Therapy Animals: Just sentimental bunkum?

Pets, the not-so-secret weapon to help patients recover from what ails them

When Scott Vande Zande had a serious stroke 15 years ago, his beloved golden retriever Hollie was key to his recovery.

“I had to learn to speak again, but there were times I couldn’t talk,” said the Seattle engineer. “I’d come home, and I was so depressed. Then, I’d see Hollie, and it took a lot of the grief away. She was just a godsend.”

After he retired from Boeing in 2015, Vande Zande wanted to share his gift. So, he got Hollie certified as a pet therapy dog and went back to the hospital stroke unit to help others.
“I brought her in and everybody fell in love with her,” Vande Zande said. “She had lost a leg to sarcoma (a type of cancer), but she was so special. I wanted to go talk to people who were going through what I went through. But first Hollie broke the ice.”

Hollie, who was named a Stroke Hero by the American Stroke Association, died in late 2016 at 13 ½. Now Vande Zande takes Katie, another golden retriever, on his rounds at Swedish Medical Center’s Cherry Hill campus, where she dispenses unconditional love and collects hugs and belly scratches in return.

Like thousands of other pets across the country – mainly dogs, but also cats, rabbits, birds and other animals – Katie is a not-so-secret weapon in helping patients recover, physically and psychologically, from their ailments.

“Lots of research shows how much the animal-human bond benefits both of us,” said Dr. David Williams, chief medical officer for Pet Partners, which trains volunteers and coordinates animal-assisted therapy in 47 states. “We see it in practice every day.”

The idea isn’t new. Reports of animals comforting humans date back centuries. In 1859, the famed nurse Florence Nightingale wrote, “A small pet animal is often an excellent companion for the sick.” Sigmund Freud reported that patients were more willing to talk when his dog Jo-Fi sat in on psychotherapy sessions.

Williams said research on animal-assisted therapy began in the 1960s, and has shown benefits ranging from lowering blood pressure, heart rates and pain levels to releasing hormones that ease depression and promote an overall sense of well-being.

“A lot has been soft research, looking at causal relationships,” said Williams, who is an emergency room physician. “We still need more, true academic-level studies looking at how AAT can benefit us at the biochemical level. Those are really just beginning now.”

Meanwhile, the practice is spreading. The American Kennel Club lists dozens of therapy dog certification groups on its website. Pet Partners, one of the organizations listed, says it has more than 10,000 volunteers and is signing on new institutions all the time.

Lovable pets raise spirits in schools, nursing homes, airports and hospices; help autistic children connect to their surroundings; lower stress in college students facing final exams; and help veterans cope with post-traumatic stress disorder.

“It’s miraculous,” said Rabbi Jodie Futornick, staff chaplain at Swedish Medical Center, who sees Katie and other pets in action. “I see people calm visibly when a dog comes in. I’ve seen people respond verbally and nonverbally when they hadn’t been responding before.”
The impact, she said, isn’t just on the patients. “If I’m having a bad day, all I need to see is Scott and Katie walking down the hall,” the chaplain said. “She’s so sweet and friendly. Nurses and doctors and the whole staff take great delight in being able to pet a dog in the middle of their day.”

Vande Zande is certain the feeling is mutual. “Every time we go to the hospital she doesn’t want to go home,” he said. “I have to pull on the leash to get her out the door.”

Not just any dog can stroll down a hospital corridor. Pet Partners’ certification program includes a seminar for the human and an audition for the animal.

“The dog has to have the rudimentary ability to sit and stay and follow commands,” Williams said. “Once you feel you and your dog are ready, it’s a two-hour test. They make sure you have good control of the dog and the dog has a good temperament. They have people act like patients, and the dog can’t be startled or scared of the process. It does exclude a lot of dogs.”

So far, it has excluded Ginger, the loving-but-rambunctious golden retriever Vande Zande hopes will succeed Katie someday. “She’s failed twice,” he admitted. “We’re working on it, but right now she just wants to be a puppy. “But she’s a great dog, and I’m still hopeful.”

Explore Further:

If you’d like to explore our range of medication-free products to support relaxation and manage your levels of stress, then you’ll find them here. If you’d like to explore our complete range of products, chosen to support  your health, wellbeing and peak performance in study, work and sport, then a good starting point would be to return to our home page, which is here

Source Material and acknowledgements:

This article was provided to us by the American Heart Association News service to which we express our gratitude. It was first published by that service on 27th April, 2018. Photographs appearing in the article were provided courtesy of Scott Vande Zende.

