Monthly Archives: May 2013

Erectile dysfunction

May 30

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Daniel Pendick

A logical approach to treating erectile dysfunction

Posted November 27, 2012, 9:28 am

Windsock at half mast

Thanks to an aging population and a lot of direct-to-consumer advertising, many American men of a certain age know to ask about the “little blue pill” or similar medications if they develop erectile difficulties. But is an erectile dysfunction (ED) drug like sildenafil (Viagra) or its competitors always the best place to start? That’s an open question, especially among men with low levels of testosterone.

Testosterone first?

Before Viagra appeared on the scene in 1998 and transformed the treatment of erectile dysfunction, testosterone was an important medical therapy for it. Testosterone is central in the male sexual response, including the desire for sex and the mechanics of triggering an erection.

To be sure, getting more of this hormone isn’t a universal solution for ED. Some men with erectile problems have perfectly normal amounts of testosterone. Many doctors won’t consider prescribing testosterone unless certain other symptoms are also present, such as decreased desire for sex (libido) and fatigue. And boosting testosterone doesn’t always improve erections. But it is an option on the table for men with low testosterone.

“It’s well established that testosterone by itself, for men with sexual dysfunction that includes erectile dysfunction, can improve erections in the majority of men who take it,” says Dr. Abraham Morgentaler, an associate clinical professor of urology at Harvard-affiliated Beth Israel Deaconess Medical Center.

Dr. Morgentaler is also the founder and director of Men’s Health Boston, which treats many men with low testosterone. At the clinic, “our first choice for men who have low testosterone and erection problems is to give them testosterone and not sildenafil,” says Dr. Morgentaler, the author of Testosterone for Life. “Improved doesn’t always mean adequate, though, so, it is not unusual to add sildenafil or a similar medication if a man still is not satisfied with quality of his erection with testosterone therapy alone.”

One potential advantage to the “testosterone first” approach is that could make it unnecessary to take a pill in the anticipation of a sexual encounter. Also, men with low testosterone and symptoms may experience extra benefits of testosterone replacement, such as more “pep” and more desire for sex in the first place.

Call in the cavalry?

The current ED medications belong to a class of drugs known as PDE-5 inhibitors. They enhance blood flow to the spongy tissues in the penis, which creates an erection. Several competitors have since leapt into this lucrative market: tadalafil (Cialis), vardenafil (Levitra), and avanafil (Stendra).

Today, one of these drugs is usually the first treatment a primary care doctor recommends for erectile complaints—not testosterone. That’s because they tend to work more reliably than testosterone, and the response is usually quicker. But like testosterone, they don’t work for about 30% of men who try one.

Questionable combination

Men with ED who also test low for testosterone may be offered a hormone boost, frequently in the form of a rub-on gel applied daily, in addition to an ED drug. Does this make a difference? To find out, a team of researchers based at Boston University Medical School conducted a study involving 140 men with low testosterone. Half took Viagra and used a daily testosterone gel, while the other half took Viagra and used a placebo gel.

Adding testosterone to Viagra didn’t make a difference. Erections, desire for sex (libido), and sexual activity were the same in both groups.

“One of the central findings of the study is that sildenafil works extremely well,” says Dr. Matthew Spitzer, the lead author of the study, which was published in the Annals of Internal Medicine.

The researchers speculate that Viagra may supercharge the process that creates erections beyond the point at which testosterone could add anything more. In other words, for these men the Viagra worked so well that there was little room for improvement. “Once a guy has a good erection,” Dr. Morgentaler says, “how are you going to make him do better on testosterone?”

A logical approach

More and more, erectile dysfunction is being viewed as a systemic medical problem. In some studies, ED is like the canary in a coal mine for a future heart attack. That’s because ED is often due to atherosclerosis—the same artery-clogging process that usually precedes heart attacks and strokes. So it should be approached more systematically than just starting with an ED drug.

If a man notices he is having trouble getting or sustaining an erection, and other things in his life are relatively stable, then a conversation with a doctor is in order. A blood test for testosterone is a good next step. If the testosterone level is low, then trying testosterone replacement makes sense. If that doesn’t improve erections, then it’s time to try an ED drug.

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Good sleep demands a good mattress.

May 29

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How to Pick the Perfect Mattress

Sleep matters — so much so that six in 10 Americans crave sleep over sex. And the key to rest that’s good enough to forgo sex just might be the mattress: Nine in 10 respondents in a sleep survey cited their mattress as an important factor in getting that coveted good night’s rest. In 2010, Americans spent more than $5.8 billion on mattresses and box springs alone.

