Monthly Archives: March 2016

The Protective Effect of Peanut, Walnut, and Almond Consumption on the Development of Breast Cancer

The Protective Effect of Peanut, Walnut, and Almond Consumption on the Development of Breast Cancer. – PubMed – NCBI// // // //

Gynecol Obstet Invest. 2015;80(2):89-92. doi: 10.1159/000369997. Epub 2015 Jul 10.

The Protective Effect of Peanut, Walnut, and Almond Consumption on the Development of Breast Cancer.

Author information

  • 1Instituto Estatal de Cancerologia, Servicios de Salud del Estado de Colima, University of Colima, Colima, Mexico.



Breast cancer is the most common gynecologic malignancy known worldwide. The consumption of certain foods may modify the risk for its development. Peanuts and other seeds have shown anticarcinogenic effects in vitro, but there are a few studies that evaluate the effect of their consumption on the development of breast cancer. The aim of the present study was to determine whether there is an association between the consumption of peanuts, walnuts, and almonds and the development of breast cancer.


We analyzed 97 patients presenting with breast cancer and 104 control subjects that did not have the pathology (BIRADS 1-2). An analysis of the main clinical characteristics and lifelong seed consumption was carried out. The association between the consumption of these foods and the risk for breast cancer was estimated by odds ratios and 95% confidence intervals, controlling other risk factors, using the Mantel-Haenszel analysis.


The high consumption of peanuts, walnuts, or almonds significantly reduced the risk for breast cancer by 2-3 times. This protective effect was not found with low or moderate seed consumption when compared with null consumption.


High consumption of peanuts, walnuts, and almonds appears to be a protective factor for the development of breast cancer. © 2015 S. Karger AG, Basel.

Common drugs can affect our minds and morals – but should we be worried about it?

Common drugs can affect our minds and morals – but should we be worried about it?

July 16, 2015 2.26pm AEST

Some welcome the possibility of drugs altering our brain for the better, others are concerned about altering our brains at all. Andrew Adermark/Flickr, CC BY

Some people welcome this prospect, while others fear it. Critics worry it threatens our sense of self, our authenticity, and that it might lead to a neglect of our proper attitude to nature and alter society in unexpected and unwelcome ways.

Most people would agree that, at the very least, we need to go slowly and cautiously here, ensuring that new technologies are not rolled out for general use until we have properly assessed their risks and benefits; established appropriate regulatory regimes; and thought through their ethical implications. But what if these technologies are already widely used, unbeknownst to those who use them?

Silent enhancers

This prospect is raised by a recent finding by researchers at University College London that normal people who take drugs commonly prescribed for the treatment of disease and dysfunction (Parkinson’s and depression) have their moral cognition altered – in a more selfish and a less selfish direction, respectively.

Whether either counts as moral enhancement is a very difficult question, most centrally because how selfish we should be remains contested. But that doesn’t seem to matter here: opposition to moral enhancement, and the counsel that we should proceed cautiously, depends more on worries about altering ourselves than on whether we’re actually altering ourselves for the better.

The study authors caution that we cannot conclude from the finding – that healthy people have their moral cognition modified by common pharmaceuticals – that sufferers from depression or from Parkinson’s are also subject to such modification.

The antidepressant used in the study (citalopram) seems to alleviate depression by changing the level of serotonin, a neurotransmitter, in the brain. Similarly, the Parkinson’s drug tested alters the level of dopamine. People who are properly prescribed these drugs have different baseline levels of these neurotransmitters to healthy controls.

As the study’s lead author Molly Crockett points out, this may mean the drugs have different effects on patients than on controls. In fact, the pharmaceuticals may be restoring patients’ former capacity for moral cognition. Or it may have no effect on their moral cognition at all; we cannot extrapolate from acute effects like these to long-term effects, given that brains are designed to adapt to persistent changes.

What our level of selfishness should be remains contested. angel and devil on blackboard, from

Still, we have at least a prima facie reason to test to see whether the drugs are having an effect on patients. What’s more, the antidepressant that Crockett and her colleagues tested is prescribed for a number of conditions besides depression and, in some of them, baseline serotonin levels are probably in the normal range.

Even more medicines

It’s not just these two drugs that affect moral cognition. In a recent paper that I published together with some Oxford University colleagues, we surveyed evidence that other drugs alter how people respond to moral dilemmas.

At least one of these medicines, Propranolol, is sometimes prescribed for hypertension (it used to be very widely prescribed). Propranolol affects normal people’s memories, making them less likely to identify an item that was previously shown to them. There are circumstances in which this could matter a lot – in a court of law, for instance.