Coffee: Help or hindrance to health? Here’s what the research have to say.

Millions of people worldwide wake up and fuel their day with it. And though consumers might be jittery about the recent court battle in California over cancer warnings, experts say most of the science actually indicates coffee could have health benefits.“The overall picture is quite clear,” said Dr. Frank Hu, chair of nutrition at Harvard University’s T.H. Chan School of Public Health. “There is no long-term increased risk of major chronic disease, including diabetes, cardiovascular disease or even cancer.”

The java confusion stems over an eight-year court case. A Los Angeles-based judge’s preliminary decision last month requires cancer warning labels because of concerns about acrylamide, a chemical produced during the roasting process. Acrylamide also is present in some fried or roasted starchy foods, including french fries, potato chips, breakfast cereals and toast. It’s also found in cigarette smoke. The judge gave the coffee industry a few weeks to file appeals and could issue a final ruling late this month.

But there’s little evidence acrylamide levels in food cause cancer in humans. Studies have found no consistent evidence acrylamide exposure in food is associated with cancer risk, according to the National Cancer Institute. The World Health Organization’s International Agency for Research on Cancer reviewed more than 1,000 human and animal studies and issued a statement in 2016 that “found no conclusive evidence for a carcinogenic effect of drinking coffee.”

“The California judge’s decision to label coffee as a cancer risk is really inconsistent with the scientific literature,” Hu said. “It’s very misleading and has already caused a huge amount of confusion in the general public. The health outcomes have been remarkably consistent.”

Hu was senior author of a 2015 study in the American Heart Association’s journal Circulation that concluded people who regularly drink moderate amounts of coffee daily — fewer than five cups — experienced a lower risk of death from heart and neurological diseases.

About four years ago, the U.S. government gave coffee its OK, too. The Department of Agriculture’s dietary guidelines for all Americans, published every five years as a go-to source for nutrition advice, said three to five cups a day, which can be up to 400 milligrams a day of caffeine, can be part of a healthy diet. The AHA suggests that people who have an arrhythmia, an abnormal heart rhythm, talk to their health care provider about caffeine intake.

“This guidance on coffee is informed by strong and consistent evidence showing that, in healthy adults, moderate coffee consumption is not associated with an increased risk of major chronic diseases (e.g., cancer) or premature death, especially from cardiovascular disease,” the federal guidelines say.

“However, individuals who do not consume caffeinated coffee or other caffeinated beverages are not encouraged to incorporate them into their eating pattern.”

More recently, a review of more than 200 studies published last fall in the BMJ concluded three to four cups a day may be “more likely to benefit health than harm.” It found a lower risk of liver disease and some cancers in coffee drinkers, and a lower risk of dying from stroke.

All of that should be good news to the people around the world who drink more than 1.1 billion cups of coffee each day.

But it’s still easy to be confused. A quick search for coffee and health online yields hundreds, even thousands, of results.

Studies abound – some funded by the coffee industry. For example, a European Journal of Nutrition study investigated the effects of coffee and its antioxidant properties and found no effect. Researchers took blood samples of 160 volunteers who drank up to three to five cups of coffee or water each day for eight weeks.

“Up to five cups of coffee per day had no detectable effect, either beneficial or harmful, on human health,” that study concluded. It was funded by Kraft Foods, which makes Maxwell House coffees.

Of course, “no one is talking about coffee as a magic bullet,” Hu said. He and other experts say it’s important to keep track of the bigger picture, with the focus on moderation and dietary patterns.

“You can’t pin anything on any one specific lifestyle behaviour, particularly with diet,” said Alice Lichtenstein, a senior scientist and director of the Cardiovascular Nutrition Laboratory at Tufts University in Boston and past chair of the AHA’s nutrition committee.

“When we talk about diet, it should really be about the whole package, not single items. Right now, the majority of the evidence suggests there may be a health benefit from drinking coffee and there doesn’t seem to be any disadvantage. Of course, with a caveat that you don’t want to add a lot of cream and sugar, or to use it as an excuse to have a few cookies or a pastry. Then, there is a downside,” said Lichtenstein, a professor of nutrition science and policy who also was an advisor on the federal dietary guidelines.

“We have a tendency to focus on one or two specific foods or beverages, and that’s when the whole floor falls out from under us.”