But is this expense justified? How important are mattresses, really? Read on for the low-down on how mattresses affect health and sleep quality.

Mattress Matters — The Need-to-Know

Perfect MattressPerfect Mattress

The first “mattresses” (read: piles of leaves, grass, or straw covered in animal skins) were invented by cave men and women. Thousands of years later, the Egyptian pharaohs discovered the luxury of raising the bedding off the ground (though common folk continued to sleep on piles of palm bows). Today, many Americans enjoy the luxury of mattress-induced sleep.

Even those who aren’t up on their mattress history know the value of a good night’s sleep. The average person spends about one third of her or his life sleeping. For those who sleep less than that, sleep deprivation can have serious health consequences, including a sour mood (what college student doesn’t know this to be truth), slower metabolism, and impaired immune function [1] [2] [3] [4] [5].

There are lots of great tips for coping with sleep deprivation, but what if the cause is right under our backs? Low-quality, uncomfortable mattresses have been linked to sleep discomfort and pain, and chronic pain can prevent quality sleep [6] [7].

Fortunately, it’s not all bad news. While mattresses can hinder sleep quality, they can also improve it. Improved “bedding systems” (a fancy way of saying “things you sleep on”) have been linked to decreased pain and discomfort, especially in women [8] [9]. Quality sleep on a good mattress may also help decrease stress [10].

The experts we spoke to said it basically comes down to personal preference. If we’re comfortable, we have a better chance of sleeping well, and if we sleep well, we’re more likely to stay healthy.

Better Bedding — Your Action Plan

When it comes to purchasing the perfect mattress, it turns out there are a lot of mixed messages out there. Some research suggests that foam mattresses create backaches; others say foam helps pain. Some studies advocate for regular cotton mattresses while others say coils create backaches and that airbeds are the way to go [11] [12]. There’s even controversy over the conventional thinking that a firm mattress is better for lower back pain [13] [14].

The reason for all this controversy is that sleep quality and comfort are so darn subjective [15]. When buying a mattress, the most important consideration is probably personal comfort. In fact, some people argue that if something else besides a mattress proves more comfortable to sleep on, we should go for it [16].

If you do find yourself in the market for a new mattress, there are still some useful tips to keep in mind. Follow these guidelines for a better shot at getting that elusive good night’s sleep.

  • Replace a mattress approximately every eight years. Keep it longer than that, and the materials might start to degrade, which might make the mattress less comfortable to sleep on. If you’re waking up in pain every day, sleeping poorly, or feeling disgruntled all the time, consider upgrading sooner [17].
  • Replace the box spring on a similar time frame. Over time, the compression of the springs (resulting from having a mattress and human bodies on top of it all the time) will start to change the structure of the spring box. Or avoid springy situations and just ditch the box spring altogether.
  • Make comfort your goal. Purchasing a mattress is all about finding the best one for you. Some people like a firm mattress; some like a soft one; others, like Goldilocks, prefer somewhere in between.
  • Try before you buy. Test “sleep” on a mattress for at least 20 minutes in a normal sleep position before making a decision.
  • Look for a mattress that fits your body. Chiropractors advocate finding a mattress that’s designed to conform to the spine’s natural curve and distribute pressure evenly across the body.  This can be tricky, because the surface curve on the mattress doesn’t necessarily represent the way your spine will curve while sleeping on it [18]. Everyone’s pressure points are different, so the best way to figure out if a mattress correctly supports the body is to bring a friend along to the store. Lie on the mattress in your normal sleeping position and ask your friend to observe whether the spine remains fairly neutral. If the spine is obviously sagging or curved exaggeratedly in any given direction, then keep searching for a mattress that helps maintain neutral spine alignment.
  • Avoid the sag. While researchers are challenging the idea that a firm mattress is essential for anyone with back pain, most experts still agree a saggy mattress isn’t the way to go [14]. To determine if a mattress has too much sag, perform the same “spine alignment observation” outlined above.
  • Don’t buy vintage. This ruIe’s especially important if you’re worried about your bed catching on fire. Only mattresses made after July 2007 must meet regulations for fire resistance.
  • Ignore brand names. Virtually all mattress coils are made by the same manufacturer. Likewise, don’t be duped by dollar signs: A higher price doesn’t necessarily mean better quality.
  • Bigger doesn’t necessarily mean better. Thickness is often just a visual ploy designed to get people to think they’re buying a comfier mattress. Listen to your body and find the bed that feels the most comfortable (not the one that just looks that way).
  • Beware of allergens. If you have allergies (particularly to dust mites, mold, and certain bacteria), read the mattress’ label to make sure that the materials don’t contain any sneaky allergens — or, better yet, look for a hypoallergenic mattress (natural latex and wool are both decent options) or a mattress cover. Worried about dust mites, bacteria, and fungi but don’t want to pay for an expensive mattress cover? Daily vacuuming might help [20].
  • Do not disturb… your partner. If you share a bed, look for a mattress that allows two people to adjust the firmness on their respective sides.
  • Give peace a chance. Even if you loved your new mattress in the store, you might not sleep better on it the first night you bring it home. It can take a couple of days to adjust to a new sleeping surface [15]. If the first night on a new mattress doesn’t transform your sleep quality, give it a few more nights before giving in to buyer’s remorse.
  • Look for a return policy. This way, you won’t be stuck with an expensive mattress that doesn’t provide the sleep of your dreams.

