March 16, 2016

Does Fat Play A Role In The Development of Alzheimer’s Disease?

March 16, 2016/ Guest User

Claire Galloway

Originally published April 9, 2015

Due to the growing prevalence of Alzheimer’s disease and limited efficacy of drugs for the associated memory-loss symptoms, scientists and non-scientists alike are interested in the potential for practical lifestyle changes such as diet to reduce the risk of developing Alzheimer’s disease and memory loss.

The food you eat can alter the chances you and your loved ones will develop diseases such as Alzheimer’s or dementia. Yet even if you’ve merely dipped your toe into the vast ocean of information on nutrition and Alzheimer’s disease, it’s easy to become confused about which foods or food-types you should add to or remove from your diet if you want to reduce your risk of developing Alzheimer’s disease.

Unlike the protective effect of some foods, such as leafy green vegetables, the role of fat and fatty foods in Alzheimer’s disease risk seems to be less understood, and controversial. What does seem to be clear is that it’s role in Alzheimer’s disease is a little complicated. Luckily, despite the present uncertainty about whether some types of fats or specific fatty foods are actually beneficial or harmful, the research on diets and Alzheimer’s disease risk does seem to coalesce around some common themes that can be translated into real-life changes. What seems most certain is that not all fats are created equal.

What fatty foods should I avoid? Red meat & Dairy.

Consumption of saturated fats – including those found in red meats and high fat dairy – has been linked to lower cognitive performance in healthy elderly people, as well as an increased risk of developing dementia or being diagnosed with Alzheimer’s disease.

Saturated fat intake may increase Alzheimer’s disease risk or exacerbate cognitive decline by degrading the integrity of the blood brain barrier (which usually protects the brain from potentially harmful agents in the blood), increasing inflammation in the brain, or decreasing the ability of brain regions important for memory to use glucose for energy.

Saturated fats also increase cholesterol, which is involved in the regulation of the beta-amyloid proteins that are thought to play a major role in driving the disease process. In short, you may want to hold off on the cheese burgers.

What fatty foods should I eat? Fatty Fish.

Several epidemiological studies have found that the more people report consuming fatty fish, the less likely they are to develop cognitive impairments and be diagnosed with Alzheimer’s disease or dementia.

The “fattiness” of the fish is likely key to the protective benefit, as the consumption of lean fish has been linked to an increased risk of developing dementia. It also seems likely that the particular fat itself found in fish, mainly polyunsaturated fats that are rich in Omega-3 Fatty Acids, may play a role in keeping the neurons in your brain healthy and communicating effectively.

Indeed, positive results from clinical trials with just Omega-3 Fatty Acid supplements corroborate the role of these fatty acids in improving cognition – or at least slowing cognitive decline in healthy elderly and Alzheimer’s disease patients. Studies in animals have found that Omega-3 Fatty Acids may also prevent Alzheimer’s disease by enabling the synthesis of Acetylcholine, a neurochemical important for attention and memory that is drastically reduced in the brains of Alzheimer’s disease patients. Omega-3 Fatty Acids may also promote the clearance of some of the pathological proteins (e.g. beta-amyloid) that likely drive the disease process.

However, the benefits of from eating fatty fish may go beyond their fattiness: Fatty fish are also a rich source of minerals that may protect against oxidative stress that occurs during aging and Alzheimer’s disease. For example, sardines contain high levels of Selenium, a mineral with antioxidant properties that is decreased in Alzheimer’s disease patients. To reap some of these promising benefits, pile your plate high with fatty fish such as salmon, sardines, and mackerel.

What fatty foods should I be cautious about? Coconut Oil.

Excitement over the health benefits of coconut oil seems to have taken the internet world by storm. It’s purported role in Alzheimer’s disease is largely driven by the testimony of one physician who reported that giving her husband coconut oil actually reversed his Alzheimer’s disease symptoms.

However, coconut oil specifically has not been linked to Alzheimer’s disease risk in epidemiological studies, and there seem to be no clinical trials that have systematically evaluated the effects of coconut oil.

In animal studies, some have found beneficial effects on cholesterol levels (e.g. less of the “bad” LDL cholesterol) and cognition, whereas others report harmful effects on cholesterol levels and cognition. There could be many reasons for these inconsistencies, but one possibility is that the optimal amount of dietary coconut oil to consume in order to ward off dementia lies within a narrow range.

