Health and Medicine – Page 24

Should you worry about HRT and cancer?

Menopausal woman A female friend of a friend started on hormone replacement therapy (to treat quite severe early postmenopausal symptoms, and on the advice of her GP to reduce the risk of osteoporosis). The symptoms have all but been relieved (although it’s difficult to separate out the effects of the HRT hormones themselves from the phytoestrogens she imbibes from soy milk and other related foods).

Either way, the recent Lancet paper, which received lots of media attention, got her all hot and bothered. She’s an earlier finisher, and is likely to be on HRT for ten years or so, is that going to mean she will get ovarian cancer. The tabloid hype surrounding the paper would seem to suggest so, but as with all statistical health studies that get pounced on by the media it’s worth taking a closer look.

Interpreting the results and scaling up to whole number women, as opposed to fractional women, over 5 years, ovarian cancer incidence for those who have never used HRT was 26 per 10,000. It was 30 per 10,000 for HRT users.

The researchers conclude that, “Women who use HRT are at an increased risk of ovarian cancer. Since 1991, use of previous has resulted in 72 additional cancers per year and 55 additional deaths in the UK.” Their results are based on the million women study, in which 500,000 were HRT and 500,000 were not.

Of course, ovarian cancer is the fourth most common cancer in women in the UK, with some 6700 developing the malignancy and 4600 dying from it every year. The high incidence of deaths is presumably down to the hidden nature of this form of cancer, which is often not detected until it has reached a lethal stage. 72 additional cancers and 55 additional deaths is a significant but not an enormous increase.

The researchers also add that, “In total, ovarian, endometrial, and breast cancer account for 39% of all cancers registered in women in the UK.1 and 2 The total incidence of these three cancers in the study population is 63% higher in current users of HRT than in never users (31 vs 19 per 1000 over 5 years, figure 6). Thus, when ovarian, endometrial, and breast cancer are taken together, use of HRT results in a material increase in the incidence of these common cancers.”

But, these are risk factors and there is simply no way of making any kind of prediction, with current medical knowledge, of whether or not a particular woman on HRT will suffer any form of cancer because of the HRT drugs she is taking. The researchers mention that as HRT use has declined in the US (partly because of the negative publicity it receives), we are also now seeing falling breast cancer rates there.

According to the author of the paper, Valerie Beral of Cancer Research UK, “It is a small but significant risk. It’s more an issue for women to think about how much they want to take HRT to relieve their symptoms against the known risks.”

However, it’s not all about hot sweats and sexual libido, as life expectancy rises in general and the aspirations of older people for a happy and active retirement rises concomitantly, it will be interesting to see whether a few less cancers will be offset by a rise in osteoporosis incidence and the other “side-effects” of the menopause (particularly early onset menopause).

An elderly neighbour of mine has been in and out of hospital with bone density issues and fractures repeatedly and at one point suffered a potentially lethal hospital-acquired MRSA (multiple-resistant Staphylococcus aureus) infection as a result. To my mind, she would most likely not have suffered in this way had she taken HRT during the early menopause. But, equally there is also the thought that had she died of cancer sooner than the osteoporosis kicked in, she would not have suffered bone density problems later in life either.

For every statistic, a counter statistic can be found and when the overall risks are very small it is difficult for the public, the media, and even the medical scientists to know for sure which way to push the agenda.

One burger could kill

Burger and fries Grandma always said, “Everything in moderation”, but then she always used to take her teeth out to eat soup, so what does she know? Apparently, even moderation can be dangerous, particularly when it comes to high fat food.

Tavis Campbell and colleagues at the University of Calgary have found that just one high-fat meal, a fast-food breakfast for instance, makes you prone to suffer the physical consequences of stress compared with someone eating a low-fat meal.

The team looked at the stress responses of two groups of students: fifteen students were fed a fatty breakfast meal (42 g fat) from a burger bar while the second group of fifteen got to dine on dry cereal with low-fat milk, cereal bars and non-fat yogurt (1 g fat). Both meals had the same number of calories and the low-fat breakfast included supplements to balance it for sodium and potassium, but the total fat content was very different.