Thanks to Joyce Walsleben, David M. Rapoport, and Nicole Lehman for their help with this article.

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Oestrogen- Villain or Heroine?

May 29

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This is my 200th blog, so it is very special one. When I started out with this web site, I never expected it to grow the way it has. In choosing topics to print, I aim for a broad audience, and things of interest to most of us. I make them as factual as possible, and of benefit to you, the reader. Mostly they have a medical/hormonal/health aspect to the blogs. Feedback would be valuable as to the sort of articles you would like. Todays post is of an article I wrote for a medical publication recently. Hope you enjoy it.

Oestrogen- 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 reappraised 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-

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Special Alert – Watch SBS this PM re Obesity and Lapband surgery. .

May 28

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Is lapband surgery worse than obesity?

Kate Finlay is a guest on SBS's <i>Insight</i> program tonight (Tuesday, May 28), 8.30pm on SBS ONE.Kate Finlay is a guest on SBS’s Insight program tonight. Photo: SBS

After a life-long struggle with weight loss, I thought lapband surgery would be the solution. I was wrong.

I was only 12 years old when my parents decided I should join Weight Watchers because I was slightly chubby. The group at my local church actually applauded me the first week I lost weight. I now see the damage this did to my body image and consequent weight gain.

By the time I was 18, I was obese. I became the “funny fat girl”, the “lucky you have a good personality” girl. Perhaps people thought I had no feelings under the fat – that I “needed” to hear it. I tried starving myself and by 20 had tried to remove fat by cutting it off of my body with a sharp scalpel.

It wasn’t until I moved to London that I started to get fit and lose weight. I attended a wedding and was excited for my family to see the real me, happy, slimmer and mature. Instead I was taunted again – “you’ve managed to gain weight”.

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When I returned to Australia, I decided I didn’t want negativity in my life any more, but slipped into old habits. Within six months I was back up to a size 16-18.

Eventually I met a man who loved me for me, via the internet, so I was judged not on looks but on personality. When our first baby was born, I had ballooned to over 100 kilos. I struggled to lose baby weight and just lived with it. After my second child was born I suffered post-natal depression and put weight on. I was told by a neighbour that I was too fat and my kids would be bullied if I didn’t lose weight. I exploded to a size 28-30. I hated myself, but had made up my mind that I was never going to lose weight, I would always be fat.

I begged my GP to get a lapband surgeon, or I would kill myself – I was better off dead. Within two weeks I was booked in and we had whacked $12,000 on the mortgage. I was given a list of complications during and after lapband surgery but I had no fear. This was going to save my life.

Kate: on drastic ways to lose weight:

In eight months, I lost 52 kilos but had to get my gall bladder removed. According to my surgeon, this was a side-effect of fast weight loss. I rolled with it. Two days after giving birth to our third child I had liver failure. This was another new side-effect of my lapband – I was not receiving all the nutrients I needed to sustain my body or my baby.

Over the next year I went days without food, weeks without using the toilet. But on the upside I was getting skinny and I had a dream – I wanted to buy clothes from a mainstream clothing store. However, the loose skin that hung on my stomach and arms were another side-effect.

Having 15 kilos of skin removed was the most intensely painful experience. The wound split open on my back and refused to heal. I was now eating less than three times a week. I was very sick, but skinny – a svelte size 12. In December I bought my first ever boutique dress. It wasn’t long before I was admitted to hospital for malnutrition. On my wedding anniversary, I was again in hospital with chronic abdominal pain. I had yet another new side-effect – an “erosion”. I was told this was very rare, but I was to find numerous online “Bandits” who had also had erosion.

