Dr Dingle's Blog / drug companies

Are your medications making you (Pharmaceutical) fat?

Are your medications making you (Pharmaceutical) fat?

Most people don't realise that a large number of pharmaceutical agents, including many over-the-counter and prescription drugs, are linked with weight gain and obesity. Drug-induced weight gain is a serious side effect of many commonly used drugs. The weight gain can be extremely high in a relative short time: sometimes more than 10 kg over 12 months. Some medications can increase appetite, cause fluid retention, or slowly lead to weight gain over a period of time due to fatigue and lower activity.
The best know impact, however, is the role of antibiotics in weight gain. The growth (fat) promoting effects of antibiotics were first discovered in the 1940s. Since then, antibiotics administered in low doses have been widely used as growth promoters in the agricultural industry worldwide. As a result, the largest use of antibiotics and related antimicrobial substances is on farms, with low doses fed to large numbers of animals used for food production, to increase weight gain by as much as 15%. If antibiotics are so effective in causing weight gain in farm animals, similar results are likely to occur in human populations. Unfortunately, antibiotic use in humans has increased markedly, often for the wrong reasons, now approximating one antibiotic course per year for the average child and most of them for the wrong reason. Antibiotics can cause many problems and we do overuse them. For a bacterial, not viral, infection always listen to you health professional; the gut microbiome can be rebuilt after the treatment finishes with super probiotics and prebiotics.
 
Blood pressure lowering medications such as Beta blockers reduce metabolic rate and slow utilization of nutrients, thus resulting in weight gain. Obesity and hypertension contribute to metabolic syndrome, which could further complicate the patient’s situation. Many of the diabetes medications can lead to weight gain. These agents may increase insulin production, which can lower blood sugar levels and result in an elevated appetite. Injectable insulin itself can also lead to weight gain, possibly due to periods of low blood sugar that stimulate appetite. Other drugs used in the treatment of type 2 diabetes can lead to weight gain and fluid retention.
Many psychotropic drugs, including antipsychotics, antidepressants and mood stabilizers, are also linked with significant weight gain. In a study of three antipsychotic drugs over 12 months, at three months haloperidol added 3.8 kg, risperidone 5.9 kg and 8.4 kg for olanzapine. After one year, all participants had gained between 9 and 11 kg. Some antidepressant drugs induce significant body weight gain, which may amount to 20 kg over several months of treatment. The older antidepressants, known as tricyclic antidepressants (TCAs) are notorious for increasing appetite and causing weight gain.
Commonly prescribed oral glucocorticoids like prednisone can also cause significant weight gain, especially when taken over prolonged durations, by causing fluid retention, stimulating appetite and increasing deposits of fat in the upper part of the body and the abdomen. Antihistamine drugs that are used to treat allergies can result in weight gain through blocking of a chemical called histamine in the brain. Weight gain is a common side effect of drugs used for headache prevention.
Statin drugs used to lower cholesterol have now been shown to be ineffective in prevention of heart disease. However, they are associated with an increase in diabetes and weight gain.
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Environmental Estrogens in cosmetics and personal care products. Breast Cancer and Toxicity

Environmental Estrogens in cosmetics and personal care products.  Breast Cancer and Toxicity

It is estimated that in the world today, there are at least 120,000 synthetic chemicals, or xenobiotics registered for commercial use and around 1,000 new chemicals are formulated each year. While many have been proven to be highly toxic and carcinogenic, little is known about the chronic effects particularly their potential to alter, or disrupt the function(s) of the endocrine system and our hormones. These synthetic chemicals are known as 'environmental estrogens', estrogen mimics, or xenoestrogens and have been found to affect hormonal functions by 'mimicking' the function of naturally occurring estrogen in the body.

Estrogens are a group of naturally occurring hormones present in both male testes and female ovaries, with females producing a considerably higher amount. They are particularly influential during puberty, menstruation and pregnancy; however they also assist in regulating the growth of bones, skin, liver and organs of the cardiovascular system. Estrogens, like all hormones, act as chemical signals and are important in helping cells in various organs to sense and respond to changing physiological conditions; therefore the right balance of hormones is critical in order to carry out the functions required of a healthy, strong body. Estrogen binds to a protein, or estrogen receptor, and the estrogen receptor complex can then bind to specific genes and by this, alter the way they are expressed, resulting in a change in cell programming 1.

