Monthly Archives: August 2013

A Simple Way to Moderate Inflammation

A Simple Way to Moderate Inflammation
Published: 5/30/2013

Chronic low-grade inflammation has been linked to the development of many age-related health conditions. Although this process may be barely noticed, there are things you can do to prevent or delay health issues related to inappropriate inflammation. Consider following an anti-inflammatory diet and taking ginger, a natural anti-inflammatory herb that may help to lessen the risks and/or symptoms of many inflammatory-related disorders. Dried ginger preparations are actually more powerful than fresh because of a chemical conversion of its constituents on drying. Capsules of dried, powdered ginger are now commonly sold in health food stores; use only those that are standardized for their content of active components. The recommended starting dose is 1 gram per day (usually two capsules), taken after a meal to avoid stomach irritation. There is no toxicity and you can stay on it indefinitely.

Why Music Makes Our Brain Sing

Gray Matter

Why Music Makes Our Brain Sing

Baptiste Alchourroun


Published: June 7, 2013

MUSIC is not tangible. You can’t eat it, drink it or mate with it. It doesn’t protect against the rain, wind or cold. It doesn’t vanquish predators or mend broken bones. And yet humans have always prized music — or well beyond prized, loved it.

In the modern age we spend great sums of money to attend concerts, download music files, play instruments and listen to our favorite artists whether we’re in a subway or salon. But even in Paleolithic times, people invested significant time and effort to create music, as the discovery of flutes carved from animal bones would suggest.

So why does this thingless “thing” — at its core, a mere sequence of sounds — hold such potentially enormous intrinsic value?

The quick and easy explanation is that music brings a unique pleasure to humans. Of course, that still leaves the question of why. But for that, neuroscience is starting to provide some answers.

More than a decade ago, our research team used brain imaging to show that music that people described as highly emotional engaged the reward system deep in their brains — activating subcortical nuclei known to be important in reward, motivation and emotion. Subsequently we found that listening to what might be called “peak emotional moments” in music — that moment when you feel a “chill” of pleasure to a musical passage — causes the release of the neurotransmitter dopamine, an essential signaling molecule in the brain.

When pleasurable music is heard, dopamine is released in the striatum — an ancient part of the brain found in other vertebrates as well — which is known to respond to naturally rewarding stimuli like food and sex and which is artificially targeted by drugs like cocaine and amphetamine.

But what may be most interesting here is when this neurotransmitter is released: not only when the music rises to a peak emotional moment, but also several seconds before, during what we might call the anticipation phase.

The idea that reward is partly related to anticipation (or the prediction of a desired outcome) has a long history in neuroscience. Making good predictions about the outcome of one’s actions would seem to be essential in the context of survival, after all. And dopamine neurons, both in humans and other animals, play a role in recording which of our predictions turn out to be correct.

To dig deeper into how music engages the brain’s reward system, we designed a study to mimic online music purchasing. Our goal was to determine what goes on in the brain when someone hears a new piece of music and decides he likes it enough to buy it.

We used music-recommendation programs to customize the selections to our listeners’ preferences, which turned out to be indie and electronic music, matching Montreal’s hip music scene. And we found that neural activity within the striatum — the reward-related structure — was directly proportional to the amount of money people were willing to spend.

But more interesting still was the cross talk between this structure and the auditory cortex, which also increased for songs that were ultimately purchased compared with those that were not.

Why the auditory cortex? Some 50 years ago, Wilder Penfield, the famed neurosurgeon and the founder of the Montreal Neurological Institute, reported that when neurosurgical patients received electrical stimulation to the auditory cortex while they were awake, they would sometimes report hearing music. Dr. Penfield’s observations, along with those of many others, suggest that musical information is likely to be represented in these brain regions.

The auditory cortex is also active when we imagine a tune: think of the first four notes of Beethoven’s Fifth Symphony — your cortex is abuzz! This ability allows us not only to experience music even when it’s physically absent, but also to invent new compositions and to reimagine how a piece might sound with a different tempo or instrumentation.

We also know that these areas of the brain encode the abstract relationships between sounds — for instance, the particular sound pattern that makes a major chord major, regardless of the key or instrument. Other studies show distinctive neural responses from similar regions when there is an unexpected break in a repetitive pattern of sounds, or in a chord progression. This is akin to what happens if you hear someone play a wrong note — easily noticeable even in an unfamiliar piece of music.

These cortical circuits allow us to make predictions about coming events on the basis of past events. They are thought to accumulate musical information over our lifetime, creating templates of the statistical regularities that are present in the music of our culture and enabling us to understand the music we hear in relation to our stored mental representations of the music we’ve heard.

So each act of listening to music may be thought of as both recapitulating the past and predicting the future. When we listen to music, these brain networks actively create expectations based on our stored knowledge.

Composers and performers intuitively understand this: they manipulate these prediction mechanisms to give us what we want — or to surprise us, perhaps even with something better.

In the cross talk between our cortical systems, which analyze patterns and yield expectations, and our ancient reward and motivational systems, may lie the answer to the question: does a particular piece of music move us?

When that answer is yes, there is little — in those moments of listening, at least — that we value more.

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Robert J. Zatorre is a professor of neuroscience at the Montreal Neurological Institute and Hospital at McGill University. Valorie N. Salimpoor is a postdoctoral neuroscientist at the Baycrest Health Sciences’ Rotman Research Institute in Toronto.

Hereditary Cancers

Familial Cancers

Breast and Ovarian Cancer Syndrome

Hereditary breast-ovarian cancer (HBOC) refers to families in which breast cancer and ovarian cancer are diagnosed frequently. It is possible that either one individual suffers from both cancers or several individuals in the pedigree suffer from one or the other cancer type. In such a case we suspect a hereditary factor to cause the pattern of breast and ovarian cancer occurrences in the family.