Two hours later, the researchers carried out standard physical and mental stress tests and recorded the students’ cardiovascular responses. They performed a mathematical test designed to be stressful, completed a public speaking exercise about something emotionally provocative, held an arm in ice water, and had a blood pressure cuff inflated around an arm, which gradually causes a dull ache.

Regardless of the task, greater CV reactivity was seen in the high-fat group, including raised blood pressure, heart rate and blood vessel resistance. “What’s really shocking is that this is just one meal,” says Campbell.

“It’s been well documented that a high-fat diet leads to atherosclerosis and high blood pressure, and that exaggerated and prolonged cardiovascular responses to stress are associated with high blood pressure in the future,” he says, “So when we learn that even a single, high-fat meal can make you more reactive to stress, it’s cause for concern because it suggests a new and damaging way that a high-fat diet affects cardiovascular function.”

Thankfully, it is not all bad news. Campbell says more research is needed to fully understand how the mechanisms work. “Telling people to never eat something is probably not a good way to promote a better diet,” he says. “At the same time we do have an epidemic of obesity in North America and it’s important that people try to make informed choices.”

Science always hedges its bets in this way. If the argument were about whether to vote left or right, the politicians and lobbyists would make full-on assertions as to even the acute effects of a one-off high-fat vote. Yes, Campbell’s team has only carried out a small preliminary trial, and perhaps underfed and stressed students are not the best control group, but there findings do hint at yet another reason why we should side-step a high-fat diet.

The case is essentially closed on cigarettes in this sense, but individuals can make their own choice. Is it not about time, that the health message were made more forcefully. Maybe one burger is not going to kill you, but some people spend a fortune on finding ways to reduce stress and warding off the effects of aging, if even an occasional high-fat meal inverts all that effort, then perhaps it is time burgers carried a health warning too.

Details of the study are published today in the Journal of Nutrition, 2007, 137, 935-939

Organic Kiwi Fruit

Organic kiwi fruit Could the claims of the “organic” farming movement be true after all? According to an international team who have analysed the antioxidant, mineral, and nitrate composition of kiwifruit, yes. Their findings published in the Journal of the Science of Food and Agriculture would suggest that growing the fuzzy green fruit using so-called organic principles leads to a higher content of health-promoting factors than those grown using conventional methods.

I asked team leader Adel Kader of the University of California, Davis, about his reasoning. “Most differences in composition between conventionally grown and organically grown fruits depend on differences in inputs,” he told us. These inputs include differences in fertilizers added and so results vary considerably from one study to the next, “In our kiwifruit study, the grower added more fertilizers to the organic kiwifruit plants than to the conventional ones and that is the reason for the higher mineral contents of the organic fruits,” he adds, “The one exception is phenolic [antioxidant] content, which has been shown in our study and in several other studies on a range of crops to be higher in organic than in conventional fruits.”

Kader believes that the difference is most likely due to the fruit having to survive against pests in the absence of synthetic pesticides. “Conventional agriculture practices utilize levels of pesticides that can result in a disruption of phenolic metabolites in the plant,” he says, “which have a protective role in plant defense mechanisms.” His hunch is further corroborated by the organic kiwifruit having thicker skins as well as the higher antioxidant activity which is thought to be a natural by-product of stress. He has a simple piece of advice for those dithering over whether to tuck into the fuzzy fruit: “My advice is that people eat more fruits regardless of whether they are conventionally or organically produced,” he told Sciencebase. More on this story in SpectroscopyNOW this week.

Obesity Gene

Obesity overweight Today’s claims in the media about the recently discovered obesity gene are at best overwrought and at worst downright dangerous. A vast study involving more than twenty research centres across the UK has allegedly demonstrated that almost one fifth of us carry a variant of the gene known as FTO that predisposes us to obesity or overweight.

