SAD

It is that time of year again when the cold weather reminds us that the change of season is upon us. It has prompted me to reassess my winter wardrobe (which is sadly lacking) and I am finding it just that bit harder to get out of bed in the morning. But then again I have children who take care of that. My mood has altered somewhat and I also find myself hoping that we will be blessed with just a few more lovely sunny days.....

As I understand it, all these feelings are normal. For some people however, there is a very real winter related disorder called Seasonal Affective Disorder or SAD for short. It is also commonly confused with the winter blues or winter depression but the two are in fact different. There has been much written on this topic since it was first defined in an article published in a Psychiatry paper in the early eighties.

The American Psychiatric Association recognizes SAD as a sub type of a major depressive disorder.

Symptoms of SAD include lack of energy, difficulty getting up in the mornings, overeating, craving carbohydrates (and weight gain), difficulty concentrating and completing tasks, withdrawal from usual social activities and friends/family. Of course this leads to depression. Symptoms typically begin in autumn, peak in winter and usually disappear in spring and summer. These people are known to experience normal mental health throughout the rest of the year.

There are four major criteria as set out by the American Psychiatric association DSM -IV which must be met in order to diagnose SAD:

Depressive episodes at a particular time of year

Remissions or mania/hypomania also at characteristic time of year

These patterns must have lasted two years with no nonseasonal major depressive episodes during that same period and

These seasonal depressive episodes outnumber other depressive episodes throughout the patient’s lifetime.

Winter blues is considered to be much more mild than SAD. Symptoms still include feeling sad and a lack of energy but the key difference is that these people can still function. People diagnosed with SAD, typically find it difficult to perform normal activities of daily living.

Apparently many more women are affected by SAD than men. While it is far more common in the Northern Hemisphere than Australia, it has been estimated that one in three hundred Australians are affected.

It is also worth noting that there are a small number of people who display depressive symptoms such as insomnia, decreased appetite, weight loss, irritability, anxiety, and decreased sex drive in the SPRING and SUMMER months (Summer SAD). These people may also have short bouts of mania/hypomania behaviour at this time of year.

Classic major depression often (but not always) presents with decreased appetite (weight loss) and decreased sleep patterns.

Research shows that it is the lack of light during the winter months which leads to SAD. The brain does not produce enough serotonin which has been found to lead to depression. Serotonin is a neurotransmitter which is produced by the brain and relays messages from one part of the brain to other parts. It has a major influence on mood, and our serotonin levels are lowest in winter. Put simply, serotonin stimulates us during the day time but it is another hormone, melatonin whose job it is to promote sleep.

In the evening the body (or more accurately the pineal gland) responds to decreased light by making melatonin. Usually the secretion of melatonin peaks in the middle of the night when we are in our deepest sleep but is switched off by the pineal gland in response to light exposure in the mornings.

During winter, people affected by SAD commonly have higher levels of melatonin during the day which leads to many of the previously discussed symptoms associated with SAD. The body’s internal body clock is out of “synch”.

Light therapy, either bright white light/blue light has been used to effectively treat SAD by suppressing melatonin and stimulating serotonin production. It helps to reset the body’s natural sleep/wake cycle. Other treatments such as taking melatonin or other antidepressants used in conjunction with light therapy have proven to be effective. Or one could just head outside for a natural dose of light – great in the summer months but harder to use effectively in the colder winter months.

During my research I was also surprised to learn that it has been estimated that up to 20% of people with SAD already have/ go on to develop bipolar disorder. Interestingly, some studies have indicated that people with dark coloured eyes react differently to light than those with light coloured eyes. Also that genetic differences in photoreceptors and glucose metabolism also play a role.

Lisa

Crouch St, South

Having our own rooms in Mount Gambier is working wonderfully. Above is a picture of the street entrance to the rooms. Patients have been full of praise commenting on how neat and tidy they are. We always appreciate to hear feedback about our service. There is car parking available around the back of the practice or there is ample parking on the street. A google map is on the website for the Crouch St, South rooms.

From June 15 2010 Dr. Bradbeer will be consulting in Mount Gambier on Tuesdays. The office is open from 9.45am-4.00pm on these days.

We are working hard to secure another full time physician to the practice and when this comes to fruition we will be able to offer two consulting days per week in Mount Gambier. Fingers crossed, that I will have some good news pertaining to this within the month.

