomal proteins. Agouti mice have yellow coats and are extremely obese, which predisposes them to cardiovascular disease, diabetes and cancer ^6,7. The pregnant mice that were given the supplements produced standard lean, healthy offspring that lived longer and weighed half that of the yellow agouti mice, even though they still had the agouti gene. These observations suggest, at least in this special case, that maternal dietary supplementation may positively affect health and longevity of offspring.

The research also shows that the epigenetic effects might go on for a number of generations; a disease you are suffering today could be a result of your great-grandmother being exposed to an environmental toxin during pregnancy. Researchers exposed pregnant rats to environmental toxins during the period that the sex of their offspring was being determined. The compounds—vinclozolin, a fungicide commonly used in vineyards, and methoxychlor. Pregnant rats exposed to these chemicals produced male offspring with low sperm counts and low fertility. Those males were still able to produce offspring, however even when they were mated with females that had not been exposed to the toxins, their male offspring had the same problems of low sperm counts and low fertility. The effect persisted through all four generations tested, with more than 90% of the male offspring in each generation affected with no additional pesticide exposures ⁸. The findings provide a new paradigm for disease etiology and basic mechanisms in toxicology and evolution not previously appreciated.

One study found that over-eating during the SGP (slow growth period of the teen years) by male grandparents led to a higher rate of diabetes and cardiovascular disease in their grandchildren ⁹. All the results indicated that these potential epigenetic traits were passed down through the male gene line ¹⁰. In a later study ¹¹, researchers also induced these alterations through maternal ingestion of genistein, the major phytoestrogen in soy, at doses comparable to those a human might receive from a high-soy diet, and found that they may also cause health problems, via additive or synergistic effects on DNA methylation, when it interacts with other substances such as folic acid. Through these and subsequent studies, it has been revealed that both the mother’s and father’s diets and environment during pregnancy and childhood, respectively, are of paramount importance to the epigenome and development of the offspring ¹².

Studies have found that epigenetic effects occur not just in the womb, but also over the full course of a human life span. In a study of 40 pairs of identical twins, ranging in age from three to 74, twins were epigenetically indistinguishable during the early years of life, while older monozygous (identical) twins exhibited remarkable differences in their overall content and genomic distribution of 5-methylcytosine DNA and histone acetylation, affecting their gene-expression portrait. That is, younger twin pairs and those who shared similar lifestyles and spent more years together had very similar DNA methylation and histone acetylation patterns. But older twins, especially those who had different lifestyles and had spent fewer years of their lives together, had markedly different patterns in many different tissues, such as lymphocytes, epithelial mouth cells, intra-abdominal fat and selected muscles ¹³. As one example, the researchers found four times as many differentially expressed genes between a pair of 50-year-old twins compared to three-year-old twins, and the 50-year-old twins with more DNA hypomethylation and histone hyperacetylation (the epigenetic changes usually associated with transcriptional activity) had the higher number of over-expressed genes. The degree of epigenetic change therefore was directly linked with the degree of change in genetic function ¹³.

Numerous studies have linked epigenetic factors to cancers of almost all types, genetic disorders and paediatric syndromes as well as contributing factors in autoimmune diseases, cognitive dysfunction, reproductive, autoimmune, respiratory disease, neurobehavioral illnesses, mental retardation and aging ^14,15. The expression and activity of enzymes that regulate these epigenetic modifications have been reported to be abnormal in the airways of patients with respiratory disease ¹⁵.

While epigenetic changes can lead to an increase in diseases it now puts us in control. Not only can we avoid so many diseases that were once thought of as in our genes but research is showing by changing our diet and lifestyle we can also reverse many of these conditions.

