Huntington Disease is a rare genetic condition that most people have never even heard of unless a) they study it b) they personally know someone with the disease or c) they are a fan of House. Luckily for me only a) and c) apply in this situation. However, I believe Huntington’s like a variety of other diseases is something the public needs to be educated about because awareness really is the greatest way to inspire research into any field.
As autosomal dominant disorder this makes Huntington’s especially dangerous because as a dominant trait a person only needs one affected allele to develop the disorder. Were the trait recessive such as the trait for hemophaelia, for example, then the likelihood of having Huntington’s is significantly lowered. When a trait is autosomal this means that it is no carried by any of the sex chromosomes (X or Y), rather is carried by any of the other 22 chromosomes the human body has. In Huntington’s the gene affected is located on chromosome 4, specially on the p (upper, shorter) arm.
The symptoms of Huntington’s has already been discussed on a previous post on basal ganglia disorders; however, in summation it results in damage to the striatum and cerebral cortex causing changes in personality including mood swings, involuntary movements known as hypokinesia and eventually dementia. As is common with most genetic disorders, the symptoms do not appear until adulthood. In Huntington’s the symptoms usually arise around mid-age, but unfortunately it can arise earlier than our 30s or 40s if unlucky. Once symptoms start appearing the person usually has about another 5 to 15 years until death. The age at which symptoms appear directly correlates with the genetics behind the abnormal gene.
Huntington’s is part of numerous diseases including varies ataxias and fragile X syndrome that result due to trinucleotide repeat. Specifically, Huntington’s is due to a repeat of the CAG trinucleotide. Normal alleles carry about 10 to 35 copies, but those suffering from Huntington’s and various other neurodegenerative diseases have more than 40 repeats. People with around 60 repeats with develop Huntington’s around the age of 20. These repeats in CAG result in the production of a “mutant protein” that eventually fill the striatum and cerebral cortex causing degeneration and ultimately death of these brain cells. In healthy individuals the gene involved in Huntington’s encodes for a large protein known as huntingtin (Htt), which when normal enhances the production of a protein (BDNF) necessary for the survival of the cells in the striatum and cerebral cortex.
Stay tuned for a post later this week on current experimental treatment on Huntington’s! Thank you for reading
Cummings, Michael. “Genetics of Behavior.” Human Heredity: Principles and Issues. 9th ed. Belmont: Brooks/Cole, 2011. 405-06. Print.
A new study lead by Professor Simon Baron-Cohen of Cambridge University suggests that girls with anorexia have a higher than average “number of autistic traits” (University of Cambridge, 2013). These traits include an “above average interest in systems” and a below average empathy score (ibid). Considering the rigid personality, attitudes and behaviours of anorexics and their obsessive thought patterns in relation to body weight, body image and eating patterns it is not difficult to see how they can be interpreted as typical of autism.
n the study, first published the Journal of Molecular Autism, Baron-Cohen et al. assessed 66 girls between the ages of 12 and 18 with anorexia but no history of autism for autistic traits. A control group of over 1,600 neurotypical teens in the same age group were also given the same assessments including the the Autism Spectrum Quotient (AQ), Systemising Quotient (SQ) and the Empathy Quotient (EQ). Results showed that compared with the control group, the anorexic girls were five times more likely to score in the autistic spectrum. More than 50% of the anorexic girls fell into the “broader autism phenotype” compared with only 15% of the control (ibid). Furthermore, the anorexic girls also scored a higher SQ and lower EQ which also points towards an autistic personality.
As interesting as these results are there is indeed a practical application. Cases of autism are far more prevalent in males; however, Baron-Cohen’s findings show that perhaps autism in young girls is being overshadowed by a diagnosis of anorexia. Dr Tony Jaffa, co-leader of the study confirms that the new correlation between autistic traits and anorexia will give health professionals and researchers a new means to help those suffering from the eating disorder. He remarks:
“For example, shifting their interest away from body weight and dieting on to a different but equally systematic topic may be helpful. Recognising that some patients with anorexia may also need help with social skills and communication, and with adapting to change, also gives us a new treatment angle”
My last post was exclusively about basal ganglia and the reason for this was to help clarify the parts of the brain directly involved in two very infamous disorders: Parkinson’s and Huntington’s Disease.