The band was removed via open surgery – my lapband surgeon blamed my plastic surgeon, my plastic surgeon blamed my lapband surgeon. I spent months trying to get answers and was handballed from one to the other. Eventually my lapband surgeon handed me to the public system, where they wanted to re-band me. I refused, concerned about the pain. The surgeons were more worried about weight gain.

I still hate what I see when I look in the mirror – I hate my fat, I hate the scars. I have been operated on once or twice a year since I was banded. I live with pain, and still eat very rarely. I spend hours a day on the toilet. I vomit between five and 15 times a week. I know I am not living well.

I wish I had known erosion was a risk. I wish I had better after-care, I wish I had made smarter choices. I wish I could sit with patients and talk to them, make them rethink the hard sell. A gastric band is a product just like the many weight-loss gimmicks we fatties invest in. Not all of these will fail, but I urge all people considering banding to be informed. Ask all the questions, and talk to lapband patients – not just the successes, but the failures too.

Kate Finlay is a guest on SBS’s Insight program tonight, 8.30pm on SBS ONE, in a discussion about the obesity epidemic, which asks whether you can be fat and healthy, and if people resort to surgery too soon

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Why it is so hard to Keep the weight lost off.

May 27

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October 24, 2012
Media Contact: Beata Mostafavi 734-764-2220

Is obesity irreversible? Timing is everything when it comes to weight loss, U-M research on mice shows

The longer that overfed-mice stayed obese, the less likely correction of their diet and activity had long-term success in normalizing weight

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ANN ARBOR, Mich. — Joint research between the University of Michigan and the Argentina-based National Council of Science and Technology (CONICET) has shed light on one of the most frustrating mysteries of weight loss – why the weight inevitably comes back.

A novel animal model showed that the longer mice remained overweight, the more “irreversible” obesity became, according to the new study that appeared online ahead of print Oct.24 in the Journal of Clinical Investigation.

Over time, the static, obese state of the mice reset the “normal,” body weight set point to become permanently elevated, despite dieting that initially worked to shed pounds, authors say.

“Our model demonstrates that obesity is in part a self-perpetuating disorder and the results further emphasize the importance of early intervention in childhood to try to prevent the condition whose effects can last a lifetime,” says senior author Malcolm J. Low, M.D., Ph.D., professor of molecular and integrative physiology and internal medicine.

Malcolm Low, M.D., Ph.D.

“Our new animal model will be useful in pinpointing the reasons why most adults find it exceedingly difficult to maintain meaningful weight loss from dieting and exercise alone.”

The lead author of the study was Viviana F. Bumaschny, M.D., assistant investigator of CONICET.

Obesity affects more than 500 million adults and 43 million children younger than age 5, while related illnesses are the leading preventable cause of death.

Individuals who are overweight have a much higher risk of type 2 diabetes, hypertension, and cardiovascular diseases.

One of the major strengths of the research was a new model of obesity-programmed mice that allowed weight loss success to be tracked at different stages and ages by flipping a genetic switch that controls hunger.

Turning on the switch right after weaning prevented the mice from overeating and ever becoming obese. Similarly, mice that remained at a healthy weight into young adulthood by strict dieting alone were able to maintain normal weight without dieting after turning on the switch. However, chronically overfed mice with the earliest onset of obesity never completely returned to normal weight after flipping the switch, despite marked reduction in food intake and increased activity.

The new findings may raise questions about the long-term success rate of severe calorie restriction and strenuous exercise used later in life to lose weight, such as the extreme regimens seen in the popular reality television show “Biggest Loser.”

“Somewhere along the way, if obesity is allowed to continue, the body appears to flip a switch that re-programs to a heavier set weight,” Low says. “The exact mechanisms that cause this shift are still unknown and require much further study that will help us better understand why the regaining of weight seems almost unavoidable.”

The findings will be published alongside a corresponding commentary “Tipping the scales early: probing the long-term effects of obesity.”

Additional authors: Marcelo Rubinstein, Ph.D., principal investigator of CONICET;  Miho Yamashita, M.D., Ph.D., postdoctoral research fellow, University of Michigan; Rodrigo Casas-Cordero, B.S., graduate student, University of Buenos Aires; Verónica Otero-Corchón, Ph.D., research laboratory specialist lead, University of Michigan; and Flavio S.J. de Souza, Ph.D., assistant investigator of CONICET.

Funding: The National Institutes of Health, USA, the Howard Hughes Medical Institute International Program for Latin America and Canada, the Argentine National Agency for Scientific and Technological Development, and the Argentine National Council of Science and Technology

Disclosures: None

Citation: J Clin Invest. 2012;122(11):4203–4212. doi:10.1172/JCI62543.