The two most common genes that are known to cause HBOC are BRCA1 (on chromosome 17) and BRCA2 (located on chromosome 13).

  • BRCA1 is a tumour suppressor gene that was first described in 1990. In its mutated form it causes breast cancer (up to 60% lifetime risk) and ovarian (up to 55% lifetime risk) cancer. Regularly BRCA1 becomes active from age 35 years onwards.
  • BRCA2 mutations also cause breast (up to 60% lifetime risk) and ovarian (up to 25% lifetime risk) cancer. Regularly BRCA2 becomes active from age 40 years onwards.

Risk assessment includes a family tree (pedigree) but family history is false negative in approx half of the cases. It is especially misleading in small families, in families with a low number of females, in families with adoption or if non-paternity could be an issue.

Genetic testing is indicated if the female concerned carries a 15% risk of carrying BRCA1 or BRCA2. Genetic testing involves a blood test. It is available in QLD publicly or privately (cost $3500).

Latest research from the Australian Ovarian Cancer Study (March 2011) confirms that 16% of all ovarian cancers are BRCA-related (inherited). This percentage is far larger than anticipated. It follows that all patients with (serous) ovarian cancer should be tested for BRCA1 and BRCA2. The implications for the patient’s family will be more significant than for the patient herself.

Clinical management options

Breast: Breast cancer screening, prophylactic surgery (mastectomy)

Ovaries: screening (very unreliable because ultrasound and tumour markers frequently are both, false positive and false negative); risk-reducing prophylactic surgery (>90% reliable, definitely recommended for women >40 years of age). Prophylactic surgery also reduces the risk of breast cancer. The earlier the ovaries are removed the higher is the protection against breast cancer.

Prophylactic surgery should be performed by an experienced laparoscopic surgeon. Both ovaries and tubes need to be removed completely through a retroperitoneal approach because BRCA-related cancers often arise in the fallopian tube. Most patients request a hysterectomy at the same time, which also can be done laparoscopically. Prophylactic surgery will induce instant menopause if performed on a premenopausal woman.

Lynch Syndrome

Lynch syndrome is an inherited cancer syndrome causing uterine, bowel, stomach and urinary tract cancers. Patients with Lynch syndrome have a 40% to 60% risk of developing uterine cancer and risk of 5% to 12% of developing ovarian cancer.

Often, patients who carry Lynch syndrome are younger and know other family members who developed different types of cancer (stomach, bladder, bowel, uterus, ovarian).

Patients who were diagnosed with uterine cancer at 50 years of age or less have an 18% chance of carrying Lynch syndrome. These patients require regular screening (e.g., colonoscopies) for the other cancer types.

Patients who were diagnosed with Lynch-related bowel cancer have a 25% risk of developing subsequent uterine or ovarian cancer. In these patients prophylactic, risk-reducing surgery to remove uterus, tubes and ovaries can be life-saving. These operations are done laparoscopically (key hole) and virtually eliminate the risk of uterine and ovarian cancer.

The first step to diagnose Lynch is an immunohistochemical test that can be done from the surgical specimen from the original uterine or bowel cancer specimen. This test is not diagnostic. However, if the test is positive, confirmatory testing should be instigated and requires a blood test. Referral to a Family Cancer Clinic is recommended.

Clinical management

Colonoscopy (every 1 to 2 years) from age 25 years (reduces colon cancer incidence and mortality by >60%)

Annual urine cytology (to detect early stages of bladder and ureteric cancers)

Endometrial sampling (yearly) only for young women who have not completed a family

Prophylactic surgery (laparoscopic hysterectomy) is the most effective way to eliminate the risk of uterine cancer; it virtually eliminates its risk and should be performed by an experienced laparoscopic surgeon.

Pharmacogenomics explains why some medicines may not work for you

2 May 2013, 11.08am EST

Pharmacogenomics explains why some medicines may not work for you

Pharmacogenomics is the study of drugs (pharmakon– the Greek word for poison or drug) and the genome. These two come together to explain why about 50% of medicines don’t work in some people and why they can sometimes be harmful, or even cause death. It’s our genetic makeup that’s often the cause. The…

Pharmacogenomics is the study of variations in our genome that alter our response to drugs. Andy Melton

Pharmacogenomics is the study of drugs (pharmakon– the Greek word for poison or drug) and the genome. These two come together to explain why about 50% of medicines don’t work in some people and why they can sometimes be harmful, or even cause death. It’s our genetic makeup that’s often the cause.

The idea that the genetic makeup we inherit from our parents can affect how we respond to a foreign chemical goes back to Pythagoras, who described people becoming very sick by eating the broad bean Vicia Faba; “favism” is due to life-threatening red blood cell breakdown.

A more visible example of how our genetic makeup impacts our reaction to things we consume (and one you might be more familiar with) is the effect of alcohol on many people of Asian ethnicity. Alcohol is broken down in our body by enzymes to acetaldehyde, which is then further broken down by another enzyme to acetic acid.

The facial flushing, and runny eyes and nose are not due to a build-up of alcohol but a build-up of acetaldehyde. People exhibiting these symptoms lack the enzyme that breaks down acetaldehyde because of a single change in the gene that makes the enzyme which breaks down acetaldehyde.

Personalised medicine

Pharmacogenomics is the study of variations in our genome (DNA and RNA) that alter our response to drugs. It has nothing to do with disease susceptibility. It helps personalise medicine by studying DNA variations to better target a drug, or its dose, to improve health and not prevent toxic reactions.