References

1. Lipton 2005

2. Willet 2002

3. Esteller 2008

4. Anway et al. 2005

5. Dolinoy et al. 2007

6. Wolff et al. 1998

7. Waterland and Jirtle 2003

8. Skinner et al. 2005

9. Kaati et al. 2002

10. Kaati et al. 2007

11. Jirtle, April 2006,

12. Morgan et al. 2008

13. Fraga et al 2005

14. Weinhold 2005

15. Adcock et al. 2006

Epigenetics and Disease

2012-10-15T18:49:00.000-07:00

References

1. Bollatti and Baccarelli 2010;

2. Dolinoy et al. 2007;

3. Isles and Wilkinson 2008;

4. Weidmann et al. 2007

5. Attig et al. 2010

6. Newbol 2004

7. Nystrom and Mutanen 2009

8. Dworkin, Huang and Toland 2009

9. Esteller 2008;

10. Shikhar, Kelly and Jones 2010

11. Herceg 2007

12. Kim 2006

13. Banerjee 2009

14. Adcock et al. 2006

15. Issa 2006

16. Ornish et al. 2008

17. Link, Balaguer and Goel 2010

18. Friaz et al. 2011

19. Ryan 2011

20. Wu et al. 2004

21. Gluekman and Hanson 2008

22. Freeman 2009

23. Levin et al. 2005

24. Muhlhausler et al. 2007

25. Levin 2008

26. Williams 2008

27. Jones PB, Rantakallio P, Hartikainen AL, Isohanni M, Sipila P

28. Brown and Susser 2008

29. Dempster, Pidsley et al 2011

Depression and B vitamins

2012-08-15T17:55:00.002-07:00

Whilst the area of nutrition is often discussed only in terms of physical health, a vast amount of research links the use of dietary supplements with positive effects on behaviour and mental health. A recent study of more than 2000 people found low plasma vitamin B-12 concentrations were associated with higher depression scores, and low vitamin B-6 concentrations were associated lower attention and executive function. ¹

In another study from the University of Sheffield regular supplementation of hospitalised older people with multivitamins and minerals improved mental health, compared to a placebo.² The prospective, double-blind, placebo-controlled study included 225 hospitalised, acutely ill older people with an average age of 75.6. Participants received either a normal hospital diet plus multivitamin and mineral supplements providing 100% of the Reference Nutrient Intakes for six weeks or a normal hospital diet plus a placebo for six weeks. Levels of folate and vitamin B12 in red blood cells and plasma, respectively, increased significantly in the supplement group but decreased in the placebo group. Beneficial effects for symptoms of depression scores were observed for patients in the supplementation group regardless of the initial level of depression of the individual. The authors wrote, “Many epidemiological and case-control studies have shown associations between folate and vitamin B12 deficiency and depression. In a study of 3,500 over-65-year-olds in Chicago over an average of 7.2 years of follow-up, the researchers noted that increased intakes of vitamins from food and supplements B6 and B12 were associated with a ‘decreased likelihood of incident depression.’” Vitamin B12 is involved in the synthesis of monoamines, some of which act as neurotransmitters and may also inhibit the accumulation of the amino acid homocysteine, which may lead to toxic reactions that enhance depression. For every 10-milligram increase in the intake of vitamin B6 and for every 10-microgram increase in vitamin B12, the risk of developing symptoms of depression was decreased by two percent per year.³

1 http://jn.nutrition.org/content/early/2012/06/26/jn.112.161828.abstract

2 Gariballa and Forster 2007

3 Skarupski et al. 2010

Fluoride lowers the IQ of kids

2012-08-13T16:08:00.000-07:00

There is increasing evidence emerging from the scientific community which suggests that mass-medication in the form of water fluoridation is in fact having a serious and adverse effect on the public’s health. A recent report from the US National Research Council ¹ concluded that adverse effects of high fluoride concentrations in drinking-water may be of concern. Animal studies have shown Fluoride may cause neurotoxicity, including effects on learning and memory ^2,3. Recent experiments where the rat hippocampal neurons were incubated with various concentrations of sodium fluoride showed that fluoride neurotoxicity may target hippocampal neurons.

Fluoride readily crosses the placenta exposing the developing brain, which is much more susceptible to injury caused by toxicants than is the mature brain, may possibly lead to damage of a permanent nature ⁴

In a study conducted by Tianjin Medical University in China, a comparison in the Intelligence Quotient (IQ) was measured between 60 children living in a high fluoride area and 58 children living in a low fluoride area. The IQ of the 60 children living in the high fluoride area was lower than that of the 58 children living in the low fluoride area. 21.6% of the children in the high fluoride area were retarded compared to 3.4% of retarded children living in the low fluoride area ⁵.

In a study at Tokyo University Medical School, water fluoridation was linked to Down syndrome. The study found that - as well as the aging of mothers - the number of excess Down syndrome births caused each year by water fluoridation was estimated to be several thousand cases throughout the world ⁶.