Environmental estrogens, are now present in everyday products such as polycarbonate plastics, food packaging and cans. However the greatest source for many people is through cosmetics and personal care products and include chemicals such as triclosan, cyclosiloxanes, parabens and phthalates which are often left on the skin to absorb and accumulate 2. Women are disproportionately exposed to many environmental estrogens like paraben and phthalates because they use more personal care products on average than men 3 and teenage girls tend to use even more products than women, averaging 17 different products per day, compared with 12 for women 4.

Since the 1980's, there has been a growing amount of research toward the potential interaction between these environmental estrogens and wild animals, with a number of reports detailing the emergence of 'feminised wildlife’ around the world, and a range of adverse effects in humans including decreased sperm count, increased cases of testicular cancer and testicular abnormalities, increased breast cancer in men and women and premature or precocious puberty. Other adverse health include headache, migraine, depression, gastrointestinal disturbances, insomnia, mastopathia, changes in vaginal bleeding 5. More chronic symptoms affect the cardiovascular system, the skin (itching, rash, abnormal pigmentation), the gallbladder, and tumours, particularly of the breast but also uterus, cervix, vagina and liver 5.

One of the most troubling is their association with breast cancer 6,7,8. Breast cancer is the major cancer affecting women in the Western world 9 and one of the most disturbing and well documented current trends is the alarming increase in breast cancer incidence over the past few decades. Fifty years ago the risk rate was one woman in 20; today it is one in 8 and approximately two-thirds of breast tumors are estrogen receptive, and environmental estrogens like parabens are known to bind to estrogen receptors. Estrogen-dependent cancers, such as breast cancer, are known to be highly responsive to estrogens for growth. Even more disturbing is the increase in numbers of young girls developing breast cancer. Although many factors such as radiation, alcohol, smoking and diet, add to the risk of developing breast cancer, the predominant influencing factor has been identified as the exposure to estrogens throughout an individual's lifetime 9.

The breast is under hormonal control and a fine balance of hormones is what allows the cell to cell communication. Interaction between these cells and the surrounding fluid of the breast tissue is what controls differentiation and growth of the breast 9. If there is a disruption of those hormones, i.e. through the use of synthetic chemicals, the balance of hormonal control is thrown and the cells do not function normally which may lead to breast cancer. In support of this clinical studies show that estrogen has the capacity to drive breast tumours to grow in laboratory studies. Animal experimental studies have also shown the role of estrogen on the growth of breast cancer cells 9. While chemicals which mimic estrogen have been shown to promote and stimulate the proliferation of breast cancer cells 2,10,11, and activate other processes involved in breast cancer 2,11,12. Recent studies have also shown other factors can dramatically increase the the toxicity of Xenoestrogens and studies of individual estrogens may seriously underestimate their growth and spreading effects in breast tissue cells and their potency to promote breast cancer, particularly at lower doses 13.

Although the vast majority of studies on breast cancer are aimed towards women, men can also suffer from the disease, indicating that they have similar risk factors, with one case in a hundred diagnosed breast cancers being a male 14. Although this number is relatively small, the rate of incidence has increased by 25% in 25 years.

Sperm count of the average male in the US or Europe has been found to be declining continuously over the past four decades, dierectly linked with environmental estrogen exposure, and today it is less than 50% of what it was forty years ago15,16. One result of this lower count is the increased rate of male infertility; which is also the single most common cause of infertility. The rate of infertility has quadrupled in the past forty years, from 4% in 1965 to at least 16% today 15.

Other conditions including undescended testes caused by prenatal estrogen exposure to environmental estrogens have also been found in studies on mice and it has been suggested undescended testes increases the rate of testicular cancer 17. The incidence of testicular cancer, namely affecting males between the ages of 20 to 30, has also seen an increase worldwide. Studies have found strong links with exposure to excessive levels of estrogen with hypospadias (abnormal congenital opening of male urethra upon under surface of the penis) 18,19, lower libido 19, congenital anomalies, cryptorchidism and testicular cancer 20,21,22.

Environmental estrogens have also been linked to early puberty in girls and increasing number of girls experiencing precocious puberty in recent years 15. A study in the United States of 17, 000 girls indicated that 7% of white and 27% of black girls exhibited physical signs of puberty by age seven, and for girls aged 10 the percentages increased to 68 and 95 respectively 16. This trend for earlier puberty has been found to be widespread, with similar cases found in the United Kingdom, Canada and New Zealand (Trankina, M. V L., 2001).

