Compound In Broccoli Could Boost Immune System, Says Study

This is just a test-tube and mice study so far but further exploration is clearly warranted. The fact that the compound worked only when eaten (not when injected) suggests that understanding of it is still at an early stage. Possible harmful effects have also not been explored

A compound found in broccoli and related vegetables may have more health-boosting tricks up its sleeves, according to a new study led by researchers at the University of California, Berkeley. Veggie fans can already point to some cancer-fighting properties of 3,3'-diindolylmethane (DIM), a chemical produced from the compound indole-3-carbinol when Brassica vegetables such as broccoli, cabbage and kale are chewed and digested. Animal studies have shown that DIM can actually stop the growth of certain cancer cells.

This new study in mice, published online Monday, Aug. 20 in the Journal of Nutritional Biochemistry, shows that DIM may help boost the immune system as well. "We provide clear evidence that DIM is effective in augmenting the immune response for the mice in the study, and we know that the immune system is important in defending the body against infections of many kinds and cancer," said Leonard Bjeldanes, UC Berkeley professor of toxicology and principal investigator of the study. "This finding bodes well for DIM as a protective agent against major human maladies."

Previous studies led by Bjeldanes and Gary Firestone, UC Berkeley professor of molecular and cell biology, have shown that DIM halts the division of breast cancer cells and inhibits testosterone, the male hormone needed for growth of prostate cancer cells. In the new study, the researchers found increased blood levels of cytokines, proteins which help regulate the cells of the immune system, in mice that had been fed solutions containing doses of DIM at a concentration of 30 milligrams per kilogram. Specifically, DIM led to a jump in levels of four types of cytokines: interleukin 6, granulocyte colony-stimulating factor, interleukin 12 and interferon-gamma. "As far as we know, this is the first report to show an immune stimulating effect for DIM," said study lead author Ling Xue, who was a Ph.D. student in Bjeldanes' lab at the time of the study and is now a post-doctoral researcher in molecular and cell biology at UC Berkeley.

In cell cultures, the researchers also found that, compared with a control sample, a 10 micromolar dose of DIM doubled the number of white blood cells, or lymphocytes, which help the body fight infections by killing or engulfing pathogens. (A large plateful of broccoli can yield a 5-10 micromolar dose of DIM.). When DIM was combined with other agents known to induce the proliferation of lymphocytes, the effects were even greater than any one agent acting alone, with a three- to sixfold increase in the number of white blood cells in the culture. "It is well-known that the immune system can seek out and destroy tumor cells, and even prevent tumor growth," said Xue. "An important type of T cell, called a T killer cell, can directly kill certain tumor cells, virally infected cells and sometimes parasites. This study provides strong evidence that could help explain how DIM blocks tumor growth in animals."

DIM was also able to induce higher levels of reactive oxygen species (ROS), substances which must be released by macrophages in order to kill some types of bacteria as well as tumor cells. The induction of ROS - three times that of a control culture - after DIM was added to the cell culture signaled the activation of macrophages, the researchers said. "The effects of DIM were transient, with cytokine and lymphocyte levels going up and then down, which is what you'd expect with an immune response," said Bjeldanes. "Interestingly, to obtain the effects on the immune response, DIM must be given orally, not injected. It could be that the metabolism of the compound changes when it is injected instead of eaten."

To examine the anti-viral properties of DIM, the researchers infected mice with reoviruses, which live in the intestines but are not life-threatening. Mice that had been given oral doses of DIM were significantly more efficient in clearing the virus from their gut - as measured by the level of viruses excreted in their feces - than mice that had not been fed DIM. "This means that DIM is augmenting the body's ability to defend itself by inhibiting the proliferation of the virus," said Bjeldanes. "Future studies will determine whether DIM has similar effects on pathogenic viruses and bacteria, including those that cause diarrhea."

The discovery of DIM's effects on the immune system helps bolster its reputation as a formidable cancer-fighter, the researchers said. "This study shows that there is a whole new universe of cancer regulation related to DIM," said Firestone, who also co-authored the new study. "There are virtually no other agents known that can both directly shut down the growth of cancer cells and enhance the function of the immune system at the same time."

Two co-authors of the study are from Michigan State University's Department of Food Science and Human Nutrition - James Pestka, professor of food science, and Maoxiang Li, a visiting research associate. DIM is currently under investigation in government-funded clinical trials as a treatment for prostate and cervical cancer. The University of California has filed patent applications on the use of DIM and its derivatives for immune modulation. Berkeley BioSciences, Inc., a company co-founded by Bjeldanes and Firestone, has licensed the related patent applications from the University of California and is researching and developing immune-enhancing nutritional supplements and therapeutics based on this discovery.

Source. Journal abstract here. The title of the original article is: "3,3'-Diindolylmethane stimulates murine immune function in vitro and in vivo"






New booster vaccine for TB

One of the most feared diseases in the world is making an alarming comeback in the UK. Cases of tuberculosis increased by 10 per cent in 2005, with 8,494 cases, and are set to continue rising, as the bug becomes increasingly resistant to drugs, and international travel extends its global reach. TB kills about 1.6 million people a year, largely in developing countries, and experts believe that its global resurgence goes hand in hand with the Aids pandemic. However, Helen McShane, a British scientist, announced today that a groundbreaking new vaccine - the first in 80 years, which has taken ten years to develop - is being tested in human clinical trials for the first time.

The areas most affected by the disease in Britain are cities such as London, Birmingham and Leicester, with immigrant communities from areas where the disease is still common: Pakistan, Bangladesh and parts of Africa. One in five cases of TB is found in new arrivals into the country. However, the disease is not something you could simply catch on a train; only frequent or prolonged contact with someone with TB puts a person at risk (hence why it's passed within families), and it can be treated with antibiotics if diagnosed quickly. Nevertheless, the Government is so concerned at the growing number of people with TB that it is considering screening visitors to the UK from countries such as China and India, it was revealed this week.

If the new TB vaccine passes its trials, as it is expected to do, it could be available in your GP's practice by 2015, when it would work as a booster for the childhood BCG injection (now given only to children in high-risk groups), conferring long-lasting immunity on all adults and thus preventing the spread of this disease.

Symptoms include a persistent cough, weight loss and fever. Before the First World War there were more than 100,000 UK cases a year, but numbers have fallen steadily since the BCG vaccination was introduced in 1953.

Dr McShane, the scientist behind this latest booster vaccine, is a 40-year-old medical doctor-turned-vaccinologist. It's impossible not to share her excitement, particularly when she describes the day in her Oxford University laboratory when she realised she was on to something. "It was a little tense," says Dr McShane, who was then 35 and five years into a project that she had started as a PhD student in 1997. "I went into the lab to check blood tests taken the day before, looked at the plates and couldn't believe my eyes. The results were excellent. We knew the vaccine would stimulate the production of some antibodies but there were ten times the number we had predicted. I ran down the corridor to show my professor immediately." Dr McShane knew she had created a vaccine that could potentially save two million lives a year worldwide. The Wellcome Trust will today announce her project as the first new vaccine for TB in 80 years.

