SWSLHD and Bowral's Health - 61

Sperm damage possible via Wi-Fi

2nd Dec 2011

Catherine Hanrahan   all articles by this author

Medical Observer

Radiation from the laptop connected to Wi-Fi was three times higher than without Wi-Fi, and at least seven times higher than control conditions.

USING a laptop connected to the internet via Wi-Fi could be decreasing men’s fertility by affecting their sperm quality, a new study suggests.

Researchers conducted a simple experiment comparing sperm samples from 29 healthy donors left under a Wi-Fi connected laptop computer for four hours with sperm samples kept away from any electronic device.

They found that progressive sperm motility was 80% in the control sperm compared with only 69% in the sperm sample exposed to the Wi-Fi laptop.

The drop in motile sperm corresponded to an increase in non-motile sperm of around 25% in the sperm exposed to the laptop, compared to 14% in the control sperm.

Similarly, more than twice the number of sperm, 8.6%, had fragmented DNA in the sample exposed to the laptop compared with only 3.3% of control sperm.

“Our findings suggest that prolonged use of portable computers sitting on the lap of a male user may decrease sperm fertility potential,” the authors from Argentina said.

Radiation from the laptop connected to Wi-Fi was three times higher than without Wi-Fi, and at least seven times higher than control conditions.

The authors speculated that the detrimental effect on sperm quality was due to radiofrequency electromagnetic waves, not a thermal effect, because temperature was controlled during the experiment.

Fertil Steril 2011; online 23 Nov

Tags: Wi-Fi, laptop, sperm, radiofrequency electromagnetic waves, fertility

COMMENTS: 

Bite-my-Lip
2nd Dec 2011
2:56pm

Most rubbish study I've read. What the papers values 0.6?

 

loomingstorm
2nd Dec 2011
5:58pm

Typical tiny under-powered sensationalised melodrama-type study. Inappropriate conclusions drawn from data with innumerable confounders that were simply ignored so that the punch line could be published. Yet another annoyingly unprofessional publicity stunt!!

 

Gina
3rd Dec 2011
10:02am

I knew I should have bought a bigger laptop
Harvey here I come

SWSLHD and Bowral's Health - 58

Many over-40s living with undiagnosed AF time bomb

28th Nov 2011

Catherine Hanrahan   all articles by this author

AT LEAST 50,000 Australians aged 40 years or more may have atrial fibrillation without knowing it

AT LEAST 50,000 Australians aged 40 years or more may have atrial fibrillation (AF) without knowing it, new data suggest.

The incidence of undiagnosed AF in the community could be as high as one in 200 in this age group, the annual scientific meeting of the Australasian College for Emergency Medicine was told in Sydney last week.

With Australian Bureau of Statistics data showing more than 10 million Australians are aged 40 or older, around 50,000 may have AF based on this estimate.

Professor Ben Freedman, professor of cardiology at Concord Hospital and deputy dean of the Sydney Medical School, told the meeting his study of more than 1000 pre-admission ECGs in over-40s patients showed 3.1% were in AF.

Of those, 0.5% were cases of incidental, unrecognised AF not associated with symptoms or elevated resting heart rate.

“This means there’s a lot of people out there who have AF who don’t know about it,” Professor Freedman told MO.

Asymptomatic AF episodes were more common than symptomatic episodes, and silent AF led to stroke.

“The first time many stroke patients knew they had AF was when they presented with stroke, and stroke is a very poor warning symptom of AF,” he said.

The study showed only half of the patients with known AF and a CHADS2 score of two or more were taking warfarin.

The CHADS2 score is calculated using history of congestive heart failure, hypertension, diabetes, stroke symptoms and age.

Professor Freedman said doctors were not anticoagulating on the basis of stroke risk, and an appreciable asymptomatic group may benefit from recognition and thromboprophylaxis to reduce future stroke.

“I think there’s been an increase in the last 2–3 years in the use of risk calculators, and it’s partly because of the realisation that there are other drugs now that could be used for anticoagulation,” Professor Freedman said.

“But there still is an evidence practice gap, and I think we still need to close it if we are serious about preventing stroke.”

The new anticoagulants may assist in closing this gap, he said.