Other drugs appear to make people more trusting. Whether this is a good or bad thing would depend on context: in some contexts, trust is a moral good that allows us to achieve shared ends (so-called “prisoner’s dilemmas” are one example). In other contexts, being trusting might leave people open to being exploited.

The drugs we surveyed have had their effects on cognition studied. Given that other medicines prescribed for physical conditions may also affect how we think (because the compounds that act as neurotransmitters also sometimes regulate bodily functions), there may be many more.

Just another unknown

So we may already be morally modified, and the time to ask ourselves whether we should change our cognition by taking medication has long passed. But it’s still important that we come to understand how we’re altering ourselves, to assess whether we ought to continue to do so. We need to understand the costs and benefits of these alterations.

There’s no reason to panic; the effects of pharmaceuticals on moral cognition are likely to be subtle and it takes sophisticated statistical analysis to uncover them. But that doesn’t mean there’s reason for complacency, either: a subtle effect at the level of individuals may make a dramatic difference at the level of a population, if enough people are taking the same compound.

And suppose we discover that we are morally modifying ourselves, should we worry? I think that depends on what the effects are. If they are generally beneficial (or, more realistically, more beneficial than costly: in a messy world, nothing comes without costs), then we should relax.

It’s worth bearing in mind that the differences between us are the product of physical forces – genes and various environmental influences – that we do not fully understand, and over which we exercise relatively little control. Moral modification by pharmaceuticals doesn’t look all that different from the kinds of influences that make us who we are.

Important Health Research Points to LDN Use

Important Health Research Points to LDN Use‬

Here is the citation for a very significant research study which was published just last month in one of the top US medical journals: Stable Peptide of the Endogenous Opioid Enkephalin Precursor and Breast Cancer Risk. By Olle Melander, MD, et al. Journal of Clinical Oncology; 2015 Aug 20;33(24):2632-8.‬ ‪ ‬

‪Olle Melander, MD, and colleagues, from Lund University in Malmo, Sweden, sought an answer to the question of whether enkephalins (opioids made in the body) had any protective effect on the development of breast cancer. In two large studies, enkephalins were measured in fasting plasma samples ‪in thousands of women. The convincing answer was a resounding “YES!”. The lower one’s enkephalins, the higher one’s risk of developing breast cancer! The results were published recently in the oncologists’ “bible”, the Journal of Clinical Oncology.‬ ‪

‪From our viewpoint, to say more enkephalin (or endorphins) is also to say “read here: LDN!” And that is because those who take LDN are surely doubling or tripling their levels of those opioids. So, this wonderful Swedish study reassures us: regular use of LDN has now been shown to be a reliable preventive against cancer—and there is no reason to think this applies solely to breast cancer. We can only continue to hope that clinical trials utilizing LDN for the prevention of cancers of any sort will eventually see the light of day.‬

An Eloquent Video, A Must See — April 2015

Norwegian, with English subtitles

At long last, a most professional, most persuasive video concerning LDN!

It was made in Norway in 2013, with English subtitles. Far from a sales pitch, it tries to tell an evenhanded story. Its sole omission, which one often finds in Europe, is the total disregard for the role of the late Bernard Bihari, M.D., who discovered the human uses of LDN in 1985. Other than that, it is nearly perfect and a joy to watch. It has led to an avalanche of LDN sales in that country (from a mere 300 users beforehand, it is now used by some 15,000 patients in Norway).

Please do not miss watching:

Enjoy it!

LDN for Multiple Sclerosis

I have been using more and more LDN (low dose naltrexone) over the last few years, with some amazing results. It works best for all forms of auto-immune diseases, but has helped in PTSD, restless legs, burning mouth/vagina syndrome, cancer, and sometimes in depression. Its main advantages are low cost and few side effects. Not everyone responds well, but most sufferers of these conditions do not have much to lose by trying it, especially in serious conditions like MS, Lupus, Cancer and Rheumatoid arthritis.

An LDN User Story: Wendy Lowe Shares Her Experience Using LDN for Multiple Sclerosis


Multiple sclerosis (MS) is a disease of nerve demyelination, in which the protective covers of nerve cells that provide insulation are damaged. The name of the disease refers to scars (sclerae—referred to these days as lesions or plaques) that often appear on the brain and spinal cord. This damage has the potential to disrupt the communication between the brain and the rest of the body, thereby causing dysfunction and damage. A wide variety of physical and/or mental impairments can result.