Indeed, a mere tablespoon of coconut oil has 12g of saturated fat – which is over half of your recommended daily intake. So what is driving all the hype? The saturated fat in coconut oil mostly consists of medium-chain-triglycerides, which may not be as harmful as the long-chain-triglycerides found in cow milk, for example. In fact, medium-chain-triglycerides are converted into ketones, which serve as an alternative energy source for the neurons in your brain. This could be especially helpful in Alzheimer’s disease, as the neural and cognitive dysfunction may be partly due to the decreased ability of Alzheimer’s disease brains to properly metabolize and use the primary energy source of the brain, glucose.

Even more promising, some studies have also found that ketones may be able to protect neurons from beta-amyloid and its associated attacks on neuronal function. Nevertheless, you may want to restrain from dousing your food in coconut oil until scientifically-rigorous research has time to catch up to the enthusiastic anecdotes that can be found on the internet. In the meantime, coconut oil in low amounts is probably a good alternative to butter and margarine, but only in those recipes in which a rich source of Omega-3 Fatty Acids – such as olive oil – simply will not do.

An important caveat to remember is that your genetic background can play an important role in the efficacy of nutritional interventions. For example, many nutritional correlations or interventions show no effect or even an opposite effect in carriers of the APOε4 allele, a gene that codes for a protein involved in blood cholesterol transport. It may be worthwhile, then, to find out whether you or your loved one is a carrier before implementing any dietary change to lower your Alzheimer’s disease risk.

Another important thing to remember is that Alzheimer’s disease normally occurs late in life, when the nutritional status and dietary patterns reflect decades of habits of eating. Not to mention other lifestyle habits – such as physical activity levels or coping with stress – that may synergistically or antagonistically interact with your diet to affect your overall risk. That is, it may not be possible to reverse 70 years of cheeseburgers with 2 years of sardines.

All things considered, it is very unlikely that we will find a secret, super-diet that will protect us all from Alzheimer’s disease and dementia. If anything, dietary changes are more likely to delay the onset, decrease the speed of cognitive decline, or otherwise lessen the severity of Alzheimer’s disease in subtle ways.

However, given the limited treatment options for Alzheimer’s disease, incorporating a few relatively inexpensive and tasty diet changes is worthwhile. Especially when a particular diet or food has other known benefits – such as reducing your risk of developing diabetes and heart disease or promoting healthy weight loss – what do you have to lose?

Edited by: Anzar Abbas

March 16, 2016

The Mystery of Alzheimer’s: is it an Autoimmune Disorder?

March 16, 2016/ Guest User

Kevin Sullivan

Originally published April 2, 2015

There is a good chance that you personally know someone suffering from Alzheimer’s disease. This is unsurprising, as it is estimated that one out of every nine people over 65 is affected, making it the most common form of dementia. Initially, someone with Alzheimer’s will show signs of forgetfulness and disorientation which may not be immediately noticeable. A person might find themselves losing their keys more often or asking the same question multiple times in a conversation without realizing it. These symptoms gradually get worse over a period of three to nine years, leading to more severe memory loss, mental and physical impairment, and eventually resulting in death. According to the 2014 World Alzheimer Report, 44 million people are living with dementia worldwide, with the number set to double by 2030. Aside from the devastating emotional costs imposed upon the individuals and their care providers, usually family members, the economic impact of dementia is an imposing figure. In 2010, the cost of care for dementia was $604 billion, with costs expected to exceed $1 trillion by 2030.

Decades of research have revealed several risk factors for the disease, such as age, head trauma, heart disease, and sex (women may be more susceptible than men). Despite information about these risk factors and studies revealing the differences between the brains of people with Alzheimer’s relative to those of healthy people, the exact cause still remains a mystery. In recent years, researchers have discovered many clues that have gotten us closer to solving this mystery. One of the key findings is that the degeneration of the brain in Alzheimer’s is associated with the presence of protein fragments called amyloid beta peptides. Amyloid beta is present in healthy brains as well, but problems arise in Alzheimer’s when these peptides become folded in an incorrect way, causing them to associate with one another and form clumps, called plaques, which deposit in the brain.