 
Tags: atrial fibrillation, stroke, undiagnosed, asymptomatic, CHADS2

SWSLHD and Bowral's Health - 48

A meaty question when it comes to mental health

24th Oct 2011 Catherine Hanrahan   all articles by this author

Medical Observer

PEOPLE who don’t eat much red meat may be susceptible to mental disorders such as depression, but eating too much red meat has a similar effect, research shows.

Researchers from Deakin University showed that among 1000 randomly selected women, those who ate both less, and more, red meat than recommended by Australian dietary guidelines, were twice as likely to have major depression or dysthymia.

The results, presented at last week’s conference, remained significant after adjusting for overall healthy diet.

Similarly, women who ate less than the recommended amount of red meat were 15 times more likely to have bipolar disorder, and those eating more were eight times more likely to have bipolar disorder.

Women who ate less red meat were also nearly twice as likely to have an anxiety disorder.

Lead author Dr Felice Jacka, NHMRC research fellow at the Barwon Psychiatric Research Unit at Geelong Hospital and Deakin University, said recognition of the role diet played in mental health was low.

“It’s certainly not part of any clinical guidelines or recommended clinical practice at this point but we think it should be based on the clinical consistency of the evidence,” she said.

Comments:

Docmus
26th Oct 2011
8:31pm

Interesting observation but you have to wonder about the reliability of the study. Is 1000 women enough to conclude anything when the number of actual bipolar cases will be pretty small? How can the women be randomly selected when a substantial number will surely decline to take part in long quizzes about diet and mental health history? The confounding variables in this study would be almost insurmountable.

 

FeliceN
26th Oct 2011
8:56pm

Hi Docmus
I wish to clarify - unfortunately my quote on this study was taken out of context. We have previously published both cross-sectional and prospective studies of the link between diet quality and mental health, and this is what I referred to as clinical consistency of the evidence (ie. regarding diet quality, not red meat). This particular report on red meat (whilst assessing confounding by other factors) did have very small numbers of BD cases and I have urged caution in over-interpreting our findings. They are very preliminary and need to be replicated before any recommendations can be made.

SWSLHD and Bowral's Health - 31

Doubt over effectiveness of domestic violence training

14th Oct 2011 Catherine Hanrahan   all articles by this author

TRAINING GPs to identify women experiencing domestic violence dramatically increases referral to specialist services, a new study shows, but experts question whether it actually benefits the victims.

In the UK study, 24 general practice teams were given prompts in their medical record software to ask women about abuse, and training sessions were delivered by domestic violence experts who also acted as the advocate for referral.

The research showed that practices trained to identify cases of domestic abuse referred 223 women to advocacy over a 12-month period, compared with only 12 referrals from practices not given the intervention.

Similarly, practices in the intervention group recorded three times more cases of domestic violence than the control group.

“We showed… clinician behaviour with regards to domestic violence – a major public health and healthcare issue that has largely been ignored in clinical practice – can be changed,” the authors said.

Associate Professor Kelsey Hegarty, who leads the University of Melbourne’s abuse and violence research program in the Department of General Practice, said in an editorial published with the study that it showed the intensiveness required to change clinicians’ behaviour.

“However, the clinical significance is unknown and therefore it is difficult to be sure whether this intervention, if replicated, will improve abused women’s health and wellbeing,” the editorial said.

The Lancet 2011; online 13 Oct

Tags: domestic violence, general practice teams, advocacy

   

Comments:

Mia
14th Oct 2011
4:59pm

When a system of management fails to work optimally at times there is a confounding variable.
It has been traditional to categorise domestic violence management under the notion of assailant and assailee.
After decades of working as a GP I tend to see the phenomenon as a dyadic or co-dependent one: That both parties have difficutlies in negotiating differences in a win-win style. Commonly one utilises their physical powers, the other chronic low grade passive aggression which causes the other to snap using the only skill that they know.
Could it be that we need to redefine the concept of domestic violence.

SWSLHN and Bowral's Health - 7

NSAIDs may block antidepressants

2nd May 2011 - Medical Observer

 
Catherine Hanrahan   all articles by this author

COMMON anti-inflammatory drugs may antagonise the effects of antidepressants, scientists have found.

US researchers analysed the effects of ibuprofen and other NSAIDs on citalopram in an animal model of depression and in a human population.