Parkinson’s disease is far more recognized that Huntington’s disease; however, thanks to the character Thirteen on the tv show House that might be changing. Parkinson’s disease effects about 1% of all people over the age of 50; however, as you can see from the video posted below, this is not always the case. Another example is actor Michael J. Fox, who was diagnosed with Parkinson’s at the age of 30. He has since become an activist for the cure of Parkinson’s, which led him to found the Michael J. Fox Foundation. It is not that uncommon to know someone with the disease. Many people can in fact recognize it based on the very characteristic tremors.
Parkinson’s is classified by hypokinesia. The symptoms of Parkinson’s include slowness of movement or bradykinesia, difficulty in initiating ‘willed’ movements or akinesia, increases muscle tone or rigidity, and of course, tremors in the hands and jaws even at rest. Many of those who suffer from the disease will eventually show signs of cognitive decline. More specifically, the substantia nigra’s input to the striatum. This input features the neurotransmitter dopamine, which facilitates the activity of the motor loop by activating cells in the putamen. As noted in the previous post, the putamen forms an inhibitory connection with neurons in the globus pallidus, which then forms an inhibitory connection with the thalamus (VLo). Due to the depletion of dopamine, the ‘funnel’ between VLo and the supplementary motor area (SMA) closes. As a result, the victim of Parkinson’s will have impaired motor function with symptoms such as ones listed above.
Treatment Options for Parkinson’s Disease
Even through Parkinson’s cannot be cured, therapies do exist to try to ease or deter the symptoms. Most therapies aim at enhancing the levels of dopamine delivered to the caudate nucleus and the putamen. The most common type of medication is known as L-dopa, which is a precursor for dopamine. This means that it participates the chemical reaction that produces dopamine. This treatment does alleviate some of the symptoms; however, it cannot do anything to stop the progressive course of the disease, nor slow the rate of cell degeneration in the substantia nigra. Currently, experiments are being conducted to test whether graftng non-neural cells, manipulated to produce dopamine, into the basal ganglia can help. Also, stem cell research shows promise to one day provide an effective treatment as well.
Whereas Parkinson’s is characterized by hypokinesia, Huntington’s is characterized by hyperkinesia or excessive movement. As tragic as Parkinson’s disease is, Huntington’s does seem far more frightening. A hereditary, progressive and always fatal disorder, Huntington’s symptoms include dyskinesia or abnormal movements, dementia and disorder of the personality. The scariest part of the disorder is that the symptoms do not appear until adulthood, so unless the person knows that they have a history of the disorder, they can easily pass on the genes of Huntington’s to their children without even knowing that they have it. Genetic tests can be performed to find out for sure, but for many people it is too late at that point. The name Huntington’s comes from the abnormal gene carried by the patient. The first and most notable sign of the disease is known chorea: spontaneous, uncontrollable movements with rapid, irregular flow resulting a flicking movement in various parts of the body. In fact, Huntington’s disease can also be called Huntington’s Chorea. The devastating effects of the disease is due to the profound neuron loss in caudate nucleus, putamen and globus pallidus as well as cell loss in any other part of the cerebral cortex. The fact that Huntington’s can strike any part of the brain means that many patients suffer a variety of different symptoms, sometimes making it difficult to diagnose without a genetic test. Damage to the basal ganglia results in a loss of inhibitory output to the thalamus (VLo) resulting in the abnormal movements.
Unfortunately, due to the progressive nature of the disorder and the genetic component, treatment for Huntington’s is virtually non-existent. Most patients with the disorder have their symptoms treated with various medications ranging from anti-depressants to sedatives and anti-psychotics.
Dendrite is Greek for “tree-like” and to explain what they do in the simplest terms possible, they receive electrochemical signals from other neurons and then pass these signal down to the soma or neural cell body. Dendrites play a critical role in determining the frequency of the action potential, which drives the electrical signal down axons of the body of the neuron towards the axon terminals. Dendrites are so essential that their architecture is a great indicator of the complexity of our neural connections. In fact, our brain function depends on strong synaptic connections, connections which are cultivated during infancy and early childhood.
Unfortunately, as with all things complex, sometimes something goes wrong in the developing process. Mental retardation occurs when there is a disruption in this early refinement of dendrites that results in cognitive impairment severe enough to disrupt adaptive behaviour. There is a wide array of genetic disorders and poor environmental conditions that can result in mental retardation. For example, Down Syndrome and PKU (both genetic disorders), accidents during pregnancy and childbirth, maternal infections with rubella, Fetal Alcohol Syndrome and environmental impoverishment. Poor environmental conditions in young children such as poor nutrition, isolation and neglect can even result in brain damage severe enough to cause damage to these sensitive dendrites.
