Disease/Health/Hot topics

Putting the Puzzle Pieces of Autism Together

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Autism spectrum disorder is the term used to describe a range of neurodevelopmental disorders characterized by communication difficulties, social impairments, and repetitive, restricted, and stereotyped behavior. The U.S. autism rate is currently 1 in 68, though it remains to be determined whether this is due to an increase in prevalence or diagnosis. The severity of autism can range from a milder form, Asperger syndrome, to the most severe form, autistic disorder. Most cases are identified before the age of 3. Hallmark features in infants are unresponsiveness to people or an intent focus on one item with the exclusion of other items for long periods of time. Children with ASD may fail to respond to their own names and avoid eye contact with other people. Additionally, ASD children engage in repetitive movements such as rocking or self-abusive behavior like head-banging or biting. They have difficulty interpreting the thoughts and feelings of others because they do not understand social cues such as facial expressions or tone of voice. A variety of influential factors contributing to the onset of ASD have been identified, though the exact cause of ASD has yet to be determined.

Autism Diagnosis

Below is a list of indicators used in the diagnostic process of autism. Severe cases of autism are usually diagnosed at a much earlier age than milder cases. Asperger’s syndrome, a mild form of ASD, is typically identified by later indicators. Individuals with Asperger’s have relatively normal intelligence and cognitive ability but impaired social functioning. Diagnosis is completed through a comprehensive evaluation by a team including a psychologist, psychiatrist, neurologist, speech therapist, and other professionals involved in ASD diagnosis.

Early indicators

  • no pointing or babbling by age 1
  • no response to name
  • poor eye contact
  • loss of social skills or language
  • no single words by 16 months or 2-word phrases by age 2
  • no smiling or social responsiveness
  • excessive lining up of objects or toys

Later indicators

  • impaired ability to initiate/sustain a conversation with others
  • impaired or absent imaginative or social play
  • impaired ability to make friends with peers
  • preoccupation with certain objects or subjects
  • repetitive, stereotyped, or unusual language use
  • restricted patterns of interest with abnormal focus and intensity
  • inflexible adherence to specific rituals or routines

Contributing Factors to ASD Onset

Although genetic factors are involved in ASD onset, they only account for 15% of autism cases. Maternal nutrition, infection during pregnancy, prematurity, and parental age are among the environmental factors implicated in ASD. Immune system abnormalities and zinc deficiency also play a role in altered synaptic transmission present in ASD.

  • Fetal brain development failures are connected to an increased autism risk. Infections associated with autism include: prenatal influenza, rubella, and cytomegalovirus infections.
  • Zinc Deficiency is present in those with ASD. Zinc is the second most abundant trace element in the body, and is implicated in processes such as cell division and differentiation. A deficiency of zinc causes neuropsychological symptoms, memory and learning impairments, behavioral issues, and enhanced glutamate excitotoxicity. Zinc deficiency is also connected to compromising the immune system, which may be connected to prenatal infection risk.
  • Abnormal melatonin synthesis may also be implicated in autism. Melatonin is a neurohormone responsible for regulating circadian rhythms, the body’s internal clock involved in regulating the sleep/wake cycle. Low melatonin levels are observed in individuals with ASD. Children with ASD have sleep abnormalities such as frequent interrupted sleep, reduced duration, and prolonged sleep onset latency. The circadian abnormalities ins ASD may be due to genetic abnormalities related to melatonin synthesis.
  • Maternal diabetes is another ASD risk factor. Obesity, diabetes, and hypertension have been found to occur more often in mothers of ASD children. Obesity has the most significant association with ASD risk.
  • Prenatal stress may also increase ASD risk. Prenatal exposure to stress hormones or psychological stress has been shown in various studies to result in abnormal infant immune function that persisted to late childhood. A high stress environment during the prenatal period can prolong the activation of the HPA axis, which is involved in the body’s stress response. Prolonged HPA activation lowers the immune system’s ability to fight off infection.
  • Prenatal exposure to valproic acid, an anticonvuslant has also been implicated in ASD onset. Valproic acid is a medication used to treat epilepsy and bipolar disorder.
  • Increased parental age in both the mother and the father are connected to ASD risk. Paternal age is linked to ASD risk due to a greater number of mutations present in older sperm that can increase ASD risk. Maternal age is connected to ASD risk through increased pregnancy complications and autoimmunity.