There are two main reasons why a new vaccine has taken so long to develop. The first is that it's a difficult bug to vaccinate against as it disguises itself efficiently in the body. There are different strains of the bug, but Dr McShane believes that they are similar enough for the vaccine to be effective against them all. The other reason for the delay, according to the charity TB Alert, is that there wasn't any funding. Until recently TB was prevalent only in the developing world and so drug companies were reluctant to plough money into a vaccine.

A potential vaccine is an achievement that Dr McShane would not have dared to imagine when she first joined Professor Adrian Hill at the Nuffield Department of Medicine in Oxford to begin a PhD. "Most students were working on a malaria project; no one was looking at a TB vaccine, so I thought it would be a good idea," she says. Dr McShane had first started to study the tuberculosis bacterium when, as a young doctor, she was working in an HIV clinic in London. The two diseases often present hand-in-hand because TB is an opportunistic infection and finds the weakened immune system of an HIV-infected person an easy way in. Dr McShane says she found it frustrating that she could offer the latest antiretrovirals for the HIV infection but she had nothing to prescribe except traditional antibiotics for the TB. She could see that as different strains of TB bacteria became resistant to these drugs, her armoury was looking more and more depleted. Surely something could be done?

She decided to take her curiosity into the laboratory. Most contagious diseases can be vaccinated against by priming the immune system to recognise the pathogen and building armies of immune cells to attack it if it invades the body. A vaccine against measles, for example, introduces a highly weakened strain of the disease into the body. This allows the immune system to target the responsible bacteria, deal with them, and prepare defences for attacks in the future.

But TB is more complicated as it is able to hide inside cells and avoid normal antibodies. Instead it requires a subgroup of white blood cells, called T cells, to be activated, which are better at seeking out the bug to destroy it. Immunologists have begun to use recombinant viruses to teach the body how to recognise TB bacteria and prepare its T cells correspondingly. These are modified viruses that carry cloned genes containing a simple protein, harvested from the disease to be fought. The "tweaked" virus is harmless to human beings. It arrives in the body, unloads the cloned protein, and dies. The protein, however, is spotted by the immune system, which prepares T cells for attack. Afterwards, the patient's body is left ready for further invasion.

Dr McShane found that her vaccine worked particularly well at boosting the weak immune response primed by the traditional BCG. "It would be fantastic if this vaccine was proven to work and became available," she says. "It's been a huge team effort with units in The Gambia and South Africa and Oxford working to a common end. The real challenges now are to see if it really does stop people getting TB, and if it does, to make sure that it gets to the people who need it."

Source

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

THE BIG BOWEL CANCER RETHINK

The current guidance is that those wonderful folates also protect against bowel cancer. So other food chemicals with a similar action to folate should be protective too -- right? Wrong! The study of choline below associated it with with INCREASED bowel polyps.

And choline is mainly found in red meat, eggs, dairy products etc. So should we all become vegetarians?

There are heaps of things that could be said about this but the reaction of the medical researchers and commentators is sure amusing. The authors themselves draw the sort of conclusion that should be drawn in EVERY epidemiological study. They conclude that the effect they found "could represent effects of other components in the foods from which choline was derived". Correlation is not causation, in other words.

The editors of the journal also showed unusual humility: "Clearly, one-carbon metabolism and its role in [cancer development] is more complicated than originally anticipated, and our understanding of the underlying mechanisms is probably incomplete. More research, and caution in developing public health policy and guidance, is warranted"

More "caution in developing public health policy" from epidemiological findings? Long overdue. There should be more of it.

Another VERY interesting comment from them: "Other reasonable hypotheses about one-carbon metabolism and colorectal carcinogenesis, based on our current understanding of the biochemistry and underlying mechanisms, have also not been proven correct. In a recently published placebo-controlled randomized clinical trial among 1021 men and women with a recent history of colorectal adenoma, supplemental folic acid at 1 mg/d for up to 6 years did not reduce the incidence of subsequent colorectal adenomas and might have increased it.

WHOA! That folate that everybody gets compulsorily added to their bread did no good and seems to have done harm?? And do we see a double blind controlled study contradicting epidemiological inferences?? Who would have believed it!

They go on to admit that two animal studies have shown that folate INCREASES cancer. Aren't you glad that your government is dosing you up with the stuff and giving you no say in the matter?

OK. I will not gloat any further. I am reluctant to let the wiseheads off the hook but I don't actually think that the particular study below tells us anything much at all. Its main value has been to squeeze out from the know-alls the long overdue admissions and cautions about folate noted above. It's certainly a pity that such admissions are so infrequent, however.

What they all seem to be overlooking is that the study is about REPORTED food intake. And we know how fraught that can be. The nurses who were surveyed would all be acutely aware that eating lots of meat, dairy and eggs is NAUGHTY, according to the current wisdom. So many would have understated what they ate in that department. So what the study really shows is that REBELLIOUS or especially honest people get more polyps. It probably had nothing to do with their choline intake at all.

So where do we go from there? Who is it who would disregard official dietary advice and eat what they like? Easy: Working class people. Nurses come from all social backgrounds and there would be plenty who would happily wrap themselves around a Big Mac with no guilt at all. And, as we repeatedly find, the workers have more health problems generally for all sorts of reasons, including not only such things as a riskier lifestyle but genetic differences as well. So all we have at the end of this study is another demonstration of that old truth: The workers have poorer health in all sorts of ways.

But the addition of folate to our bread is more and more looking like an iatrogenic disaster to come. I think I should note that I have previously reported that the addition of folate to bread seems to have caused an upsurge in bowel cancer.

Dietary Choline and Betaine and the Risk of Distal Colorectal Adenoma in Women

By Eunyoung Cho et al.

Abstract

Background: Choline and betaine are involved in methyl-group metabolism as methyl-group donors; thus, like folate, another methyl-group donor, they may be associated with a reduced risk of colorectal adenomas. No epidemiologic study has examined the association of intake of these nutrients and colorectal adenoma risk.

Methods: We investigated the relationship between intakes of choline and betaine and risk of colorectal adenoma in US women enrolled in the Nurses' Health Study. Dietary intake was measured by food-frequency questionnaires, and individual intakes of choline and betaine were calculated by multiplying the frequency of consumption of each food item by its choline and betaine content and summing the nutrient contributions of all foods. Logistic regression models were used to calculate adjusted odds ratios (as approximations for relative risks) and 95% confidence intervals (CIs) of colorectal adenoma. All statistical tests were two-sided.