It’s because of the Human Genome Project that we can now work out the genes that affect how a drug works or leads a drug to cause harm. Mapping the genome was the first step; we needed a picture of the genetic make-up of humans before pharmacogenomics could be possible.

DNA variations affect how well a drug is broken down by the liver, transported around the body to its site of action and the actual site the drug targets. The frequency of these drug genetic variations is very different between Caucasians, Asians, Africans and people from the Middle East. Virtually nothing is known about the genetic variations and their frequency in our Aboriginal population.


So why is pharmacogenomic testing not part of routine testing before a doctor writes a prescription? Well, for most drugs, a person’s genetic makeup plays a very small role in how a drug will affect her. Other factors such as her age or what stage she is in her illness are more significant.

But your genetic make-up is important for some drugs and Medicare funds tests for them. HIV medicine Abacavir, for instance, is not prescribed unless a genetic test is done to rule out a life-threatening reaction.

In some inflammatory diseases (rheumatoid arthritis, inflammatory bowel disease), an old drug called azathioprine can cause a life-threatening drop in bone marrow cells in one in 300 people. A genetic test before starting treatment tells the doctor the best dose to avoid this toxic reaction.

More than meets the eye

There are many genes linked to drug toxicity or poor response. And whether or not we should test these genes before prescribing a drug is hotly debated.

All together, pharmacogenomic testing requires experts in genetic testing, pathologists, and experts in medicines (clinical pharmacologists and pharmacists). Just providing the results of a genetic test is not only inadequate but potentially useless. The results need to be interpreted and doctors need to be advised on what they should do to ensure patient safety. That’s the role of medicines experts.

Determining the cost-benefit of genetic testing for medicines needs large and international studies, the funding of which is difficult, especially in Australia.

Although the US FDA (Food and Drug Administration) has championed pharmacogenomics, and a 2008 Deloitte Economics report suggested such testing would deliver a net economic benefit of $12 billion over five years, the Australian government has not taken any action in this area.

But this is likely to change as our knowledge of drug-genome interaction increases and the cost of genetic testing falls. There will come a time when your doctor will not only test your liver or kidney function but also check your DNA variations to optimise the medicines you need to take and their doses

Natural treatment Erectile Dysfunction.

5 natural ways to overcome erectile dysfunction

Can you run as fast as you did when you were 20 years old? Hit a baseball as far as you once could? Bash a tennis ball with the same speed and spin?

Probably not.

As we age, there are still plenty of ways to stay in the game and enjoy it. That’s as true of sex as it is of sports.

Erectile dysfunction (ED) can occur for many reasons. Sometimes it is as simple as the side effect of a particular medication. But for roughly 75% of men, the cause is more complex. ED may result from vascular disease, neurological disease, or diabetes, or the result of prostate-related treatments or surgeries.

Whether you suffer from ED or are hoping to sidestep this condition, try these tips for better health and a better sex life.

1. Start walking. According to one Harvard study, just 30 minutes of walking a day was linked with a 41% drop in risk for ED. Other research suggests that moderate exercise can help restore sexual performance in obese middle-aged men with ED.
2. Eat right. In the Massachusetts Male Aging Study, eating a diet rich in fruit, vegetables, whole grains, and fish — with fewer red and processed meat and refined grains — decreased the likelihood of ED. Another tip: a chronic deficiency in vitamin B12 may contribute to erectile dysfunction. A daily multivitamin and fortified foods are the best bets for those who absorb B12 poorly, including many older adults.
3. Pay attention to your vascular health. High blood pressure, high blood sugar, high cholesterol and triglycerides can damage arteries in the heart (causing heart attack), in the brain (causing stroke), and leading to the penis (causing ED). Low levels of HDL (good) cholesterol and an expanding waistline also contribute. Check with your doctor to find out whether your vascular system — and thus your heart, brain, and penis — is in good shape or needs a tune-up through lifestyle changes and, if necessary, medications.
4. Size matters, so get slim and stay slim. A trim waistline is one good defense — a man with a 42-inch waist is 50% more likely to have ED than one with a 32-inch waist. Getting to a healthy weight and staying there is another good strategy for avoiding or fixing ED. Obesity raises risks for vascular disease and diabetes, two major causes of ED. And excess fat interferes with several hormones that may be part of the problem as well.
5. Move a muscle, but we’re not talking about your biceps. A strong pelvic floor enhances rigidity during erections, and helps keep blood from leaving the penis by pressing on a key vein. In a British trial, three months of twice-daily sets of Kegel exercises which strengthen these muscles, combined with biofeedback and advice on lifestyle changes — quitting smoking, losing weight, limiting alcohol — worked far better than just advice on lifestyle changes.

From Healthbeat, Harvard University. For more on diagnosing and treating ED, purchase What to do about Erectile Dysfunction by Harvard Medical School.

Old veggies.

Using Older Produce

Next time you contemplate tossing out those limp greens, softening grapes or spotted bananas, you may want to reconsider. A study found that fruits and vegetables don’t lose any antioxidant capacity in the days after purchase, and still provide abundant nutrients, including antioxidants, up until the time that they begin to spoil.

Belgian researchers purchased an assortment of fresh produce and measured its antioxidant content, then stored them at room temperature or refrigerated them. They continued to check the antioxidant levels of both groups until spoilage occurred, and found that the fruits and vegetables did not lose any phenolic compounds, ascorbic acid or flavanols – the trio of chemical types associated with antioxidant content. And in some cases, the total count of phenolic compounds actually increased prior to spoilage.

Instead of tossing produce, try cooking methods that exploit their softened state – you can easily turn older fruits into jams, add limp greens to soups and stews, and overripe bananas are perfect for banana bread or smoothies!

