Complimentary and Sustainable Medicine

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 

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

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.

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.

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

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