Between 2 and 2.5 million people are affected with multiple sclerosis globally. The disease usually begins between the ages of 20 and 50 and is twice as common in women as in men.[1] The cause of MS is not yet clear, and there is no known cure. Treatments try to prevent new “attacks” and improve symptoms/functioning after an attack. Medications used to treat MS have varying degrees of efficacy, but can have serious negative effects and be poorly tolerated. Many people with MS seek out alternative treatments for their disease.

Wendy LoweWendy Lowe, who lives in Sheffield, UK, offered to share her experience using LDN as a treatment for her multiple sclerosis.

How and when did your health difficulties start?

When I was 22, and in training as an Occupational Therapist, I went through episodes in which I would get lost, be confused, and have hallucinations. It was terrifying. My general practitioner (GP) laughed at my terrifying account, “You’re a student, aren’t you? Lay off the drugs!” I’m a Mormon. I don’t even drink alcohol, tea or coffee, let alone do drugs! I was furious. I continued having (what was later discovered to be) “partial complex” seizures that would cause me to wander about, kind of like sleep-walking. Later, my hometown GP sent me to a specialist in epilepsy who did an MRI; the scan revealed scarring in my brain and possible evidence of mini-strokes. He put me on carbamazepine, a standard seizure drug, and I experienced a brief respite from my seizures.

A few months later, I woke up with very disturbed vision: there were hundreds of black “floaters” (little black blobs) in my vision. I couldn’t read. My optician said in a grave voice, “You need to go straight to the Emergency Room. You may have detached your retina.” The staff at the hospital didn’t tell me the reason why I couldn’t see properly out of my eye. I was told that the hundreds of floaters might fade over time, turning into grey shadows I might be able to read through. They said there was nothing they could do for me. They covered my eye with a patch and I looked like a pirate!

When and how did you receive your diagnosis?

One day at work, I was having a student take notes for me because I was not able to hold onto a pen. The head of our Mental Health team (a psychiatrist) patiently watched me struggle through the conference, and then later told me to go home (via the hospital!). After having an MRI done, I was immediately diagnosed with multiple sclerosis. Was it a big horrible shock? No. I felt like shouting it from the rooftop! My frequent mystery illnesses finally had a name. I was relieved because I knew enough neurology to know that MS was the not the worst of the neurological conditions I had been tested for. It had taken 7 years to get a correct diagnosis.

What treatment did your health care team recommend?

Later that year after I had another relapse that landed me in the hospital for a week, my neurologist explained there were new drugs on the horizon for MS, but told me the best treatment she could prescribe for me at that moment was “to get pregnant”! My husband and I had been married for 8 years; I explained to him that we needed to get pregnant, and we did. That year, 2004, I had never felt so well in my whole life. We had a little girl, whom I breastfed for a year. I then decided to take the neurologist’s advice to start taking medicine. I had the full range of disease modifying drugs to choose from, but she strongly advised that since my MS was “aggressive” Rebif® (interferon beta-1a) would be my very best hope.

How did the recommended treatment protocol work for you?

I took Rebif® for 5 years but continued to relapse. My weight was at times dangerously low due to having vertigo/vomiting relapses. Additionally, in 2006, I developed optic neuritis in both eyes at the same time, and became totally blind. The doctors told me to expect the worst because my optic nerve had been so repeatedly damaged with each relapse and inflammatory exacerbation. Eventually, my vision started to return very, very slowly. My color vision was still weird, but I could see well enough to recognize people, which was a huge improvement.

I hated the every-other-day Rebif® injections. They hurt, bruised badly, and gave me very intense fake-flu symptoms. These years were full of every infection you could possibly imagine. I had lots of ear infections, chest infections, pneumonias, and even a C-Difficile (hospital superbug) infection. I had been taking the disease modifying drug Rebif® for 5 years and although I believe it had not made me any better, my disease was indeed “modified”: it had developed lots of other conditions to keep it company!

How did you find out about LDN and what did you think of it?

I’d known about LDN for about 3 years from a friend at the MS therapy center. However, being so deep in the “medical model” due to my profession, I considered the only adequate proof of medical benefit to be a double-blind clinical trial, repeatable and large-scale. Since LDN had no such research, and anecdotal claims didn’t really “touch” me, I could ignore it quite easily. Given my professional background, I have some sympathy for doctors who respond to reports of LDN efficacy by saying “it cannot possibly be true.” But, yes, it can be.

Were there other obstacles to choosing LDN as a treatment?

I was under the incorrect impression that one could not take LDN if one also needed to take opioid medications in the same day. I was taking heavy duty pain killers to get through the day and I was too scared to forgo them, so LDN had not seemed like an option. What I did not understand was that there are ways to use heavy pain killers and LDN by staggering the medications appropriately (consult your healthcare professional about this). The irony was, once I actually started taking LDN, my pain was so relieved that just ibuprofen and acetaminophen worked fine, and I haven’t needed the heavy duty stuff anymore.