Use antidepressants

I get very concerned when I note how many of my patients are on antidepressants prescribed by their own doctor. Very rarely are they told about the many side effects of the antidepressants. The evidence is they are not all that effective either. My big gripe is that alternative treatments for “feeling blue” are not explored or offered. Unfortunately, it is easier for the doctor to give a pill and then move on to the next patient, than it is to go into alternatives. Welcome to Medical Practice 2013 !!.
25 January 2013, 6.57am AEST

Are antidepressants over-prescribed in Australia?

The British Medical Journal (BMJ) has just published two opposing views on the vexed question of whether antidepressants are being over-prescribed. The issues raised by debate are by no means unique to the United Kingdom; increasing rates of antidepressant prescribing are apparent in most developed countries…

Antidepressant prescribing has been increasing in most developed countries since the the late 1980s and early 1990s. PrettyPills/Flickr

The British Medical Journal (BMJ) has just published two opposing views on the vexed question of whether antidepressants are being over-prescribed. The issues raised by debate are by no means unique to the United Kingdom; increasing rates of antidepressant prescribing are apparent in most developed countries, including Australia.

The BMJ discussion was precipitated by recent UK prescribing data, which reported a 9.6% increase in antidepressant prescriptions in 2011 – the largest increase in prescriptions of all medication classes for that year.

Arguing that the figures indicated over-prescribing, general practitioner Des Spence writes, “I think that we use antidepressants too easily, for too long, and that they are effective for few people (if at all).”

In the opposing camp, professor of psychiatry Ian Reid contends, “Given recent demonstrations that depression is still under-recognised and under-treated, the claim that antidepressants are over-prescribed needs careful consideration.”

Situation in Australia

A recent report on prescribing patterns of antidepressants and other psychotropic medications (drugs for mental illnesses) has aroused similar controversy in the local media. The study’s authors reported a 58.2% increase in the dispensing of psychotropic drugs over the period from 2000 to 2011, including a 95.3% increase in antidepressants.

Echoing the argument that antidepressants are being over-prescribed, the authors raised concern about “ … the dramatic increase in antidepressant prescriptions despite questions about the efficacy of these drugs in mild to moderate depression.”

These recent UK and Australian data are not surprising; they are consistent with the major increase in antidepressant prescribing that’s been occurring in most developed countries since the introduction of the SSRI (selective serotonin reuptake inhibitor) antidepressants in the late 1980s and early 1990s.

An international trend

In 2000, my colleagues and I wrote one of the first major reports of this global trend. We found an approximately threefold increase in antidepressant prescribing in Australia from 1990 to 1998. The increase reflected what was occurring in most major Western countries and coincided with the widespread introduction of SSRI antidepressants such as Prozac, Zoloft, Aropax and Cipramil during that period.

In a another paper, we examined a longer timeframe (1975 to 2002) finding a 1.1% annual increase in antidepressant prescribing from 1975 to 1990, an acceleration to 29% in 1995, then a slowing down to 6.6% in 2002.

There’s no doubt there’s a continuing increase in the use of antidepressants in developed countries such as Australia and the UK, in the range of between 6% and 9% annually. The critical question, though, is whether this substantial increase in prescribing is justified at both a national public health and the individual clinical level.

Benefit or harm?

In Australia, we are able to look at the question of benefit or harm by examining national epidemiological and suicide data.

In terms of adequacy of depression treatment, a 2007 national survey found that 6.2% of individuals had experienced a mood disorder (mainly depression) over the prior 12 months, but over half (51.2%) did not access any services for mental health problems in that time. This indicates a substantial unmet treatment need for depression, rather than over-treatment.

It’s important to consider whether the increase in prescribing is justified at both a national public health and the individual clinical level. Erin DeMay

While it’s not possible to identify rates of antidepressant prescribing, as such, from the survey, the rate of use for psychological services was 23.2% for those with a mood disorder. This is a substantial increase from the 11.8% in an analogous 1997 survey, suggesting that doctors were readily utilising psychological services via Commonwealth-funded schemes such as Better Access.

Overall, these data do not indicate that there’s over-prescribing of antidepressants in Australia.

Antidepressants and suicide

A second potential measure of the value or otherwise of this increase in antidepressant use is its impact on suicide rates.

We examined this question in 2003, and found there was a significant correlation between changes in antidepressant prescribing rates from 1991 to 2000 and the rates of suicide. We also found that people in age and gender groups with increased rates of prescribing demonstrating lower suicide rates.

This same finding has also been reported in the United States and Scandinavia, indicating that greater rates of effective treatment for depression in a population have a significant impact on suicide.

We interpreted our findings broadly – that effective treatment of depression, whether by medication or psychological treatment can lead to a measurable benefit (here a fall in suicide rates), even at a whole population level.

Issues around effectiveness

Another issue raised in the BMJ debate is the current state of knowledge about the effectiveness of antidepressants for those with mild depression – the most common form in the community. Unfortunately, current evidence is inconsistent and dependent on the methodology used by researchers.

A highly publicised 2008 meta-analysis of published and unpublished antidepressant trials found that only those with severe levels of depression benefited more from antidepressants than a placebo.

But a recent report examining longitudinal data from individual patients in a series of large antidepressant trials found no relationship between likelihood of benefit from antidepressants and the initial severity of depression. In other words, patients benefited at similar rates independently of how severely depressed they were.

These inconsistent findings indicate the jury is still out on whether those with mild depression benefit from antidepressants.

What to make of it all?

So, where does this leave us in determining whether current rates of antidepressant prescribing are excessive? While rates of prescribing are undoubtedly increasing, data from national surveys suggest continuing high rates of untreated depression as well as increased use of psychological services. And, as discussed above, findings from a number of developed countries, including Australia, indicate the public health benefit of reduced suicide rates.