Environmental estrogens are also suspected of disrupting thyroid functioning, sexual differentiation of the brain in foetal development and cognitive motor function 23. It is also believed that high levels of environmental estrogen exposure results in lower birth weights, smaller head circumferences, poorer neuromuscular maturity and visual recognition, delays in psychomotor development, short term memory problems, and growth retardation in newborn babies 24.

Prenatal exposure to environmental estrogens also poses a serious health risks to developing fetus and children as evidence of adverse effect on birth outcomes, childhood obesity, and intellectual disability are increasing 25. The placental barrier has been shown to allow these chemicals to cross as many of them have been measured in human fetal cord blood and tissue. More importantly, because organogenesis begins at the time when the fetus is solely dependent on maternal supply, early life exposure to environmental estrogens may lead to adverse short or long term health outcomes due to fetal reprogramming 26.

From testing on animals it has further been proposed that excessive estrogen levels could cause anxious behaviour 27,28, altered fecundency 29, reduced penis size 30 and increased embryo mortality 24. Environmental estrogens are not only capable of binding to estrogen receptors on cell membranes but are also able to bind to neurotransmitters such as epinephrine, neuroepinophrine and dopamine enabling estrogens to influence the body's central nervous system (CNS) 31. Environmental estrogens have also been shown to effect the body’s immune system 30. A large number of studies have also environmental estrogens to contributing to obesity and diabetes, independent of poor diet and physical inactivity; such chemicals including ingredients found in personal care products and cosmetics such as phthalates and phenols 32,33.

More recently studies have found effects of direct exposure to products instead of just individual chemicals. Extensive observational studies have indicated a relationship between certain hair product use and hormonally imbalances including early menache (puberty) 34,35 and uterine fibroids  36 as well as enlargement of breast tissue in boys and men 37.

 

However, estrogenic (or anti-estrogenic) effects of the personal care products as commercial mixtures have rarely ever been evaluated. In a study of eight commonly used hair and skin products four of the eight personal care products tested (Oil Hair Lotion, Extra-dry Skin Lotion, Intensive Skin Lotion and Petroleum Jelly demonstrated detectable estrogenic activity 38. The estrogenic activity of these products was not predictable by examining their listed ingredients. However, perhaps the most surprising finding about any one product was the estrogenic activity of SP4 (Petroleum Jelly). Petroleum jelly products are also often used on infants as low-cost therapies for common problems such as diaper rash and is manufactured by refinement of the crude petroleum product. While other studies have shown that hair oil use as a child was significantly associated with earlier menarche and hair relaxer use and uterine fibroids among participants in the 36. A third study found an elevated incidence of endometriosis and use of personal care products containing benzophenone-type UV filters 39.

 

Fortunately, studies have also shown it is relatively easy to reduce exposure by reducing personal care use or using safer products. In one study of around 100 girls they replaced their personal care products with safer alternatives for 3 days. The replacement products were chosen on the basis of whether their ingredient lists included triclosan, benzophenone-3, or parabens. Phthalates are not listed on ingredient lists, but they are often found in scented products. So the researchers avoided products that listed “fragrance” as an ingredient unless they were specifically labeled as phthalate free.  More than 90% of the participants had detectible levels of phthalates, parabens, and benzophenone-3 before they started using the replacement products. After using the alternative products for 3 days urinary concentrations of methyl and propyl paraben decreased by 43.9% and 45.4%, respectively, mono-ethyl phthalate decreased by 27.4%, and triclosan decreased by 35.7%. However, there were increases in concentrations of butyl and ethyl paraben, which were detected in about half the girls. These chemicals might have been unintentional contaminants or unlabeled ingredients in replacement products, which they acknowledge they were unable to ensure were paraben free 40.