What ultimately made you change your mind about trying LDN?

I was so ill from fake flu symptoms caused by the Rebif® that I was living my life around side effects. I was not going to do that while my sister was visiting in 2009- I wanted to spend time with her. So I decided to not take my Rebif® during her visit. I felt so much better. After being off it for a month, I decided to quit it totally. My little girl was starting school for the first time, and I thought: she’s got a new life starting, maybe this is my chance to start a new life too. I decided I had nothing to lose by trying LDN.

What were your doctors’ opinions about LDN?

I spoke to my neurologist about it, and she said that there are three types of drugs she would definitely not prescribe: “the mad, the bad, and the dangerous”. She said LDN was certainly not dangerous, and not bad (illegal or people making a lot of money off it), so that just left “mad” (crazy). I responded, “Well, so is MS, and so am I! So it will suit me well.” She made it clear she did not agree with my decision and claimed LDN was “just a placebo.” But I had heard what I needed to from her: it wasn’t dangerous. So I was going to go for it.

How much LDN do you take, and what changes in your condition have you experienced?

Although I now take 3.5mg of liquid LDN each night, I started with 2 mg. On Day 1, a miracle happened. Almost every night, I experienced severe arm and hand spasms. I would look like I’d had a stroke: my right arm would curl around as tightly possible and I’d wake with my right hand clawed into a spastic curl so tight I was unable to move it. I had to wear a splint on my arm so tight that it would frequently dislocate my shoulder. It was very painful. But after the first dose of LDN, none of that happened. I had a comfortable, mobile right arm and a basically functional right hand. My right hand was slightly swollen for about an hour, which was unusual, but I took one look at that arm and that hand– and I knew that this was definitely not just a placebo effect. From the first dose of LDN, my nightly arm spasms had gone.

Also that first morning, I opened my kitchen blinds and saw my garden fence for the first time in three years: my distance vision had improved overnight. My eyes were also not uncomfortable for the first time in longer than I can remember- years and years. They had hurt so much (a shock of pain through the back of my eyes) when I’d look left to right or up and down. But since that first day on LDN, I’ve had no pain. When my family and friends would ask me, “How are you, Wendy?” I would joke, “Things are looking up!” because for the first time in ages, looking up didn’t hurt. I still think it’s wonderful to have pain-free vision.

I also used to need round-the-clock medication to be comfortable, but upon starting LDN I was immediately able to begin reducing those medications. I have not experienced another day with the daily pain I used to have. Now, I have no pain and so much more energy. I have a more functional body that does what I expect it to do.

Did you experience any side effects from LDN, and if so, how did you manage them?

I had nightmares the first couple of weeks, and I kept thinking “Wow! Stephen King would be proud of that one!” But because I’d been through such horrible side effects and illnesses from other medications, it didn’t faze me. Having a silly dream from time to time is a really mild side effect. Also I find that if I take the LDN when I’m wide awake, I tend to stay awake until 4am. So I wait for myself to start yawning, and then I know I’m tired enough to take it, and go straight to bed. This way it doesn’t disturb my sleep.

What overarching message would you like to give about LDN?

I would encourage people to strongly consider taking it. You’ve got nothing to lose. Actually, you do have something to lose. LDN stopped my disease progression in its tracks. I wish I had started it sooner as I may have avoided a lot of the irreversible damage my disease caused during the years I was not taking it. I want people to be aware of this so it doesn’t happen to them. I even carry cards with information about LDN to give out. I tell people: just go and inform yourself. There is help, but you have to pursue it and be persistent.

I wish everyone the courage to do what’s best for you,
Wendy Lowe

More about Wendy:

Our little family consists of me, my super husband, our daughter, and our cat. We live on the edge of Sheffield, the fourth largest city in the UK. I “should be” housebound, I suppose, but I’m too nosy! I go outdoors and do things. I have lots of friends. I go to church. I’m quite happy really.

Sadly, due to my illness, I only managed an Occupational Therapy career for seven years. I loved my job so much- especially the creativity of finding solutions to challenges. When I developed MS, I learned to do this first-hand by treating myself as a patient. One day I couldn’t get my leg to move whilst walking home- it dragged as I attempted to walk. I wondered if a short circuit in the ‘walk’ program of my brain could be overcome by using a non-reflex, learned movement like skipping. It worked. I skipped home! Helping patients by finding solutions like this was a big part of what gave me joy from my work. I dreaded the idea of giving it up and it took me a long, long time to come to the conclusion that I wasn’t going back. But I’ve discovered that there is life beyond work. My life is okay. It’s good. There are a lot of other things I can do to be happy and be helpful to other people.