Explore More:

If you’d like to explore ways to support your psychological, physical and intimate health with our range of medication-free products, please return to our home page by clicking here

Source:

This article was first published by the American Heart Association on 24th April, 2018, and is reproduced here with permission. The article has had minor alterations for length.

Irritable Bowel Syndrome: What is it exactly?

Answering some common questions about IBS and possible solutions

Abdominal pain and digestive issues are often uncomfortable to talk about, but irritable bowel syndrome (IBS) affects a large number of people. For example, a recent review in the United States1, estimated that between 10 to 15 percent of adults there complain of the disorder. The figures for the UK are likely to be very similar. Here are some of the more commonly asked questions about IBS:

What is irritable bowel syndrome?

Irritable bowel syndrome (IBS) is a group of symptoms that occur together, including repeated pain in your abdomen and changes in your bowel movements, which may be diarrhoea, constipation, or both. With IBS, you have these symptoms without any visible signs of damage or disease in your digestive tract.

IBS is a functional gastrointestinal (GI) disorder. Functional GI disorders, which doctors now call disorders of gut-brain interactions, are related to problems with how your brain and your gut work together. These problems can cause your gut to be more sensitive and change how the muscles in your bowel contract. If your gut is more sensitive, you may feel more abdominal pain and bloating. Changes in how the muscles in your bowel contract lead to diarrhoea, constipation, or both.

Does IBS have another name?

In the past, doctors called IBS colitis, mucous colitis, spastic colon, nervous colon, and spastic bowel.

Are there different types of IBS?

Three types of IBS are based on different patterns of changes in your bowel movements or abnormal bowel movements. Sometimes, it is important for your doctor to know which type of IBS you have, although your doctor may still diagnose IBS even if your bowel movement pattern does not fit one particular type. The three types of IBS are:

IBS with constipation (IBS-C)
With IBS-C, on days when you have at least one abnormal bowel movement
more than a quarter of your stools are hard or lumpy and
less than a quarter of your stools are loose or wateryIBS with diarrhea (IBS-D)
In IBS-D, on days when you have at least one abnormal bowel movement
more than a quarter of your stools are loose or watery and
less than a quarter of your stools are hard or lumpyIBS with mixed bowel habits (IBS-M)
In IBS-M, on days when you have at least one abnormal bowel movement
more than a quarter of your stools are hard or lumpy and
more than a quarter of your stools are loose or watery

Bear in mind that many people with IBS have normal bowel movements on some days and abnormal bowel movements on other days.

Who is more likely to develop IBS?

Women are up to two times more likely than men to develop IBS.1 People younger than age 50 are more likely to develop IBS than people older than age 50.2

Factors that can increase your chance of having IBS include:

  • having a family member with IBS
  • a history of stressful or difficult life events
  • having a severe infection in your digestive tract

What triggers IBS?

Whilst factor like stress make it more likely that a person will develop IBS, the immediate triggers to the condition are uncertain, and seem to vary. Likely triggers include the development of food sensitivities or intolerances, changes in gut bacteria (for example after treatment with a course of antibiotics) and carbohydrate malabsorption.

What other health problems do people with IBS have?

People with IBS often have other health problems, including1

  • certain conditions that involve chronic pain, such as fibromyalgia , chronic fatigue syndrome and chronic pelvic pain
  • certain digestive diseases, such as dyspepsia and gastro-oesophageal reflux disease
  • certain mental disorders, such as anxiety , depression and somatic symptom disorder

What treatments will help my IBS?

A range of lifestyle changes can keep people with IBS comfortable. These may include altering diet to avoid large and high-fat meals or any other known trigger foods. Adding probiotics and increasing fibre intake are also helpful to many.

Learning to relax, managing stress, improving sleeping habits and getting more exercise are also know to be beneficial.

When should you see a doctor?

It’s always advisable to see your general practitioner if you have symptoms suggestive of IBS, in order to confirm the diagnosis and rule out any other possible causes of your symptoms.

Symptoms which are not commonly associated with IBS and which should prompt an immediate visit to the doctor include significant or progressive abdominal pain, weight loss, rectal bleeding or bloody diarrhoea. Episodes of diarrhoea that wake you from sleep should also be further investigated.

You should also see your doctor if you have symptoms suggestive of IBS and also a family history of inflammatory bowel diseases like Crohn’s or ulcerative colitis, or you have suffered from anaemia, vitamin deficiencies or electrolyte disturbances.

