21 December 2012

Was the mother right to refuse treatment?

 Supports Chapters One and Two?

Everyone (in the UK at least) must know of Neon, the seven-year-old boy who has a brain tumour, medulloblastoma, and of Neon's mother, Sally Roberts, who is fighting for her son not to have radiotherapy and chemotherapy because of the danger, she says, of adverse side effects which could damage his brain and destroy his quality of life. 

The Daily Mail, today, put it this way:

Cancer boy Neon WILL have radiotherapy against his mother's wishes after High Court ruling.

  •     Mr Justice Bodey said he was worried Sally Roberts judgement had 'gone awry'
  •     Mrs Roberts had tried to claim her son should have alternative treatment to radiotherapy
  •     Experts brand her alternatives 'completely unethical'
  •     She conceded that her argument is 'weak' under questioning

I don't intend to take sides on this issue (although you can probably guess which side I might be on). But if you are wondering if Mrs Roberts has a case, here is the abstract from a 2003 study about the long-term effects on survivors of exactly the treatment a judge has decided her son must have:

Macedoni-Luksic M, Jereb B, Todorovski L. Long-term sequelae in children treated for brain tumors: impairments, disability, and handicap. Pediatr Hematol Oncol. 2003; 20: 89-101.


Sixty-one long-term survivors, treated for brain tumors in childhood, were evaluated in term of neurological impairments, disability, and handicap.

Thirty-eight patients (pts) (62%) had at least one impairment.

Visual impairment was detected in 14 pts (24%), associated with recurrence (p = .012).

34r pts (56%) had motor impairment, associated with sex (female) in irradiated patients;

13 (21%) had epilepsy, associated with supratentorial tumor site (p = .001).

The same number of patients had brain atrophy; risk factors were hydrocephalus at diagnosis and perioperative complications.

16 pts (30%) had IQ score < 80, associated with young age at first treatment (p = .006) and recurrence (p = .043).

27 out of 61 of our patients (44%) were disabled: 12 mildly, 14 moderately, and 1 severely.

Epilepsy was the most important risk factor for disability.

Cognitive impairment, motor impairment, and epilepsy were associated with employment (43%);

Cognitive impairment was also associated with education.

 So is Mrs Roberts right to be worried about her son's having conventional treatment? Has her judgement 'gone awry'? You decide.


15 December 2012

Fluoride drugs and violent deaths

This week and last week saw the violent deaths of many people including young children, at the hands of young men on the rampage in the USA. Understandably, there are calls for changes in the gun laws. But the fact that American can carry guns is not the cause of the problem.

It isn't guns that kill people; it is people who kill people.

The US has a long history of such outrages. And is pretty much alone as a country to suffer in this way, despite the fact that guns are carried, legally, in other countries - whose citizens don't go around on killing sprees.

So, instead of blaming the weapons, wouldn't it be more profitable to research the cause? To ask why some people feel the need to go kill a bunch of others and then (usually) themselves?

In the 1990s I was researching fluoridation of water supplies. But as I did my research, I came across examples of the harm that fluoridated drugs could do. Just like the killings in last two weeks, there have been examples of children going on a killing sprees and shooting their parents, school friends, teachers, other people and then themselves for decades.

I don't know whether the recent perpetrators of these outrages were on drugs but back in the last century, I found that many, if not all, of them appeared to be taking the SSRI drug, Prozac.

Below is an extract from my book, Fluoride: Drinking ourselves to death? I wrote this in 1999; it is still relevant today. Searching PubMed today, I could find no medical research that addresses the problem. Perhaps it is about time there was some!