[1] Milo R, Kahana E. Multiple sclerosis: geoepidemiology, genetics and the environment. Autoimmun Rev. March 2010: 9 (5):A387–94

Recurrent thrush: how some women live with constant genital itching

Recurrent thrush: how some women live with constant genital itching
February 9, 2016 6.10am AEDT .

For about 5% of women, the symptoms of thrush recur or never really go away.  ..
Cathy Watson
Honorary Researcher, General Practice and Primary Health Care Academic Centre, University of Melbourne

Disclosure statement

Cathy Watson does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond the academic appointment above.
Imagine. You are on a two-week walking tour in Thailand and the unthinkable happens. An episode of vaginal thrush hits like a tsunami.

Every step is agonising and it’s hard to resist the urge to scratch your genitals incessantly. To make it worse, your tour guide is a male with limited English and there is no pharmacy within a day’s walk.

This is how Debra (not her real name) described her extreme experience to me at a consultation.

Debra’s may sound like an extraordinary circumstance, yet women with vaginal thrush can suffer extraordinarily, no matter where they are at the time.

Although most women will have experienced one or more episodes of uncomplicated thrush that results in temporary discomfort, some suffer from recurrent episodes. The persistent physical symptoms of these can be shameful and often debilitating.

Uncomplicated thrush

Uncomplicated thrush is common. About 75% cent of women will have vaginal thrush in their lifetime.

Thrush is caused by a fungal infection (Candida albicans) that lives in the vagina, often without causing symptoms. Why some women develop symptoms is unclear. When symptoms do occur, they include itching, burning and a “cottage cheese-like” discharge.

Vaginal thrush mostly occurs during a woman’s reproductive years. It is uncommon before her first menstrual cycle and after menopause (when periods cease), so hormones are likely implicated.

When symptoms of thrush occur, women may experience itching and burning in the genital area. from

Many have thrush at a particular time of the month, specifically before menstruation. It also often occurs following a course of antibiotics and is common in women with diabetes.

Medications are available without a prescription so many women treat themselves. Treatment consists of antifungal creams or vaginal tablets, which are put inside the vagina with a special applicator.

There is also the choice of oral tablets, which are more expensive and not recommended for pregnant women.

But it’s important that women see their doctor if these treatments don’t work or symptoms recur. This is because they may be suffering from an entirely different infection, which requires different treatment.

Although women can effectively be treated with medications available over the counter, there are about 5% for whom the symptoms recur or never go away.

Recurrent thrush

Recurrent thrush refers to four or more diagnosed episodes of vaginal thrush within 12 months. Because the four episodes have to be identified with a swab test, research into this area is difficult and costly.

Compared with research into uncomplicated thrush, the published studies for recurrent thrush are few and of poorer quality. No research so far has found a cure that works for all women.

Women with recurrent thrush always need to have their emergency supplies. from

This also means we don’t know exactly how long women may go on having experiences of recurrent thrush. Anecdotal evidence shows episodes can come and go for many years.

For people like Debra, who forgot to pack “emergency supplies” before her trip, recurrent thrush can cause relentless itching, constant pain and embarrassment.

Some women need to take time off work. Others find their self-esteem and confidence suffers when the condition flares up. Some women may find sexual intercourse extremely painful and others have attributed relationship difficulties or breakdown to the condition.

Many have reported frustration about seeing doctors who “fob them off”, advising them to take another course of anti-fungal treatment, or telling them that they just have to “put up with it”.

Recommended treatments

Some women benefit from long-term treatment, but relief remains elusive for others.

The only treatment of recurrent thrush supported by a large study is “suppression and maintenance” therapy. Symptoms are suppressed with a high dose of anti-fungal treatment followed by a maintenance dose (weekly or monthly) for up to six months to prevent remission.

Treatment is often inconsistent between practitioners. This perhaps reflects the lack of confidence in available guidelines, based on the above study.

In Australia, the Pharmaceutical Benefits Scheme (PBS) does not cover the recommended long-term treatment, making it unaffordable for many. If women use the vaginal creams or pessaries, the cost over a six-month period would be around A$600. Taking the oral treatment could set them back over A$900.

Some women are reluctant to take anti-fungal medications for long periods, as they can have some side-effects, including abdominal pain. Because of this and the expense, many turn to alternative therapies to combat thrush.