Spriometry, gas transfer and bronchial provocation tests are also available on consulting days in Mount Gambier.

Jessica

More bariatric surgery

It’s not rocket science.

Evaluation of patients prior to bariatric surgery is largely a matter of common sense. The goal is to identify any problems that are able to be modified with non-surgical intervention, and to introduce treatment to reduce risk. As I explain to patients, the fitter they are prior to surgery the less likely they are to get really crook if they encounter unforeseen complications, and the better they will do afterwards when it comes to getting on their feet and losing weight. However, for most patients the good stuff really happens post-operatively. Diabetes resolves, hypertension improves, sleep apnoea is cured…. For that reason, we really want to identify and treat only those problems which will significantly increase the risks of surgery. All other problems should be addressed after surgery. For example, diabetic control preoperatively does not need to made perfect, as it almost universally improves dramatically after surgery.

Guidelines as to whom we should consider suitable for bariatric surgery were introduced nearly 20 years ago – and have not altered since. Now there’s a situation that has to change with the times! In any case, the National Institutes of Health in the US came up with the following recommendations:

Bariatric surgery should be considered in individuals with:
- BMI of 40kg/m2 or greater
- BMI of 35 to 39kg/m2 with severe comorbid conditions such as life- threatening cardiopulmonary problems or diabetes.
- BMI of 35 to 39kg/m2 with obesity-induced physical problems interfering with lifestyle (e.g joint disease which is treatable but for the obesity)
- No underlying endocrine abnormality that can contribute to obesity, ongoing substance abuse or uncontrolled psychiatric disturbance
- An ability to understand the surgery and its consequences and comply with post-operative dietary modification
- No illness that greatly reduces life expectancy


In our clinical evaluation of patients preoperatively we want to ensure that there is no undiagnosed cardiac, respiratory or endocrine disease that will significantly increase the risk of perioperative complications. The population of patients undergoing bariatric surgery is at particular risk of coronary artery disease, cardiomyopathy, uncontrolled hypertension, hypothyroidism, obstructive sleep apnoea or obesity hypoventilation syndrome, asthma or chronic obstructive pulmonary disease or undiagnosed diabetes. Not every patient will require the same specific workup. However, investigation which we frequently request include exercise testing, echocardiography, lung function tests and diagnostic sleep studies. Everybody has blood tests, including coagulation studies, iron studies, blood glucose and thyroid function, lipid studies and full blood count as well as an ECG. (Most of our patients have had these investigations requested by their general practitioners).

In 2007, a useful clinical risk-stratification tool was suggested by DeMaria and colleagues in a paper published in the journal of Surgery for Obesity Related Disease. This score reminds us that mortality rates are generally very low for bariatric surgery, but are significant in some patient groups.

The score takes into account the following variables:
- BMI >50
- Male gender
- History of hypertension
- Increased risk for pulmonary embolism ( variable included previous PE, inferior vena cava filter, right heart failure, obesity hypoventilation syndrome)
- Age 45 years of more

One point is awarded for each variable, with mortality rates as follows:
- score 0-1, mortality rate 0.31%
- score 2-3, mortality rate 1.90%
- score 4-5, mortality rate 7.56%

This scoring system was, however, created from one particular retrospective analysis in one institution and validated in another institution. The PE risk variable is not straight forward, and less than 1% of patients scored all 5 points. The operation involved was gastric bypass, which is a much more complicated procedure than gastric banding or vertical gastroplasty, which are the major procedures performed in Hamilton.

A much bigger study of qualified surgeons in the US, which was published in the New England Journal of Medicine last year and which included gastric bands, showed very low mortality rates, as per the attached table. In that study, only very high BMI, history of pulmonary embolism, and perhaps history of OSA, were associated with increased risk of mortality.

A study published in the NEJM in 2007 suggested that long-term mortality in very obese patients was reduced by 40% in patients who had gastric-bypass surgery. The slightly – increased risk of dieing post-operatively should, perhaps, be considered in light of that sobering, dramatic statistic.

Andrew

I’ve been reading about obesity. More specifically, I have been reading about bariatric surgery.

As I have the privilege of reviewing many of the patients who undergo bariatric surgery locally (either laparoscopic adjustable gastric band insertion or vertical banded gastroplasty), I was invited to speak to some of the local medicos last week on the preparation of patients for these surgical procedures.