Explore Further:

To read more articles from our Health Information Centre, the main index is here
If you’d like to explore our range of medication-free products to support relaxation and manage your levels of stress, then you’ll find them here
References:
[1] Chey WD, Kurlander J, Eswaran S. Irritable bowel syndrome: a clinical review. Journal of the American Medical Association. 2015;313(9):949–958.
[2] Lacy BE, Mearin F, Chang L, et al. Bowel disorders. Gastroenterology. 2016;150(6):1393–1407.
Source Material:
National Institute of Diabetes and Digestive and Kidney Diseases and Dr. Stephanie A. McAbee, from the Vanderbilt University Medical Centre Digestive Disease Unit.

Artificial sweeteners: Link to diabetes & obesity seems likely but…

By James Brown & Alex Conner

Many countries have introduced a sugar tax in order to improve the health of their citizens. As a result, food and drink companies are changing their products to include low and zero-calorie sweeteners instead of sugar. However, there is growing evidence that sweeteners may have health consequences of their own.

New research from the US, presented at the annual Experimental Biology conference in San Diego, found a link with consuming artificial sweeteners and changes in blood markers linked with an increased risk of obesity and type 2 diabetes in rats. Does this mean we need to ditch sweeteners as well as sugar?

Sweeteners are generally “non-nutritive” substances meaning we can’t use them for energy. Some of these compounds are entirely synthetic chemicals, produced to mimic the taste of sugar. These include saccharin, sucralose and aspartame. Others sweeteners are refined from chemicals found in plants, such as stevia and xylitol. Collectively, sweeteners are being consumed in increasing amounts with most diet or low-calorie food and drink containing some form of non-nutritive sweetener.

Combating or fuelling the obesity crisis?

Artificially sweetened foods and drinks have become popular largely due to the growing worldwide obesity crisis. As sugar contains four calories per gram, sweet foods and drinks are normally highly calorific. In principle, by removing these calories we reduce energy intake and this helps to prevent weight gain.

Increasingly, however, evidence suggests that consuming artificially sweetened products might be associated with an increased risk of being overweight or obese, although this is controversial. If true, it suggests that using sweeteners is fuelling, not fighting obesity. Research has suggested that consuming lots of artificial sweeteners scrambles the bacteria in our gut, causing them to make our bodies less tolerant to glucose, the main building-block of sugar.

The new research, from the Medical College of Wisconsin and Marquette University, looked at some biological effects of sweeteners in rats and in cell cultures. They wanted to know if artificial sweeteners affect how food is used and stored. These are called metabolic changes and the research combined many different aspects of metabolism to build an overall picture.
The team also looked at the impact of sweeteners on blood vessel health by studying how these substances affect the cells that form the inner lining of blood vessels.

The scientists gave rats food that was high in either sugar (glucose or fructose) or calorie-free artificial sweeteners (aspartame or acesulfame potassium). After three weeks they saw significant negative changes in both groups of rats. These changes included the concentrations of blood lipids (fats).

They also found that acesulfame potassium, in particular, accumulated in the blood and harmed the cells that line blood vessels. The study authors state that these changes are “linked to obesity and diabetes”. These results suggest that consuming sweeteners change how the body processes fat and gets its energy at a cellular level.

Many countries have introduced a sugar tax in order to improve the health of their citizens. As a result, food and drink companies are changing their products to include low and zero-calorie sweeteners instead of sugar. However, there is growing evidence that sweeteners may have health consequences of their own.

New research from the US, presented at the annual Experimental Biology conference in San Diego, found a link with consuming artificial sweeteners and changes in blood markers linked with an increased risk of obesity and type 2 diabetes in rats. Does this mean we need to ditch sweeteners as well as sugar?

Sweeteners are generally “non-nutritive” substances meaning we can’t use them for energy. Some of these compounds are entirely synthetic chemicals, produced to mimic the taste of sugar. These include saccharin, sucralose and aspartame. Others sweeteners are refined from chemicals found in plants, such as stevia and xylitol. Collectively, sweeteners are being consumed in increasing amounts with most diet or low-calorie food and drink containing some form of non-nutritive sweetener.

Combating or fuelling the obesity crisis?