 

 

  1. McLachlan, J. A. & Arnold, S. F., 1996
  2. Darbre, 2003
  3. February 2015
  4. 24 September 2008
  5. Ternes et al 2004
  6. Darbre and Harvey 2008;
  7. Vandenberg et al. 2012;
  8. Zoeller et al. 2012
  9. Darbe 2006
  10. Okubo et al. 2001;
  11. Wróbel and Gregoraszczuk 2013
  12. Gomez et al. 2005
  13. Pan S, et al 2016
  14. Williams, R. M., 2004
  15. Sax, L., 2001,
  16. Trankina, M. L., 2001
  17. Christiansen et al, 1996
  18. Paulozzi 1999
  19. Calzolari et al, 1986
  20. MeLachian et al, 1984)
  21. Rapp, 1996
  22. Bernstein, 1988
  23. Ayotte and Bonefeld‑Jorgensen, 2003
  24. Trankina, 2003
  25. Godoy, et al. 2014
  26. Skinner M. K., et al. 2011
  27. Arabo et al, 2005
  28. Caston et al, 2001
  29. Vos et al, 2000),
  30. Brooks et al, 2007
  31. Fuentes et al, 2000
  32. Song Y, et al 2014;
  33. Carwile JL, et al 2011
  34. James-Todd. 2011
  35. Tiwary CM. 1998
  36. Wise LA, 2012
  37. Gottswinter JM, 1984
  38. Myers et al 2015
  39. Kunisue T, et al. 2012
  40. Harley KG, et al. 2016

 

 

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ADD and ADHD are not a disease

ADD and ADHD are not a disease

Attention Deficit Disorder (ADD) and Attention Deficit Hyperactive Disorder (ADHD) are a group of symptoms and not a disease. Children are classified as ADD when they show signs of inattention, such as a lack of close attention to detail, difficulty in sustaining attention or are easily distracted. Some children may be underactive (hypoactive), inflexible, suffer from speech disorders and have poor short term memory, and show sleep and appetite changes. ADHD has the added signs of hyperactivity such as fidgeting, being always ‘on the go’, disruptive or demonstrate other signs of hyperactivity. While there are more precise definitions for these conditions, they are mostly subjective and open to a large amount of interpretation. ADD/ADHD are relatively new conditions and were probably defined as soon as a pharmaceutical company had a drug to use.

As more investigation is done on these disorders, more controversy is raised about possible origins and causes. It’s likely that ADD/ADHD occurs because of a complex of factors, including illnesses and a combination of susceptibility factors such as genetics, maternal diet during pregnancy and length of breast feeding. The child’s exposure to various chemicals in both food and the environment and their current diet are also probable contributing factors. Some chemicals and foods may act as a trigger for the disorder. Whatever the cause, it seems likely from the nature of the symptoms that ADD/ADHD has many contributing factors. No cases are identical, especially when dealing with children. ADD/ADHD however, is definitely not a deficiency of Ritalin or any other drug.

Surveys suggest that as many as 49 per cent of boys and 27 per cent of girls are described as inattentive by their teachers, while serious deficits in attention appear to occur in at least three to 10 per cent of school-age children, making inattention among the most prevalent of all childhood neuro-psychological disorders. Many of these children are diagnosed as having ADD/ADHD.

Many studies identify a worseing of symptoms with certain foods or food additives; others link lead contamination, smoking and alcohol in pregnancy to developmental disorders in children. The possibility of chemical substances in the diet and the environment influencing ADD/ADHD is highly likely.

Sadly, little real evaluation of ADD/ADHD children is actually carried out. They are not routinely evaluated for chemical, nutritional or allergic factors, or assessed for behavioural or environmental issues arising from their home environment. Instead they are given drugs. This is despite the fact that there is growing body of scientific literature showing significant nutritional deficiencies in many of these children. There is growing evidence that a significant number of ADD/ADHD sufferers have a high body burden of heavy metals, particularly lead, mercury, cadmium and possibly even the trace element copper. These metals are potent toxins which block thousands of important chemical reactions in the body and can play havoc with the nervous system. At even moderate concentrations, lead can lower a child’s IQ. Recent research links infant and maternal exposure to lead with higher rates of schizophrenia.

 

Nutritional deficiency is an underlying cause of  ADD/ADHD in a significant number of children. Correcting these deficiencies and inbalances can make substantial improvements in childrens’ behaviour. Sometimes improvement is almost immediate.