Alternative treatments

Although some women may find the folk remedy of yoghurt soothing, there is no strong evidence to support its use. Some recommend formulations such as aci-gel or vinegar to restore the normal pH of the vagina. But contrary to popular belief, the vaginal pH of women with thrush is usually normal.

There is no strong evidence to support the effectiveness of yoghurt for thrush. Matthew W.S. Christensen/Flickr, CC BY

Other natural treatments include tea tree oil and garlic. But using tea tree oil can lead to nasty allergic reactions, while garlic can burn.

Sometimes simple remedies such as ice packs applied to the area for up to ten minutes can bring relief. As alternative treatments, doctors usually recommend cotton underwear and avoiding feminine hygiene products, if possible.

Seeing a health professional who understands the complexities of this condition can be helpful, along with setting realistic expectations about management. Some hospitals have specialised vulval disorders clinics that women can attend with a doctor’s referral.

It is impossible to predict how long persistent thrush may last for individual women, but the good thing is most will respond to long-term therapy, and it will eventually ease.

A longer duration of estrogen deficiency increases fibrosis risk among postmenopausal women with nonalcoholic fatty liver disease.

I have shown the multiple benefits of oestrogen to women in the menopause, in my blogs over the last few years. They are too many to list here as the include nearly every part of the body. A search of “Oestrogen for women”  and Öestrogen benefits”on my web site will show them. Here is another interesting benefit- it looks to be of help to our livers (especially after a drink or two :))
Hepatology. 2016 Feb 26. doi: 10.1002/hep.28514. [Epub ahead of print]

A longer duration of estrogen deficiency increases fibrosis risk among postmenopausal women with nonalcoholic fatty liver disease.

Author information

  • 1Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR.
  • 2Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN.
  • 3Gastroenterology and Hepatology, Duke University, Durham, NC.
  • 4Dept. of Pathology, Duke University, Durham, NC.
  • 5Dept. of Pathology, University of California San Francisco, San Francisco, CA.
  • 6NASH CRN Data Coordinating Center, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
  • 7Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
  • 8Dept. of Pediatrics, Columbia University, New York, NY.
  • 9Division of General Internal Medicine, Johns Hopkins Bloomberg School of Public, Health, Baltimore, MD.
  • 10Gastroenterology, Central Arkansas Veterans Healthcare System, Little Rock, AR.
  • 11Gastroenterology and Hepatology, University of Arkansas for Medical Sciences, Little Rock, AR.


Post-menopausal women with nonalcoholic steatohepatitis (NASH) are at an increased risk of hepatic fibrosis when compared with premenopausal women. Whether duration of estrogen deficiency in postmenopausal state dictates individual’s fibrosis risk remains uninvestigated. We aimed to assess the associations of age at menopause and time from menopause with fibrosis severity in postmenopausal women with nonalcoholic fatty liver disease (NAFLD). Data from 488 post-menopausal women with 1) histologic diagnosis of NAFLD and 2) self-reported information on age at menopause were analyzed. The associations of premature menopause (age at menopause of <40 years) and time from menopause (age at study enrollment – age at menopause, years) with fibrosis severity (stage 0-4) were assessed using multiple ordinal logistic regression models with and without adjusting for clinical confounders. Among the participants (age at menopause: 43.7 ± 8.6 years), women with premature menopause (29.3%) were younger at enrollment (p<0.001) and used hormone replacement therapy (HRT) more often (p<0.003). After adjusting for age at enrollment, race, waist circumference standardized by body mass index, current smoking, current alcohol use, hypertension, diabetes/impaired fasting glucose, homeostatic model assessment of insulin resistance, and HRT, premature menopause was associated with an increased likelihood of having more severe fibrosis; adjusted cumulative odds ratio and 95% confidence interval (ACOR [95%CI]) was 1.9 [1.3-2.7], p=0.001, while time from menopause was directly associated with an increased likelihood of having more severe fibrosis (ACOR [95%CI] for 5-year unit=1.2 [1.1-1.3], p=0.002).


Duration of estrogen deficiency in postmenopausal state confers fibrosis risk among post-menopausal women with NAFLD. This article is protected by copyright. All rights reserved.

© 2016 by the American Association for the Study of Liver Diseases.


hepatic fibrosis; menopause; nonalcoholic fatty liver disease; nonalcoholic steatohepatitis; premature menopause

Stick to good science, so you can generate anecdotes like this..

Stick to good science, so you can generate anecdotes like this..