In the most recent meta analysis of 27 eligible epidemiological studies found that children in high fluoride areas had significantly lower IQ scores than those who lived in low fluoride areas ⁷. The conclusions of the study “support the possibility of an adverse effect of high fluoride exposure on children’s neurodevelopment.”

Some of the other adverse health effects of fluoride include lowered levels of collagen synthesis, depleted energy reserves and lowered immunity, irritable bowel syndrome,thyroid disorders, Skeletal fluorosis, Osteosarcoma, Osteoporosis and bone fractures as well as Alzheimer's disease.

1 NRC (National Research Council). 2006. Fluoride in drinking water: a scientific review of EPA’s standards. The National Academies Press, Washington, DC

2 Chioca LR, Raupp IM, Da Cunha C, Losso EM, Andreatini R. 2008. Subchronic fluoride intake

induces impairment in habituation and active avoidance tasks in rats. Eur J Pharmocol

579:196-201

3 Mullenix PJ, Denbesten PK, Schunior A, Kernan WJ. 1995. Neurotoxicity of sodium fluoride in rats. Neurotoxicol Terator 17:169-177.

4 U.S. EPA. 2011. EPA and HHS announce new scientific assessments and actions on fluoride/agencies working together to maintain benefits of preventing tooth decay while preventing excessive exposure

5 Lu, Y; Sun, ZR; Wu, LN; Wang, X; Lu, W; Liu SS (May 2000) “Effect of High Fluoride Water on Intelligence in Children” , Fluoride (Journal) Volume 33, No 2, pp 74 – 78.

6 Takahashi, K (May 1998) “Fluoride-Linked Down syndrome Births” , Fluoride (Journal) Volume 31, No 2, pp 61 – 73.

7 Choi AL, Sun G, Zhang Y, Grandjean P 2012. Developmental Fluoride Neurotoxicity: A Systematic Review and Meta-Analysis. Environ Health Perspect :-. http://dx.doi.org/10.1289/ehp.1104912

Medical vested interests. Can you trust the doctors

2012-08-10T17:18:00.000-07:00

A recent article ¹ highlights the lack of openness in medical research and reporting. The study found that “only one in seven authors fully disclosed their conflict of interest in their published articles….. and that approaches to controlling the effects of conflicts of interest that rely on author candidness are inadequate and furthermore, journal practices are not robust enough and need to be improved.

The problem with this is that “high-profile “opinion leaders” may exert considerable influence on prescribing practices of doctors and the doctors may not even be aware that the opinion leaders are getting paid by the pharmaceutical companies.

For the doctors, researchers and politicians, as well as the pharmaceutical companies, “vested interests” include billions of dollars spent marketing to doctors and interns each year. It is money-based medicine. In fact it’s more than $10 billion each year in the U.S. alone. The term “marketing” is perhaps a little loose because this spending involves sponsored holidays, retreats, conferences (all expenses paid), gifts—some non-taxed of course, like expensive bottles of wine—and the list goes on. The major medical journals recognise this now and call a medical professional who receives only $10,000 (U.S.) from a single pharmaceutical company “independent.” If you do a few bits of independent work for a few big companies, as long as you get only $10,000 from each one, it is considered acceptable. No other profession is allowed to do this.

It is usually not your general practitioner who receives the extra money, but the specialists and key figures in the area. It is a little scary when you recognise that the people who are outspoken on a health topic may be receiving some benefits from these big organizations, but even worse, no one can scrutinise their research because, as the medical journals recognise, the pharmaceutical industry has very deep pockets. I have written extensively on this in my book The Great Cholesterol Deception. An entire chapter of the book is devoted to researchers’ vested interests, another to doctors’ vested interests and another to the influence of the pharmaceutical industry.

After two decades as an editor of The New England Journal of Medicine, one of the most prestigious medical journals in the world, Marcia Angell wrote, “It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines.” In 2008 she wrote, “Over the past two decades, the pharmaceutical industry has gained unprecedented control over the evaluation of its own products. Drug companies now finance most clinical research on prescription drugs, and there is mounting evidence that they often skew the research they sponsor to make their drugs look better and safer.”¹ This is a person on the front lines of the best medical research in the world. Little wonder the rest of us lack confidence in the research.

1 Conflict of Interest Reporting by Authors Involved in Promotion of Off-Label Drug Use: An Analysis of Journal Disclosures. http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.1001280

Dr Peter Dingle

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