According to the researchers, “Obesity is a serious international health problem that increases the risk of several common diseases.” Fair comment. They add that, “The genetic factors predisposing to obesity are poorly understood.” Another fair comment.

They then report that while carrying out a genome-wide search for type 2 diabetes susceptibility genes among 13 groups of almost 40000 participants they have identified a common variant in the FTO gene that predisposes to diabetes through an effect on body mass index (BMI).

Additionally, the team reports that there is a cumulative, or additive, association of the variant with BMI. They found that 16% of the adults with the risky genetics weighed about 3 kilograms more than the others and were almost twice as likely to be obese, when compared to people without the risk allele. Moreover, the team says that they observe this genetic risk factor in individuals age 7 years and older and say that it reflects a specific increase in fat mass.

But, all this talk of obesity being down to genes will provide many individuals with an excuse along the lines of “it’s my glands”, which has become something of a serious cliche for some people who simply refuse to reduce the calorie intake and to add serious amounts of exercise to their daily routine.

The politics of obesity aside, I contacted metabolic expert Jeremy Nicholson of Imperial College London who recently discovered that calorie restriction in dogs extends life, reduces the risk of diabetes and metabolic disorders, and could be due to a change in the behaviour of microbes in the gut. He is less than impressed with the response of the media to the Science paper on FTO. “Basically, no amount of genetics can explain how humans have got fat so fast,” he told me. I would have to agree, genetics has long-term effects one usually does not see major changes in body function and form happening across a single generation.

So, might there be an alternative explanation for the apparent obesity epidemic in the developed world? Nicholson thinks so. “Changes in the gut microbes and caloric bioavailability probably could be the explanation,” he says. If we are suffering severe disturbances in the profile of gut bacteria – either they have changed behaviour or the species have changed – then those heading for overweight or who are already obese could be absorbing far more calories even from the same amount of food because of it.

Liposuction, like Vaser, Smartlipo and laser liposuction is one option, but could a dose of live yogurt or an antibiotic regimen be the solution to obesity? We are only just starting the hors d’heuvre when it comes to understanding the interplay between our bodies and microbes. Much more work into metabolism and the role of the guy microflora needs to be done before we can cast aside obesity as yet another genetic construct and so abandon sufferers to the realm of the untreatable.

Nicholson explains that the microflora in our gut are laid down in infancy and there is not a lot we can do about that. However, he says, “The real secret is eating a lot of beans and pulses (lentils etc) – lots of them every day, they keep the lower gut microbes very happy and the products of their
breakdown (catabolism) do not cause diabetes.” Nicholson laments that the windy side-effects of such a diet are far less malign than the problems associated with a diet deficient in beans and pulses.

Genetics, microbes, and beans aside, Nicholson has what I think has to be the final word on the debate: “Even genes and bugs added together still fade into insignificance if you sit on your butt all day eating pork rinds – you will get fat but its not genetic!”

It’s a dog’s life

Puppy dog Cutting out the French fries, burgers, chips, candy, beer, soda, and other delicious yet largely non-nutritious food and drink from your diet is generally a good idea. One of the reasons, health experts suspect, is that somehow a reduced-calorie diet leads to a longer life. Now, researchers at Imperial College London have looked at a dog’s life and discovered why dietary restriction could lead to a longer life.

Jeremy Nicholson and colleagues followed 12 “pairs” of dogs in which one partner in each pair was given 25% less food than the other. Nicholson and his colleagues found that the dogs who had less food lived almost 2 years longer (that perhaps equates to between 10 and 14 years). They also found that those dogs suffered less diabetes and osteoarthritis, and were older on average when plagued by the common diseases of old age.

But, why?

The scientists believe that differences in the populations of microbes in the dogs’ guts could partly explain the metabolic differences. The dogs that were not on a restricted diet had increased levels of potentially unhealthy aliphatic amines in their urine, the team found. The presence of higher levels of these compounds indicate reduced levels of choline, the compound essential for metabolizing fat. Such a microbial profile has, in other studies, been associated with the development of insulin resistance and obesity in humans.