 Take-Home Message

The extensive list of possible contributing factors and recent statistics regarding autism is daunting, but it is important to note that the presence of one factor does not necessarily guarantee ASD onset. The identified factors are implicated in ASD, but their relationship to one another is not fully understood. One ASD factor that has been affirmatively ruled out is vaccination. This is NOT connected to ASD in any way, though this idea still seems to continue to circulate. The researcher who conducted the vaccination study was stripped of all medical practicing abilities after it was revealed that the study and data were fabricated. Individuals with ASD greatly benefit from treatment such as social skills training, speech therapy, and applied behavioral analysis. Some medications can be used for side effects such as obsessive-compulsive disorder or anxiety, though the presence of these side effects vary from one case to another. Hopefully with continued research, we can identify the link between the contributing factors and perhaps determine the cause of ASD.
For more information on autism:  http://www.ninds.nih.gov/disorders/autism/detail_autism.htm
http://www.autismspeaks.org/
Sources:
Image link: http://img.washingtonpost.com/news/to-your-health/wp-content/uploads/sites/26/2014/03/1-in-68-graphic-with-logo-296×398.jpg

Disease/Health

A Disorder of Growing Uncertainty: Autism

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Global rates of autism have been increasing, and although we have identified several genes and environmental factors with development of the disease, the ultimate cause is yet to be determined.  One might argue that this global increase in autism rates is due to increased diagnosis and classification of the disease.  While this could be true, it is not the whole story.

There have been many different genes associated with autism.  Most of these genes are caused by certain mutations that occur within the genome.  While parents may not carry the mutation themselves, it is possible for the mutations to occur in their reproductive cells or to the baby during pregnancy.  Many different environmental factors have been connected with increased risk of gene mutations.  As you can see in the figure below, mutations can be attributed to Mendelian Disorders, rare de novo mutations, and chromosome abnormalities.

The question that is trying to be answered now is what makes up the remaining 77% of genetic mutations?  Studies have shown connections between environmental factors during pregnancy and early development and rates of autism. These environmental factors include:
Prenatal Viral Infection: Maternal infection and complication of immune system health during pregnancy has been integrally linked with development of autism.
Zinc Deficiency:  Zinc deficiencies have been observed in autistic children.  This deficiency could play a large role in gene expression.
Abnormal Melatonin Synthesis:  Inability to produce sufficient melatonin has been observed at high rates in autistic patients.  This abnormal melatonin synthesis leads to complications in the circadian rhythm, leading to abnormal sleep patterns.
Maternal Diabetes:  Maternal diabetes during pregnancy has lead to a twofold increased risk of the child developing autism.
Prenatal and Perinatal Stress:  High levels of stress have been associated with increased risk of autism.
Toxins: Many toxins have also been associated with gene dysfunction and the development of autism.
Parental Age:  The age of both mother and father have a profound influence on the development of autism.  The older the parents are, the more likely complications will occur in pregnancy, leading to autism.
Postnatal Risk factors:   Gastrointestinal abnormalities, allergies, exposure to drugs, infection, and heavy metals have also been associated with development of autism after birth.
 
Many different causes have been proposed, and currently there is no one cause that stands out as the one and only cause to the disorder.  Further research must be done to better understand autism and how it can be prevented.  However one thing is certain.  Vaccination has been discounted as a source of autism.  So parents, DON’T HESITATE, VACCINATE!!

Disease/Health

Incidence of Autism linked to Stress?