They showed that in 1500 patients with depression who took citalopram over a 12-week period, 55% of those who had taken an NSAID at least once were treatment-resistant to citalopram, compared with 45% who had not taken an NSAID.

The clinical data was supported in a mouse model, where all the NSAIDs and analgesics tested blocked the antidepressant effect of citalopram.

In vitro studies showed the anti-inflammatories antagonised p11, a biochemical marker for depression. This protein was regulated by frontal cortical levels of the cytokines tumour necrosis factor alpha and interferon gamma, which were also abolished by ibuprofen.

Clinical pharmacologist Professor  Ric Day, from St Vincent’s Hospital and the University of NSW, said the findings may explain why a large proportion of patients are resistant to antidepressants.

However, Professor Ian Hickie, executive director of the Brain and Mind Research Institute, University of Sydney, said the results were contrary to other cytokine hypothesis studies. “Most people have tended to think the opposite – that cytokines appear to be increased in some people with depression and might be driving… things like sleep disturbance, changed body temperature and lack of energy,” he said.

The clinical data could be confounded if taking NSAIDs indicated medical conditions which made patients less likely to respond to standard treatments, he added.

PNAS 2011, online first

Comments:

ondocfarm
2nd May 2011
1:49pm

At the Sydney 11th IASP World Congress on Pain (2005) it was shown that NSAIDS interfere at the midbrain ( RVN & PAG level) level with the opioids and can stop them working. Reference: Workshop 394 Page 154 Abstracts. Christopher Vaughan Uni of Sydney Royal North Shore........ So people on higher doses of opioids should never be given doses of NSAIDS concurrently. I have had a few whose pain levels exploded when given NSAIDS by an unwary doctor!

SSWAHS = SWSLHN and mental health in the Southern Highlands - 9

Brain volume declines with antipsychotic use

15th Feb 2011

Catherine Hanrahan all articles by this author

THE largest and longest study linking the use of antipsychotics to the loss of brain volume has Australian experts divided over the impact of early treatment initiation.

The Iowa Longitudinal Study found the use of antipsychotics was correlated with smaller brain volume after controlling for illness severity, duration of follow-up and substance misuse.

The prospective study, which followed 211 patients with schizophrenia for a median seven years, found higher doses of antipsychotics were associated with smaller brain volume on MRI.

Professor Louise Newman, developmental psychiatrist at Monash University, said the study should flag the need for caution when initiating antipsychotics.

“It suggests very careful consideration of antipsychotic use before we have clearly established symptoms [in individuals],” she said.

The publication of the Iowa study coincides with a British Journal of Psychiatry editorial by Dr Joanna Moncrieff, co-chair of the UK’s Critical Psychiatry Network. She cites mounting evidence that antipsychotics are linked to brain volume reduction, suggesting early use in young people is not justified.

But Professor Patrick McGorry, executive director of Australia’s Orygen Youth Health, said there was no consensus on the clinical significance of brain volume changes. “It would be very destructive to say that just because the brain issue is not clear, young people shouldn’t get any help,” he said.

Professor David Le Couteur, president of the Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, said the relevant clinical outcome was long-term cognitive effects.

“[Let’s] see whether these changes in brain volume, which are just a surrogate marker, in fact pan out to have an impact clinically,” he said.

Arch Gen Psychiatry 2011; 68:128-37; B J Psychiatry 2011; 198:85-87

Comments:

big bug
15th Feb 2011
7:06pm

Brain shrinkage in drug-treated psychotic patients (both scz and bipolar) is in no way caused by the genes (which are only for mild schizotypy and benign hypomania). The most likely cause is persistently fatty diet--especially chocolate and cheese--often aggravated by co-morbid anxiety (cortisol alone can shrink the hippocampus, given time). The anxiety--about half of this population--comes from fatty maternal diet, in pregnancy, which also promotes gestational diabetes (which, alone, raises scz risk for offspring SEVEN FOLD). Fatty personal diet, which causes the typical insulin resistance in scz, seems to precipitate acute psychotic episodes, by causing brain inflammation--as in depression. The problem with antipsychotic drugs is that they can increase appetite--for fatty foods already on the menu. The result will be weight gain, diabetes, vascular risk, treatment resistance and a shortened lifespan. Drug-based psychiatry has a poor future. Drug-free management of first-episode psychosis at Soteria House in California led to more patients being employable, after 12 months, compared with hospital-treated cases. To convert scz back to the pure, harmless schizotypy phenotype, use a strict low-fat diet, and for co-morbid anxiety use Inositol supplement 5 gm/day. Using this regimen, I now have 5 formerly scz patients showing obvious improvements in cognition and insight, whose drug doses may now be reduced safely, and even stopped.