December 10, 2015 12.35pm AEDT

Paul suffered a workplace injury eight years ago that was pretty awful. He was trapped for some time under a large oxygen cylinder which had fallen on him. He escaped relatively uninjured apart from some bruising around his chest wall and an area of intense burning pain between his shoulder blades. Understandably, he was psychologically traumatised by the ordeal, not helped by being the object of a very public tirade of abuse which occurred a couple of weeks later when his soon-to-be-ex employer spotted Paul in the main street of the small town where they both lived.

Numerous interventional procedures, medication trials and hundreds of hours of psychology sessions later, Paul remained out of work and although he could get by passably well on a good day, the burning pain in the middle of his back persisted essentially unchanged. During this time, his family went through disclosures of sexual abuse, life-threatening illnesses and major financial hardship caused by Paul’s ongoing inability to find an employer willing to take on a late middle-aged man with a work-related bad back.

It was not only his prospective and former employers who discriminated against him. He was surveilled by private detectives on a number of occasions and accused in court of malingering. During the time he was on high-dose opioid patches, he was regularly accused by locum GPs of being a drug addict. His regular GP had known him before the accident and could see, as I did, that he was doing his best through some very difficult times. A few years ago, he stopped using medications and undertook an intensive CBT-based pain program which certainly helped him become a capable self-manager of his pain. The injections we had done were capable of giving him new complete relief for a few hours at a time due to the effect of the local anaesthetic. Our shared frustration was not being able to manufacture even a modest reduction in the intensity and unpleasantness of the pain to allow him to use his self-management skills to much better effect.

Having sat through some presentations about the new generation of neuromodulation devices (implantable electrical stimulators) at conferences, I raised the possibility of a trial with Paul a few months ago. We had previously discussed such things but Paul was worried about the invasive nature of the treatment, and I did not feel the evidence warranted much optimism for the sort of pain that he had.

Instead of simply aiming to scramble pain signals in the spinal cord like first-generation devices, modalities such as high-frequency and burst stimulation aim to feed misinformation into the nervous system to affect pain processing upstream in the brain. They are some of the first fruits of the blossoming of pain research in the last 20 years.

My colleague ushered me with a barely concealed smirk of satisfaction into his office where Paul stood like a man transformed. Gone was the haunted, hunted look I had become very familiar with. He had driven an hour and a half to the appointment and was barely in any discomfort. He reported knowing that his pain was still there but more like a dull ache than a savage howling in his head. For the last two weeks, he had been able to dial the stimulation up or down as the situation demanded, and for the first time in eight years he felt in control of his pain. He had energy, optimism and contentment I had not seen in him the whole eight years I have been his doctor.

Paul’s wife, who has stood by him with dignity and love through the ordeals and innumerable petty humiliations of those years simply thanked us quietly for giving her her husband back.

Unfortunately for Paul, his trial leads will come out today and he will need to go back to coping as best he can until the implantation is arranged. I dearly hope when he is implanted that he will go on to take his place among the legion of inconspicuous triumphs generated by good scientific medicine.

Smarter treatments, rigorously evaluated and then introduced sustainably into practice with care and compassion are what the medical profession does at its best. Although not at all cheap, the cost-effectiveness argument for these implantable devices is overwhelming. Getting a single taxpayer back in the workforce pays for the implant within a couple of years in saved costs, including future pension costs and extra superannuation savings. Even if you can’t get everyone economically productive, shouldn’t freedom from needless pain be a universal right?

The effect of new technology intelligently applied on the lives of those who live with pain and their families can be priceless.

Note : Paul is clearly not his real name, and his medical history is used with his permission

Testosterone and Alzheimer’s Disease

More evidence for the benefit of testosterone for the aging male. Note that testosterone has been shown to benefit women’s brain function and memory. ( search Testosterone and memory on my web-site for the references)

Testosterone-lowering therapy for prostate cancer may increase Alzheimer’s risk

Penn Medicine, 12/08/2015

Finding comes from a study of biomedical data from patient records by Penn Medicine and Stanford researchers. Men taking androgen deprivation therapy (ADT) for prostate cancer were almost twice as likely to be diagnosed with Alzheimer’s disease in the years that followed than those who didn’t undergo the therapy, an analysis of medical records from two large hospital systems by Penn Medicine and Stanford University researchers has shown. Men with the longest durations of ADT were even more likely to be diagnosed with Alzheimer’s disease. The findings, published in the December 7 issue of the Journal of Clinical Oncology, do not prove that ADT increases the risk of Alzheimer’s disease. But the authors say they clearly point to that possibility, and are consistent with other evidence that low levels of testosterone may weaken the aging brain’s resistance to Alzheimer’s.