Another major finding is that tau proteins, which normally help to stabilize the structural components of cells, can become defective in Alzheimer’s disease, causing them to get tangled up and deposit in the brain. Both amyloid beta plaques and tau protein tangles are quite toxic to nerve cells and eventually result in the death of the neurons that make up the brain. Despite these and a variety of other clues that have been discovered, Alzheimer’s is plagued by the classic chicken-or-egg question: which of the observed problems are causes of the disease, and which ones are a result of the disease process? So far, this question has been very difficult to answer. Only one form of Alzheimer’s, known as early onset familial Alzheimer’s disease, has a definite cause involving a mutation in specific genes that produce amyloid beta proteins. However, these mutations are the cause of only 1 to 5 percent of cases, while the origin of the rest of the cases remains unclear.

The field of Alzheimer’s research is rapidly advancing, with new discoveries made nearly every day. One intriguing recent discovery suggests that an immune response may be responsible for the progression of Alzheimer’s disease. In a March 2015 review published in Nature Immunology, a group led by Michael T. Heneka from the University of Bonn explained some of these recent findings. One of these hypotheses proposed explains that, because amyloid beta is found in several different viruses and bacteria, the body developed an immune system response to the peptide in order to fight off these pathogens. In some cases, the immune response can become misdirected and targets the amyloid beta found in human tissue instead of that of an invader, which is known as an autoimmune response. When the immune system attacks tissue within the brain, it causes damage to the local neurons and leads to destruction of brain tissue.

The immune response in the brain is controlled by cells called microglia. These cells act as the guard dogs of the central nervous system, both defending against infections and scavenging damaged cells and waste found around the brain. Much like certain dogs, they can have extremely strong reactions to even small disturbances. This sensitivity, while quite advantageous for quickly responding to threats, can also have major consequences if they become so sensitive that they start attacking human tissues. Once the microglia are activated, they release molecules that trigger inflammation in surrounding tissue. Inflammation is a process that normally helps to eliminate the initial cause of an injury and help with tissue repair, but persistent inflammation will result in significant cellular damage. Moreover, this response actually makes it more difficult for the body to clear beta amyloid plaques, causing a negative feedback loop that results in even more plaque deposition in the brain.

Adding more evidence to this theory, a new study published in the Journal of Alzheimer’s Disease on February 2015 by the Bieberich lab at Georgia Regents University demonstrated that an autoimmune response might be responsible for the progression of the disease. Researchers have discovered that a molecule called ceramide, mainly found in membranes surrounding cells throughout the body, can be targeted by the immune system. This immune response causes an increase in antibodies that destroy ceramide in the brain. The researchers found that when amyloid beta plaques start to build up in the brain, certain cells begin producing more ceramide. The ceramide is then targeted by the immune system, causing inflammation and increasing the amount of amyloid beta in the brain. These new studies suggest that our own immune response, then, may be what is ultimately responsible for the advancement of the disease.

While we may still not know the root cause behind the mystery of Alzheimer’s disease, these new findings have revealed another important clue, which is that autoimmune responses may play a significant role in the progression of the disease. One of the exciting aspects of this research is that it opens up a whole new set of opportunities to treat Alzheimer’s using therapeutics that target the microglia or reduce inflammation in the brain, which may be able to slow down the progression of the disease. More effective treatments are sure to significantly address the mounting healthcare costs associated with the growing population afflicted with this disease. More importantly, these new treatments have the potential to provide life-altering relief to those currently suffering from Alzheimer’s.

Edited by: Marika Wieliczko

March 15, 2016

Possessed: Demons of the Mind

March 15, 2016/ Guest User

Kristen Thomas

Originally published October 31, 2014

One day your teenage son becomes convinced that someone is in his head. This person provides a running commentary on your son’s life and every move he makes. Your son can hear this voice as clearly as yours when you stand before him. Your son socially withdraws from you, his friends, and everyone else, and this voice becomes his only companion. When your son does speak to you, it seems disjointed and confused. Then one day reveals that the voice in his head belongs to a demon, and this demon has taken control.

Although this may sound like the first 30 min of the latest exorcism movie, psychiatrists would recognize these behaviors as symptoms of schizophrenia, a neurodevelopmental disease that affects approximately 1% of the world’s population. Hallucinations (e.g. hearing voices) and delusions (e.g. believing someone possesses control over a person’s actions) are perhaps most commonly associated with schizophrenia, but the symptoms of schizophrenia are diverse and complex. Other symptoms may be cognitive (e.g. disorganized thinking and speech) or negative (e.g. social withdrawal and depression). No two patients have exactly the same symptom profiles. Most patients first develop symptoms in their late teens or early 20s and battle this disease for their entire lives.