Healthy dendrites have spines that look like small balloons that hang of the dendrite. In cases of mental retardation dendritic spines are very thin and long, resembling the dendritic spines of a fetus. This is clearly seen in the top most image, a) and c) are healthy dendrites. This clear difference reflects the failure of normal circuits in the brain’s development. Studies by Marin-Padilla and Purpura have discovered a correlation between extent of dendritic spine damage and degree of mental retardation.
Bear, Mark F., Barry W. Connors, and Michael Paradiso. “Neurons and Glia.”Neuroscience: Exploring the Brain. Baltimore, MD: Lippincott Williams & Wilkins, 2006. 43. Print.
Images courtesy of google images.
Anatomical references are not only important in surgery, but knowing them facilitates speech and orientation in various fields.
Anterior or rostral (Latin for ‘beak’): direction pointing towards head
Posterior or caudal (Latin for ‘tail’): direction pointing towards feet
- The spinal cord runs anterior to posterior with a ventral and dorsal side.
Dorsal (Latin for ‘back): direction pointing upwards; think dorsal fin
Ventral (Latin for ‘belly’): direction pointing downwards
Bilateral symmetry: the right side of the brain and spinal cord is the mirror image of the left side
Midline: invisible line running down the middle of the nervous system
- Medial: structures closer to the midline
- Lateral: structures further from the midline
Ipsilateral: two structures that are on the same side of the midline
Contralateral: two structures that are on opposites sides of the midline
Making Sections of Tissue
The standard approach when making sections or slices of tissue is to cut parallel to one of the three anatomical planes.
- Midsagittal plane: plane of the section resulting from splitting in the brain into left and right halves
- Coronal plane: splits in the brain into dorsal and ventral halves
- Horizontal plane: splits the brain into anterior and posterior halves
Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. Neuroscience: Exploring the Brain. Philadelphia, PA: Lippincott Williams & Wilkins, 2007. Print.
Sleep is a confusing topic of study because despite every human needing it, no one really knows with 100% certainty why we do it. There is no single theory that is accepted by the entire scientific community; however, two main hypotheses seem most fitting. First, the restoration hypothesis proposes that we sleep to rest and recover, a preparation for when we wake. What is being restored remains unclear. The second hypothesis proposes that sleep is an adaptive process that keeps us out of trouble for a large chunk of the day: hiding us from predators and conserving our energy reserves. The only thing we do know about sleep is that we cannot survive without it.
The majority of our sleep (75%) is spent in non-REM (rapid-eye movement) sleep and occurs in four stages. An entire sleep cycle takes approximately 90 minutes and is classified as a form of ultradian rhythm (faster than circadian which is a 24 hour cycle).
Stage 1: The Transitional Stage
Stage 1 is known as the transitional stage as it is when our brain waves become less regular and begin to wane. If you were to look at an EEG we would pretty much look wide awake. You have probably felt the sensation of shifting between the two stages if you have ever fallen asleep in class or in front of the TV. That sense of falling is due to the slowing of our brain waves. Activity levels begin to change from alpha to theta waves; they are high amplitude but very low frequency. Due the small difference, however, stage 1 is the lightest stage of sleep and we are easily woken. Our eyes are making slow, rolling movements and the whole stage only lasts a few minutes. All in all though, it only occurs at the beginning of sleep and only lasts 5-10 minutes.
Stage 2: The First NREM Stage
Stage 2 marks the true beginning of non-REM sleep. During stage 2, our brain waves become slightly deeper and occasional variations in wave movement (oscillations) occur between 8-14 Hz occurs. These oscillations are called sleep spindles and are produced by thalamic pacemaker cells. It is proposed that sleep spindles occur because the brain is trying to inhibit processing to ease the transitional into sleep. Another characteristic stage 2 indicator is the K-complex. K-complexes are a high-amplitude, sharp wave and the largest brain event during sleep. Scientists believe that K-complexes help suppress arousal and aid in memory consolidation. Lastly, another indicator of transition from stage 1 to stage 2 sleep is that eye movements cease.