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Autism is a neurodevelopmental disorder that is characterized by impairment in communication and social behavior and by repetitive behaviors.  Like most any other disease that affects someone for the majority of their life, a large portion of the cause of autism is due to genetic factors but genetics is unable to account for all cases of autism.  So this brings up the effects that our environment has and its implications in the onset of autism.  The most critical time for the environment to have it effects on an individual causing autism is while the mother is carrying her child during pregnancy.  Recent research has shown many imbalances due to environment during pregnancy lead to autism and in particular the mother being stressed.
Normally during pregnancy a woman has elevated levels of cortisol which is the body’s natural stress hormone, but this slight elevation during pregnancy is important for a normal pregnancy.  If, for some reason, the cortisol levels of the pregnant woman were to increase to abnormally high levels research has shown that cortisol from the mother that is able to reach the fetus may potentially alter fetal development and growth, which in the case of neurodevelopment could be extremely detrimental.  It has been shown that the cortisol levels of pregnant women can increase to abnormally high levels during particularly stressful situations such as major storms or natural disasters.  Research has also shown that the placenta is also affected by stress by releasing Corticotropin releasing factor that can cross the blood brain barrier and cause damage to the function and integrity of the hippocampus of the developing fetus.  Another stress to the mother that could be harmful to the fetus is sickness.  Research has shown that if the mother contracts a virus or bacteria that are able to reach the fetus likelihood of the fetus developing autism is much higher.
After reading this article I think that it is very important to make sure that the environment that a fetus is developing in is as stable and safe as possible to ensure the healthiest offspring possible, but at the same time I don’t think that it is something to be so worried about that people start to panic and quarantine their pregnant woman to prevent disease.  If you think about it the fact that there aren’t more diseases or incidence of autism is amazing because there are so many things and ways that things can go wrong in the development of a fetus that a completely healthy newborn is in itself a miracle.  I think that is just a testament to how amazing the human body is and well it does what it does.

Health

Autism: An Environmental Perspective

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Autism is a spectral disorder that is becoming commonly diagnosed. In fact, 1 in 68 children are diagnosed as part of the spectrum. This brings up the question whether the criteria for diagnosing are becoming fine-tuned and therefore more accurate or whether people are stretching the diagnosis because parents demand an answer to why their child is “different.”  Because it is a spectrum disorder, autism includes a broad range of social, behavioral, and cognitive deficits. From high-functioning cases of individuals with high IQs and low social skills to cases where communication is not possible, there is no one way to define autism.
Just as with all facets of development, there is a balance between genetics and environment that plays into expression of hereditary traits. There are a number of genes that predispose an individual to becoming autistic, but what is most interesting is the role of environmental factors. Since most cases of autism of diagnosed in early childhood, it is possible that fundamental structures in the brain are altered while in utero, but are not noticed until key developmental periods. Parents might see cognitive deficits from delayed speech progression, abnormal social behaviors, repetitive behaviors, etc. The phenotype for autism lies in the neurological changes in the brain which include alteration of important synaptic proteins needed for long term potentiation. In addition, autistic individuals have a smaller amygdala and hippocampus.  The amygdala is important for emotions, emotional behaviors, and motivation while the hippocampus is important for long-term memory. This week’s article focused on how prenatal environment affects the neurological development of the autistic brain.
The author suggests two central components to environmental factors are immune system abnormalities and zinc deficiencies. Maternal stress is one contributor to the altered immune system and changes within the brain. Specifically, mothers under stress have high levels of cortisol which cross the placenta and alter the neurological development. The small hippocampus of autistic patients also leads to high cortisol secretion which may also contribute to abnormal growth. Parental age of both the mother and father contributes to the increase the risk for autism in the offspring. Mothers over 30 years old are more likely to have an autoimmune disorder. The antibodies of these mothers may inappropriately target the growing fetus during critical periods of development. Fathers have an increased risk of sperm mutations with age. Lastly, prenatal infections such as influenza may cause inflammation of the brain. The other major factor for autism, zinc deficiency, actually plays into the altered immune system because low levels of zinc promotes inflammation and impairs immune responses. In addition, zinc deficiency causes gastrointestinal abnormalities commonly linked to autism.
There are many hypotheses for how these abnormalities lead to autism. The immune system alters long term potentiation, a mechanism required for learning and memory. In addition, pro-inflammatory cytokines can affect neurotransmitter release and the ability to send neurological signals.  The modification of NMDA receptors necessary for excitation of the neuron is another possible mode of action. There are many other mechanisms touched on in the paper, but I focused on the immune system mechanisms.
Many factors increase the risk for autism, but there is not a complete understanding of the mechanism. Does a zinc deficiency cause autism, or is it merely a side effect? More research is required to form the complete picture of the genetic and environmental causes. Autism might be diagnosed more and more because parents want a single answer to certain quirks or abnormalities of their child. However, autism might be expressed to greater degree because of our culture. Our generation starts families later in life to allow time to establish their careers. In addition, our fast-paced society may contribute to the stress of mothers, producing a dangerous environment for a fetus. No longer are people in the dark or misinformed about what causes autism. I think education is the first step in understanding autism spectrum disorder and moving towards a better understanding.
Resources:
http://www.autismspeaks.org/what-autism