The Dark History of Schizophrenia and Mental Illness

According to a 2008 survey, 85% of people understand that schizophrenia is an illness with a physical basis, yet throughout history schizophrenia and other forms of mental illness were thought to be the result of demonic possession or witchcraft. During the Middle Ages and Renaissance, the Catholic Church promoted the view that people who suffered from mental illness should be treated through religious means: confession in the case of witchcraft or exorcism to remove the demon spirit. Perhaps consequently, those who suffered from mental illness were treated with fear and disgust.

The first asylums opened in the 14th century and used brutal means to control its mental patients. Patients were often chained to the walls or fastened to their beds. In extreme cases flaming pitch was applied to the patient’s head. Mental patients only began to experience more humane treatment in the 18th and 19th centuries. However, even these “humane” treatments included bloodletting, a prolonged withdrawal of blood that also sedated unruly patients by weakening them. Throughout history the horrors suffered by mental patients have been far more worthy of Hollywood’s horror film genre than the behaviors of the patients themselves.

Although schizophrenia patients receive more humane treatment today, the belief that their condition may be the result of demonic possession rather than a brain disorder still resurfaces. Any Google search for “demons and schizophrenia” will yield a variety of spiritual and occult websites claiming to be able to differentiate demonic possession from schizophrenia. In June of this year, the Journal of Religion and Health published an article by the Turkish researcher M Kemal Irmak. According to the author, demons reside in a parallel world, unseen by most humans, but they may also possess and control humans. He also claims that many modern cases of demonic possession have been misdiagnosed as schizophrenia and urges medical doctors to enlist the services of faith healers in such cases.

A Scientific Interpretation: Debunking the Demon Myth

Science is equipped to deal with exploration of physical phenomena within our own world––not that of demons. However, decades of research have shown that the symptoms of schizophrenia are due to physical changes within the brain, and they may be treated using medical rather than religious means.

The first antipsychotic medications were introduced during the 1950s. Early and modern antipsychotics alleviate positive symptoms as well as some of the cognitive symptoms of schizophrenia by blocking the activity of dopamine, a signaling molecule within the brain. No approved antipsychotics treat the negative symptoms, which are often debilitating. Fortunately, many schizophrenia patients are still able to lead productive, independent lives under a lifelong treatment regime.

The last few decades have also greatly expanded our understanding of the physical basis of this disease. Schizophrenia is highly heritable: if one identical twin is diagnosed with schizophrenia then the other twin has about a 50% chance of also developing the disease. The genetics of schizophrenia are highly complex, and thousands of different genes have been linked to schizophrenia, many of which have also been linked to autism, Tourette’s syndrome, or other cognitive disorders. Environmental factors, including early life stress and drug abuse, also appear to interact with genetic factors to further influence disease development.

Perpetuating the Stigma of Schizophrenia

Despite the advances made in our understanding and treatment of schizophrenia, the average patient experiences a nine year delay between their first symptoms and first diagnosis and treatment. Part of the problem is misdiagnosis: other mental diseases, including major depression, can have similar symptoms. Furthermore, many physicians are reluctant to diagnose a patient with schizophrenia due to the stigma that many patients experience following diagnosis.

Schizophrenia is one of the most highly stigmatized diseases in our society. Many patients are reluctant to tell others about their diagnosis because many people are afraid to work with, date, or admit that they are related to someone with schizophrenia. This stigma not only delays diagnosis but also means that at any given time more schizophrenia patients are homeless or imprisoned than in a mental hospital. Stigma also affects the allocation of research funds: schizophrenia receives less funding per person affected than other mental disorders, e.g. Alzheimer’s disease or depression, yet schizophrenia is one of the most costly diseases to society.

If most people recognize that schizophrenia is a physical illness, then why does this stigma still exist? After millennia of association with supernatural and often evil forces, our society has been slow to accept the mentally ill without fear or reservation. The news media reinforces this stigma by reporting on crimes committed by those suffering from untreated mental illness, though patients are far more likely to harm themselves than others. As you view The Exorcist and similar horror flicks this Halloween, ask yourself whether these films also perpetuate the stigma. The myth of demonic possession and the history of schizophrenia have been closely entwined for centuries, and science must continue its work to disentangle them within our society.

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