Results: Among 39246 women who were initially free of cancer or polyps and who had at least one endoscopy from 1984 through 2002, 2408 adenoma cases were documented. Increasing choline intake was associated with an elevated risk of colorectal adenoma; the multivariable relative risks (95% CIs) for increasing quintiles of intake, relative to the lowest quintile, were 1.03 (0.90 to 1.18), 1.01 (0.88 to 1.16), 1.23 (1.07 to 1.41), and 1.45 (1.27 to 1.67; Ptrend less than .001). Betaine intake had a nonlinear inverse association with colorectal adenoma; the multivariable relative risks (95% CIs) for increasing quintiles of intake were 0.94 (0.83 to 1.07), 0.85 (0.75 to 0.97), 0.86 (0.75 to 0.98), and 0.90 (95% CI = 0.78 to 1.04; Ptrend = .09). Among individual sources of choline, choline from phosphatidylcholine and from sphingomyelin were each positively related to adenoma risk.

Conclusions: Our findings do not support an inverse association between choline intake and risk of colorectal adenoma. The positive association between choline intake and colorectal adenoma that we observed could represent effects of other components in the foods from which choline was derived and should be investigated further.

JNCI Journal of the National Cancer Institute 2007 99(16):1224-1231

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

Hanoi Jane was wrong about aerobics too

Remember those Jane Fonda workout videos in the 1980s? Turns out high-impact aerobics was the worst thing people could do to their knees, CBS News reported:

Sheila Wares remembers the high impact aerobics well - and still keeps a library of titles under her television, although they've all been banned from her VCR thanks to a bad knee. "It's amazing when you think about your knee and how much it affects so much of everything when it comes to exercise, even with yoga you know," she told The Early Show medical contributor Dr. Emily Senay. "Try and do a downward dog on a knee that won't cooperate."

According to Wares' doctor, Jennifer Solomon, she isn't alone. Many baby boomers are experiencing this problem. She sees many patients with similar over-use injures at New York's Hospital for Special Surgery. "These are the people who did the aerobics classes five or six days a week, the high impact aerobics, the step aerobics with three tiered steps," said Dr. Solomon, a physiatrist. "These are the people who thought they were doing the right thing and following the trend of the '80s."

Dr. Solomon says the repetitive nature of high impact aerobics has had an adverse affect on many of the once devoted Fonda fans like Wares. "They have knee problems," she said. "They all have early arthritis, or have terrible arthritis where they can't go up and down stairs."

Ah, those workout videos. They were empowering women. They were going to make everyone live longer and healthier. It turns out this was the wrong way to exercise. The scientific consensus of a quarter-century ago turned into the arthritic nightmare of today.

Dr. Solomon said these high impact exercise techniques are basically defunct because we now know how to exercise smarter. "You go into any health club and take a look at their schedule you'll see that step aerobics is no longer there. High impact activity is no longer there," she said. "People are now into core stability and power workouts, which is less stressful on the joints."

Today the only exercise Wares gets are the daily walks with her dog Maxine, which is far from the high level of activity she used to enjoy. "You were under the impression that you were doing the right thing and keeping yourself healthy," she said, "but it turns out to be a cruel irony in the long run, and did the opposite of what you were striving for."

Let's see, wrong on Vietnam. Wrong on Jonestown. Wrong on high-impact aerobics.

Source





Meth abuse may speed brain degeneration

YOUNG people who abuse methamphetamines may put themselves at risk of parkinson-like movement disorders later in life, a new animal study suggests. In experiments with mice, scientists found that animals deficient in a protein called glial cell line-derived neurotrophic factor (GDNF) were especially vulnerable to long-term movement problems after being exposed to the neurotoxic effects of a methamphetamine "binge".

GDNF is needed for the proper functioning of dopamine, a brain chemical involved in regulating movement. Both GDNF and dopamine are depleted in the brains of people with Parkinson's disease.

Because methamphetamines can damage dopamine-producing cells in the brain, researchers have speculated that young meth users may be at elevated risk of parkinson-like movement disorders as they age. The new findings, reported in The Journal of Neuroscience, support that theory. "The study in mice tells us that people who make less GDNF protein may be more vulnerable to the motor deficits caused by methamphetamine and that those effects may not be revealed until we get older," explained principal author Dr Jacqueline McGinty, a professor in the department of neurosciences at the Medical University of South Carolina in Charleston.

For their study, Dr McGinty and her colleagues used both normal mice and mice missing one of their genes for GDNF. Two weeks after being exposed to a meth binge, the animals tended to show dopamine depletion and other signs of brain damage, with the GDNF-deficient mice being especially vulnerable. Similarly, these mice were more likely to have movement impairments when they were 12 months old - old age for rodents.

No one knows what percentage of the population has an abnormal GDNF gene, Dr McGinty said, but individuals certainly vary in how much GDNF protein their genes make. It's possible, she and her colleagues said, that young people with naturally lower levels of the protein may be susceptible to long-term brain damage and Parkinson-like symptoms at an older age. "Motor deficits during aging may be accelerated if young adults are exposed to an environmental toxin like methamphetamine," Dr McGinty said.

Source

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

STATINS FOR ALZHEIMERS?

Whether there were any double-blind procedures is unclear. In any case it appears to be the usual epidemiological nonsense of assuming causation from correlation. Once again that wicked social class is ignored, for instance. Poor people are much less compliant with drug regimes (particularly nasty ones like statins) and may seek medical help less so may be given less statins -- and poor people have worse health generally (and some might have more scrambled brains to begin with) so might have more brain tangles. So is this just documenting another correlate of poverty? See also more cautions here. Journal abstract follows media report below

Taking statins may help to prevent Alzheimer's disease, a study has directly suggested for the first time. Researchers in the US claim to have uncovered clear evidence that the cholesterol-lowering drugs - taken daily by about three million people in Britain - could ward off the illness. The large-scale study, conducted at Boston University from 2002, found that the drugs may cut the risk of getting Alzheimer's by as much as 79 per cent, even in people thought to be genetically susceptible to the disease. The lead author, Gail Li, said the study was the first to compare the brains of people who had received statins with those who had not.

Previous research has indicated that Alzheimer's may be caused by poor blood flow and vascular changes in the brain, which statins may help to prevent. Dr Li, from the University of Washington School of Medicine in Seattle, and her colleagues examined the brains of 110 Americans who had died aged between 65 and 79, and had donated their organs for research.

The two changes in the brain considered the hallmarks of Alzheimer's are known as brain "plaques" and "tangles". These are protein deposits that appear to spread in the brain, although the cause of Alzheimer's is not yet fully understood. The researchers found significantly fewer tangles in the brains of people who had taken statins than those who had not, even allowing for variables such as age, gender and past health.