Community/Disease/Health/Hot topics

Obesity: What happens when you can't trust your gut

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Obesity is frequently demonized as a disease of laziness – one that people could avoid if they would only get off the couch and eat healthier. Recent research, however, has identified several brain-related components to this disease, possibly enough to categorize it as a brain disorder. While it is true that some individual responsibility is required for overcoming obesity, several other factors must be understood in order to really tackle this issue.
Much of the brain dysfunction that occurs in obesity does appear to come as a result of high-fat diet. Chronic intake of high amounts of fat can inflame and damage some parts of the brain, including the hypothalamus, which controls hunger (among other homeostatic processes, like sleep).  Inflammation in the rest of the brain will eventually lead to a cascade of events resulting in loss of memory function. Overconsumption of carbohydrates, another obesity-associated eating behavior, can lead to insulin resistance, which has been shown to have a negative effect on cognition and induces type 2 diabetes. But if an unhealthy diet causes obesity and so many other health issues, how can people not be expected to assume more responsibility for themselves?
First to consider are the social issues linked with obesity. There is the obvious issue of fast food and other generally unhealthy food being usually cheaper than more nutritional food. This especially affects low-income communities: one 2010 study found that BMI and income were inversely related, indicating a correlation of low wages to increased risk for obesity. Not only are there many factors that can predispose people to being obese, but once weight gain begins, it can be hard to go back. This is especially true when exposure to high-fat foods begins early in life. For example, rats exposed to a high-fat diet when nursing or pregnant leads to overweight offspring. Additionally, another study found that when rats are exposed to the same type of diet during the postnatal growth period, they tend to favor high-fat foods in their adult lives, leading to an increase in risk for obesity.
Perhaps the most interesting element involved in obesity is the modulation of metabolism and intestinal signaling by microbiota which naturally occur in the digestive system. Bacteria play a role in the speed by which food is transferred from the mouth through the rest of the gut, an activity which happens more quickly in obesity. This leads to feeling hungry sooner after eating as well as altered absorption of certain nutrients. Interestingly, a study found that by simply transferring bacterial cultures from obese mice to nonobese mice, they developed symptoms associated with metabolic syndrome – one of which is obesity.
Perhaps it can be said that obesity begins with poor nutritional choices – but these choices can be influenced by society and perpetuated by alterations to brain morphology and predisposition to metabolic disorders. By understanding the complexities underlying obesity and how societal pressures, differences in biochemistry, and even nonhuman microorganisms can affect the body’s response to how it handles overnutrition (too many carbs, too much fat, etc.), we can begin to make obesity more about personal medicine rather than personal morality. After all, we don’t treat depression as the result of an unwillingness to be happy; while this can perpetuate the illness, it is accommodated for and worked around in current therapies. If obesity could be resulting from a combination of effects not directly related to personal choice, why can’t we treat it the same way?
 
For more information on gut bacteria, a great summary can be found here.