Fluoride drugs and violent deaths
Many antidepressive drugs contain fluoride because of its profound effect on mood. Fluanxol, Motipress, Motival, Parstelin and the biggest seller, Prozac, are all highly fluorinated. Hypothyroidism, which they produce, can induce almost any psychiatric symptom or syndrome, including rage, fear ranging from mild anxiety to frank paranoia, mood swings and aggression.
      Recently the USA has seen an alarming rise in apparently motiveless killings where individuals - usually men, but also children - have taken a gun and shot several people before shooting themselves.
      The number of people, including preschool children, prescribed antidepressants and stimulants rose in the mid-1990s despite limited knowledge about the effects of such drugs on young children. The reasons for prescribing such medications in young children include pain relief, anxiety associated with medical, pre-surgery and dental procedures, bed wetting and attention-deficit/hyperactivity disorder in children aged three years and older. Yet, 'Unresolved questions involve the long-term safety of psychotropic medications, particularly in light of earlier ages of initiation and longer durations of treatment'.1
      In an early case, a young defendant was found not guilty because he committed a murder 'in the course of a hypothyroid psychosis'. . . 'He was later judged to be not guilty by reason of insanity, although he was clearly sane at the time of his trial.'2
      The University of Maryland looked at 200,000 patients in three areas of the country. It found that use of stimulants and antidepressants rose in all the areas between 1991 and 1995. Julie Zito, principal author of the study, said that some of the drugs' uses are not included in warnings on drug packages. While this is not uncommon with some drugs for adults, there is no information on how these psychotropic drugs work for children.
      In a recent rampage that has become frighteningly familiar in the USA, a fifteen-year-old Springfield, Oregon, student, Kip Kinkel, dressed in a trench coat, ran through a crowded school cafeteria firing his rifle from the hip. He killed a classmate and critically wounding several others. The Associated Press headline read:


This was frighteningly similar to a violent episode which took place in Louisville, Kentucky in 1989. Joseph Wesbecker stepped out of an elevator at work firing an AK47 semiautomatic assault rifle. Twelve people were wounded and eight killed before Joseph Wesbecker took his own life. One victim described him as 'totally devoid of human element and human soul.'
      Kip Kinkel was restrained before he could take his life, but begged others to shoot him when they tackled him. Both men were taking Prozac at the time.
      Prozac's manufacturer, Eli Lilly has repeatedly claimed that Prozac is safe. The International Coalition For Drug Awareness (ICFDA), a non profit group that warns of potential serious adverse reactions to prescription medications, reports that there is abundant evidence in medical literature showing a link between Prozac and violence, as well as suicide.
Dr. Ann Blake Tracy, director of ICFDA, and author of Prozac: Panacea Or Pandora?, has testified as an expert witness since 1992 in Prozac and other antidepressant related criminal cases. Dr. Tracy poses the question, 'How many patients have ever been warned that even something as simple as mixing most major cough syrups with their use of these medications can produce PCP (Angel Dust) like reactions?' 'We are sitting in the middle of this nation's most dangerous drug problem and have not yet awakened to the seriousness of this situation.'
Wesbecker and Kinkel are only two of a growing number of violent cases committed by people taking Prozac or one of its clones:

  1. A mother on Prozac in San Francisco smothered her three small daughters by wrapping their hands and faces with duct tape and attempted to take her own life
  2. A man in Los Angeles on Prozac committed suicide in front of TV cameras.
  3. A lottery employee taking Luvox (a Prozac clone) in Connecticut shot and killed four fellow workers before taking his own life
  4. A man in Wyoming taking Paxil (another Prozac clone) shot and killed his wife, daughter and baby grand-daughter before he took his own life.

      Now four more are dead and Kinkel is facing a life without his parents and several classmates. He also faces spending the rest of his life in prison while he slowly comes to a realization of what he did in this drug-induced stupor.
      According to internal company documents made public in court cases filed against Eli Lilly, in 1990 they attempted to protect their 'golden goose' (Prozac was bringing in over $6 million a day). Dr Leigh Thompson went 'against the advice of his staff' and told the board of directors that suicide and hostile acts committed by Prozac users were, in all probability, caused by the patients' underlying disorders rather than Prozac. On 7 November 1990 he asked, 'What are our priorities?'
      Of course priority number one for Eli Lilly was to protect Prozac.
      In December 1993 the world heard that Prozac had been found 'not guilty' in the murderous rampage and suicide of Joseph Wesbecker. But, in fact, Eli Lilly had paid millions of dollars to settle out of court. The judge was so upset about the secrecy and deception surrounding the case that he called for an additional hearing to force Lilly to admit this publicly. He succeeded, and Lilly and the plaintiffs were forced to admit that this was indeed a settlement and not a 'not guilty' verdict for Prozac.
      In another Prozac case against Lilly (Forsyth v. Lilly) currently being tried in Federal District Court in Hawaii, Judge Alan C. Kay ruled:

  • 'Lilly falsified reports of side effects of suicide attempts by reporting them as overdoses.'
  •  'material issues of fact exist as to whether Lilly deliberately suppressed adverse studies.'
  • 'The Court finds that Plaintiffs have presented sufficient evidence to show that Lilly may have acted wantonly, oppressively, or with such malice as implies a spirit of mischief or criminal indifference.'