Artificially sweetened foods and drinks have become popular largely due to the growing worldwide obesity crisis. As sugar contains four calories per gram, sweet foods and drinks are normally highly calorific. In principle, by removing these calories we reduce energy intake and this helps to prevent weight gain.

Increasingly, however, evidence suggests that consuming artificially sweetened products might be associated with an increased risk of being overweight or obese, although this is controversial. If true, it suggests that using sweeteners is fuelling, not fighting obesity. Research has suggested that consuming lots of artificial sweeteners scrambles the bacteria in our gut, causing them to make our bodies less tolerant to glucose, the main building-block of sugar.

The new research, from the Medical College of Wisconsin and Marquette University, looked at some biological effects of sweeteners in rats and in cell cultures. They wanted to know if artificial sweeteners affect how food is used and stored. These are called metabolic changes and the research combined many different aspects of metabolism to build an overall picture.

The team also looked at the impact of sweeteners on blood vessel health by studying how these substances affect the cells that form the inner lining of blood vessels.The scientists gave rats food that was high in either sugar (glucose or fructose) or calorie-free artificial sweeteners (aspartame or acesulfame potassium). After three weeks they saw significant negative changes in both groups of rats. These changes included the concentrations of blood lipids (fats).

They also found that acesulfame potassium, in particular, accumulated in the blood and harmed the cells that line blood vessels. The study authors state that these changes are “linked to obesity and diabetes”. These results suggest that consuming sweeteners change how the body processes fat and gets its energy at a cellular level.

Limit your intake

What does this mean for the average consumer of artificial sweeteners? As the study was performed in animals and not humans it would be wrong to draw firm conclusions about what might happen in people. The findings of the study do, however, add to the growing body of research that suggests that sweeteners are not benign alternatives to sugar.

The European Food Safety Authority suggests a daily limit to most artificial sweeteners of around five milligrams per kilogram of body weight, per day. With so many foods including artificial sweeteners now, it is relatively easy to reach this limit.

It is important to note that not all sweeteners are equal. This recent study focused on artificial sweeteners, like most of the research that has identified negative effects. Some sweeteners are associated with health benefits. Stevia, for example, has been shown to improve blood pressure and glucose tolerance while xylitol has been shown to help prevent tooth decay. This means that choosing the type of sweetener that you use may be more important than choosing a sweetener over sugar.

It is likely that the best advice is the blandest: everything in moderation. There is no such thing as good or bad food, only good or bad amounts. Maybe avoid consuming too much of either sugar or sweetener, especially in drinks.

Explore Further:

If you’d like to explore ways to support your psychological, physical and intimate health with our range of medication-free products, please return to our home page here

About the authors and source material:

James Brown is senior lecturer in biology and biomedical Science, Aston University, Birmingham; Alex Conner is senior lecturer in biomedical sciences, University of Birmingham. This article was first published in the online academic discussion journal ‘The Conversation’ on 23rd April, 2018. The original article, with active links and references, may be viewed here

SAD: Treating “Winter Blues” with light AND sound

The Application of Audio-Visual Entrainment for the Treatment of Seasonal Affective Disorder

By David Siever, Edmonton, Alberta, Canada.

Abstract: Seasonal Affective Disorder (SAD) strikes all people from all nations, not just those near the poles of the earth as might be thought. The treatment of SAD has traditionally involved the use of anti-depressants, and more recently, light box therapy. Audio-Visual Entrainment (AVE) has also been shown to be beneficial in the treatment of this genetically based affective disorder and its related anxious/depressive/dietary conditions.

Introduction: Each year, 6% of northern populations are affected with Seasonal Affective Disorder (SAD) and another 14% have a milder form of SAD, called the winter blues. Surprisingly, SAD may occur at any time of year and in equatorial regions although the ratio of northerners with SAD as compared to those living in the tropics is about 10-1. People in the southern USA experience SAD in the summer from staying indoors where air conditioning allows them to escape the unbearable summer heat. People have also experienced SAD moving into a basement suite or an office on the north side of a building or after painting the interior of their home a darker shade of color. People have experienced SAD following the development of cataracts or after wearing sunglasses for an extended period of time and during overcast, rainy periods (Rosenthal, 1993).

The common symptoms are depression, anxiety, extreme fatigue, hypersomnia, carbohydrate cravings, and weight gain. Women between the ages of 20 to 40, their sexually reproductive years, are most susceptible (Rosenthal, 1993). The first controlled study using light therapy to treat SAD was published in 1984. SAD was officially accepted as a clinical malady in 1987 by the American Psychiatric Association and described in its then current diagnostic manual, the DSM-III-R. Since that time, a great number of studies on the topic have been completed.