Stage 3 and 4: The Delta Rhythm Stages
During stage 3, an EEG would show large-amplitude, low rhythm delta waves. Eve movements as well as body movements will be usually be absent. Stage 3 can also be seen as a transitional stage but between light and deep sleep. As we enter into deep sleep our body and brain become increasingly less sensitive to stimuli and less susceptible to arousal. Common childhood sleep issues such as bed wetting, night terrors and sleep walking tend to occur towards the end of stage 3. The main difference between stage 3 and 4 is the amount of delta waves. When less than 50% of deep sleep is delta, we are in stage 3. When more than 50% of our brain activity is delta waves, we are in stage 4 of sleep. As delta waves correspond with very deep sleep, a person in stage 4 of sleep is the hardest to wake. This can be extremely scary if a person is sleep walking or a child is having night terror. They may seem awake but they are completely unresponsive to external stimuli. Stage 4 of sleep only happens during the first cycle as such, our sleep becomes lighter throughout the night. This is extremely helpful as it prepares our body for waking. From an evolutionary stand point this makes sense. Our ancestors certainly could not set an alarm clock, the noise of other animals and the rising sun needed to be sufficient to wake us.
REM sleep is probably the most exciting and important of all the stages of sleep. REM stands for rapid eye movement and is suitable name for this stage as an EOG would show rapid eye movement under our eyelids. During this phase we also experience dreaming. Our brain activity mimics waking, showing a myriad of different brain waves: alpha, beta and dysynchronous waves. Despite our brain activity showing an incredible change in activity, our muscles are actually paralysed. A scary albeit common phenomenon known as sleep paralysis is when we wake-up during REM sleep and our muscles remain effectively paralysed. During sleep however, this “paralysis” is known as sleep atonia. It is a beneficial process as it prevent us from acting out our dreams and putting ourselves in harms way. Certain neurons in our brain stem (specifically the tegmentum) known as REM sleep-on cells release monoamines inhibit motor neuron activity. Another curious attribute of REM sleep is the incredible recall of a person woken from it. Our dream world becomes as real and vivid as the real world. As REM mimics wakefulness, waking someone during REM means they will feel very alert. The exact reason for REM sleep is as elusive as sleep itself; however, scientists do know that like sleep, it is vital. When a person is repeatedly disturbed during REM sleep or does not get enough sleep in general, we go through a process called REM rebound. In other words, we spend the majority of our following sleep in REM. Lastly, scientists have also discovered that newborns and foetuses spend the majority of their sleep in REM. All in all, these findings suggest REM is vital to proper human functioning and development.
As we progress through the night we spend increasingly less time in stages 3 and 4. After the first cycle stage 1 of sleep is replaced by REM sleep and the amount of time spent in REM sleep increases. Even though the reason why we sleep is unclear, the change in brain activity and the determent of not sleeping is enough to say with certainty that sleep is necessary for normal human function.
Bear, M., & Connors, B. (2007). Neuroscience: Exploring the brain (3rd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
Dement, W.C. (1978). Some must watch while some must sleep. New York: W.W. Norton.
Hall, R. (1998, January 1). Stages of Sleep. Retrieved September 14, 2014.
K-complex. (2014, August 24). Retrieved September 14, 2014, from http://en.wikipedia.org/wiki/K-complex
Pinel, J.P.J. (1992). Biopsychology. Needham Heights, MA: Allyn & Bacon.
Sleep spindle. (2014, August 24). Retrieved September 14, 2014, from http://en.wikipedia.org/wiki/Sleep_spindle
Communication at any age requires a skill set including the obvious such as a proper vocabulary and grammatical accuracy. For a child, a conversation is far more difficult because vocabulary and grammar are not the only things that are still developing. The five years leading up to this communicative breakthrough also depends on the phonological and social development of the child.
Component 1: Phonological Development
Firstly, the quintessential ingredient to verbal speech of any kind is phonological development. When infants are born they all have the ability to perceive the sounds and tones used in all languages. Experience with their own language over the first year of their life, slowly allows them to tune into the phonemic contrasts between their own language over others (Smith et al. 2011). For example, when a Japanese baby is 8 months old, they can distinguish /r/ and /l/ sounds; however, by the time they are one, they no longer can (Purves, 2001).
This may not seem like a useful skill; however, it is necessary for an infant to become an expert at their own mothertongue. Adults play a quintessential role by building on the biological rhythm of their babies developing speech. By 10 months, the canonical babbling comes to reflect the prosody of their surrounding language of their parents (De Boysson-Bardies, 1993). Clearly when infants are this young, it is essential for close proximity between caregiver and infant. Characteristics of contingent talk such as exaggerated facial expressions, repetition and eye-contact ensure optimal attention. Without this attention, the infant would not gain the benefits of contingent talk and their vocabulary acquisition would suffer.