1. Julie Magno Zito; Daniel J. Safer; Susan dosReis; James F. Gardner; Myde Boles; Frances Lynch. Trends in the Prescribing of Psychotropic Medications to Preschoolers. JAMA. 2000;283:1025-1030.
2. Easson WM. Myxedema psychosis – insanity defense in homicide. J Clin Psychiatry 1980; 41: 316-8.
3. http://www.drugawareness.org/oregon.html. Accessed 15 April 2000

08 December 2012

Link Between Vitamin D And Women's Cognitive Performance

Supports Chapter 11:  Our irrational fear of sunlight

As part of the concept of a 'healthy' lifestyle foisted on us in the 1980s, sunbathing became a no-no, unless you were fully clothed, or slathered in sunscreen, or the sun wasn't shining, or preferably all three! 

Not long after, the numbers of cases of Alzheimer's dementia began to rise. Today, in the UK at least, dementia has become the number one health concern, not just for the misery it causes to sufferers and their families, but the sheer cost in terms of both money and health resources needed to look after the growing number of people with dementia.

And so to December 2012:

Two new studies have just been published in the Journals of Gerontology Series A: Biological Sciences and Medical Sciences which show that vitamin D may be a vital component for the cognitive health of women as they age.

Higher vitamin D dietary intake is associated with a lower risk of developing Alzheimer's, according to research conducted by a team led by Cedric Annweiler, MD, PhD, at the Angers University Hospital in France.

Similarly, investigators led by Yelena Slinin, MD, MS, at the VA Medical Center in Minneapolis found that low vitamin D levels among older women are associated with higher odds of global cognitive impairment and a higher risk of global cognitive decline.

Slinin's group based its analysis on 6,257 community-dwelling older women who had vitamin D levels measured during the Study of Osteopathic Fractures and whose cognitive function was tested by the Mini-Mental State Examination and/or Trail Making Test Part B.

Very low levels of vitamin D (less than 10 nanograms per milliliter of blood serum) among older women were associated with higher odds of global cognitive impairment at baseline, and low vitamin D levels (less than 20 nanograms per milliliter) among cognitively-impaired women were associated with a higher risk of incident global cognitive decline, as measured by performance on the Mini-Mental State Examination.

Annweieler's team's findings were based on data from 498 community-dwelling women who participated in the Toulouse cohort of the Epidemiology of Osteoporosis study.

Among this population, women who developed Alzheimer's disease had lower baseline vitamin D intakes (an average of 50.3 micrograms per week) than those who developed other dementias (an average of 63.6 micrograms per week) or no dementia at all (an average of 59.0 micrograms per week).

Another case of 'cause and effect', as a result of incompetent health advisers.

n.p. (2012, December 4). "Link Between Vitamin D And Women's Cognitive Performance." Medical News Today. Retrieved from

04 October 2012

Fraud In Published Scientific Papers Rises Dramatically

Supports Chapter One: Trick to Treat

In the first chapter of Trick and Treat, I outlined the vast amount of fraud, ghost-writing, and spin that was to be found in medical journals' articles. 

I wrote that in 2008. As this article from Medical News Today, Weekly Newsletter - 3 October 2012, points out, little has changed. In fact the problem might well be getting worse.

Article Date: 02 Oct 2012 - 12:00 PDT

Fraud, suspected fraud, plagiarism and duplicate publications are the main reasons why scientific papers are retracted today, researchers from the Albert Einstein College of Medicine reported in PNAS (Proceedings of the National Academy of Sciences) today.