It’s not intuitive that obesity is a problem which warrants drastic intervention. It probably needs to be reiterated that the following medical problems, which no-one really wants to suffer from, are associated with obesity, and can be a major cause of suffering in our community, as well as an increasing burden on our health-care infrastructure:
- coronary artery disease
- insulin resistance and type two diabetes
- cancer (endometrial, breast and colon)
- hypertension
- dyslipidaemia
- stroke
- liver and gall bladder diseae
- obstructive sleep apnoea and respiratory disorders
- osteoarthritis
- gynaecological problems (infertility, polycystic ovarian syndrome, menstrual irregularity)
- pseudotumour cerebri



One might also wonder what all of the fuss is about. How much of a problem is this, really? I think the accompanying graph speaks for itself. (The measurement tool that we most commonly use to assess weight / obesity is the body mass index. While this tool may be, to some extent, flawed it is pretty standard. BMI over 30 defines obesity, with BMI over 40 being labelled 'morbidly obese'. It is the tool used in collection of the data that go into compiling a graph such as this).

My professional exposure to people who struggle with obesity, and my reading around the topic, has caused me to become less and less optimistic that lasting control of weight problems can be achieved with non-surgical measures (ie diet and exercise). Professor Joe Proietto, from Melbourne, spoke at the recent World Congress of Internal Medicine in Melbourne (I wasn’t there but got the DVD!) and at the Australasian Sleep Association meeting last year. Wow, if you want to hear someone who presents a scientific basis for the failure of non-surgical weight loss and the inevitability of continued increase of the obesity epidemic in our society, then Joe is the man!

He explained that the hypothalamus, the part of the brain where appetite is ‘controlled’, seems to be programmed to hunt for food. There is only one hormone (chemical messenger) which we know of which circulates in the blood stream and is designed to stimulate appetite. It is called Ghrelin, and is secreted mainly from cells in the stomach. There is a number (around nine) of hormones that suppress appetite. The two we probably know most about are Leptin (secreted by adiopose tissue) and cholecystokinin (made and secreted in the small bowel in response to ingestion of food). Prof Joe P has convincing experimental data that demonstrate how prolonged low-calorie diet is accompanied by weight loss (no surprises there) and a reduction in secretion of leptin and CCK (ie less suppression of appetite). At the end of a prolonged period of low calorie diet, experimental subjects have their appetites unleashed and choose to eat high protein and high fat foods. In real life, this is called “Yo-yo dieting”. Seems it’s not just a matter of willpower.

Current thinking is that bariatric surgery impacts on the secretion of the above hormones, and others involved in suppression of appetite, in ways that are sustained. This facilitates long term dietary modification. It also contributes to the rapid resolution of complications of obesity, and in particular diabetes, following bariatric surgery. To my disappointment a recent review article in Nutrition journal found no good studies to date testing this hypothesis.

Bariatric surgery certainly is, however, the only intervention which regularly results in sustained weight loss. I used to be hesitant to refer patients for these procedures. Now it is often an issue discussed at the initial consultation.

Next post: What are the indications for bariatric surgery? What are the risks? What does a pre-operative evaluation entail?

Andrew

Additional respiratory appointments

As I am sure we are all well aware the burden of disease for respiratory illness is high. COPD is the 4th leading cause of death in the world (behind heart disease, cancer and stroke)and researchers estimate by 2020 its will be the 3rd leading cause of death world wide.

It is also estimated that by 2020 it will be the 5th leading cause of morbidity (DALY).

From these figures it is no surprise that the demand for respiratory consulting is high, hence to meet this demand we are very fortunate to have some Melbourne based physicians providing consulting services for Regional Respiratory Medicine.

Over the next month Dr. Daniel Steinfort will be consulting in Horsham. Daniel has been consulting in Horsham for 18 months. In Melbourne he is based at the Royal Melbourne Hospital and is currently undertaking his PHD.

Dr. Camelia Borta will begin consulting with us during May and has undertaken to visit the practice for fortnightly periods approximately every six weeks. Camelia is currently working at Casey Hospital, Berwick. This will enable us to provide extra consulting to Mount Gambier.

Jessica

Hamilton Sleep Disorders Centre

The Hamilton Sleep Disorders Centre opened its doors in May 2005, hence is approaching it 5th birthday. Happy Birthday!