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Autism: More Than Just Genetics

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A lack of understanding has surrounded autism until recently, as the newest research has begun to shed a light on the potential causes of the disorder iconic of Sheldon Cooper from the Big Bang Theory. Autism is a spectral disorder, meaning its manifests itself in a wide variety of forms, affecting people in a several different ways. There are several genetic mutations that are thought to be associated with the neurological disease, as well as many environmental factors that play a role. As of late, researchers have identified that most of these factors are interrelated, generally resulting in zinc deficiency and/or immune system abnormalities. In turn, dysfunctional synapses in the brain can occur, leading to the impaired social interactions and unique behavioral characteristics we see in those with autism. Some of the many environmental causes identified as risk factors for autism include parental age, prenatal viral infection, maternal diabetes, pre- and perinatal stress, as well as gastrointestinal abnormalities, often called “leaky guy syndrome”.
For example, increased parental age has been shown to increase the likelihood of autism in the child. This is due to the fact that as parents age, there is an increased rate of mutation in the sperm from the father, leading to genetic mutations in the child. When a pregnant mother contracts various bacterial or viral infections there is also an increased risk of autism. Influenza, rubella, and cytomegalovirus are the most common of these infections. Maternal diabetes during pregnancy has been cited to cause a two-fold increased risk of autism in the child. In terms of stress, pregnant mothers release hormones when under stressful situations, which can cross the placenta and affect neurodevelopment of the fetus, resulting in an increased risk for autism. Lastly, several studies have listed gastrointestinal abnormalities as a risk factor for autism as many parents report digestion issues in their children affected by autism.
In addition, many skeptics argue that vaccinations may cause some sort of increased risk of autism. However, an abounding amount of research has argued the opposite: that there is no relationship between vaccines and risk of autism. Yet it seems so often we hear of new studies investigating the possible link. So my question is why are we still funding research on vaccines and autism? Is it worth the money we spend searching for a scare that has been denied by study after study? How are those that choose not to get vaccinated affecting our population and immunity as a whole? All questions quite debatable, and multi-faceted certainly, but how can we ignore the scientific evidence that ultimately says there is no link between autism and vaccination? Definitely something to think about and consider, especially for all the expecting parents out there.

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Autism: Aging Parents Reflect Increasing Rates

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According to CNN, Autism diagnosis rates have increased 30% in the last two years in the United States.  More than ever, researchers have been attempting to find the causes and disrupted pathways that lead to the development of autism.  There is a noticeable stigma surrounding autism.  People have a difficult time understanding the disorder as well as handling those with it in an acceptable manner.  What is causing the increase in diagnosis?  What causes the disorder?  There are many theories surrounding the increase in diagnosis of autism.  One is the obvious theory, autism rates are actually increasing in children.  I’m more on board with this theory.  Other theories however are far more interesting and controversial.  There are financial incentives for those diagnosed with learning disorders or autism because of government aid as well as insurance covered services.  It is also believed that people push for physicians to diagnose their children with a learning disorder in order to explain them being “different”.
It is believed that many parents push for diagnoses of their children in an effort to receive financial aid or special treatment in learning environments for their child.  What allows this theory to have any sort of strength is that autism is seen across a very broad spectrum.  There are some extremely high functioning people who are diagnosed as autistic and you’d never know unless someone told you.
The idea that parents push for diagnoses to explain their kids being “different” is fueled by the fact that we as humans have a fundamental flaw.  We don’t like being the ones to blame.  If we can push the blame onto others or else push the blame onto a disorder then we will.  If it explains why our child is not like everyone else’s then we can accept that fact.
The science behind autism shows that it is a neurological disorder resulting in a decrease in synaptic plasticity in areas of the brain such as the amygdala and the hippocampus.  The amygdala controls fear, arousal, and other behavioral functions while the hippocampus controls learning and memory.  Synaptic plasticity in autism is reduced due to malformed synapses.  These synapses are held tightly together by scaffold proteins like nuerexin and neuroligin.  A mutation in the mRNA that forms these proteins causes mutations rendering these proteins unable to properly perform their job.  This causes synapses to no longer be held tightly together, reducing the activity of the synapse and thus its synaptic plasticity.  The risk of mutation in these proteins is increased with the age of the parents at age on conception, primarily the father’s.
It has been found that paternal mutations in offspring occur at higher rates than those from the maternal side.  De novo mutations (mutations that form throughout someone’s life and are passed down to their offspring causing genetic mutations, however, don’t cause a condition in the parent) increase in men at an exponential rate once they’ve reached 30 years old.  It is estimated that the total number of mutations in a man will double in about 16.5 years, once they’ve reached 30 years old.  These findings suggest age as a primary factor leading to the development of autism in offspring.
Though I have primarily covered age as a cause for increased rates of autism, this is not the only cause.  Environmental factors such as stress during pregnancy, viral infections in the mother during pregnancy, and Zn2+ deficiencies have all been found to be a possible cause of autism.
I personally believe that age is one of the most easily avoidable causes of autism.  The younger you are as a parent, the better chance you have of not conceiving a child with autism.  As education beyond high school is growing, people are starting careers before they start families.  People are having children at older ages and autism rates are reflecting this.  However, I am not naïve enough to believe this is the only cause given what science has uncovered thus far.
Until next time,
Sebastian