Nicholson explains: “This fascinating study was primarily focused on trying to find optimized nutritional regimes to keep pet animals such as dogs healthy and as long-lived as possible. However these types of life-long studies can help us understand human diseases and aging as well, and that is the added bonus of being able to do long-term non-invasive metabolic monitoring.”

So, might this study be applicable to humans and should we too be cutting down on our doggy treats and Pedigree Chum? Potentially, yes. Despite superficial appearances and the sometimes disgusting things dogs choose to eat, the flora and fauna of our guts are very similar. It all depends on whether cutting your burger and soda intake by 25% is worth it for those extra 10 to 14 dog years.

Details of the study are published today in the Journal of Proteome Research. The paper is one in a special issue of the journal in “Metabolomics, Metabonomics, and Metabolic Profiling in Complex Organisms: The Portals to “Real-Life” Systems Biology”.

Choline chemical structure
InChI=1/C5H14NO/c1-6(2,3)4-5-7/h7H,4-5H2,1-3H3/q+1

In totally, unrelated canine news, scientists from the University of Utah and seven other institutions have identified a piece of doggy DNA that reduces the activity of a growth gene, ensuring that small breeds stay small. More on that via Newswise.

Workout limits

Do you workout hard? Is “no pain, no gain” your exercise ethos? Do you feel like you are not getting the fitness results you expect? Your brain could be to blame.

Yagesh Bhambhani and Rohit Malik of the Faculty of Rehabilitation Medicine, at the University of Alberta, Edmonton, Canada and Swapan Mookerjee of Bloomsburg University, Bloomsburg, Pennsylvania, USA, have monitored the oxygen levels of blood flowing in the brains of healthy volunteers while they worked out using near infrared spectroscopy.

NIRS can evaluate changes in blood volume and oxygen levels in the brain while people exercise by measuring the absorption of this form of electromagnetic radiation by the blood, which varies depending on how much oxygen is present.

The team has found that even if you are healthy, there could be an upper limit on just how hard you can push yourself, because brain activity begins to be affected detrimentally as you push harder and harder.

The study watched blood flow and volume as well as measuring carbon dioxide breathed out during an incremental exercise test. In the tests, exercise intensity is gradually stepped up until the volunteers reach exhaustion and must stop. The observed fall off in carbon dioxide levels coincided with decreased blood flow to the brain, which affects exercise capacity, the researchers say.

You can find out more about the science behind the exercise threshold here. Of course, if you are not pushing your exercise regime to the limits, then you probably have nothing to worry about. More to the point, the research is aimed at fine tuning finely tuned athletes and others, not providing the sedantary or mediocre with an excuse to give up half way through their treadmill cycle. (Ahem, mentioning no names…)

Beating Heart Disease with Vitamin B Drugs

Niacin is involved in the metabolism or carbohydrates, fats and proteins, but at high dosage it can increase HDL more than a third and reduce levels of “artery-clogging” triglycerides by half.

Graeme Semple of Arena Pharmaceuticals, San Diego, reports how new drugs that raise high-density lipoproteins, so-called good cholesterol might be developed by following the lead of familiar B vitamin, niacin.

Researchers at Arena and elsewhere are trying to develop new drugs that are even more effective than niacin and so could have greater potential to protect at-risk people against heart attacks and stroke. Semple discusses the latest developments at the ACS annual meeting today.

You can read more about the biochemistry of niacin and LDL cholesterol in Sciencebase.

InChI=1/C6H5NO2/c8-6(9)5-2-1-3-7-4-5/h1-4H,(H,8,9)/f/h8H

Magnetizing a Baby

It is possible to magnetize a baby with a few drops of water, some ordinary sugar and a teether. It’s all down to changes that take place in the brain when the baby tastes the sugar.