Eric Larson, a co-author of the study, said: "These results are exciting, novel and have important implications for prevention strategies." He said further studies were needed to confirm the findings but praised the researchers' reliance on automated records and postmortem examinations of people with and without dementia. Dr Li said: "Statins are probably more likely to help prevent the disease in certain kinds of people than others. Some day we may be able to know more precisely which individuals will benefit from which types of statins."

In June, the National Institute for Health and Clinical Excellence (NICE) published draft guidance suggesting millions of people should be assessed to find out how many more would benefit from statins, which are estimated to prevent up to 7,000 deaths a year from heart attacks and strokes. Information collected routinely by GPs should be used to identify those most at risk of developing cardio-vascular disease, it said. Adults who have a 20 per cent or greater risk of developing heart disease over the next decade should be offered statins, it added. Such a move would double the number of people prescribed the drug to about six million. Final guidance from NICE is expected in January.

Other studies suggest a downside to statins. They are known to interact with other drugs and can have side-effects, including abdominal pain, diarrhoea and nausea. In July researchers in Massachusetts found that people who took statins had a slightly increased risk of cancer. Statins reduce levels of low-density lipoprotein, an enzyme involved in the transportation of "bad" cholesterol.

There are currently 700,000 people with dementia in Britain, of whom about two thirds have Alzheimer's.

Source

Statin therapy is associated with reduced neuropathologic changes of Alzheimer disease

By G. Li et al.

Background: Treatment with 3-hydroxy-3-methylglutaryl-coenzyme-A reductase inhibitors ("statins") has been associated in some epidemiologic studies with reduced risk of Alzheimer disease (AD). However, direct evidence of statin effects on neuropathologic markers of AD is lacking. We investigated whether antecedent statin exposure is associated with neuritic plaque (NP) or neurofibrillary tangle (NFT) burden in a population-based sample of human subjects.

Methods: Brain autopsies were performed on 110 subjects, ages 65 to 79 years, who were cognitively normal at enrollment into the Adult Changes in Thought Study. Neuropathologic findings were compared between statin users with ~ prescriptions of ~ 15 pills of simvastatin, pravastatin, lovastatin, or atorvastatin vs nonusers, based on pharmacy dispensing records.

Results: After controlling for age at death, gender, cognitive function at study entry, brain weight, and presence of cerebral microvascular lesions, the odds ratio (OR) for each unit increase in Braak NFT stage in statin users vs nonusers was 0.44 (95% CI: 0.20 to 0.95). The OR for each unit increase in Consortium to Establish a Registry for Alzheimer's Disease (CERAD) staging of NPs did not deviate significantly from unity (OR 0.69; 95% CI: 0.32 to 1.52). However, the risk for typical AD pathology (Braak stage ~ IV and CERAD rating ~moderate) was reduced in statin users (OR 0.20; 95% CI: 0.05 to 0.86).

Conclusions: These findings demonstrate an association between antecedent statin use and neurofibrillary tangle burden at autopsy. Additional study is needed to examine whether statin use may be causally related to decreased development of Alzheimer disease-related neuropathologic changes.

NEUROLOGY 2007;69:878-885





Autism progress

Within the next year a new study is expected to identify many of the genes that underlie autism for the first time. At the same time, two new theories are challenging established thinking about autism genetics in ways that could ultimately transform diagnosis and treatment. "The medics tell me we are at a tipping point," said Dame Stephanie Shirley, the millionaire computer entrepreneur and philanthropist, who is the chairman of the research charity Autism Speaks and the mother of an autistic son.

That genetics are the chief cause of autism has been known for three decades. It was in 1977 that Professor Michael Rutter, of the Institute of Psychiatry at King's College London, published a twin study that transformed the understanding of its origins. Twin studies are one of the mainstays of genetics. Because identical twins share all of their genes while fraternal twins share only half, and both share broadly similar environments, comparisons can tease out the relative contributions of nature and nurture. Professor Rutter found that if an identical twin was autistic, it was highly likely that the other twin was autistic too. Fraternal twins, however, were no more likely to share the diagnosis than ordinary siblings. This made it certain that genes played a large role and it is now thought that autism is among the most heritable of all psychiatric disorders. Genetics account for most of the variance and, although environmental factors matter too, they are less important.

The condition, however, has remained a genetic paradox. For all the certainty that genes are heavily involved, it has proved impossible to discover which ones are guilty. In the 30 years since Professor Rutter's study, hundreds of genetic mutations that affect health have been found. Most are single-gene disorders, where inheriting a rogue gene invariably means developing a disease such as Huntington's, which affects the central nervous system. Most of the others have involved very high risks: women with abnormal variants of the BRCA1 gene, for example, have an 80 per cent risk of developing breast cancer.

Autism does not work like that: the search for genes with such large effects has failed. It might be influenced by dozens of genes, each of which raises the risk by amounts too small to have been detected. Or it could be the result of spontaneous mutations instead of more easily tracked defects that are passed from generation to generation. Science does not yet know. [Or it could be that there is no such thing -- merly a number of different disorders with one ort two common symptoms]

The scientific success story of 2007 has been the coming of age of a new method of gene-hunting that can find the sort of genes with weak effects that are thought to influence autism. These genome-wide association studies compare the DNA of thousands of people who have a disease with healthy controls, using tools called "gene chips" to screen the entire human genome for hundreds of thousands of tiny genetic variations that differ between the two groups. In recent months, the technique has revealed scores of genes that subtly influence common conditions such as diabetes, heart disease, breast cancer and multiple sclerosis, often raising the risk by as little as 10 per cent.

Autism is the next target. The Autism Genome Project (AGP), an international consortium that studies more than 1,000 families with at least two autistic members, is about to apply the tool to its database. "We have been waiting ten years for the technology to do this," said Anthony Monaco, of the University of Oxford, one of the project's leaders. "We were never likely to understand until we were able to screen very large numbers. The probability has always been that autism is highly genetic, but highly heterogeneous - that lots of different genes are involved. We now have a great chance of picking them up."

The AGP's genome-wide association study is a classic example of win-win science. Even if it draws a blank, it will still shed new light on the genetic origins of the condition. No results would mean one of two things. It could be that the effects of the genes responsible are even tinier than suspected and bigger samples are needed. Or it could be that a radical new theory of autism genetics is correct.

Professor Michael Wigler, of Cold Spring Harbour Laboratory in New York state, believes that autism might be the result of single genes with big effects after all. These mutations, however, are not quite the same as the inherited ones that cause diseases such as Huntington's. According to his model, most cases of autism are caused by random, spontaneous mutations in the sperm or eggs of parents that are passed on to individual children. Most of these then develop the condition but some, particularly girls, do not. They are somehow resistant and, although they carry a potentially harmful mutation, they do not suffer its consequences.