Still, we must remain vigilant in monitoring such prescribing and avoid mindless use of antidepressants, particularly for milder levels of depression where psychological treatments are probably more appropriate.

If you think you may be experiencing depression or another mental health problem, please contact your general practitioner or in Australia, contact Lifeline 13 11 14 for support, beyondblue 1300 22 4636 or SANE Australia for information.

Cosmetics and Breast Cancer

It horrifies me when I go into various homes to find a cupboard(or more) full  of various cleaning products, deoderisers, sterilising, coloring and other chemical products claiming to do myriad things. Even keep the toilet bowl clean and smelling good. This all attests to the power of the advertising industry, to sell us things we do not need. Unfortunately, these same things are hurting us and our families. See this story below:
The Washington Monthly / By John Wasik

Did Make-Up Give My Wife Breast Cancer? The Ugly Truth Hidden by the Cosmetics Industry

The virtually unregulated beauty industry puts potential carcinogens in their products. Then they shower us with pink ribbons.
May 8, 2013  |

When Kathleen felt a lump in her right breast she began a journey that millions have experienced—or, sadly, will experience. After a painful biopsy and other tests confirmed it was cancer, my wife was thrown into a cauldron of tears, doubt, and fear for herself and her loved ones. Our two daughters were then just eight and twelve.

Like many cancer patients, Kathleen also experienced a stranglehold of guilt. Was it something she did or didn’t do that fed the tumor? Was it the meat in our diet? Our water? The air? Her genes? I assured her that we couldn’t be at fault. We had banned soda pop and anything with high-fructose corn syrup from our house more than a decade before. We tried to eat organic food, we were transitioning to more vegetarian fare, and she did yoga and took regular walks. We didn’t even have cable.

After a test showed that Kathleen didn’t have the BRCA breast cancer gene, her surgeon, Dr. Sonya Sharpless, suggested that environmental factors might be implicated. But what could they be? Kathleen had already thrown out a bevy of household cleaning products and plastic containers.

Then she discovered the work of the Breast Cancer Fund, a San Francisco-based advocacy group that for the last ten years has been focusing on cancer-causing agents in personal care products. Through a coalition of health and environmental groups called the Campaign for Safe Cosmetics (of which the Breast Cancer Fund is the principal sponsor), the organization has been drawing attention to the fact that known carcinogens—substances like formaldehyde—are used as preservatives in everything from suntan oil to makeup. Kathleen frantically threw out her all her expensive Clinique and Shiseido cosmetics.

Did a lifetime of using cosmetics cause or contribute to Kathleen’s breast cancer? We don’t know. But here are some facts that every American woman and her loved ones should absorb. The European Union bans nearly 1,400 chemicals from personal care products because they are carcinogenic, mutagenic, or toxic to reproduction. But in the United States, the Food and Drug Administration entrusts safety regulation of cosmetics to a private entity that is housed and funded by the industry’s trade association. To date, this entity has found only eleven chemicals to be “unsafe for use in cosmetics.” The FDA has no oversight of cosmetics products before they come on the market and, unlike the EU, leaves it to the cosmetics industry to determine which ingredients should be banned.

Because the American cosmetics industry is largely self-regulated, American women have to worry that they may be exposed to all sorts of cosmetics ingredients that may be dangerous to their health. Without greater powers for the FDA to regulate cosmetics, there is just no way that people like Kathleen who have cancer, or those who fear getting it, can know for sure. Indeed, even while in the hospital cancer patients are exposed to cosmetic products that the FDA has never evaluated and that activist groups like the Campaign for Safe Cosmetics say contain known or suspected carcinogens.

This happened to Kathleen. During her first round of chemo in 2009, some volunteers at the hospital came calling with a little red bag that contained products from Clinique, Estée Lauder, and Del Laboratories. Everything from eyeliner pencils to blush was in the bag, accompanied by a brochure that provided helpful advice on skin care and wig purchases.

Her well-meaning visitors were part of the Look Good Feel Better program (LGFB), which involves 16,000 volunteers who hand out $10 million worth of personal care products every year to women being treated for cancer. Behind this effort is a Who’s Who of the personal care industry: Alberto Culver, Avon, Chanel, Coty, Aveda, Johnson & Johnson, Neutrogena, L’Oreal, LVMH, Mary Kay, Procter & Gamble, and Unilever, among others. The sponsors, as Kathleen learned from the brochure, are the American Cancer Society and the Personal Care Products Council (PCPC), the leading national trade association representing the global cosmetic and personal care products industry, which, through its tax-exempt foundation, kicked in $8.6 million to LGFB in 2011.

Oestrogen- Villain or Heroine?

I wrote this article for a local medical publication recently. Most women would be unaware of these facts.

Oestogen- Villain or Heroine?

Many of my patients express concern about taking oestrogen (E2), as it is firmly fixed in their minds that it causes Breast Cancer. After all, the breast has cancers that are E2- receptor positive. Does that not say it all? However, it is not that simple (it never is).

Quality of Life: E2 increased feeling of well-being in several trials[1],[2]. It also showed an improvement in Health related QOL in symptomatic women though an alleviation of symptoms[3].

Longevity: The Leisure World Cohort study[4] found that long term E2 users had a reduction in death from all causes of 15%. They state that “results of recent clinical trials and other observational studies, suggest that after an initial period of increased risk, the use of E2 therapy may be without excess adverse effect.”

Alzheimer’s disease: The Cache County memory Study[5] concluded that taking E2 use for more than 10 years reduced the risk of Alzheimer’s disease, if treatment commences at the onset of menopause. Another study found an enduring protective role of endogenous and exogenous E2 on memory in older postmenopausal women[6].