Component 2: Acquisition of Vocabulary
Hand in hand with phonological development is the acquisition of vocabulary. The first step of any child’s vocabulary acquisition is contingent talk. Contingent talk is when a caregivers ‘scaffolds’ learning by talking about what the infants is already attending to (Carpenter et al. 1998). Various forms exist including child-direct speech, following in, expansion and clarification and all of these forms help co-regulate intentions (Fogel, 1993). In other words, both the child and the caregiver work together to improve the language of the child. As the name suggests, scaffolding language allows the caregiver to just teach their child new words, but also to improve the quality of their word choice and the coherence between words.
Furthermore, contingent talk is instrumental in the development of theory of mind (Astington & Baird, 2005). In relation, understanding the intention of a caregiver also helps build in a child’s vocabulary. As a paradigm, when an experimenter tells an 18-month-old that they are looking for a ‘toma’ and then proceeds to look for it, rejecting objects until settling, with satisfaction for a final object, the majority of 18-month-olds will infer that this final object is the ‘toma’ (Tomaselo, 2003). Lastly, what all of these skills lead up to is the 100 word transition phase. After a child learns his or her first words, the next couple of months consistent of holophrases such as “nomore” until they have learnt about 100 words. Beyond this point, at around 18 months, children switch from holophrases to telegraphic speech (Bates et al. 1995). Three to four word phrases then begin around 24-27 months, the stage when grammar acquisition becomes important.
Component 3:Acquisition of Grammar
Grammar becomes increasingly more important around 24 months because now word order actually begins to change the meaning of speech. The two major components of grammar are syntax and morphology. Syntax is the organisation of words into larger structure like sentence; who did what to whom. Understanding knowing who did what to whom or the agent-patient relationships is vital to communication. Around the age of three, children start to show understanding on this relationship. Tomasello et al. (1998; 1999) taught children made-up verbs and by age three, the children were able to act out appropriate actions and modify the agent-patient relationships to fit new scenes.
Once this skill has been attained, children can also start using synaptic bootstrapping; using grammatical information to infer the meaning of unfamiliar words (Gleitman, 1990). This is particularly useful when a child is having a conversation with anyone with a broader vocabulary, allowing them to carry on speaking without actually knowing every word. To continue, understanding morphology or word structure like plurals, possession, tense etc. allows children to use words productively in conversation. The wug test (Berko, 1958), suggests that understanding morphemes develops between the age of four and five. Understanding both syntax and morphology helps a five year old get around the barriers of having a conversation with someone more versed than them.
Component 4: Developing Pragmatics
Finally, the acquisition of pragmatics is also a necessary tool for holding a conversation, regardless of age. The first pragmatic skills occurs even in infants, maintaining eye-contact with the people speaking to them. Maintaining eye-contact and eventually responding with smiles and sounds lets the other speaker know that the child is paying attention. Eventually, around 11 months this skill helps develop joint attention whereby the child can actually direct their caregivers attention (Smith et al. 2011). By a child is five, expressing intent is necessary to get their point across, setting the topic and for taking turns in speaking (Bates, 1976; Strivers et al. 2009). Finally, developing an understanding for implicature and referencing is also a necessary skill for conversation. Studies show that by age five children have learnt that they can use pronouns to refer to people, persons and things which are clearly seen or recently spoken off (Matthews et al. 2006). Until this age, to refer to things children will point to remain ambiguous. Understanding implicature like “I ate some cake” meaning “some” and not “all” also develops by around five years of age. Both of these skills are extremely helpful tools for a five year especially for clear communication and reduces ambiguity and confusion. Fortunately, by this age, should ambiguity remain, a five-year old will actively search the scene for clues that will reduce confusion. In other words, by age five, children have learnt the pragmatic skills to steer them through must conversational confusion.
Astington, J. W., & Baird, J. A. (2005). Why language matters for theory
of mind. Oxford, England: Oxford University Press.
Bates, E. (1976). Language and context: Studies in the acquisition of pragmatics. New York: Academic Press.
Berko, J. (1958). The child’s learning of English morphology (Doctoral dissertation, Radcliffe College).