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The Pelvic Examination

May 26

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I am sure many women will be pleased about this bit of information.
J Womens Health (Larchmt). 2011 Jan;20(1):5-10. doi: 10.1089/jwh.2010.2349. Epub 2010 Dec 31.

Do new guidelines and technology make the routine pelvic examination obsolete?

Source

Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, NY 10032, USA. clw3@columbia.edu

Abstract

Routine pelvic examinations are the core of the periodic gynecological examination and widely tolerated as a necessary part of health maintenance. Is this examination beneficial for asymptomatic women? Justifications for the pelvic examination include screening for Chlamydia (or gonorrhea) infection, evaluation before initiation of hormonal contraception, screening for cervical cancer, and early detection of ovarian cancer. Current nucleic acid amplification tests for Chlamydia and gonorrhea permit the use of urine and self-administered vaginal swabs, which most women prefer over a pelvic examination. Pelvic examination findings do not affect the decision to prescribe or withhold systemic hormonal contraception; a pelvic examination is not needed to initiate these contraceptives. Recent American College of Obstetricians and Gynecologists (ACOG) guidelines recommend less frequent cervical screening, thus decreasing the frequency of a speculum examination for cervical screening. Bimanual examinations for palpation of the uterus and ovaries are also routinely performed in the United States. Clinical trial data, however, show these examinations do not lead to earlier detection of ovarian cancer. No evidence identifies benefits of a pelvic examination in the early diagnosis of other conditions in the asymptomatic woman. Speculum and bimanual examinations are uncomfortable, disliked by many women, and use scarce time during a well woman visit. Eliminating the speculum examination from most visits and the bimanual examination from all visits of asymptomatic women will free resources to provide services of proven benefit. Overuse of the pelvic examination contributes to high healthcare costs without any compensatory health benefit.

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Bali holiday

May 20

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My holiday is coming to an end unfortunately. Back to work next week. This is what we will miss.IphoneBali 006

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Homeopathy- does it work.?

May 9

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This will be my last post for the next two weeks as I am going to be away (Bali).
When practising medicine, it is important to make sure the evidence supports the treatment given. This does change over the years, as new research is produced, changing the way we do things. Who wants to go back to the days of castor oil? Homeopathy fails all these tests, unfortunately. An expensive placebo. At least it does no harm.
17 April 2013, 3.38pm AEST

World Homoeopathy Awareness Week Has Passed

Illustrating Homoeopathic dilutions using coffee Ian Musgrave

World Homoeopathy Awareness Week has just passed (10 April to 16 April), but I would still like to take this opportunity to make people aware that Homoeopathy is expensive placebo that has been failing clinical trials since 1835.

I’ve written about homoeopathy before*, showing that homoeopathic treatments, which either have no trace of active ingredient or levels so low as to be biologically meaningless, have no good evidence of therapeutic benefit.

This video on homoeopathy covers a lot of similar ground to my articles. You may be amused at the sight of me taking an overdose of homoeopathic sleeping pills (around 3:52 into the video). That sequence had a great missed opportunity moment. When Frank Pangallo asks me if I feel sleepy, I should have replied “if this was real medicine, we would be in hospital now”.

There are a number of other discussions relevant to World Homoeopathy week. This article at Science Based Pharmacy about the implications of homoeopathic products for Pharmacists is thought provoking reading. The Guardian’s report that even homoeopaths disavow homoeopathic vaccination should give you pause as well.

There are several relevant videos aside from the one linked above. Here’s Richard Dawkins investigating homoeopathy. James Randi’s TED talk on homoeopathy, and this video from CBC marketplace.

For more general infomation on homoeopathy start at the 10:23 campaign for a good one-stop basic information source. For further detail, over at Science Based Medicine, there is a good, easily readable series on homeopathy.

Then there is the weighty House of Commons Science and Technology Committee (STC) report, Evidence Check 2: Homeopathy, which concludes that there is no evidence that homeopathy works any better than placebos (commentary here). A more general article is the Ars Technica report on homoeopathy.

If you are wondering why people would use homoeopathy when it doesn’t work, this article might help you understand.

For some light relief, a homoeopath explains how physics works, then there’s an amusing poster from the Centre for Inquiry Canada and a song from Australia’s Tim Minchin (warning: rude words).

*My Conversation article ‘Doctors’ orders: debunking homeopathy once and for all’, was included in The Best Australian Science Writing 2012 anthology.