Community/Health/Hot topics

You Are What You Eat: Early Life Diet and Obesity Risk

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Obesity and sedentary behaviors are commonly viewed as a reflection of cultures with widespread availability of cheap high-calorie and high-fat foods, often in developed countries like the U.S. Behavioral patterns of overeating are often viewed as a conscious choice, but research has found that consistent food choices may lead to hard-wired obesity predisposition, particularly through prenatal and early life exposure to high-fat and high-calorie diets. Obesity may be a series of poor choices that lead to permanent brain changes that impact not only the obese individual but also the development and fate of their children. Perhaps not only you, but also your children, are what you eat.
Over-nutrition in prenatal and early life diets has been found to cause brain abnormalities that predispose children to obesity and development of cognitive and memory impairments. Numerous studies using mice models have revealed alarming impacts from high-fat diets both in utero and during the weaning (nursing) period. Pregnant female mice on high-fat diets during pregnancy and weaning resulted in offspring that were hyper-insulemic and hyper-leptinemic. Offspring were also heavier at birth and remained heavier during the weaning period.
High-fat diets increase resistance to leptin, an important hormone involved in sending signals to the brain to stop eating. Leptin acts on receptors in the hypothalamus to inhibit hunger signals. Leptin resistance impairs food-reward-related brain signaling, so individuals have a higher food intake threshold they need to reach in order to feel satisfied. The hypothalamus is the area of the brain involved in hunger drives. Excessive feeding in early life leads to hypothalamic dysfunction, which intensifies eating drive into adulthood, resulting in weight gain. Insulin is a hormone that allows your body to use glucose from food to provide energy for cells. High-fat diets lead to insulin resistance, predisposing children to early development of type II diabetes. 
High-fat diets can also induce local pro-apoptotic (cell death) signaling in the hippocampus. Reduced hippocampal size in obesity may accelerate later life cognitive impairment and potentially increase the risk of developing neurodegenerative diseases such as Alzheimer’s disease. The hippocampus is an area of the brain vital for cognition, learning, processing of short to long term memory, spatial navigation, as well as emotions. A poorly developed or damaged hippocampus results in a reduction in executive functioning and attention, decreasing global functioning and lower IQ.
Impacts of Maternal and Paternal Obesity on Childhood Brain development
Maternal obesity during pregnancy reduces production of hippocampal BDNF, an important regulator of neuronal development survival, memory and cognitive ability; it also suppresses food intake. BDNF levels are reduced by inflammatory cytokines. Production of inflammatory cytokines is increased in obese individuals, leading to impaired hippocampal function by decreasing levels of important regulators like BDNF. Genetic obesity is also linked to reduced hippocampal BDNF expression and increased cytokine expression and hippocampal inflammation.
There are also paternal connections to obesity predisposition. A mice study revealed fathers who were obese at the time of conception can pass on obesity predisposition to their children and the next generation. Obese male mice were mated with normal diet and normal weight females. Analysis of microRNAs in the sperm of the obese fathers revealed that high-fat diet changes the molecular makeup of sperm, which program embryos for increased risk of obesity.
What does this mean?
Essentially, when children’s brains develop in an environment of excess nutrition,  the brain needs that same level of nutrition to feel satisfied. High-fat diets during prenatal and postnatal development as well as genetic influences from the mother and father have drastic effects on a child’s ability to eat properly and function normally. The brain may be hard-wired for high-fat diets, increasing the likelihood of developing obesity. Obesity not only affects physical functioning, but has stark impacts on cognitive abilities as well. Children exposed to high-fat diets may have reductions in executive functioning and attention, decreased global functioning and lower IQ’s.
What can we do?
Unfortunately, prenatal and early life over-nutrition is an issue that cannot be solved simply by telling people to eat healthier. Accessibility to healthy food varies due to factors such as socioeconomic status. Foods high in fat, salt, and preservatives are cheaper than fruits and vegetables, and those of lower SES face the dilemma of letting their family go hungry or feeding them unhealthy food. As research in the realm of obesity continues, a greater call to action is needed to change the food system by which our country is built around, which is no easy task. But how long are we willing to sacrifice the bodies and brains of our children before we make a change?
 