Carpenter, M., Akhtar, N., & Tomasello, M. (1998). Fourteen-through 18-month-old infants differentially imitate intentional and accidental actions. Infant Behavior and Development, 21(2), 315-330.
Caselli, M. C., Bates, E., Casadio, P., Fenson, J., Fenson, L., Sanderl, L., & Weir, J. (1995). A cross-linguistic study of early lexical development. Cognitive Development, 10(2), 159-199.
De Boysson-Bardies, B. (1993). Ontogeny of language-specific syllabic productions (pp. 353-363). Springer Netherlands.
Fogel, A. (1993). Developing through relationships. Chicago: University of Chicago Press.
Gleitman, L. (1990). Structural sources of verb learning. Language Acquisition, 1, 1-63.
Matthews, D., Lieven, E., Theakston, A., & Tomasello, M. (2006). The effect of perceptual availability and prior discourse on young children’s use of referring expressions. Applied Psycholinguistics, 27(03), 403-422.
Purves, D., Augustine, G. J., Fitzpatrick, D., Katz, L. C., LaMantia, A. S., McNamara, J. O., & Williams, S. M. (2001). The Development of Language: A Critical Period in Humans.
Smith, P., & Cowie, H. (2011). Understanding children’s development (5th ed.). Chichester, West Sussex: Wiley.
Stivers, T., Enﬁeld, N. J., Brown, P., Englert, C., Hayashi, M., Heinemann, T., Levinson, S. (2009). Universals and cultural variation in turn-taking in conversation. Proceedings of the National Academy of Sciences, 106(26)
Tomasello M. 1998. Reference: intending that others jointly attend. Pragmat. Cogn. 6:219–34
Tomasello M. 1999. Perceiving intentions and learning words in the second year of life. See Bowerman & Levinson 1999. In press
Tomasello, M. (Ed.). (2003). The new psychology of language: Cognitive and functional approaches to language structure (Vol. 2). Psychology Press.
Our bodies rely on food for energy but also for biosynthesis. Biosynthesis is the production of complex molecules within living organisms or cells; a process necessary for self-maintenance. For example, the synthesis of protein from neuropeptides. Two necessary precursors for biosynthesis are organic carbon (such as from sugar) and organic nitrogen (such as from amino acids). For a diet to be sufficient, therefore, it must supply chemical energy, organic molecules and finally essential nutrients.
For energy, animals ingest and digest nutrients such as carbohydrates, proteins and lipids to get enough ATP necessary for cellular respiration and energy storage. Essential nutrients are ingested as precursors to complex molecules and as minerals and vitamins. Unlike complex molecules, essential nutrients cannot be synthesised from raw materials. Thus, they must be ingested.
Amino Acids and Fatty Acids
Four types of essential nutrients exist: amino acids, fatty acids, vitamins and minerals. Approximately, half of the 20 amino acids are required for humans including: methionine, valine, threonine, phenylaline, leucine, isoleucine, tryptophan, lysine and histidine. Meat, fish, poultry, dairy products are considered complete proteins because they contain all essential amino acids. However, vegans and vegetarians or even meat-eaters can get all their essential amino acids by eating a full diet consisting of beans, legumes, nuts, seeds and vegetables. Insufficient amounts of amino acids causes protein deficiency, which can be severely detrimental to healthy development. Therefore, if you stop eating meat, it is important to make sure you are eating a diet that contains all your essential amino acids.
Essential fatty acids are also required. Only two are known to be essential for human survival: alpha-linoleic acid and linoleic acid. Alpha-linoleic acid is a long-chain omega-3 fatty acid and is high in food such as salmon, tofu, shrimp, flax seeds and walnuts (fish, seeds, grains and vegetables). Linoleic acid is a long-chain omega-6 fatty acid and is found nuts, grains, cereals and poultry. Insufficient amounts of omega-3 and omega-6 contributes to impaired cellular functioning and heart disease.
Vitamins and Minerals
The final two essential nutrients are vitamins and minerals. Vitamins come in two, organic forms: soluble and water-soluble. Fat-soluble vitamins are found in fatty foods such as animal products, vegetable oils, etc. They include vitamin A, D, E and K and are stored in our liver and fatty tissue. Deficiency in certain vitamins cause different issues (a future post will discuss this in more detail). Water-soluble vitamins, on the other hand, are not stored in the body and so need to be consumed more frequently. These means that when we urinate, these vitamins leave our body. Fortunately, that means it is hard to consume too many water-soluble vitamins. Too many fat-soluble vitamins can cause toxicity. Water-soluble vitamins include vitamin C, B and folic acid and can be found in foods such as fruit, vegetables (especially greens) and grains. As water-soluble vitamins are sensitive to heat and air, boiling can destroy the vitamins. Foods high in fat-soluble vitamins are far more durable.