Animals are more sensitive to the seasons than humans, as they go through migration, mating, molting and hibernation. For instance, hamsters can sense the difference between a 12-hour day when their gonads don’t grow versus a 12-hour and 15 minute day when their gonads begin growth. It is thought that humans aren’t as sensitive as animals because humans originated in and around Africa where solar fluctuations are much more minimal than those near the Earth’s poles (Wright, 2002).

Tick-Tock Goes the Clock: It must be understood that circadian timing has nothing to do with the sense of time lapsing between events, nor the ability to notice differences in timing between two events, such as two tone-bursts or other sensory stimulation. Stimulation from events initiates an attentional cortical reset, which in turn synchronizes brain activity. More specifically, about 300 milliseconds later, the brain generates an attentional spike known as the P300 response. This spike starts a timing loop, initiated in the substantia nigra, a part of the basal ganglia, which in turn sends a burst of the neurotransmitter dopamine to another part of the brain called the striatum. The striatum contains “spiny” cells, which oscillate at different frequencies. Over time, the differences or “beats” add up. When attention is once again initiated, the count is recorded, providing a “time stamp” for that interval, which higher levels of the brain then interpret into a sense of timing (Wright, 2002).

The Captain and Pineal: All species studied to date, from single-celled organisms to humans, have been observed to have a biological clock. This clock is essential for survival, regulating various types and levels of arousal to provide cues for alertness, eating, sleep and the release of hormones. Light waves striking the retina activate electrical output that is sent down the optic nerve to the brain for visual processing. A secondary, smaller nerve tract from the retina, originating from specialized cells that utilize a light detecting pigment called melanopsin, also carries signals to the suprachiasmic nucleus (SCN) of the hypothalamus. The SCN, in turn, sends nervous outputs to various parts of the brain including the pineal gland. Four genes that govern circadian cycles in flies, mice and humans have been discovered that not only reside within the SCN, but in all cells of the body. When cultured in a petri dish under constant lighting, these cells continue with gene activity, hormone secretion and energy production in a 24-hour cycle that varies less than 1% (Wright, 2002).

In the mid 70s, Dr. Alfred Lewy of the National Institute of Mental Health (NIMH) discovered the neurotransmitter melatonin. The wake/sleep cycle in animals and humans is controlled by melatonin, which is produced by the pineal gland, a structure the size of a pea and located in the mid-brain. Every night, the pineal gland excretes melatonin into the bloodstream and continues to do so until dawn. However, under normal exposure to sunlight, secretions of melatonin follow the earth’s light/dark time frame and therefore more melatonin is typically released during the long dark hours of the winter months. Henceforth, the pineal gland is in charge or “captains” our wake/sleep arousal states.

Knowing if We Have SAD: Although most anxiety and depression inventories could be used to detect SAD, one popular SAD test is the Seasonal Pattern Assessment Questionnaire or SPAQ, developed by Rosenthal and his colleagues at the NIMH. The SPAQ is a self-assessment questionnaire that evaluates one’s level of SAD from four basic categories:

1) Pattern of seasonality
2) Degree of seasonality
3) The degree that seasonal changes are a problem for you
4) Evaluating other related information

SAD and Brain Function: Few PET or SPECT studies of brain metabolism in SAD persons have emerged and they are inconsistent in results. Both Cohen, et al’s, (1992) positron emission tomography (PET) study and a single photon emission computerized tomography (SPECT) study by Murphy, et al. (1993) were inconsistent in results. The results of electroencephalographic (EEG) studies are also inconsistent and involve few electrode sites (Volf & Passynkova, 2002). One such study suggests increased left frontal alpha activity as compared to the right (Allen, et al., 1993), which is consistent with common understandings of depression. Another found all activity except alpha was higher in the left posterior region (Teicher, et al., 1996) while another study showed increased theta-alpha at C3 (Cajochen et al., 1996). Volf sought to finally put the debate to rest by comparing 16 site QEEGs of 31 depressed SAD patients against those of controls. Barring technical issues (a digital filtering concern of aliasing error, possibly invalidating all data, arises within the study), he found asymmetries of delta, theta and alpha involving heightened EEG activity in the right parietal and temporal regions. An asymmetry of heightened beta EEG occurred in lateral frontal regions (F7 & F8).