Amateur Observer
20th Feb 2011
2:47pm

"Big bug" having just searched the medical literature, I can find no randomized controlled trial of low-fat diet as a treatment. There are also several studies suggesting NO benefit of inositol in chronic schizophrenia. Can you confirm that you practice evidence-based medicine?

sceptical
17th Feb 2011
12:24pm

With all due respect to those who are attempting to treat young schizos, bi-polars, uni-polars, anxiety, we have not been told about the social habits of these unfortunate young people. Perhaps recreational substances use, including alcohol from the legal age of 18 (binge-drinking excluded), are the cause of many falling prey to these mental health disorders?

Amateur Observer
20th Feb 2011
2:52pm

Agree - with almost 100% of schizophrenics being cigarette smokers one would have to be suspicious of nicotine having a role in the pathogenesis (in susceptible individuals).

Richard Cranium
21st Feb 2011
3:48pm

I appreciate your viewpoint Big bug. To Amateur Observer, who would fund a randomized controlled trial of a low fat diet anyway? Who funded the several studies suggesting NO benefit of inositol in chronic schizophrenia? I know on the two occasions I have commented on your comments I have asked you to answer questions but I don't get how someone who is seemingly scientifically minded doesn't ask them also.

It is up to each and every scientist (and I'm not but I am definitely interested) to ask the questions: "Says who and why do they say it?" I'm sure those who take the time to look in to it will find out that there are a number of ways to skin a cat and that some are more humane than others so even if it takes longer and costs more, it's better!

Richard Cranium
21st Feb 2011
3:58pm

I appologise Amateur Observer, it was not your comment I commented on last time, it was a comment made by "Another amateur observer", honest mistake.

big bug
21st Feb 2011
7:53pm

To Amateur Observer: Science, said Charles Darwin, consists in grouping facts, so that general laws and conclusions may be drawn from them. Medicine, with no intellectual appetite for nutritional and epidemiological facts, can do no grouping, so cannot explain or prevent disease, but manages to eke out a living on a meagre diet of Random-allocation Controlled Trials. If you want an RCT of healthy (probably low-fat) diet in scz, check Sherryn Evans, 2005 ("evans s and schizophrenia" on PubMed). Her intensive diet group (in Melbourne!) gained only 2 kg in 6 months on Zyprexa, and reported better energy and mental contentment than the control group given minimal diet advice, who gained 9 kg. We know that fatty diet causes diabetes (H Himsworth, CLIN SCI, 1936: The Diet Of Diabetics Prior To The Onset Of The Disease); that glucose intolerance is common in scz (first reported in 1924); and that scz cases do eat fatty diets (several reports), and often develop diabetes. Malcolm Peet, in the UK, claims to have observed worse scz symptoms when the diet is low in polyunsaturated fatty acids, which agrees with studies showing that sat fats impair cognition, reduce dendritic branching, lower BDNF levels in hippocampus, and cause brain inflammation.
As for Inositol, 2 studies in Israel showed no improvement in ANERGIC (deficit cases--untreatable?) scz cases, given Inositol for only 4 weeks, so longer trials are a must, in more typical cases. Inositol has two potential uses in scz: to treat co-morbid anxiety (up to 65% of cases); and to provide specific anti-ageing benefits (J Barger, 2008) for brain, already shown in caloric restriction animal models--increased neurotrophins like BDNF (to enhance synapse formation and plasticity), increased antioxidant enzymes, enhanced neuronal energy (got to be good!), and increased autophagy and replacement of oxidation-damaged mitochondria. NHMRC-funded low fat diet trials are planned for depression and bipolar in Geelong (Prof M Berk), and clearly should be extended to scz as well.