This may explain why autism is an overwhelmingly male disorder, four times more common among boys than girls. It fits with data showing that the children of older parents are at higher risk: sporadic mutations of this sort increase with age. It also points towards an intriguing explanation for the existence of high-risk families with more than one autistic child. Professor Wigler's research suggests that in these families, a mutation first occurred in one of the parents, usually the mother. While she was immune, probably because of her gender, her sons were not so lucky: half of them would be autistic, depending on whether they inherited the rogue gene. "Sporadic autism is the more common form of the disease and even the inherited form might derive from a mutation that occurred in a parent or grandparent," the professor said.

If mutations of this sort are responsible, they would not show up in the AGP: they are new and unique to individuals and families, so will not surface from large comparisons of DNA. "That is one of the exciting things about our work," Professor Monaco said. "If we find genes, it is interesting and if we don't find genes, it is interesting too."

What Professor Wigler's theory does not account for is another aspect of new thinking about autism: that it may not be a single disorder. For autism to be diagnosed, children must meet three criteria: they must show social impairment, communication difficulties and nonsocial problems such as repetitive and restricted behaviour. Yet there is an emerging consensus that these traits do not always go together and that there are people who meet the criteria for one or two characteristics but who do not receive any diagnosis. Autism, in short, may be the confluence of three separate developmental conditions. Only when they occur together is the result devastating.

Research by Angelica Ronald, Francesca Happe and Robert Plomin, of the Institute of Psychiatry, has suggested that each of these three problems is influenced by different sets of genes. The twin studies have shown that while each trait is highly heritable, they do not often overlap. "The label autism is something that was applied to a set of behaviours that were first described in the 1940s," said Dr Ronald, who is funded by Autism Speaks. "It's not necessarily a label for a clear biological entity and in research it may be a misnomer to assume it's one thing."

This has important implications for gene-hunting. It could be that genes have not been found because scientists have been treating autism as a whole. If different genes affect the communication and social elements of the disorder, finding them might involve looking at people who are not autistic, but who have mild versions of one of the problems. "We need to tackle whether we should look at autism as a single phenomenon, or whether it would be better to look, for example, just at autistic social problems," Dr Ronald said. Such an approach would also be valuable by shedding immediate light on what any genes that are found actually do.

Dr Ronald added: "If we split up the symptoms, we can know that these genes are going to be involved in social problems and those ones in nonsocial problems. That is obviously going to be valuable when we look towards diagnosis and treatment." An understanding of which genes are involved in which parts of autism should help doctors to spot the condition earlier. It would also prepare parents for the way their child is likely to develop and it could help with the design of therapies.

Dame Stephanie is excited by the pace of change. "It is quite possible that in five to ten years, we will have a real understanding of this disorder," she said. "That's a timescale that means today's children may be helped."

Source

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

GETTING SLIMMER? YOU MAY BE DEMENTED

This is such fun that I am going to let it stand without comment:

Incident dementia in women is preceded by weight loss by at least a decade

D. S. Knopman et al.

Background: Although several studies reported weight loss preceding the onset of dementia, other studies suggested that obesity in midlife or even later in life may be a risk factor for dementia.

Methods: The authors used the records-linkage system of the Rochester Epidemiology Project to ascertain incident cases of dementia in Rochester, MN, for the 5-year period 1990 to 1994. The authors defined dementia using the criteria of the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). Each case was individually matched by age (~1 year) and sex to a person drawn randomly from the same population, and free from dementia in the index year (year of onset of dementia in the matched case). Weights were abstracted from the medical records in the system.

Results: There were no differences in weight between cases and controls 21 to 30 years prior to the onset of dementia. However, women with dementia had lower weight than controls starting at 11 to 20 years prior to the index year, and the difference increased over time through the index year. We found a trend of increasing risk of dementia with decreasing weight in women both at the index year (test for linear trend; p < 0.001) and 9 to 10 years before the index year (test for linear trend; p = 0.001).

Conclusions: Even accounting for delays in diagnosis, weight loss precedes the diagnosis of dementia in women but not in men by several years. This loss may relate to predementia apathy, loss of initiative, and reduced olfactory function.

NEUROLOGY 2007;69:739-746





Crazy hours for doctors are dangerous

Although most people are aware of their impaired function after going without one or two nights of sleep, the most common form of "sleep loss" is shortening of sleep hours. Everyone encounters some nights of reduced sleep length but when this persists and there is no or little recovery sleep, problems occur. Recent research has highlighted that shortening sleep to four or even six hours per night over a two-week period is associated with increased lapses in attention due to "microsleeps". More worrying is that individuals who have restricted sleep seem to have an inability to monitor their own deterioration in performance, resulting in overconfidence in their ability to undertake tasks. So a sleep-restricted person may behave in the same way as a person who has had too much alcohol to drink, both underestimating their impairment and thinking they are fit to drive a car or some other responsible task, like complicated medical surgery.

Indeed, the hospital workplace is one setting where the risk of sleep loss has increasingly attracted attention from medical researchers. Professor Charles Czeisler and his team from Harvard University have recently published a series of landmark papers in The New England Journal of Medicine and other leading medical journals. These papers have provided direct evidence that working extended shifts in the hospital intensive care unit results in more errors, especially medication orders. Shorter split shifts with time allowed for napping resulted in fewer errors. In a nationwide US survey of 2737 interns, the Harvard group found extended shifts were linked to a greater rate of needlestick injuries and near-miss or actual driving accidents.

How does this relate to the hospital workplace in Australia? Although, in general, work-hour regimes are kinder here than in US hospitals, 15 per cent of all doctors in Australia report working more than 80 hours per week. Problems arise in rural areas or in specialised settings where individuals may be on call all week. We know that even being on call without being called in can impair sleep and often little is done to acutely monitor on-call specialist trainee work hours. These trainees are few in number and in high demand. Even more worrying is who monitors the sleep-wake schedules of their bosses. Watching a senior hospital specialist fall asleep at a lunchtime meeting often provokes a laugh but perhaps ignores the underlying problem. No patient would consent to surgery if they noticed their doctor's breath smelt of alcohol. However, how many patients ask their surgeon how much sleep they've had lately?

Hospitals are often imbued with a cultural mix of altruism, machismo and denial. Many of us who have worked in hospitals have bored our friends and family with tales of stoical never-ending shifts and battling to stay awake in a sleepy fog. The reality is that we can't kid ourselves that this is safe and any hospital administration that tolerates this situation is at fault. The current shortage of doctors in the health system has resulted in "moonlighting", with some doctors working for two or sometimes three employers. At the moment hospitals in Australia are probably more concerned where their doctors left their last SIM card but they should also be asking where else do you work, how many hours do you work and how much sleep do you get?