In that time the centre has conducted over 2000 sleep studies ranging from diagnostic, cpap implementation, cpap reviews, MSLT, and MWT.

The centre draws patients to Hamilton from the Wimmera, Limestone Coast and Greater Green Triangle area. In the last year Portland District Health has also opened the doors to a in-laboratory sleep services, which is helping to service the demand in the region.

The vast majority of diagnosis that come through the sleep centre doors are Obstructive Sleep Apnoea and although the centre has seen a great deal of patients there is still a significant amount that have OSA and don't realize.

A common comment I hear at the sleep centre is 'I think I've actually had this for years'. What sparks them to be investigated is varied from doctors referral, bed partner nagging (due to snoring or witnessed apnoeas), friend being diagnosed and realising their story sounds similar to their own, job requirements or their own motivation.

So, I thought this was a good opportunity to refresh everyone minds about some OSA Stats.

The Quick Facts
1. OSA is said to be prevalent in 5% of the population but some studies have predicted it may be present in up to 10% of middle aged men.

2. Patients on 3 or more Blood Pressure medications are 70% more likely to have OSA.

3. Around 23% of patients with Type II Diabetes have OSA

4. OSA suffers are seven times more likely to have an accident

5. Depression is strongly linked to OSA and insomnia

6. 50% of snorers have OSA

When OSA is diagnosed and successfully managed it can have a positive impact on hypertension, type II diabetes, snoring, accidents, depression and the risk associated with cardiovascular disease.

It is very important to keep Obstructive Sleep Apnoea on the agenda.



Jessica

Restless Legs Syndrome

Frustration. Exhaustion. Inability to rest or sleep without twitchy or uncomfortable legs. An overwhelming urge to move affected limb.

Many people would not realize that these distinctive symptoms actually have a name and therefore go undiagnosed and untreated resulting in restlessness, difficulty in sleeping and daytime sleepiness.

Restless legs syndrome (RLS) is a central nervous disorder possibly with some genetic predisposition or related to an imbalance of dopamine in the brain. Dopamine is a brain chemical that affects movement and as levels normally drop at night this may explain why RSL is worse at this time. Iron is a significant factor in the production of dopamine which may account for the link between low iron levels and RLS symptoms.
RSL may be acerbated, but not caused by stress or psychiatric conditions.

As indicated RLS usually affects the legs particularly the calves but some people may experience symptoms in the upper legs, feet, hands or arms.

Primary RSL seems to have no cause. Those affected may have developed the condition during childhood and this may have been attributed to growing pains (or even ADHD). There is a tendency for the condition to increase with age with significant increase in severity often seen after age 50.

With secondary RLS there is usually a link to another condition. These include anaemia, kidney disease, Parkinson’s disease, pregnancy, thyroid problems, neurologic lesions, sleep apnoea or narcolepsy, and alcoholism.
There are certain medications that when taken may trigger or increase RSL symptoms, as may the withdrawal of some drugs.

Diagnosis is usually made on the basis of reported symptoms and medical history. The four established criteria are:
• Irresistable urge to move your legs along with uncomfortable sensations (may be described as creeping, crawling, pulling, tingling, itching, pain, burning)
• Symptoms commence or get worse at rest (sitting, lying down)
• Symptoms are partially relieved by activity (stretching, walking)
• Symptoms are worse at night

Blood tests or other investigations may be done to exclude other possible causes.

RSL doesn’t lead to other serious conditions but symptoms can become incapacitating for some sufferers especially excessive tiredness from sleep deprivation.

There is no cure for RLS but there are treatments available that can manage the condition and relieve discomfort. This may involve treatment of underlying conditions, lifestyle techniques which may require changes in daily behavior or habits, use of support groups and in severe cases transcutaneous electric nerve stimulation (TENS) for a short time at night may be of help. Medications are commonly prescribed but there is no one drug that works for everyone and they should always be used with caution as may have side effects or increase the symptoms of RSL. Usually the drugs prescribed are ones used for other conditions but have been found to be beneficial with symptoms of RLS. They may include dopaminergic agents, Benzodiazepines, non benzodiazepine sedatives, opiates and narcotics and hypertensive medications.

RSL may necessitate referral to a sleep specialist for further evaluation. This may require observation overnight at a sleep clinic where sleep can be monitored for periodic limb movements during sleep. However a diagnosis can usually be made without a sleep study.

Irene