Misconduct occurs at ten times the rate it used to in 1975 among scientific papers - scientific papers refers to articles that are published in academic journals. Two thirds of all retractions today are due to misconduct.

Senior author Arturo Casadevall, M.D., Ph.D., the Leo and Julia Forchheimer Chair and professor of microbiology & immunology and professor of medicine at Einstein, and also editor-in-chief of mBio said:
"Biomedical research has become a winner-take-all game-one with perverse incentives that entice scientists to cut corners and, in some instances, falsify data or commit other acts of misconduct."
A survey carried out by the BMJ (British Medical Journal) in January 2012 revealed that 13% of doctors and scientists had seen colleagues deliberately fabricate or change data during their research to make sure that it was published.

The authors examined 2,047 articles that had been retracted from biomedical literature up to the end of May 2012. They had set out to find out why retractions occur. They consulted several secondary sources, including the NIH (National Institutes of Health, the Office of Research Integrity, as well as Retractionwatch.com.

The authors found that:
21% of retractions were due to mistakes (error)

67% of retractions were due to misconduct, which was broken down as:
   - fraud or suspected fraud 43%
   - duplicate publication 14%
   - plagiarism 10%
   - unknown or "miscellaneous" reasons 12%

The problem with very skillful fraud, Dr. Casadevall said, is that it is hard to discover. There are probably several fraudulent papers still published and not retracted because misconduct has not yet been detected.

The authors explained that previous studies that underestimated the extent of scientific misconduct had relied completely on notices of retraction issued by the journal, which are written by the authors of the papers themselves.

Dr. Casadevall said:
"Many of those notices are wrong. Authors commonly write, 'We regret we have to retract our paper because the work is not reproducible,' which is not exactly a lie. The work indeed was not reproducible - because it was fraudulent. Researchers try to protect their labs and their reputations, and these retractions are written in such a way that you often don't know what really happened."
The report showed that higher-impact factor journals seem to have especially high retraction rates. Dr. Casadevall said that today scientists are disproportionately rewarded for publishing lots of papers, which should ideally appear in prestigious journals - most likely this kind of pressure has contributed to the growing number of retractions.

Dr. Casadevall said:
"Particularly if you get your papers accepted in certain journals, you're much more likely to get recognition, grants, prizes and better jobs or promotions. Scientists are human, and some of them will succumb to this pressure, especially when there's so much competition for funding. Perhaps our most telling finding is what happened after 2005, which is when the number of retractions began to skyrocket. That's exactly when NIH funding began to get very tight."
Dr. Casadevall had put forward a number of solutions to address the problem of scientific misconduct in the journal Infection and Immunity, which included:
  • There should be more emphasis on the quality of publications rather than how many are published
  • When rating journals, there should not be so much emphasis on impact measures
  • The research community should aim for more cooperation and collaboration
  • More sustainable, stable and reliable resources for research funding should be developed
  • Career pathways should offer scientists more flexibility to make sure talented professionals are not loss due to poor funding
Retractions come from very few laboratories

The authors stressed that not all is gloom and doom. Dr. Casadevall explained that 38 laboratories accounted for 43% of all retractions last year. There are thousands and thousands of labs whose scientists publish articles in academic journals.

Dr. Casadevall said:
"So while we're not looking at a systemic disease, so to speak, in the scientific community, our findings do indicate a significant problem that needs to be addressed."

27 June 2012

Study Finds that Carbs Prevent Energy Use

Supports Chapter 19: 'Healthy eating' is fattening

A few days ago, England’s Euro 2012 football team lost a quarter-final match to Italy on penalties. This scenario has happened so regularly that one might call it the ‘England finish’.

It has also happened so regularly that it hasn’t been difficult to see a pattern emerging for some years: England just run out of energy; they aren’t able to sustain 90 minutes of football.

The question is: Why? And the answer, which I have been convinced of for some years, was their rubbish carb-based diet. I am no lover of football, so have never watched a game, but commentaries on news bulletins spell out the form. To précis it, the England team always seem to start the game full of bounce, have most of the possession and often take the lead, then I all goes wrong. At half time they fill up on Jaffa cakes - and are so rubbish during the second half that they lose. But this, is exactly what I would expect. Carbs not only result in reactive hypoglycaemia (you run out of blood glucose), they also raise serotonin, a hormone that makes you sleepy and slows you down. This is why people are advised to have a carb meal before going to bed. But both of these conditions are the last thing you should eat if you have to work – or play football.