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A soda a day keeps the doctor in pay: soft drinks and diabetes

May 8

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A soda a day keeps the doctor in pay: soft drinks and diabetes

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Drinking one can of soft drink a day is linked to a 20% increase in the risk of developing diabetes. Damien Ayers

Recent research linking soft drinks to type 2 diabetes reminds us, once again, that we are what we put in our mouths. This large study from Europe found drinking a 12 ounce (about 355 ml) can of soft drink, or soda, a day was associated with a 20% increase in the risk of developing diabetes. This same effect has previously been observed in populations from the United States, Finland and Singapore.

If this is a real effect, as increasingly looks to be the case, it has massive implications. Half of eight-year-olds in the United States already drink this amount of soda, and teenage males consume more than double that. In conjunction with soft drink consumption among American adults, this represents tens of millions at risk of diabetes in the United States alone. Hundreds of millions more people are affected in other developed and developing countries worldwide.

There’s an obvious reason why soft drink consumption causes diabetes – more sweetened drinks equal more calories, which equals weight gain. Excess weight is the single most important factor in the global diabetes epidemic. While soft drinks may have effects on diabetes independent of obesity, this latest study (again) implicates weight gain as a key factor.

The study’s apparently anomalous finding of an association between diet sodas and diabetes likely reflects “reverse causation” – a phenomenon whereby people switch to diet soft drinks once they start to get the health problems caused by regular ones. So it’s the development of disease that’s causing people to drink diet soft drinks, not the diet soft drinks causing disease.

The real concern is that soft drinks are just the tip of the ice cube when it comes to diet-related ill health.

Like much of the rest of the world, Australians now consume vast amounts of processed foods purchased at major retailers and restaurant chains. Invariably high in salt, sugar or fat, these products have very clear and extremely serious consequences for health.

Where rats and mosquitoes were once the carriers of disease, it’s now the tobacco and alcohol industries and the major food and beverage corporations that are the purveyors of global ill health. Convenience, cost and corporate profits now rule at the expense of physical well-being.

The heart of the problem is that commercial success for these industries is public health disaster. This is a catastrophic failure of the market. As a New York Times investigative reporter and author of Salt Sugar Fat: How the Food Giants Hooked Us so convincinglydescribed on ABC TV’s Lateline, these foods and drinks are designed to achieve the “bliss point” at which consumption is maximised. Solely in pursuit of profit, and regardless of the adverse effects they might cause.

The health problems attributable to unhealthy food and drink are widely recognised. TheWorld Health Organization recently agreed the goal of a 25% reduction in preventable deaths by 2025. Six out of the eight targets defined to deliver this objective are aimed at lifestyle–based problems, and only two cover clinical management issues.

In Australia, the government’s solution to diet-related disease is the Food and Health Dialogue, an initiative that brings the food industry, government and non-governmental organisations together to improve the food supply and reduce diet-related ill health. The initiative relies on the voluntary participation and self-regulation of the food and beverage industries to achieve its goals.

Its priorities are food reformulation on sugar, salt, fat, energy, fibre, wholegrains and fruit and vegetable content, as well as consumer nutrition education and standardisation of portion sizes issues. In the four years since it was established, it has managed to reach targets for salt reduction in a handful of food categories. No substantive action has been reported on any other nutrient, and has been achieved for education or portion size.

Given there is a $100 billion business at the table that perceives itself at risk from the dialogue’s goals, the lack of progress isn’t really surprising. Why would businesses that maximise margins and shareholder value by adding sugar salt and fat to their products seriously engage in any such initiative? The bigger, unanswered question is why government hasn’t acted faster or more effectively when there’s so much at stake.

As a first step, the food and beverage industries must be removed from the policy-setting table. Like tobacco and alcohol, the conflicts are just too great and the public health problems too large. And just as for tobacco, the end game has to be regulation that controls the food and beverage industry – until that happens there will be no decline in diet-related ill health.

Industry will of course argue that it’s all about personal choice and individual responsibility. And that it’s not the role of the state to interfere with what people desire. It will use its massive influence and enormous marketing budget to talk up its success stories and sweep its failures under the carpet.

But sooner or later the problems will get too big to hide, the outrage too great and a significant step forward will have to be taken. We no longer buy industry’s arguments for tobacco and one day we won’t for soft drinks. Let’s just hope it doesn’t take us 50 years, half a million premature deaths, and a hundred billion health-care dollars spent on diabetes before we achieve this.