Sources:
Female mice research article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671057/
Male mice research article:
http://www.eurekalert.org/pub_releases/2013-07/foas-odp071113.php

Disease/Health/Hot topics

Are we predisposed to being obese?

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Common convention has each of us believing that being overweight or obese as a sign of being lazy, apathetic, or even just slovenly.  When we walk down the street and see an individual who is severely overweight, we tend to pass judgment without a second thought.  We automatically assume that they don’t care, eat everything in sight, refuse to exercise, and pretty much don’t care.  Here is a shocker; maybe it’s not that simple!  There are so many more factors involved with being overweight that we don’t even know to think about.  There are many factors that play a role in obesity, but for this post I will focus mainly on genetic predisposition, pre-birth factors, and most importantly for us in America, our food policies.
Lets take a look at the first two, genetic predisposition and pre-birth factors.  There is not one individual in the world that is able to control either of these, but both have strong impacts on our lives – the great nature or nurture debate.  Some things I didn’t know prior were for example the importance of leptin.  Leptin is a hormone that is secreted to tell us we are full, and the gene is located on chromosome 7.  The way it works is it binds to Neuropeptide Y (NPY) and inhibits its actions.  NPY is the peptide that causes fat growth and increases our food intake.  A decrease in leptin increases our weight.  Well then, why is there a decrease in leptin?  If your dad was overweight when you were created is one factor.  Poor diet in men has been shown to change the molecular make up of the semen in mice leading to overweight offspring.  If that’s not enough to question what we already thought, how about looking at the mother.  Pregnant rats on a restricted diet had the remaining nutrition supplemented by either a high carbohydrate or high fat diet.  Not surprisingly, the high fat offspring were heavier at birth.  Surprisingly, the high carb babies had a higher level of NPY.  Over 20 weeks, the high carb rats surpassed the other rats in weight, fat, and fell behind in metabolism.
Our food policies and regulations tend not to be regulatory regarding content of the food, but rather making sure everyone has food.  Take a look at our school lunch programs, where the main factors are not necessarily what is on the plate, but making sure everyone has a plate.  The regulatory agencies such as the FDA approve anything that meats the safety standard, but not much else.  It was only a few years ago that trans fats were removed from public diets.  The amount of calories are very seldom regulated, and the nutritional content is definitely not regulated more than just identifying what is in there.  Take for example this video showing Irish people trying American snacks, https://www.youtube.com/watch?v=-Vjd4YtAImM.  It clearly shows how we have conditioned our culture to accept anything.  And you never know, it may tie into how we as individuals become addicted to the things like simple sugars and fats.
So is obesity a neurological or biological disease.  I wish the answer is as simple yes or no.  What I just finished writing about only scratches the surface of obesity.  There are factors that are definitely within our control that I didn’t mention, such as exercise, consciously choosing foods that are healthier for us, and remaining educated about all the factors involved.
Source:
https://moodle.cord.edu/pluginfile.php/390940/mod_resource/content/0/obesity%20a%20brain%20disease.pdf