Health administrators may be held criminally liable for their sleepy doctors in the same way that a transport company may be held criminally liable for fall-asleep accidents caused by its drivers. The first step to prevent this is to recognise the risk, use scientifically proven strategies to deal with the problem and finally to recognise that the best treatment is to sleep like a dog.

Source

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

Eating healthy fruit, vegetables won't stop cancer

This has been known for years (e.g here). It's just that people do not want to believe it. It gives people a sense of power to think that what they put in their mouth matters. The researchers below are not bold enough to tell the whole truth about "obesity", though -- that it is only the grossly obese who are at slightly higher risk

FRUIT and vegetables provide no protection against cancer, according to latest Australian research that has shocked nutritionists. In a discovery that turns conventional advice on its head, experts have admitted there is "zero evidence'' that eating fruit and vegetables can help people avoid a disease that kills nearly 40,000 Australians every year.

Research presented for the first time at last week's CSIRO Prospects for Cancer Prevention Symposium shows that what people eat is far less important in cancer prevention than previously believed. Instead, the three prime risk factors driving up Australian cancer rates have been identified as obesity, drinking too much alcohol and smoking. Staying within a healthy body weight range was found to be more important than following particular nutritional guidelines. This means a slim person who doesn't eat enough fruit and vegetables would probably have a lower risk of developing cancer than someone who is overweight but eats the recommended daily amount of fruit and vegetables.

The findings emerged from the Cancer Council's Melbourne Collaborative Cohort Study, an ongoing research project involving 42,000 Australians who have been monitored since 1990. Revealed exclusively to The Sunday Telegraph, they challenge widespread belief in the power of juices and vegetable-based ``anti-cancer'' diets to avoid or fight various types of the disease.

Dr Peter Clifton, director of the CSIRO's Nutrition Clinic, told The Sunday Telegraph there was ``zero evidence'' that eating fruit and vegetables could protect against cancer. Heart disease is Australia's biggest killer, so fruit and vegetables are still regarded as important in maintaining health. Professor Dallas English, of the Cancer Council of Victoria, told the symposium that despite decades of research, there was no convincing evidence on how Australians could modify their diet to reduce the risk of cancer. ``The most important thing about diet is limiting energy (kilojoule) intake so people don't become overweight or obese, because this has emerged as a risk factor for a number of cancers, including breast, prostate, bowel and endometrial (uterus),'' he said. The link between eating red meat and bowel cancer was ``weak'' and the Cancer Council supported guidelines advising people to eat red meat three or four times a week, Professor English said. His advice comes after Health Minister Tony Abbott last week backed a report, funded by Meat & Livestock Australia, on the dietary role of red meat.

Surprisingly, fibre was deemed to have no significant benefit in avoiding bowel cancer _ although calcium was associated with a 20 per cent reduced risk. Likewise, a high intake of fat, considered a prime culprit since the 1970s, was found to have only a ``modest'' link to breast cancer. Smoking caused one in five cancer deaths, while regularly drinking too much alcohol boosted the risk of several cancers including breast and bowel, Professor English said.

He and Dr Clifton acknowledged that eating fruit and vegetables might help people avoid obesity, as they were lower in kilojoules than other foods. ``The risk of every type of cancer is increased by obesity,'' Dr Clifton added. Both experts predict a surge in cancer as a result of Australia's obesity epidemic, but say exercise can play a vital role in cutting cancer rates, potentially halving the risk of some cancers.

Source




The "Mindfit" claim

Don't line the pockets of the lady below until an independently replicated double-blind evaluation of it emerges in the journals. It's theoretically possible that it is helpful but my guess would be that the effects in adults are marginal and temporary

Baroness Susan Greenfield, the neuroscientist, is to launch an exercise programme for the brain that she claims is proven to reverse the mental decline associated with ageing. Greenfield, who is also director of the Royal Institution, maintains that Britain's baby-boomers are discovering that concentrating on physical fitness is no longer sufficient preparation for old age. "What concerns me is preserving the brain too," she said. "There is now good scientific evidence to show that exercising the brain can slow, delay and protect against age-related decline."

Greenfield will launch MindFit, a PC-based software program, at the House of Lords next month, for the "worried but well" - people in their middle years who are healthy and want to stay that way. Created by researchers in Israel and already on sale in America, it offers users inter-active puzzles and tasks that are claimed to stimulate the brain just as using a gym exercises the body's muscles. "There is evidence that such stimulation prompts brain cells to start branching out and form new connections with other cells," said Greenfield.

The baroness's decision to lend her name to MindFit and to take a significant stake in Mind-Weavers, the company promoting it, could raise eyebrows among fellow scientists. Her high profile in the media has rankled with some and she was twice snubbed by the Royal Society.

The idea that the performance of the brain can be improved by exercises or potions has a long and controversial history. There have also been scientific battles over the claims made for dietary supplements, especially fish oils, and so-called smart drugs. The latter have been shown to cause a short-term increase in IQ but the long-term secondary effects are unknown.

Greenfield's decision to promote MindFit, which will retail for around 70 pounds, follows the release of new scientific research apparently showing clear benefits. In the latest research, conducted at the Sourasky Medical Centre at Tel Aviv University in Israel, 121 volunteers aged over 50 were asked to spend 30 minutes, three times a week, on the computer, over a period of two years. Half were assigned to use MindFit and the other half played sophisticated computer games. The results, released at a recent academic conference and due for formal publication shortly, showed that while all the volunteers benefited from using computer games, the MindFit users "experienced significantly greater improvement in short-term memory, visuo-spatial learning and focused attention".

Greenfield, who also runs an Oxford University laboratory researching the causes of degenerative brain diseases such as Alzheimer's, found out about MindFit through her extensive links with Israel and decided to bring it to Britain. "It is clear that there is no drug on the horizon to treat Alzheimer's or age-related mental decline so I have long been interested in seeing whether stimulating the brain might offer a way of Greenfield is launching a program designed in Israel. Kidman, left, is the new face of Nintendo, which already sells Brain Training games slowing down these changes," she said.

Other researchers are also convinced that people can rejuvenate their brain with exercise. Ryuta Kawashima, professor of neuroscience at Tohoku University in Japan, spent 15 years investigating how mental exertion helps the brain grow. His work became the basis of the Brain Training and More Brain Training computer games, produced by Nintendo, the console manufacturer. Nicole Kidman, the actress, fronts its latest British advertising campaign. Nintendo itself makes no formal scientific claims for the programs but Kawashima said in a recent book: "My brain exercises increase the delivery of oxygen, blood and various amino acids to the prefrontal cortex. The result is more neurons and neural connections, which are characteristics of a healthy brain."

Other researchers accept such ideas in principle but warn that any system claiming to boost mental ability must prove itself in clinical trials.