The basic problem appears to be deficient levels of neurotransmitters (chemicals that coordinate many of the body’s and mind’s activities) in brain cells. Various chemical substances affect the transmission of messages across the synapse, the gap between individual nerve cells. Acetylcholine, adrenalin, noradrenaline, dopamine, gamma-aminobutyric acid (GABA) and serotonin are all examples of neurotransmitters. Some of these chemicals are responsible for other chemical secretions and uptake. They control muscular activity, mood and behaviour. So you can see how they might be involved in ADD/ADHD.

Over-prescription of drugs, (particularly the amphetamine Ritalin, one brand name for methyl phenidate) that manage the symptoms of the disorder, is common. In Western Australia the annual use of prescription amphetamine-like tablets prescribed for ADD/ADHD has exploded. There are many problems associated with taking these drugs. They include anorexia, weight loss, insomnia, lability of mood, nervousness and irritability, abdominal discomfort, excessive withdrawal symptoms, heart arrhythmias, palpitations and psychological dependence. Suicide is also a major complication of withdrawal from amphetamine-like drugs. Children on Ritalin are more prone to become addicted to smoking and illicit drugs. These drugs don’t deal with the underlying cause. The US National Institute of Health has concluded that there is no evidence that Ritalin brings about any long-term benefit in scholastic performance.

These drugs have a noradrenaline-like action. Noradrenaline normally acts to coordinate many nervous system functions. It’s thought to filter out unimportant stimuli, reducing the number of distractions sensed by the child. If ADD/ADHD is a noradrenaline shortage, it could be measured, but no one seems to want to do this. It’s much easier (and more profitable?) to prescribe drugs. If it’s a noradrenaline shortage, it can at least to some degree, be corrected by dietary measures.

There are many reasons as to why a child may have a poor nutrition. These include being breast-fed for only a short period of time. Infant milk formulas and cows’ milk  are not the same as human milk. Cows’ milk is great for a calf that needs to put on weight directly after birth. A cow’s brain does not grow after birth. The human brain continues to grow substantially up to the age of three, and then more slowly, up to 18 years of age. It’s not surprising then, that human milk is high in Essential Fatty Acids (EFAs) and choline, along with many other ingredients essential for the development of a healthy brain and nervous system. Both these nutrients are severely deficient in many infants’ and children’s diets, particularly if the diet is high in grains and processed foods.

One explanation for the higher rates of ADD/ADHD in males is that males have a higher demand for EFAs (Omega 3 oils). Males don’t appear to absorb them well and are less efficient at converting them to an important group of chemicals called prostaglandins. Prostaglandins regulate many activities in the body and play an essential part in others. Many of the foods that are linked with ADD/ADHD also inhibit the conversion of the EFAs to prostaglandins. Foods such as wheat, dairy and salicylate-containing foods, including some of the food colours. Conversion is also blocked by deficiencies in Vitamins B3, B6, C, biotin, zinc and magnesium. There are many studies now that show the benefit of supplementing the diet with fish oils and flax seed oil, not only for adults but for kids being treated with Ritalin. What’s also interesting about the EFAs is that many of our parents were dosed with them once or twice a week in the form of cod liver oil.

ADD/ADHD children appear to be deficient in a number of nutrients:

Vitamin C;

Vitamin B3;

Zinc;

Magnesium; and,

Essential fatty Acids (Omega 3 rich oils).

It may be that there is an absence of these nutrients in the diet. It may be the effects of medication, stress, and other lifestyle factors, including exposure to some environmental contaminants, that have lead to nutritional deficiencies. For example, the use of antibiotics has been shown to have an effect on the nutritional status of children, as they deplete the body’s levels of zinc, calcium, chromium and selenium. Antibiotics, other medication and  food preservatives can also have a serious detrimental effect on the healthy gut bacteria which in turn affects the ability of the gut to absorb nutrients.

Academic performance and behavioural problems improve significantly when children are given optimal nutrition and nutritional supplements. In one study, supplementing with just 200 milligrams of magnesium for six months improved magnesium status and significantly reduced hyperactivity. Magnesium plays a key role in the production of noradrenaline. One of the main sources of magnesium in our diets is green vegetables, but few kids get enough of these. Other nutrients involved in the production of noradrenaline include manganese, iron, copper zinc, Vitamin C and Vitamin B6.

Noradrenaline formation may be affected by an absence of the amino acids L-phenylalanine or L-tyrosine, which are its building blocks. Vitamins B1, B2, B3, B6, Vitamin C, Folic acid and the minerals zinc, magnesium and copper are necessary for the conversion of phenylalanine and tyrosine to noradrenaline.