Amateur Observer
25th Feb 2011
5:28pm

I believe the assertion that "Medicine ... no intellectual appetite for nutritional and epidemiological facts ..." is completely false. And respectfully, the criticism of "medicine managing to eke out a living on RCTs" won't earn you much support here in a GP website!

Surprisingly you didn't even mention the one herbal therapy which has good evidence in reducing actual schizophrenia symptoms (ginseng), but strung together a hodge podge of nearly-related studies not supporting your original view. Regarding glucose-intolerance, this is also an unfortunate, but well-known side effects of common anti-schizophrenia medications (eg Olanzepine) thus the obvious "chicken or the egg?" question.

SSWAHS = SWSLHN and mental health in the Southern Highlands - 6

Better Access debate rages

21st Feb 2011

Catherine Hanrahan all articles by this author

2 comments

CONTROVERSY continues to dog the Better Access mental health program, with two new studies reporting conflicting results about equity of access for disadvantaged people.

University of Newcastle researchers found between 88% and 99% of a sample of 15,000 women reporting a mental health condition had not used MBS mental health items, including those from the Better Access program.

The study, linking data from the Australian Longitudinal Study on Women’s Health (ALSWH) with Medicare records, found those who did not use the MBS items, despite having mental health conditions, were more socioeconomically disadvantaged than those accessing the services.

The findings conflicted with data published in the British Journal of Psychiatry by researchers from the Universities of Queensland, NSW and Melbourne.

They used data from more than 8000 respondents from the 2007 National Survey of Mental Health and Wellbeing.

To assess Better Access use, they determined who had seen a mental health professional, paid partly or fully by Medicare, and whether or not they had a disorder.

Among the 1521 respondents who had a mental health disorder, they found there was no difference in socioeconomic disadvantage between those who used Better Access psychological services, other mental health services or no services.

However, in general agreement with the ALSWH study, the BJP study did show that 92% of respondents with a mental health disorder did not use Better Access mental health services.

Professor Ian Hickie, executive director of Sydney’s Brain and Mind Institute, said the women’s health study data showed the Better Access program had the same issues as specialist mental health systems.

“It’s really driven by those who already have the greatest access getting more access and many of those who need, missing out,” he said.

Dr Caroline Johnson, mental health spokesperson for the RACGP, said neither survey was designed specifically to assess the Better Access program.

“We need to know more about the population who report mental health concerns but are not accessing care,” she said. “[And] what we don’t know is whether being in the scheme makes more of a difference than usual care.”

Meredith Harris, lead author of the BJP study, said it controlled clinical factors in the socioeconomic analysis, whereas the women’s health study did not.

Sebastian Rosenberg, senior lecturer at Sydney’s Brain and Mind Research Institute, said that unlike the women’s health study, the BJP study didn’t use Medicare data.

“When it’s Medicare data and it’s public information, then it’s possible to recreate and confirm,” he said.

BJ Psych 2011; 198:99-08

MJA 2011; 194:175-79

Comments:

Bibiana

22nd Feb 2011
9:59am

Just wonder is there any study which examines the 'stigma' associated with accessing mental health services? Since the 'beyondblue' - the National initiative to combat depression first established in 2000, de-stigmatization of clinical depression in mainstream Australia has been very successful. However, I was recently told by an Australian-born Chinese wanting to see a psychologist through the Better Mental Health Access Program that her GP asked her to think carefully whether she really wanted to do so. The reason being it will be entered in her Medicare record that she is a person needing mental health service.
I then shared my personal experience with her about the benefit of seeing a psychologist. However, I also told her that if she was really concerned, she could self-refer and pay the fees out of her own pocket. As a mental health researcher for nearly 10 years, I am very aware of the stigma of mental illness perceived by people from Culturally and Linguistically Diverse communities. This is another aspect of access issues not picked up by the mainstream radar.

wenz
23rd Feb 2011
5:10pm

It is quite clear to myself that the better educated and probably, financially better off patient is able to access psychology care. For a lot of disadvantaged patients, a 20 to 40 dollar copayment per visit to a psychologist is beyond their means - and there are very few bulk billers available. I understand that a small co payment might weed out the client with less commitment - but it also weeds out the sort of patients that require our assistance.