Source

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

WHY DO HEART ATTACKS KILL MORE BLACKS?

It's racism! would be the Sharpton/Jackson explanation. Not really, says the study below. It turns out that blacks are only a tiny bit nore likely to have heart attacks than are whites of the same age but that blacks are much less likely to survive after the attack. "Demographic factors" (coming from rough areas where cocaine use is more prevalent?) and "prior functional status" (general poor health due to lifestyle?) were among the reasons why but the main reason is that black heart attacks are different to start with: "lower prevalence of ventricular fibrillation as the initial cardiac rhythm". Sadly for Sharpton/Jackson, inferior medical attention was not a factor

Explaining Racial Disparities in Incidence of and Survival from Out-of-Hospital Cardiac Arrest

By: S Galea et al.

Abstract

A prospective observational study of 4,653 consecutive cases of out-of-hospital cardiac arrest (OOHCA) occurring in New York City from April 1, 2002, to March 31, 2003, was used to assess racial/ethnic differences in the incidence of OOHCA and 30-day survival after hospital discharge among OOHCA patients. The age-adjusted incidence of OOHCA per 10,000 adults was higher among Blacks than among persons in other racial/ethnic groups, and age-adjusted survival from OOHCA was higher among Whites compared with other groups.

In analyses restricted to 3,891 patients for whom complete data on all variables were available, the age-adjusted relative odds of survival from OOHCA among Blacks were 0.4 (95% confidence interval: 0.2, 0.7) as compared with Whites. A full multivariable model accounting for demographic factors, prior functional status, initial cardiac rhythm, and characteristics of the OOHCA event explained approximately 41 percent of the lower age-adjusted survival among Blacks. The lower prevalence of ventricular fibrillation as the initial cardiac rhythm among Blacks relative to Whites was the primary contributor. A combination of factors probably accounts for racial/ethnic disparities in OOHCA survival. Previously hypothesized factors such as delays in emergency medical service response or differences in the likelihood of receipt of cardiopulmonary resuscitation did not appear to be substantial contributors to these racial/ethnic disparities.

American Journal of Epidemiology 2007 166(5):534-543





Romancing Opiates

Post below lifted from Noodlefood. See the original for links

I just began reading Theodore Dalrymple's recent book Romancing Opiates. So far, it's excellent. Most surprising is the fact that -- contrary to all popular belief, fictional portrayals, and media reports -- the symptoms of physical withdrawal from heroin are extremely mild. The addict is not in any danger of dying whatsoever, as with serious alcohol withdrawal. He's not even in any real physical distress.

The distress that addicts do feel is based solely on their beliefs about the withdrawal of the drug: it's purely psychological. Studies have shown that addicts aren't able to tell whether they've been given morphine or placebo, such that symptoms like nervousness and restlessness came and went based on what they were told about the contents of their injection (28).

However, addicts are extremely adept at faking such distress in the hopes of wheedling a prescription from the often-gullible doctor. Most doctors accept the standard view that withdrawal from opiates is a terrible ordeal, despite substantial evidence to the contrary, such as the addicts displaying no great signs of distress when secretly watched by the doctor. So the doctors routinely prescribe the addict drugs like methadone.

In contrast, when the addict is confronted with a doctor like Dalrymple, who refuses such prescriptions and clearly explains his reasons why, some will not only cease their performance of distress, but even "smile and admit with a laugh that anyone who says that cold turkey is a terrible ordeal is lying and more than likely trying to bluff his way to a prescription" (25). Once that is done, other addicts in the ward don't even bother with the attempted deception.

In recent years, doctors have tried to alleviate the non-existent horror of opiate withdrawal by "ultra-short opiate detoxification." (If I recall correctly, this method was featured on House.) Basically, the addict is administered "an opiate antagonist, naloxone, under general anesthesia, followed by continued administration of naloxone for a further forty-eight hours. This [method] ... turns a trivial medical condition, namely 'natural' withdrawal from opiates, into a potentially fatal one, since quite a number of deaths are known to have occurred as a result of it, some clinics that use it having recorded as many as ten deaths" (29). Yikes!

The failure to consider the obvious implications of perceptual observations can have serious consequences in any area of life. In this case, that failure on the part of those in the business of addiction treatment means that a voluntary psychological dysfunction is treated with ineffective, counterproductive, and even life-threatening methods. Lovely, no?

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

CHILDREN NEED THEIR FATHERS

One would think it obvious that children need their fathers but there are Lesbians who deny it so perhaps the study below helps a little. The study concludes that involvement of the father in family life can even make up for a dysfunctional mother. The study has unusually good sampling so the conclusions are more generalizable than most

Maternal Depressive Symptoms, Father's Involvement, and the Trajectories of Child Problem Behaviors in a US National Sample

By Jen Jen Chang et al.

Abstract

Objective: To examine the effect of maternal depressive symptoms on child problem behavior trajectories and how the father's positive involvement may modify this association.

Design: Secondary data analysis using data from the National Longitudinal Survey of Youth.

Setting: A nationally representative household sample of men and women from the National Longitudinal Survey of Youth.

Participants: The study sample includes 6552 mother-child dyads interviewed biennially between January 1, 1992, and December 31, 2002; children were 0 to 10 years old at baseline.

Intervention: Past-week maternal depressive symptoms in 1992.

Main Outcome Measures: Maternal self-reports of child internalizing and externalizing behaviors were assessed repeatedly using a modified Child Behavior Checklist.

Results Linear growth curve models indicate that the adverse effects of maternal depressive symptoms on child problem behavior trajectories become negligible after controlling for the father's involvement and other covariates, including the child's age, sex, and race/ethnicity; the mother's educational level; maternal age at child birth; number of children; poverty status; urban residence; and father's residential status. Positive involvement by the father was inversely associated with child problem behavior trajectories. The effects of maternal depressive symptoms on child problem behaviors varied by the level of the father's positive involvement.

Conclusion: When the father actively compensates for limitations in the depressed mother's functioning, the child's risk of problem behaviors may be reduced.

Arch Pediatr Adolesc Med. 2007;161:697-703





MORE EVIDENCE THAT SOCIAL CLASS DOES MATTER

The study below is not particularly striking of itself but it is refreshing to see the role of social class recognized. Race is the doubtful factor in the study. It would have been nice to see results presented separately for blacks and whites. Poor blacks, for instance, are less exceptional than poor whites so poor blacks may well have been more robust than poor whites. The effects may have been stronger if whites only had been studied. The conclusion of the study is that poor mothers are more likely to give birth to babies with damaged brains. As poor mothers are more likely to engage in risky behaviours that is not inherently surprising but genetic factors could be involved too

Neonatal Encephalopathy and Socioeconomic Status: Population-Based Case-Control Study

By Heidi K. Blume et al.