Colon Cancer: What is often forgotten is the proven reduction in colon cancer in women on HRT of 33%[7],[8],[9]

Heart disease: A study in the BMJ showed a significant reduction in mortality, heart failure and myocardial infarction in women on HRT for over 10 years[10]. Keep in mind that 50% of women over 50 will die of heart disease. This is over 7 ½ times the number that fall victim to breast cancer[11]. Further studies show that if women have HRT initiated within 6 years of menopause, they have a reduction of myocardial ischaemia and hypertension of 40-60%[12],[13],[14]

Osteoporosis:  Every study confirms that E2 are the most effective way of increasing bone density and preventing osteoporotic fractures[15],[16],[17]. It is more effective and beneficial than the biphosphonates that are frequently used by bone physicians as first choice and by GP’s unsure about the safety of E2 therapy, according to Professor Studd. Furthermore, studies from several centres have shown conclusively that E2 prevent collagen from being lost from the intervertebral discs thus maintaining their strength and function. This important protective effect of E2 seems to be unique as biphosphonates and the other non-hormonal treatments of low bone density do not have beneficial effects on the discs.

Depression: There are certain types of depression in women that are effectively treatable with E2, although psychiatrists seem to have closed their minds to this possibility to an extent which becomes dangerous for women[18]. Transdermal E2 and serotonergic and noradrenergic antidepressants are efficacious in the treatment of depression and vasomotor symptoms in symptomatic, midlife women[19]. Transition to menopause and its changing hormonal milieu are strongly associated with new onset of depressed mood among women with no history of depression[20],[21].

Libido: E2 certainly improves libido by helping vaginal dryness and painful intercourse. Even without these characteristic symptoms, estrogens can improve sexual desire[22],[23],[24]

Hair skin and Nails: The loss of E2 in menopause causes thinning of the skin and loss of Hair. As our understanding of the molecular and hormonal controls on the hair follicle has grown, there has been increased interest in the various modulators of hair growth, including the potential role of E2[25]

Osteoarthritis: Evidence is accumulating about the very positive effect of E2 on joints and preventing OA. In study from Denmark, they referred to E2 as a possible magic bullet in preventing OA. They found” The female predominance of polyarticular osteoarthritis (OA), and in particular the marked increase of OA in women after the menopause points to a likely involvement of female sex hormones in the maintenance of cartilage homeostasis. This is in complete alignment with clinical data using biochemical markers of joint degradation which demonstrated approximately 50% inhibition of cartilage destruction (with E2). These finding were recently validated in WHI, where women taking E2 had significantly less joint replacement[26].

Frailty:  There is solid evidence that E2 prevents loss of musculoskeletal tissue mass and quality, and the ability to respond to mechanical and metabolic stressors, like exercise.[27]

Voice: HRT seems to counteract the vocal changes caused by menopause. The type of HT did not affect the outcome in this study[28].

Weight Gain:  The hormonal changes across the perimenopause substantially contribute to increased abdominal obesity which leads to additional physical and psychological morbidity. There is strong evidence that E2 therapy may partly prevent this menopause-related change in body composition and the associated metabolic sequelae[29].

Diabetes:  HRT reduces the risk of diabetes and, through improving insulin action in women, with insulin resistance[30],[31],

Neuroprotection:  Ovarian hormones can protect against brain injury, neurodegeneration and cognitive decline[32]. Studies suggest that women are “protected” against stroke relative to men, at least until the years of menopause, when E2 levels fall. Studies further reveal that endogenous E2 production has a neuroprotective role in the brain against cerebral ischemia[33],[34]. E2 is intimately associated with neuronal survival, mitochondrial function, neuroinflammation and cognition through genomic as well as non-genomic pathways[35], E2 has been documented to be effective in treating the symptoms of Parkinson’s disease[36]. However, it is crucial that E2 replacement start at menopause or sooner. Any delay causes the neuroprotective benefits to be lost.

It is time that the medical profession reappraises our attitude to E2 as a result of these recent studies. Our patients also deserve to have this information so that they can make better informed decisions about using HRT containing E2, and the potential long-term benefit of taking E2.

[1] Quality of life of postmenopausal women on a regimen of transdermal estradiol therapy. Am J Obstet Gynecol 1993;168:824-30.

[2] Menopausal symptoms  and treatment-related effects of estrogen and progestin in the WHI. Obstet Gynecol 2005; 105:1063-1073

[3] NIH Conference Management of menopause related symptoms Ann Intern Med 2005;142:1003-1013

[4] The increased longevity in older users of postmenopausal estrogen therapy: the Leisure World Cohort Study, Menopause 2006 Jan-Feb;13(1):12-18 Gynecol 1993;168:824-30

[5] Hormone Replacement therapy and incidence of Alzheimer disease in older women: the Cache County Study. JAMA 2002 Nov 6;288(17):2123-9-

[6] Lifelong estrogen exposure and memory in older postmenopausal women. J Alzheimers Dis 2013 Jan 1;34(3):601-8

[7] Hormone replacement therapy and the risk of colorectal cancer: a meta-analysis. Obstets Gynecol 1999;93:880-8

[8]Postmenopausal hormone therapy and the risk of colorectal cancer: a review and meta-analysis. Am J Med 1999:106:574-82

[9] Slattery et al HRT and improved survival among postmenopausal women diagnosed with colon cancer; Cancer causes control 1999;10:467-473.

[10] BMJ 2012;345:e6409.

[11] Cancer statistics 2010 Cancer j Clin 2010;60:277-300

[12] CEE and coronary heart disease The WHI. Arch Intern Med 2006;166:357-36

[13]Postmenopausal HRT and the risk of CVD by age and years since menopause JAMA 2007; 297:1465-1477

[14] HRT and CVD in the early menopause – the WHI data revisited. Climacteric 2007;10:195-196

[15] Ten reasons to be happy about hormone replacement therapy: a guide for patients. Studd,J.Menopause international 2010; 16; 44-46.