Viruses don’t deserve their bad rap: they’re the unsung heroes you never see

Associate Professor, Griffith University

The word “virus” strikes terror into the hearts of most people. It conjures up images of influenza, HIV, Yellow Fever, or Ebola. Of course we worry about these viruses—they bring us disease and sometimes an excruciatingly painful death.

But the 21 viral types that wreak havoc with the human body represent an insignificant fraction of the 100 million viral types on earth. Most viruses are actually vital to our very existence. No-one seems to stick up for the good guys that keep ecosystems diverse and balanced (although I did recently in a TEDx talk in Noosa).

The sheer number of these good viruses is astonishing. Their concentration in a productive lake or river is often 100 million per millilitre – that’s more than four times the population of Australia squeezed into a ¼ of a teaspoon of water.

Globally the oceans contain 1030 viruses. If you lined them all up they would extend for 10 million light years, or 100 times the distance across our galaxy. Collectively they would weigh as much as 75 million blue whales.

In short, there are a lot.

What are viruses?

Viruses are not living organisms. They are simply bits of genetic material (DNA or RNA) covered in protein, that behave like parasites. They attach to their target cell (the host), inject their genetic material, and replicate themselves using the host cells’ metabolic pathways, as you can see in the figure below. Then the new viruses break out of the cell — the cell explodes (lyses), releasing hundreds of viruses.

The viral cycle Peter Pollard

Viruses are very picky about who they will infect. Each viral type has evolved to infect only one host species. Viruses that infect bacteria dominate our world. A virus that infects one species of bacteria won’t infect another bacterial species, and definitely can’t infect you. We have our own suite of a couple of dozen viral types that cause us disease and death.

A deadly dance

Algae and plants are primary producers, the foundation of the world’s ecosystems. Using sunlight they turn raw elements like carbon dioxide, nitrogen and phosphorus into organic matter. In turn, they are eaten by herbivores, which are in turn eaten by other animals, and so on. Energy and nutrients are passed on up the food chain until animals die. But what ensures that the primary producers get the raw elements they need to get started?

The answer hinges on the viruses’ relationship with bacteria.

A virus doesn’t go hunting for its prey. It relies on randomly encountering a host — it’s a numbers game. When the host, such as a bacterial cell, grows rapidly, that number increases. The more of a bacterial species there is, the more likely it will come into contact with its viral nemesis — “killing the winner”. This means that no single bacterial species dominates an ecosystem for very long.

In freshwater, for example, you see very high rates of bacterial growth. You would think this high bacterial production would become part of the food chain and end up as fish food. But that is rarely the case.

We now realise that the bacteria actually disappear from these ecosystems. So where do the bacteria go?

The answer lies in the interaction of the bacteria and viruses. When a virus bursts open a bacterial cell its “guts” are spewed back into the water along with all the new viruses. The cell contents then become food for the neighbouring bacteria, thereby stimulating their growth. These bacteria increase in numbers and upon coming into contact with their viral nemesis they, too, become infected and lyse.

Viruses make the world go ‘round

This process of viral infection, lysis, and nutrient release occurs over and over again. Bacteria are, in effect, cannibalising each other with the help of their associated viruses. Very quickly, the elements that support the food web are put back into circulation with the help of viruses, as you can see in the graphic below.

How nutrients are recycled. Peter Pollard

This interaction ensures inorganic nutrients are readily available to algae and plants on which ecosystems depend. It’s the combination of high bacterial growth and viral infection that keeps ecosystems functioning. This explains why we don’t see bacteria in food webs. Viruses short circuit bacterial production passing higher up the food chain so it doesn’t become fish food in freshwater ecosystems.

Most of the food (dissolved organic carbon) that drives the very high bacterial growth in freshwater comes from the terrestrial environment. Indeed, freshwater viral/bacterial interactions appear to be a critical link in carbon cycle between the land and atmosphere.

Soil viral ecology studies lag way behind water research. Viral dynamics in terrestrial ecosystems are complicated as soils can bind and inactivate viruses to limit their ability to infect other organisms. We may well be relying on freshwater processes to complete the global carbon cycle, as shown in the graphic above.

In freshwater, viruses are enhancing the rate of bacterial decomposition whereby complex organic matter is quickly and efficiently mineralised into their simple inorganic components such as carbon dioxide, nitrogen, and phosphorus.

Thus viruses are a critical part of inorganic nutrient recycling. So while they are tiny and seem insignificant, viruses actually play an essential global role in the recycling of nutrients through food webs. We are only just now beginning to appreciate the extent of their positive impact on our survival.

One thing is for sure, viruses are our smallest unsung heroes.