Minerals on the other hand are inorganic and include calcium, iron, phosphorus, magnesium, sulphur, sodium, potassium and chloride. Minerals also come in two forms: macro or major minerals and trace elements. Macrominerals include electrolytes and the body stores about 5 grams of each one on hand. In order to stay healthy, a person to consume about 100mg a day to maintain the 5 gram store and equalise the loss. Trace elements are found in much smaller quantities, hence their name and include iron, zinc, iodine, selenium, copper, manganese, fluoride, chromium and molybdenum. Minerals are essential because they serve as reinforcers for bone growth, strong teeth, maintaining homeostasis and synthesising energy from food. A great source of minerals is from plants such as fruits, vegetables and nuts as they get minerals directly from the soil they grow in. Grains, meats, cereals, dairy, etc. also contain minerals but in a diluted amount due to processing or because they have already been used by the animal itself.
All in all, a proper diet needs to incorporate all essential nutrients for proper health and functioning.
Campbell, N. A., & Reece, J. B. (2008). Animal Nutrition . Biology (8th ed., ). San Francisco: Pearson, Benjamin Cummings.
Rinzler, C. A. (2006). Nutrition for Dummies (4th ed.). Indianapolis, IN: Wiley Pub.
Vitamins and minerals . (2012, November 26). . Retrieved June 24, 2014, from http://www.nhs.uk/conditions/vitamins-minerals/Pages/vitamins-minerals.aspx
The Ebola Virus has been getting a lot of news coverage recently with a massive outbreak in West Africa. As of March this year the death toll is the highest of any Ebola outbreak ever recorded. The exact number is still increasing, but over one thousand individuals have been exposed with causalities now around 800 (Sender, 2014). Obviously this virus is deadly and scary, but what exactly is it? My family and I were discussing these outbreaks over dinner, and I thought that a great way to learn about it is to do some research.
Firstly, the Ebola virus causes Ebola virus disease (EVD) or Ebola haemorrhagic fever (EHF) in humans. It is part of Genus Ebolavirus and the Filoviridae family. The Genus Ebolavirus consists of five distinct species:
- Zaire ebolavirus (EBOV)
- Bundibugyo ebolavirus (BDBV)
- Reston ebolavirus (RESTV)
- Taï Forest ebolavirus (TAFV)
- Sudan ebolavirus (SUDV)
Not all of these species are dangerous to humans. However, BDBV, EBOV and SUDV are all associated with mass outbreaks of EVD in Africa. Out of these three, EBOV is the most deadly. According to the World Health Organisation (World Health Organization, 2014) the RESTV species can infect humans, but they do not cause severe illness or death as is the case with the other three. Since 1994, EBOV and the TAFV species has infected chimpanzees and gorillas (WHO, 2014). Outbreaks of severe EVD have also been found in macaque monkeys in the Philippines in 1989, 1990 and 1996. Not only do outbreaks in non-human primates cause concern for them, but it also creates concern that one day EVD in humans can be brought on by the TAFV species.
EVD in humans first appear in 1976 in Western Africa. The virus occurred in two simultaneous outbreaks in two different villages, in Nzara, Sudan and Yambuku, Democratic Republic of Congo. The outbreak in the DRC fell along the Ebola River, hence the name.
As mentioned above, the Ebola virus is a virological taxon part of Genus Ebolavirus. The Ebola virus, as an a cellular virus, replicates through a host cell. The virus attaches itself to the host cell’s receptors through glycoproteins. Then it fuses its own viral membrane with the cell’s membrane. This fusion process allows the virus to release its nucleocapsid (which contains the virus’ genetic material) into the cytoplasm of the host cell. Using the cellular machinery of its host, the virus creates viral proteins and then as the protein levels rise, new nucleocapsids are also created (Noda et al. 2006). As the new genetic material rises in number, budding occurs. Budding is where the virus, creates an “envelope” using the host’s cell membrane. Essentially, creating a new virus from the host itself (ibid). Eventually, as more and more viruses are created from the host, the host will be destroyed.