It has been proposed for many years that food additives and other food constituents can contribute to ADD/ADHD. While this is refuted by the food additive industry, there’s growing evidence that this is the case. It’s also becoming apparent that there are biochemical explanations as to why some foods and food additives, particularly the food colours, may be contributing factors. For example, salicylates inhibit the conversion of the EFAs to the protective prostaglandins, as mentioned earlier. Many foods that contain salicylates - tomatoes and granny smith apples, as well as aspirin and the food colours like tartrazine (102) - may exacerbate ADD/ADHD.

Food additives linked with ADD/ADHD can also deplete the body of vitamins and minerals. Tartrazine decreases blood levels of zinc and increases its excretion in the urine.

Food additives to avoid are

102, 107, 104, 110, 120, 122, 123, 124, 127, 129, 132, 133, 142, 151, 153, 155, 160b, 168, 173, 250, 251, 252, 282, 320, 321, 420, 421, 621 (MSG) 622, 624, 627,631, 635, 951 (Nutrasweet®, Aspartame®).

The diet of the pregnant and breast-feeding mother is very important. Infant and early childhood health conditions have a big role in the health of middle childhood.  This is supported by research on alcohol exposure at various stages of pregnancy, hence the importance of good foetal and childhood nutrition.

 

What to do about food

For any child with ADD/ADHD it’s important to identify foods that may be causing a problem. This is best done with a professional such as a naturopath. or a doctor specialising in nutritional and environmental medicine. With these professionals you can devise an elimination diet to identify potential environmental and dietary culprits. Some of the culprits are shown below.

The main foods causing sensitivities and allergies include:

  • Cow’s milk and associated dairy products;
  • Some legumes – soybeans, peanuts;
  • Nuts and seeds –pistachio nuts, cashews, macadamia nuts, cottonseed;
  • Crustaceans – shellfish, shrimps;
  • Fruits (non-citrus) – cherry, apple;
  • Citrus Fruits – oranges, lemons, limes;
  • Wheat and Other Grains – corn, rice, rye, oats, barley, buckwheat;
  • Cola nut products – chocolate, cola;
  • Spices – cinnamon, bay leaf, peppers, peppermint, oregano, sage, thyme, cumin;
  • Food Additives – coal tar dyes, preservatives, flavour enhancers, artificial sweeteners; and,
  • Caffeine – coffee, tea, chocolate, cola drinks.

The brain uses only glucose for energy. The research on sugar suggests that it may not be a major factor in ADD/ADHD. However, brain glucose that comes in waves of high highs and low lows is likely to affect a kid’s mood.

 

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Lowering cholesterol is not the answer

Lowering cholesterol is not the answer

Of the last 50 years we have seen a decrease in saturated fat, salt and cholesterol levels yet we continue to see increases in cardiovascular disease. We are doing more than ever before but still the disease continues to increase. Fortunately there appears to be the decreases in deaths as a result of cardiovascular disease primarily due to the early intervention once someone has had a heart attack or stroke. Because we have been targeting at risk population we would expect to see a decrease in cardiovascular disease within a few years of any program yet more people have heart attacks and strokes than ever before.

Maybe the time has come to separate out all the vested interests and silver bullet solutions and deal with the problem. Already in previous articles I have described to you that cholesterol is not the killer it is just a messenger. It is like a warning light on the car. When the light comes on you can fix the problem before it gets any worse, or you can get some tape and cover it over. Unfortunately we have become very adept at covering our own personal health warning light.

The reason we have become so fixated with lowering cholesterol is that it is a multi-billion-dollar industry in Australia alone. The costs of the drugs to the public and individuals is estimated to be about $1.5 billion each year. Add on to that the cost of monitoring and all the blood checks, another billion dollars then you can understand why it is almost impossible to stop this juggernaut. There is just too much money invested in it. Then you also have two consider all the cholesterol lowering foods, the claims made and organisations involved and you realise that the total is probably closer to $10 billion each year.

The outcome we are after is the lowering of cardiovascular disease not cholesterol. If we have not succeeded at this then we need to go back to the drawing board and start again and not just reinvent another cholesterol theory or a new cholesterol-lowering drug. The last 30 years has been an abject failure that has cost a fortune in money and lives.

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