Treatment: A number of coping techniques are used to reduce the symptoms of SAD. These include long walks outside, aerobic exercise, a diet rich in complex carbohydrates and protein, relocating to sunnier locations, winter vacations to tropical areas, and frequenting sun-tanning centres. Light-based clinical interventions include light box therapy and audio-visual entrainment.

“Light box” therapy has been used to reduce the symptoms of SAD in 60% to 80% of SAD patients (Lam, 1999). White light therapy, using intensities of 2,500 lux, requires exposure times from 2 to 6 hours, a considerable behavioral investment for the user (Terman, et. al., 1989). Light exposures in the intensity of 10,000 lux for 30-minute exposures have been found to be more effective than 2,500 lux intensity with exposure times of several hours (Terman, et.al., 1990). Some people have reported that over-use of light therapy can leave them feeling “wired” and restless (Rosenthal, 1993).

Audio-Visual Entrainment (AVE) using flashing lights and pulsing tones has been shown to enhance EEG activity at the stimulation frequency. However, a lesser known attribute of AVE lies in its inhibition effect at roughly the half-frequency of stimulation (Siever, 2003). In QEEGs (brain maps) collected at our office of those with SAD, we have observed long spindles of 10 Hz alpha brain wave activity, globally, with particularly increased activity in the left frontal regions, consistent with Allen’s findings. In light of these findings, we had chosen to utilize 20 Hz AVE as a treatment modality for SAD.

SAD Study Using Audio-Visual Entrainment: Method: The Digital Audio-Visual Integration Device (DAVID) Paradise by Comptronic Devices Limited (now Mind Alive Inc.) was used in a 4-week randomized study of 74 SAD sufferers (52 females and 22 males, avg. age = 38.5 years) to reduce the symptoms of SAD through the application of AVE. The participants were screened according to the DSM-IV, SAD requirements. The study accepted participants from November 1998 to March 1999 from Edmonton, Alberta (which is located approximately 53.5 northern latitude).

Procedure: The Beck Depression Inventory (BDI) and the Anxiety Sensitivity Index (ASI) were used for the pre-test, post-test (placebo), and the post-post-test (treatment) results. A daily diary was maintained to record total sleep time, sociability at work and with the family, eating, appetite and carbohydrate intake, cravings, energy and body weight.

The participants were divided into two groups: a Control Group (CG) that did not receive the DAVID AVE unit and the Treatment Group (TG) that received “placebo” and treatment sessions. The Treatment Group received sub-delta (placebo) frequencies of 1 Hz for two weeks followed by beta frequencies (treatment sessions) of 20 Hz for two weeks. Fifty-eight treatment participants and 16 control participants finished the study. Paired t-tests were used in the within group measurements, and the analysis of variance (ANOVA) was used in the between group measurements.

Results: The pre-test BDI score for both groups was 20.1. A score above nine indicates at least mild depression. Depression within the CG increased by 28% to a score of 26.1. A reduction in depression for 36% of the participants was observed in the TG during the placebo condition and during actual treatment (the beta AVE group) 100% of the participants had reduced depression (BDI = 7.3, p<0.001), as shown in Figure 1.

Figure 1 Comparison of BDI scores between controls, placebo & treatment groups

Of these, 84% became clinically non-depressed. The AVE male population anxiety sensitivity (AS) decreased significantly from 21% to 60% (p<0.001) from post to post-post, respectively while the control male population had a 7% increase in AS. The AVE female population showed decreased AS, from 15% to 34% (p<0.001) from post to post-post respectively, while the control group showed a mild reduction of 6%

Figure 2 Comparison of ASI scores between pre, post and post-post results.

Daily diary results (Figure 3) indicated marked improvements. Positive moods improved by 20%. Sociability at home with the family and at work improved by 22% and 40% respectively

Figure 3 Comparison of measures from pre to post-post conditions.

As shown in Figure 4, AVE participants’ food intake changed; over eating decreased by 18%, appetite decreased by 12%, and carbohydrate intake decreased by 15%. The participants also reported happiness with their increased energy (average increase of 18%)

Figure 4 Comparison of pre and post-post measures.

The daily diary results also showed that by using AVE, some participants lost considerable weight. A group of 12 participants (8 females and 4 males) reported that their average weight gain during the winter months was 15 pounds. During the placebo condition, they had an average weight loss of 3 pounds (1.36 Kg) plus an additional average weight loss of 6.5 pounds (4.3 Kg) during the two-week treatment condition.