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The Flu shot explained

May 7

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FYI – I had my flu shot a month ago. I have for the last 25 years. I have not had the flu in that time(touch wood). Used to get the flu yearly before that.

from: Leigh Cowart
TO: The Feel Smarter Desk
Date: Nov 14th, 2012

Experts: If You Don’t Get A Flu Shot, You’re Stupid. And A Dick

Asheville, NC: I finally got my flu shot yesterday, and in my post-vaccination low-grade fever haze, I was reminded how much misinformation exists about flu shots.

But this dispatch isn’t about how much I hate the anti-vaccine movement and how the triumph of public health has led to masses of pampered, scientifically illiterate hippies believing the kind of stuff that makes homeopathy look sane by comparison. No, this is about the nitty gritty of seasonal influenza vaccinations. Give me your tired, your poor, your huddled masses yearning to breathe free: let us speak of flu!

First things first: influenza is an asshole. It hates you and wants to shred the lining of your lungs, turning you into its own private incubator of nasty, drowning you in a froth of dead cells, bodily fluids, and the refuse of your own immune response. In your average year, the flu will kill 250,000 to 500,000 people worldwide. However, in an above average year, flu can be a mass killer. For example, the Spanish Flu pandemic of 1918 killed between 20 and 50 million people. And that was before airplanes. So yes, in case you were wondering, you should definitely care about flu.

Flu belongs to the Orthomyxoviridae (Greek for straight mucus viruses) family of RNA viruses, which contains the three genera of Influenzavirus: Influenzavirus A, which infects humans, birds, and other mammals; Influenzavirus B, which infects humans and seals; and Influenzavirus C, which infects humans and pigs. All of them suck. Some of them suck more than others.

Influenza A viruses are the culprits in all flu pandemics, and are thus a very big deal, so let’s take a closer look. You’re probably somewhat familiar with the subtype (or serotype) nomenclature, for example H1N1 or H3N8. But here’s what those letters and numbers actually mean…

The classification of Influenza A viruses is based on two viral surface proteins: hemagglutinin (HA or H) and neuraminidase (NA or N). Influenza hemagglutinin is a glycoprotein with antigenic properties: antigens are substances that can trigger the production of one or more antibodies, so for the purpose of this explainer, you can just think of antigen as a synonym for “bad guy”.

Influenza hemagglutinin is the thing that is responsible for binding the virus to the cell that is it trying to infect. Without this viral surface protein to bind sialic acid on the cell membranes in your upper respiratory tract, the Big Bad Flu would just float around in your lungs doing diddly squat. Hemagglutinin is the flu glue that allows the viral particles to stick to a healthy cell, then grapple-hook its way inside, entering the cell in a bubble, or vesicle, of the cell’s own membrane. By entering the cell instead of fusing with the cell, influenza evades the immune system, hiding in the very place it’s going to hijack for its own reproduction.

Next: viral neuraminidase, which is what allows the influenza virus to be released from its cozy host cell, post-replication. Once the virus has gotten busy inside the cell, hijacking the cellular machinery to make copies of itself, it needs a way to bust out all the freshly minted virions. This is where neuraminidase comes in. Neuraminidase makes it possible for the virus to be released from the cell by cleaving an important group, the sialic acids, thus allowing brand new baby flu virions to float free until their hemagglutinin surface proteins find a sticky, healthy lung cell to hook into and start the entire thing all over again. Without neuraminidase, the new virons that burst forth could get stuck to the sialic acid in the dead cell’s membrane, ruining their dreams to replicate inside of and destroy a new host cell. No neuraminidase, no escape.

Here’s where it gets nasty: Sixteen hemagglutinin subtypes and nine neuraminidase subtypes have been identified for influenza A viruses. Not only that, but out of all the parts of an influenza virus that change, or mutate, the hemagglutinin and neuraminidase surface proteins do it the fastest. This little rapidly mutating surface protein thing is pretty unique to influenza: Other viruses can mutate, but it’s typically not their surface proteins that change. This is why you can’t get the measles twice: your body knows measles’ surface proteins and recognizes them every time measles shows up. Influenza, on the other hand, changes its surface proteins all the fucking time, making it hard for your immune system to recognize and destroy.

The myriad influenza serotypes like to hang out in different combinations, like a particularly grotesque swingers party. To use the nomenclature, swine flu, or H1N1, has hemagglutinin serotype 1 and neuraminidase serotype 1. So, when someone starts talking about “strains of flu”, these specific combinations of HA and NA surface proteins are usually what they are referencing.

Which brings me to flu shots. Obviously, influenza viruses are complicated little assholes. With so many combinations of surface proteins, researchers have to decide which strains to put in each year’s seasonal flu vaccine. They do this by monitoring strains of influenza in circulation and making – yes you guessed it – supremely educated guesses. Most years the strains of flu in the vaccine closely match the flu strains in circulation. And when the match is good, the vaccine is incredibly effective.