Neal Barnard MD, founder of the Physicians Committee for Responsible Medicine (PCRM), explains the process. Of course it’s not really magnetization, it’s the release of opiates in the brain, natural versions of morphine and heroin, that make us feel good. Barnard discusses the science underlying food addictions. Personal willpower is not necessarily to blame, chocolate, cheese, meat, and sugar all release these opioids. substances. Dr. Barnard also discusses how industry, aided by government, exploits these natural cravings, pushing us to eat more and more unhealthy foods. He suggests that a purely plant-based (vegan) diet is the solution to avoid many of these problems.

He points out how cheese and other dairy products contain natural compounds closely related to morphine, perhaps as a natural bonding chemical to ensure suckling mammals “enjoy” the suckling process. The presence of tiny quantities of these compounds in so many foods could explain why dairy products, chocolate, wheat, meat, nuts, onions, corn, tomatoes, onions, bananas, citrus fruits etc are common dietary triggers of migraine, for instance, users are simply overdosing on the opiates and then suffering withdrawal symptoms. And, as to cardiovascular disease, stroke, and heart attack…cardiologists know that if a man in his fifties presents with impotence, there is a one in four chance that he will have a heart attack or stroke within two years. Barnard blames our addiction to meat and even got cattle ranchers in the mid-west to prick up their ears when he relayed that fact and had them asking for his tofu recipes and tips on cooking brown rice.

Anyway, it’s a long video (40 minutes) but makes very interesting viewing.

Stimulating dyscalculia adds up

An international team of scientists have discovered that the brain’s right parietal lobe is responsible for the disorder, dyscalculia, a kind of numerical dyslexia. The discovery made by researchers at University College London, University of the Negev, Israel, Birkbeck Centre for Brain and Cognitive Development, London, Maastricht University, Netherlands, and the Max Planck Institute for Brain Research, Germany, could ultimately lead to new methods of diagnosis and management of the disorder through remedial teaching.

Dyscalculia is as common as dyslexia and attention deficit hyperactivity disorder (ADHD) with about one in twenty people affected. However, dyscalculia has been given little regard in the mainstream despite its potentially debilitating impact on quality of life. Roi Cohen Kadosh, of UCL’s Institute of Cognitive Neuroscience explains the implications of his study, which involved inducing dyscalculia: “This is the first causal demonstration that the parietal lobe is the key to understanding developmental dyscalculia,” he explains, “Most people process numbers very easily — almost automatically — but people with dyscalculia do not.” The team stimulated for a few milliseconds the right parietal lobes of volunteers carrying out an arithmetic test, using neuronavigated transcranial magnetic stimulation (TMS) . The stimulation essentially knocked out activity in that part of the brain and left the volunteers unable to react as quickly to the test.

“This provides strong evidence that dyscalculia is caused by malformations in the right parietal lobe and provides sold grounds for further study on the physical abnormalities present in dyscalculics’ brains,” adds Cohen Kadosh, “It’s an important step to the ultimate goal of early diagnosis through analysis of neural tissue, which in turn will lead to earlier treatments and more effective remedial teaching.”

The researchers will publish details of their findings in the April 17 issue of the journal Current Biology

Anorexia and Kidney Disease

Anorexia nervosa is a serious and potentially fatal eating disorder usually characterized by a severely reduced appetite and often a total aversion to food. In the mainstream media, it is most commonly associated with teenage girls and the celebrity quest for a “size zero” figure. However, it is a serious and life-threatening disorder that goes far beyond the realm of body image and extreme dieting. Important clues as to the underlying causes of this disorder may be found in its association with chronic kidney disease.

According to Peter Stenvinkel of the Division of Renal Medicine, Karolinska University Hospital at Huddinge, Sweden, anorexia is observed frequently in kidney dialysis patients. The condition worsens as kidney disease progresses leading to severe muscle wasting and malnutrition, with all its associated health problems. Scientists had suggested a link to defective central nervous system control of appetite, so Stenvinkel and his colleagues have done an analysis of various biomolecules, including natural inflammatory compounds and sex hormones. Their results suggest that inflammation is closely linked to the development of anorexia in kidney patients and is more common in men than women.

Read the full story in today’s SpectroscopyNOW.