Now a study just published in the Journal of the American Medical Association finds another good reason why the carbs, so favoured by the England team’s nutritionists, are so devastating to their game: Carbs, it now appears, as well as everything else that is wrong with them, actively slow down the rate at which your body can use its energy.

Here is the abstract of the study – and an explanation as it is a bit convoluted:

Ebbeling CB, et al. Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance. JAMA 2012;307(24):2627-2634

Context Reduced energy expenditure following weight loss is thought to contribute to weight gain. However, the effect of dietary composition on energy expenditure during weight-loss maintenance has not been studied.

Objective To examine the effects of 3 diets differing widely in macronutrient composition and glycemic load on energy expenditure following weight loss.

Design, Setting, and Participants A controlled 3-way crossover design involving 21 overweight and obese young adults conducted at Children’s Hospital Boston and Brigham and Women’s Hospital, Boston, Massachusetts, between June 16, 2006, and June 21, 2010, with recruitment by newspaper advertisements and postings.

Intervention After achieving 10% to 15% weight loss while consuming a run-in diet, participants consumed an isocaloric low-fat diet (60% of energy from carbohydrate, 20% from fat, 20% from protein; high glycemic load), low–glycemic index diet (40% from carbohydrate, 40% from fat, and 20% from protein; moderate glycemic load), and very low-carbohydrate diet (10% from carbohydrate, 60% from fat, and 30% from protein; low glycemic load) in random order, each for 4 weeks.

Main Outcome Measures Primary outcome was resting energy expenditure (REE), with secondary outcomes of total energy expenditure (TEE), hormone levels, and metabolic syndrome components.

Results Compared with the pre–weight-loss baseline, the decrease in REE was greatest with the low-fat diet (mean [95% CI], –205 [–265 to –144] kcal/d), intermediate with the low–glycemic index diet (–166 [–227 to –106] kcal/d), and least with the very low-carbohydrate diet (−138 [–198 to –77] kcal/d; overall P=.03; P for trend by glycemic load=.009). The decrease in TEE showed a similar pattern (mean [95% CI], −423 [–606 to –239] kcal/d; −297 [–479 to –115] kcal/d; and −97 [–281 to 86] kcal/d, respectively; overall P=.003; P for trend by glycemic load<.001). Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin, P<.001; 24-hour urinary cortisol, P=.005; indexes of peripheral [P=.02] and hepatic [P=.03] insulin sensitivity; high-density lipoprotein [HDL] cholesterol, P<.001; non-HDL cholesterol, P<.001; triglycerides, P<.001; plasminogen activator inhibitor 1, P for trend=.04; and C-reactive protein, P for trend=.05), but no consistent favourable pattern emerged.
Conclusion Among overweight and obese young adults compared with pre–weightloss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low–glycemic index diet, and least with the very low-carbohydrate diet.
What it means
This is a study looking at weight loss, but in a different way from normal. Usually, scientists look at the amount of weight lost and/or for how long. This one is different; here they are considering how the different macronutrients affect energy usage. To make it confusing, the authors don't talk about energy usage, they talk in terms of 'decrease' in amount of energy used.

The study looks at two aspects of energy usage. A person has to use a certain amount of energy just to keep their body alive: These are things like the heart beating, brain working, keeping the body warm, etc, which they call “resting energy expenditure” (REE). This is relatively constant at approximately 1,500 kcals for an average-sized person. On top of that is the amount of energy we use when we do work or exercise. The total of the two is the total energy expenditure (TEE).

Here we have three different diets with same amount of calories, but with different ratios of carbs, proteins and fats. In this respect it is similar to the Dunlop & Lyon study of 1932 and Kekwick & Pawan’s 1956 study, both of which found that the lowest carb diet was the best for weight loss. With a similar finding, this latest study tells us why. When they ate the 60% carb diet, the participants used the least energy. It even cut the amount of energy used to maintain the body (REE). The diet on which they used the most energy (both REE and TEE) was the diet which had the least carbs and most fats.