Community/Disease/Health/Hot topics/Uncategorized

Obesity Epidemic: Pointing Fingers, But Is It Really Their Fault?

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Obesity has been high up on the discussion topics list lately, as an “obesity epidemic” is taking over America. I believe that the term “epidemic” is an appropriate description for the enormous rise in obesity, including that of children, which we are seeing in the United States. Obese people have a higher risk of heart disease, depression, sleep apnea, cancer and/or diabetes.  A large number of obese adolescents plus an increasingly high number of obese adults equals an extremely high number of people who are at a high risk of getting one or all of these illnesses. So what is being done about this “epidemic”? There has been talk of mandating a ban on foods that are bad for people, as well as the ever-popular recommendation that an obese person just needs to eat better and exercise. But would either of these options have an effect? Some say no, absolutely not. Recent research may indicate that obesity is not something that can necessarily be controlled but in fact is a brain disorder.
Studies have shown the negative consequences of a high fat diet on subjects including weight gain, insulin resistance, inflammation of the hypothalamus, increased oxidative stress in the brain, decreased volume of the hippocampus and leptin resistance. Leptin is a hormone created by fat cells and controls the amount of fat stored in the body by suppressing appetite (hunger). Drawing your attention to insulin and leptin, these two molecules are responsible for making sure we know to stop eating when we are full. When there is a resistance to these two molecules, which is found to be the case in obese people, there is an absence of the signal telling them they are no longer hungry. This leads to a continued cycle of overconsumption and resistance.
In addition to this type of scientific research, there are also studies which investigate the genetic aspects of leptin, the reward pathway in the brain and the blood brain barrier. The genetic aspects of leptin have to do with the gene that encodes for leptin not being produced; therefore a person has the feeling of being continually hungry.  With regard to the reward pathway, research has shown that if there is not enough dopamine released into the brain it is more difficult to achieve the “satisfaction” level of eating. Finally, with regard to the blood brain barrier, triglycerides can disrupt the blood brain barrier to the point where leptin and insulin cannot cross its boundaries. I discussed earlier the effects of the resistance of leptin and insulin.
This research that exists is essentially saying that obesity is a brain disorder and not just an outcome of an unhealthy lifestyle, but do you buy it?
Personally, I do to a certain extent. Prior to reading this paper I was the type of person who believed a person was obese solely due to their lifestyle choices. After having read information and research studies suggesting there is a clinical and/or genetic abnormality potentially at play here, my opinions have changed. There are definitely neurological factors that contribute to extensive eating and the inability to reach the point of satisfaction when consuming food. This has caused me to believe that in reality, being obese is not completely the person’s fault. I think of obesity as a habit that is hard to break, like for instance smoking. Obese people have neurological responses they have to work against to achieve a healthy lifestyle and in no way will I dispute that breaking this “habit” would be anything but extremely hard. On the other hand, I still believe that there are certain things that an individual can do to decrease their risk.  I understand that obtaining a healthy lifestyle is very difficult but I still do believe/hope that some are willing to work extremely hard to avoid obesity and its consequences.  I also believe that exposing children from a young age to healthy eating and exercising will better instill a lifelong habit of good health. Once bad habits start and are continuous, it is a hard to recover.
Although the debate still exists as to whether or not obesity is due to lifestyle choices or caused by a brain disorder, there is no question we are experiencing an “obesity epidemic” here in America and something needs to be done to combat it.

Picture obtained from: http://obesityinamerica.org/wp-content/uploads/2013/01/map_tape.jpg

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