Your immune system, elegant bastard that it is, can recognize virus particles via its immune receptors, little do-dads that are tailor-made to identify and bind to the antigens on the virus’ surface. It’d be kind of like having an incredibly specific home security system, except that instead of just calling the cops whenever trouble showed up, your house would remember intruders and deploy a counterattack system uniquely suited to the exact nature of the disturbance. So, if there was a very tall man that kept trying to break into your house, your house would learn that each time he showed up all it had to do was quickly drop the ceilings a foot or two to knock him out.

However, in the case of this metaphor, influenza is a collective of burglars with varying skill sets. Sometimes influenza is SAS, sometimes it’s the Navy, sometimes it’s a bunch of punk kids with flaming bags of shit. Your house, unable to protect against every burglar in this weird super villain group hell-bent on stealing your flat screen, must hedge its bets and prepare for the burglars it thinks are most likely to show up. Which is essentially what the scientists developing each year’s seasonal flu vaccine do. Researchers predict which viruses to include in the vaccine, and despite the fact that flu viruses are constantly changing, a phenomenon called “antigenic drift”, they are usually able to predict pretty close matches between viruses in the vaccine and the circulating viruses. Impressive.

Each year’s flu vaccine is trivalent, meaning they protect against three influenza viruses. This season’s vaccine is made from an H1N1 and H3N2-like strains of influenza A, as well as a strain of influenza B. And before you get all huffy because you got a flu shot last year with H1N1 in it, know that the H3N2 and influenza B strains are different from those in last year’s vaccine. So you still need this year’s flu shot.

But Leigh, I’m a healthy adult that never gets sick! Why on earth would I let a stranger jab me with a needle and deposit killed, inactivated viral particles in my perfectly toned deltoid?

Well, I’m glad you asked. As Dr. Zubin Damania (or as you may know him, ZDoggMD) reminds us in his charmingly bizarre video, One Injection: The Flu Shot, up to half of people with documented influenza viral infection are asymptomatic. These lucky bastards get the flu but don’t experience any symptoms, then spread the flu to the vulnerable populations who will definitely experience symptoms. So even though that asshole yapping on Bluetooth, spraying spittle all over the cream and sugar counter at your neighborhood chain coffee shop may seem physically robust, he could in theory be spreading flu to vulnerable members of the community, like little kids and old people. “These folks should get immunized,” notes Dr. Damania in our email correspondence, “Or else they are dicks.”

Per the CDC, everyone six months of age and older should get vaccinated for seasonal influenza, especially those at high risk of developing serious flu-related complications. According to Dr. Damania, those most at-risk for developing flu-related complications include the very young, the very old, those with immune system problems like HIV and cancer patients, and sufferers of other chronic diseases such as diabetes, COPD, and CHF.

However he is careful to note that during the H1N1 outbreak, they saw “young, healthy people dying all over the place from the flu.” So everyone should get immunized, unless they have a severe chicken or egg allergy, have had a severe reaction to an influenza vaccine, or a history of Guillain-Barré Syndrome, or are under six months of age. These unlucky folks can’t get immunized and will just have to hope that everyone else gets a flu shot, giving them a chance to cash in on some community immunity.

(Community immunity, also referred to as herd immunity, is a fantastic perk that can result from mass vaccination. Says Dr. Damania: “When everyone that can be immunized is immunized, the virus really has nowhere to hang out, so the more vulnerable members of society (very young, very old) for whom vaccines are less effective due to weaker immune response, etc. are protected by proxy.” However, current seasonal flu vaccination rates are too low to confer this fantastic and life-saving benefit.)

Still not convinced that flu shots work? Dr. Damania has some friendly advice. “Take an adult education class on basic biology. Then take another class on basic statistics. Then review the literature on flu vaccine efficacy (particularly Japanese studies), and the data showing benefit. Now, since I know nobody is actually going to go through all that trouble, outsource the education/research to someone who does this for a living (a doctor, epidemiologist, immunologist, the CDC, etc) and listen to their recommendations.”

And no, you absolutely cannot get the flu from a flu shot. You might have to suffer through a low-grade fever, headache, or body aches, but that’s just your immune system ramping up and making some priceless influenza antibodies. However, I’m sure that enterprising readers can milk some sympathy courtesies out of their weenie, post-vaccine state. I know I sure did.

See Desknotes for the complete interview with Dr. Zubin Damania.

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