Conclusion: White light AVE at 20 Hz produced significant results. Although sub-delta frequencies are non-effective at generating entrainment, sub-delta frequencies can affect both dissociative mind states and cerebral blood flow (Fox & Raichle, 1985). In addition, the “placebo effect” could also explain the sub-delta significance. The “placebo effect” has been shown to reduce anxiety, increase endorphin production, conditioning, and expectancy (Godfroid, 1998). Being that inadequate light elicits depression in SAD sufferers, the “placebo effect” via photic stimulation is possible.

The AVE Group’s depression decreased while the Control Group’s depression increased. Sensitivity to anxiety decreased in both male and female AVE groups. Although the female control participants had decreased sensitivity to anxiety, the female AVE population showed significance between the 1 Hz and 20 Hz stimulation.

Most control group participants claimed that they gained weight whereas an additional benefit of AVE is weight loss. One participant claimed that, “after using the 20 Hz session for 2 weeks, the taste of sweets in my mouth was repulsive.” Follow-up reports indicate participants’ SAD symptoms returned within an average of 2 weeks after discontinuing use of the DAVID AVE device.

Explore more:

To view our range of Audio-Visual Entrainment (AVE) devices, manufactured by Mind Alive Inc, the world’s leading developer of the technology, please click here

References: 

Allen, J., Locono, W., Depue, R., & Arbisi, P. (1993). Regional encephalographic asymmetries in bipolar seasonal affective disorder before and after exposure to bright light. Biological Psychiatry, 33, 642-646.

Cajochen, C., Brunner, D., Krauchi, K., Graw, P., & Wirz-Justice, A. (2000). EEG and subjective sleepiness during extended wakefulness in seasonal affective disorder: circadian and homeostatic influences. Biological Psychiatry. 47, (7), 610-617.

Cohen, R., Gross, M., Nordahl, T., Semple, W., Oren, D., & Rosenthal, N. (1992). Preliminary data on the metabolic brain pattern of patients with winter seasonal affective disorder. Archives of General Psychiatry, 49, 545-552.

Fox, P. & Raichle, M. (1985). Stimulus rate determines regional blood flow in striate cortex. Annals of Neurology, 17, (3), 303-305.

Godfroid, I. O. (1998). Placebo II. Psychiagenia and the brain organization. Annales Medico-Psychologiques [French], 152 (2), 108-114.

Lam, R .W. (1999). Information about seasonal affective disorder (SAD). University of British Columbia/VHHSC Mood Disorder Clinic. Retrieved on www.psychiatry.ubc.ca/mood/md_sad.html.

Murphy, D. G., Murphy, D. M., Abbas, M., Palazidou, B., Binnie, C., Arendt, J., Campos Costa, D., & Checkley, S. (1993). Seasonal affective disorder: response to light as measured by electroencephalogram, melatonin suppression and cerebral blood flow. British Journal of Psychiatry, 163, 327-331.

Rosenthal, N. E. (1993). Winter blues: What it is and how to overcome it. New York: Guildford Press.

Siever, D. (2003). AVE session protocol guide for professionals. Available from Mind Alive Inc., Edmonton, Alberta, Canada.

Teicher, M., Glod, K., & Ito, Y. (1996). Hemispheric asymmetry of EEG and T2 relaxation time in seasonal affective disorder (SAD) pre and post-light therapy. In: SLTBR: Abstracts of the Annual Meeting of the Society for Light Treatment and Biological Rhythms. p. 9.

Terman, M., Terman, J., Quitkin, F., McGrath, P., Stewart, J., & Rafferty, B. (1989). Light therapy for seasonal affective disorder: a review of efficacy. Neuropsychopharmacology, 2, 1-22.

Terman, J., Terman, M., Schlager, D., Rafferty, B., Rosofsky, M., Link, M., Gallin, P., & Quitkin, F. (1990). Dentification, assessment, and treatment of seasonality in mood disorders. Psychopharmacology Bulletin, 26, 1, 3-11.

Volf, N. & Passynkova, N. (2002). EEG mapping in seasonal affective disorder. Journal of Affective Disorders, 72, 61-69.

Wright, K. (September, 2002). Times of our lives. Scientific American, 287 (3), 59-65.