[16]. The comparative effect on bone density , endometrium and lipids of continuous HRT (CHART) study. Speroff et al JAMA 1996;276:1397-1403

[17] Ultra-low micronized beta estradiol and bone densityand bone metabolism in older women. Prestwood et al..JAMA 2003:290:1042-1048

[18] A guide to the treatment of depression in women by estrogens Climacteric 2011 Dec;14(6):637-42

[19] Depression during the menopausal transition. Menopause Int 2008 Sep;14(3):123-8

[20] Associations of hormones and menopausal status with depressed mood in women with no history of depression Arch Gen Psychiatry  2006;63:375-82

[21] Summary of the National Institute on Aging-sponsored conference on depressive symptoms.Menopause 2010;17:815-22

[22] The Seattle Midlife Women’s Health Study J Womens Health 2010 Feb;19(2) 209-18

[23] Sexuality in Midlife J Midlife Health 2012 Jul;3(2):61-5

[24] The use of estrogen therapy in women’s sexual function. J Sex Med 2009;6:603-1

[25] Managing hair loss in midlife women. Maturitas 2012 Nov 24 S0378-5122(12)00368-4

[26] The pathogenesis of osteoarthritis involves bone, cartilage and synovial inflammation:may estrogen be a magic bullet? Menopause Int 2012 Sep 28.

[27] Menopause, estrogens and Frailty. Nedergaard et al. Gynecol Endocrin 2013 May;29(5):418-23

[28] J voice. Sep;2012 26;(5) :671

[30] Updated IMS recommendations on postmenopausal hormone therapy. Climacteric 2011;14:302-320

[31] Effects of estrogen plus progestin on the incidence of diabetes in postmenopausal women. Results from the WHI study. Diabetologia 2004; 47:1175-1187

[32] Neuroprotection by ovarian hormones in animal models of neurological disease. Endocrine 2006 Apr; 29(2):217-31

[33] Estrogen signalling and neuroprotection in cerebral ischemia. J Neuroyndocrinol 2012 Jan;24(1):34-47

[34] Neuroprotection by estrogen. Ann N Y Acad Sci 2003 Dec:1007:89-100

[35] Effects of estrogen in the brain:is it a neuroprotective agent in Alzheimer’s disease? Curr Aging Sci. 2010 Jul; 3(2):113-26.

[36]From clinical evidence to molecular mechanisms underlying neuroprotection afforded by estrogens. Pharmacol Res 2005 Aug:52(2):119-

Vitamins That Cost Pennies a Day Seen Delaying Dementia

Vitamins That Cost Pennies a Day Seen Delaying Dementia

 By Andrea Gerlin – May 21, 2013 3:03 AM GMT+0800

Brain scan comparison of Alzheimer’s disease. Photograph: Lawrence Berkeley National Library

A cheap regimen of vitamins in use for decades is seen by scientists as a way to delay the start of Alzheimer’s disease and dementia, a goal that prescription drugs have failed to achieve.

Drugmakers including Bristol-Myers Squibb Co., Pfizer Inc. (PFE) and Eli Lilly & Co. (LLY) have spent billions of dollars on ineffective therapies in a so-far fruitless effort to come up with a treatment for dementia and Alzheimer’s.

Now, in the latest of a steady drumbeat of research that suggests diet, exercise and socializing remain patients’ best hope, a study published today in the Proceedings of the National Academy of Sciences shows that vitamins B6 and B12 combined with folic acid slowed atrophy of gray matter in brain areas affected by Alzheimer’s disease.

“You don’t have any other options for these patients, so why not try giving them this cocktail of B vitamins?” says Johan Lokk, a professor and head physician in the geriatric department at Karolinska University Hospital Huddinge in Sweden, who wasn’t involved in the study.

Alzheimer’s disease and dementia mostly affect older people. As people live longer, the number afflicted by the conditions is growing. Delaying dementia with an inexpensive vitamin regimen may help stem the surge in cases, which the World Health Organization predicted would more than triple from 36 million worldwide in 2010 to 115 million in 2050, as well as the cost, estimated at $604 billion in 2010 by Alzheimer’s Disease International.

Vitamin Market

Vitamin makers and retailers such as Pfizer’s consumer health-care unit and GNC Holdings Inc. (GNC) in the U.S. and Reckitt Benckiser Group Plc and Holland & Barrett Holding Ltd. in Europe stand to benefit. The Nutrition Business Journal estimates the global market for vitamins, minerals and supplements was $30 billion in 2012 and forecasts sales will grow 3.6 percent by 2017.

In the PNAS study, researchers tracked 156 people ages 70 and older who had mild memory loss and high levels of a protein previously linked to dementia. Among people with elevated homocysteine, the study found that the amount of gray matter declined 5.2 percent in those taking a placebo, compared with 0.6 percent in those who took the vitamin cocktail. The supplements cost about 30 cents a day in pharmacies and health-food stores.

First Look

“It’s the first and only disease-modifying treatment that’s worked,” said A. David Smith, professor emeritus of pharmacology at Oxford University in England and senior author of the study. “We have proved the concept that you can modify the disease.”

The U.S. Food and Drug Administration hasn’t cleared new drugs for memory loss conditions in a decade. Approved medicines such as Eisai Co.’s Aricept ease symptoms without slowing or curing dementia. A joint U.S.-European Union task force in 2011 found that all disease-modifying treatments for Alzheimer’s in the previous decade failed late-stage trials “despite enormous financial and scientific efforts.”