Ultimately, the number of viruses in the body begins to wreak havoc. In humans and other primates, the virus eventually causes extreme hemorrhagic fever and in most cases, death.
Ebola is transmitted to humans through contact with infected bodily fluids (ie. blood, secretions). Contact can be direct through broken skin or mucous membranes or indirectly with environments contaminated with theincubation period (2 to 21 days) means that people can get infected by a person that does not even know they are ill. It is natural that family and friends want to mourn their recently deceased loved ones; however, the mourning process can become a high risk activity. Often, the burial ceremonies involve direct contact with the deceased person before the virus has died. In other words, healthy individuals are being infected by their infected, deceased loved one (WHO, 2014). Other common ways Ebola is transmitted is through recovered individuals and working in the healthcare field. Any one that has sex with a man recovered from Ebola can become infected from their semen. The semen carries the Ebola virus up to seven weeks after recovery, hence the man will feel healthy, engage in sexual activity and unknowingly, infect others (WHO, 2014). Healthcare professions are at high risk when the proper sanitary precautions are not enforced or possible. Lastly, people that work with infected primates or pigs can also become infected with the disease; however, the likelihood lesser than contact with a diseased human. As stated above, not all viruses that have infected animals are capable of causing EVD in humans.
Currently there is debate that fruit bats, in particular genera Hypsignathus monstrosus, Epomops franqueti and Myonycteris torquata are natural hosts for Ebola. This hypothesis is based on an overlap between the EVD outbreaks and the geographic distribution of fruit bats in Africa.
Symptoms and Diagnostics
A major concern when treating Ebola is that it carries symptoms similar to many other diseases. According to the World Health Organization (2014) “malaria, typhoid fever, shigellosis, cholera, leptospirosis, plague, rickettsiosis, relapsing fever, meningitis, hepatitis and other viral hemorrhagic fevers” all need to be ruled out. Of course with equipment available in the Western world, this process is quite simple. Ebola can be precisely diagnosed by running a variety of diagnostic tests including but not limited to electron microscopy, antigen detection tests and virus isolation by cell culture (WHO, 2014). These diagnostic tools can rule out other disorders by checking for low white blood cell and platelet counts plus elevated liver enzymes (WHO, 2014).
In Africa, however, these diagnostic tools are not always available. Therefore, it is important that the symptoms are clearly laid out and understood. EVD causes “severe acute viral illness” with symptoms including headache, muscle pain, weakness, fever and sore throat. These initial symptoms then progress into vomiting, rash, diarrhea, reduced kidney and liver function and sometimes internal and/or external bleeding.
Treatment and Prevention
Currently there is no vaccine for EVD despite many being tested. Those infected with EVD are being treated with various drug therapies, which are always being improved and remedied. Until a vaccine or a truly efficient treatment has been discovered, patients with EVD are being treated in intensive care where they are holistically cared for, keeping them hydrated through IV with an electrolyte solution.
As the mortality rate for Ebola is so high (as high as 90%) the best way to treat Ebola is to prevent it from happening in the first place (BMC, 2014). In other words, the best way to handle Ebola is to prevent it. For the general public this means educating them on how the disease is transmitted, teaching them proper sanitation procedures and providing them with ways to keep clean and safe such as making condoms and cleaning products readily available.
For more information do your own research or check out some of the websites in my bibliography.
Thank you for reading!
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Ebola virus. (2014, May 8). Retrieved August 6, 2014, from http://en.wikipedia.org/wiki/Ebola_virus
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Ebola Virus. (2014, June 17). Retrieved August 6, 2014, from https://www.bcm.edu/departments/molecular-virology-and-microbiology/ebola
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Noda, T., Ebihara, H., Muramoto, Y., Fujii, K., Takada, A., Sagara, H., … Kawaoka, Y. (2006, September 29). Assembly and Budding of Ebolavirus. Retrieved August 6, 2014, from Noda, T., Ebihara, H., Muramoto, Y., Fujii, K., Takada, A., Sagara, H., … Kawaoka, Y. (n.d.). Assembly and Budding of Ebolavirus. Retrieved August 6, 2014.
Sender, H. (2014, July 31). Where Is The Ebola Virus? Outbreak Map Shows Virus Deaths In West Africa. Retrieved August 6, 2014, from http://www.ibtimes.com/where-ebola-virus-outbreak-map-shows-virus-deaths-west-africa-1645012