Objective: To investigate the association between maternal socioeconomic status and the risk of encephalopathy in full-term newborns.

Design: Population-based case-control study.

Setting: Washington State births from 1994 through 2002 recorded in the linked Washington State Birth Registry and Comprehensive Hospital Abstract Reporting System.

Participants Cases (n = 1060) were singleton full-term newborns with Comprehensive Hospital Abstract Reporting System International Classification of Diseases, Ninth Revision diagnoses of seizures, birth asphyxia, central nervous system dysfunction, or cerebral irritability. Control cases (n = 5330) were singleton full-term newborns selected from the same database.

Main Exposures: Socioeconomic status was defined by median income of the census tract of the mother's residence, number of years of maternal educational achievement, or maternal insurance status.

Main Outcome Measures: Odds ratios estimating the risk of encephalopathy associated with disadvantaged socioeconomic status were calculated in 3 separate analyses using multivariate adjusted logistic regression.

Results: Newborns of mothers living in neighborhoods in which residents have a low median income were at increased risk of encephalopathy compared with newborns in neighborhoods in which residents have a median income more than 3 times the poverty level (adjusted odds ratio, 1.9; 95% confidence interval, 1.5-2.3). There was also a trend for increasing risk of encephalopathy associated with decreasing neighborhood income (P<.001). Newborns of mothers with less than 12 years of educational achievement had a higher risk of encephalopathy compared with newborns of mothers with more than 16 years of educational achievement (adjusted odds ratio, 1.7; 95% confidence interval, 1.3-2.3). Newborns of mothers receiving public insurance also had a higher risk of encephalopathy compared with newborns of mothers who have commercial insurance (adjusted odds ratio, 1.4; 95% confidence interval, 1.2-1.7).

Conclusion: Disadvantaged socioeconomic status was independently associated with an increased risk of encephalopathy in full-term newborns. These findings suggest that a mother's socioeconomic status may influence the risk of encephalopathy for her full-term newborn.

Arch Pediatr Adolesc Med. 2007;161:663-668

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************

THE LATEST CHANT IN THE "DIET GIVES YOU CANCER" FAITH

The abstract is below. What it shows is that nice middle class patients who do what the health gurus tell them live longer. But you would never guess that from what they say below. No hint of control for social class even though we already know that the poor have more health problems, live more dangerously and die younger. It's always these inconclusive epidemiological studies which support the "bad fat" religion. The double blind studies are the real criterion and they are un-co-operative with the men of faith. See the right-hand column of this blog on that

Association of Dietary Patterns With Cancer Recurrence and Survival in Patients With Stage III Colon Cancer

By: Jeffrey A. Meyerhardt et al.

Abstract

Context: Dietary factors have been associated with the risk of developing colon cancer but the influence of diet on patients with established disease is unknown.

Objective: To determine the association of dietary patterns with cancer recurrences and mortality of colon cancer survivors.

Design, Setting, and Patients: Prospective observational study of 1009 patients with stage III colon cancer who were enrolled in a randomized adjuvant chemotherapy trial (CALGB 89803) between April 1999 and May 2001. Patients reported on dietary intake using a semiquantitative food frequency questionnaire during and 6 months after adjuvant chemotherapy. We identified 2 major dietary patterns, prudent and Western, by factor analysis. The prudent pattern was characterized by high intakes of fruits and vegetables, poultry, and fish; the Western pattern was characterized by high intakes of meat, fat, refined grains, and dessert. Patients were followed up for cancer recurrence or death.

Main Outcome Measures: Disease-free survival, recurrence-free survival, and overall survival by dietary pattern.

Results: During a median follow-up of 5.3 years for the overall cohort, 324 patients had cancer recurrence, 223 patients died with cancer recurrence, and 28 died without documented cancer recurrence. A higher intake of a Western dietary pattern after cancer diagnosis was associated with a significantly worse disease-free survival (colon cancer recurrences or death). Compared with patients in the lowest quintile of Western dietary pattern, those in the highest quintile experienced an adjusted hazard ratio (AHR) for disease-free survival of 3.25 (95% confidence interval [CI], 2.04-5.19; P for trend <.001). The Western dietary pattern was associated with a similar detriment in recurrence-free survival (AHR, 2.85; 95% CI, 1.75-4.63) and overall survival (AHR, 2.32; 95% CI, 1.36-3.96]), comparing highest to lowest quintiles (both with P for trend <.001). The reduction in disease-free survival with a Western dietary pattern was not significantly modified by sex, age, nodal stage, body mass index, physical activity level, baseline performance status, or treatment group. In contrast, the prudent dietary pattern was not significantly associated with cancer recurrence or mortality.

Conclusions: Higher intake of a Western dietary pattern may be associated with a higher risk of recurrence and mortality among patients with stage III colon cancer treated with surgery and adjuvant chemotherapy. Further studies are needed to delineate which components of such a diet show the strongest association.

JAMA. 2007;298:754-764.





DOES SMOKING SEND YOU BLIND?

The following study shows that smokers have a considerably higher risk of one sort of blindness but whether that is because smoking is strongly class-related we do not know. It's mostly dummies who smoke these days as its contribution to lung cancer is clear. And intelligence IS related to mortality, unfashionable though it is to mention that

Smoking and the Long-term Incidence of Age-Related Macular Degeneration

Jennifer S. L. Tan et al.

Objective: To assess the association between smoking and long-term incident age-related macular degeneration (AMD).

Methods: Of 3654 Australians 49 years and older examined at baseline (January 14, 1992, through December 18, 1993), 2454 were examined 5 years later (January 11, 1997, through February 23, 2000), 10 years later (July 10, 2002, through November 4, 2005), or both. Retinal photographs were taken to assess AMD. Smoking status was recorded at each interview.

Results: After controlling for age, sex, and other factors, current smokers had a 4-fold higher risk of late AMD than never smokers (relative risk, 3.9; 95% confidence interval, 1.7-8.8). Past smokers had a 3-fold higher risk of geographic atrophy (relative risk, 3.4; 95% confidence interval, 1.2-9.7). Joint exposure to current smoking and (1) the lowest level of high-density lipoprotein (HDL) cholesterol, (2) the highest total to HDL cholesterol ratio, or (3) low fish consumption was associated with a higher risk of late AMD than the effect of any risk factor alone. However, interactions between smoking and HDL cholesterol level, ratio of total to HDL cholesterol, and fish consumption were not statistically significant.

Conclusion: Smoking strongly increased the long-term risk of incident late, but not early, AMD, with a possibly greater effect in persons with a low HDL cholesterol level, a high ratio of total to HDL cholesterol, and low fish consumption.

Arch Ophthalmol. 2007;125:1089-1095

****************

Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

*********************