Since then, at least four more experimental treatments have failed. New York-based Bristol-Myers dropped development of avagacestat in December after data showed the therapy wasn’t effective enough to move into the final stage of testing. Solanezumab, from Indianapolis-based Lilly, failed to meet the main goal of two large studies last year, though the company plans to conduct further research.

Bapineuzumab from Pfizer, Johnson & Johnson and Elan Corp. failed to improve patients’ memory or thinking, according to test results released in August. This month, Baxter International Inc. said Gammagard, which is used to help patients with immune disorders, didn’t help Alzheimer’s patients in a late-stage study.

Meanwhile, scientists are exploring the use of experimental drugs to prevent Alzheimer’s. Independent trials will begin this year and run for three to five years.

Shrinking Brains

Older people’s brains shrink about 0.5 percent a year from the age of 60, and faster in people with vitamin B12 deficiency, mild cognitive impairment or Alzheimer’s disease, Smith said. If that pace can be significantly slowed before full-blown Alzheimer’s develops, it may delay the disease’s progression so that older people can enjoy better lives until they die from another cause.

“If you delay the onset by five years, you can halve the number of people dying from it,” says Jess Smith, a research communications officer at the Alzheimer’s Society, a U.K. charity. She isn’t related to A. David Smith.

The Oxford group studied people in the Oxford, England, area who had mild cognitive impairment, also known as MCI, or some memory loss. One in six people over 70 have MCI and about half of those develop dementia within five years, A. David Smith said. Alzheimer’s accounts for 50 percent to 80 percent of all dementias, according to the Alzheimer’s Association.

Vitamin Cocktail

Study volunteers were given either a placebo or 0.5 milligrams of vitamin B12, 20 milligrams of vitamin B6 and 0.8 milligrams of folic acid. Their brains were scanned using magnetic-resonance imaging and blood levels of the protein homocysteine were measured at the start of the trial and two years later. The MRI scans compared how much gray matter was lost in brain regions most affected by Alzheimer’s disease.

“It’s a big effect, much bigger than we would have dreamt of,” A. David Smith said. “I find the specificity of this staggering. We never dreamt it would be so specific.”

Brain Atrophy

The research reinforces previous findings that supplements slowed brain atrophy and cognitive decline in the group.

Smith and his colleagues at Oxford reported in 2010 that the atrophy rate in patients’ whole brains was reduced about 30 percent in those taking the vitamins and 53 percent in those on the vitamins who also had elevated homocysteine. They published study results in 2012 of memory tests that found people on the treatment who had high homocysteine were 69 percent likelier to correctly remember a list of 12 words.

The studies, known as Vitacog, were funded by seven charities and government agencies and vitamin maker Meda AB (MEDAA) of Solna, Sweden. Smith is an inventor on three patents held by Oxford University for B vitamin formulations to treat Alzheimer’s disease or MCI.

Vitamin B12 is found in liver, fish and milk and folic acid in fruit and vegetables. Deficiency of folate and B vitamins is already linked to dementia. Researchers such as Smith are studying whether less-than-optimal levels of B vitamins and folic acid contribute to its development.

Possible Benefit

“If you have somebody who has outright Alzheimer’s disease, this isn’t really going to help them much,” said Joshua Miller, a professor in the department of nutritional sciences at Rutgers University in New Brunswick, New Jersey. “If you can catch them at an earlier level, they may be able to benefit from it but only if you have elevated homocysteine.”

A U.S. study published in 2008 found that people who had moderate or severe Alzheimer’s didn’t benefit from the supplements. There’s no evidence that B vitamins enhance cognitive function in healthy people, A. David Smith said.

Doctors in Sweden began measuring homocysteine in people who report declining memory about two years ago, said Lokk at Karolinska. Swedish patients with high homocysteine are given folic acid and B vitamins, even if they aren’t deficient.

Taking Offensive

“We think the increased homocysteine level could be deleterious to the brain,” Lokk said. “We wanted to be on the offensive in diagnosing and treating patients. In our opinion, it is harmless and cheap.”

Vitamin B12 is probably the key to slowing the brain’s shrinkage and cognitive decline, Miller said. The FDA said in 1998 that folic acid had to be added to breads, cereals and other products that use enriched flour, to reduce neural tube defects such as spina bifida in newborns. A study by Miller and his colleagues in people of Mexican and South and Central American ancestry age 60 and older in Sacramento, California, the following year found their homocysteine was still high and that very few had low folate. Europe doesn’t require fortification of flour and breads.

Other studies have suggested that folic acid stimulates the growth of existing cancer cells. The data aren’t conclusive, so people at risk of cancer should avoid extra folic acid, Lokk said. This could include men older than 70 who may have undetected prostate cancer, A. David Smith said.

“We’re not suggesting everyone over 60 take this; we’re suggesting it should be targeted to people over 70 with high homocysteine and memory problems,” he said.

Too Early

It’s too early to put everyone on B vitamins, said Jess Smith of the Alzheimer’s Society.

“The evidence for supplementing is just not there yet,” she said. “We need bigger studies and more evidence that looks at what homocysteine is doing and what is actually going on in the brain.”

A. David Smith agrees. He plans a study of B vitamins in 1,200 people over 70 with MCI and elevated homocysteine. He needs 6 million pounds ($9.1 million) to pay for it. Miller plans another large study and wants to see if folic acid in flour in the U.S. leads to different results there. Meanwhile, the lack of blockbuster-drug potential presents funding hurdles.

“The pharmaceutical companies aren’t going to make any money on this and the supplement companies aren’t going to have enough money to do it,” Miller said. “This would have to be government-funded. I’m just not sure the climate is right for it now.”