Diet and exercise
So, if you are counting calories and exercising to lose weight, as the ‘experts’ say you should, then, obviously, when you exercise, you want to use as much energy as possible. There isn’t much point in jogging lots of boring miles if you are not going to use up energy – and thus weight - right? But this study shows that if you eat the diet these incompetent ‘experts’ advise you to eat, you won’t lose as much as you would if your diet was high-fat, low-carb!

And if you are an England footballer, you really don’t want to have to eat a diet that destroys your ability to use all your energy. Or a nutritionist/dietician who insists on it!

19 June 2012

Now, Statins May Increase Heart Attack Risk!

Supports Chapter 2: What's Behind The Screens?

It is widely believed that atherosclerosis, the 'furring up' of the arteries, narrows the coronary arteries and makes a heart attack more likely in two ways: Firstly, a clot in a partially blocked artery is more likely to block it completely, cutting off the blood supply downstream; and secondly, the atherosclerosis itself may block the artery with a similar result.

Many laymen have been led to believe that cholesterol is to blame for the blockage, or 'plaque', but this is hotly disputed. Much more likely, it seems, is that calcification of the artery wall, which hardens the artery wall making it less pliable, is the cause.

Statin Use Tied to Faster Plaque Buildup

A small observational American study of war veterans with diabetes and advanced coronary heart disease has found that those who regularly took statins had accelerated progression of calcification. This current analysis included 197 participants with type 2 diabetes from the Risk Factors, Atherosclerosis, and Clinical Events in Diabetes (RACED) study, a substudy of the Veterans Affairs Diabetes Trial (VADT) study.

Study participants who were frequent statin users were found to have significantly more coronary plaque advancement than those who were less frequent users (P<0.001), according to Aramesh Saremi, MD, and colleagues from the Phoenix VA Health Care System in Arizona.

The results remained the same even after adjusting for age, duration of diabetes, hypertension, cardiovascular events, baseline coronary artery calcium, race and ethnicity, blood pressure, total cholesterol/high density lipoprotein cholesterol (HDL-C), and body mass index, Saremi's team reported here at the annual meeting of the American Diabetes Association.

But Cam Patterson, MD, from the Center for Heart and Vascular Care at the University of North Carolina at Chapel Hill, and who was not involved in this study, warned that it would be a 'horrible mistake to infer that strict compliance with statin use is somehow causally associated with progression of atherosclerosis. Adding that he thought that such a conclusion is definitively a false one.

'The patients who were more compliant with statin therapy had much higher calcium scores at baseline, so these are obviously patients who had a substantially greater propensity for atherosclerosis to begin with,' Patterson said. He suggested that patients who already have vascular disease are more likely to be compliant with their statins.

Saremi does not disagree with Patterson; the progression of calcification may be linked to the healing of soft plaque initiated by statin therapy.

'It's important now to determine whether this progression of calcification leads to cardiovascular events.

She also suggested that if diabetics are put on statins earlier in the course of their disease, when their calcium scores are low, there may not be such a rapid advancement of calcification. But this is unsupported supposition.

In this substudy, 36 patients reported less frequent statin use, while 161 reported more frequent use. The mean age of patients was 61 and the average follow-up was 4.6 years.
In the unadjusted model, researchers found that every 10% increase in statin use was associated with a 0.41 mm3 increase in coronary calcium progression (P<0.01), which did not change much in the adjusted model: 0.33 mm3 increase (P=0.04).

When researchers excluded those with prior or new cardiovascular events, the risk for calcium progression remained the same.

Saremi and colleagues speculated that statins may enhance the density of calcification as part of the healing process, potentially contributing to plaque stabilization and decreased cardiovascular disease events . But this is more unsupported speculation (they don't like to give up on statins, even though statins have also been shown to increase diabetes risk). However, they did also suggest that the advancement of plaque in type 2 diabetics who frequently took statins may lessen the medication's overall benefit.


Saremi A, et al. Progression of vascular calcification is increased with statin use in the Veterans Affairs Diabetes Trial (VADT)" ADA 2012; Abstract 426-P.