The good mood food: Is it a real thing?

            We have all been there, we have a hard day and we go to chipotle to get a huge delicious burrito to cheer us up: good mood food. But is this smart to eat 2200 calories in one sitting and does it actually cheer us up? We learned in Dr. Campisi’s class that the average 70kg male needs 2100 calories per day to sustain his weight and metabolic activity, you can get this in one meal at chipotle! So what actually cheers you up? Surprisingly, this is actually a highly studied branch of science.

            When we eat a delicious burrito from chipotle, we are eating a large amount of an essential amino acid called tryptophan. Tryptophan is important to our mood because it is a precursor of serotonin, a neurotransmitter that transmits the signal of “wellbeing” and “happiness (Hulsken et al 2013).” Sounds easy right? Eat a meal and be happy, to bad it’s not that easy. The more saturated fat, sodium, and carbohydrates that are in a meal the happier we may be for the next couple hours, but studies have shown that your mood will be significantly dampened for two whole days after (Hendy 2012). Another review article looked at the most common good mood food, chocolate. The researchers looked at six studies that included chocolate and found that in all but one, chocolate was able to improve mood significantly (Scholey and Owen 2013). The article failed to research what happens one and two days after administration but there are many factors that lead me to believe no negative mood affect would arise from eating chocolate.

            When you eat a chipotle burrito you consume on average 28 grams of total fat, 1420mg of sodium, and 76 grams of carbohydrates. Your body has to work hard to digest all of this and dilute that massive amount of sodium. When one eats a Hershey’s candy bar you are only eating 13 grams of fat and 35 mg of sodium, you get a lot more “pick me up” for a lot less work in digestion and absorption.

Hendy H. Apr 2012. Which comes first in food-mood relationships, foods or moods? Appetite. 58(2): 771-775

Hulsken S, Martin A, Mohajeri MH and Homberg JR. Dec 2013. Food-derived serotonergic modulators: effects on mood and cognition. 26(2): 223-234

Scholey A and Owen L. Oct 2013. Effects of chocolate on cognitive function and mood: a systematic review. Nutrition Reviews. 71(10): 665-681

https://www.chipotle.com/en-us/menu/nutrition_calculator/nutrition_calculator.aspx

http://www.hersheys.com/pure-products/details.aspx?id=3480&name=HERSHEYS+Milk+Chocolate+Bar

The Effect of Artificial Light on Sleep

      Insufficient sleep plagues many people in today’s non-stop world. Surprisingly, however, poor sleep is significantly due to the prevalence of artificial light—including computer screens, television, and cell phones—in our daily lives. Many people are attached to devices that emit artificial light. Consequently, this dependence on technology has an adverse effect on how well people sleep.

      One of the functions of the eye, other than sight, is the resetting of the circadian clock (Czeisler 2013). The circadian clock is the biochemical mechanism that regulates our sleep cycles. When we stare at a computer screen or constantly look at a phone throughout the day, sleep-promoting neurons are inhibited, as is the release of the sleep-inducing hormone melatonin (Czeisler 2013). Furthermore, artificial light stimulates the release of the neurotransmitter orexin, which causes one to feel aroused and awake (Czeisler 2013).

      I have noticed this effect of artificial light on my sleep cycles. During the school year, when I constantly use my computer and phone throughout the day, I routinely stay up until midnight or later without feeling very tired at all. In contrast, on a camping trip for example, I usually begin to feel sleepy an hour or so after the sun goes down. The main difference between my behavior in these two scenarios is that I don’t use any electronics while camping. One blogger, J.D. Moyer, explains and experiment in which he and his family went a month without artificial light—other than computers to do work. He says that other than not getting as much work done as usual, due to the darkness, he and his family slept much longer and felt much better as a result of this. In light of Czeisler’s explanation, these two observations about sleeping better without artificial light usage make sense. Without artificial light stimulating wakefulness and inhibiting the release of melatonin, our circadian clocks are on time and cause us to fall asleep and sleep longer.

      Though it would be nice to be able to sleep longer at night, some may argue that this is impossible by simply cutting out artificial light. Personally, I would not be able to fulfill all my obligations without using devices that submit me to artificial light. Admittedly, we could all probably reduce the amount of time we spend using computers and phones. I think many would agree that the result of longer, better sleep would be worth sacrificing time on electronic devices.

References:

Czeisler, Charles A. “Casting Light on Sleep Deficiency.” Nature. 497(S13).

Moyer, J.D. “Sleep Experiment: A Month With no Artificial Light.” Systems for Living

            Well. March 4, 2013. Blog.

Vascular damage and stents: promoting endothelial repair

During our cardiac lectures, we discussed coronary artery bypass graft and angioplasty as ways to restore proper coronary circulation and heart function. Coronary artery bypass graft, known as a heart bypass, is a surgical procedure that uses a section of a healthy blood vessel to bypass a blocked coronary artery (1). An angioplasty, also known as percutaneous coronary intervention or percutaneous transluminal coronary angioplasty, uses a small balloon-like device that is inserted into the femoral artery and navigated to the coronary artery, where the balloon is inflated at the site of a clot or narrowed artery. The inflation of the balloon breaks up the clot and allows for a cleared vessel (1). To keep the vessel open, often times a stent, a small metal cylinder, is inserted into the site (2). This stent should in theory keep the vessel open and allow for proper blood flow.

Sometimes the trauma of inserting a stent induces inflammation along with growth factors and cytokines, causing the smooth muscle, tunica media, to thicken (3). This muscular thickening then narrows the vessel, completely reversing the effects of the angioplasty. A risk for scar tissue is also a major problem as well. To prevent scar tissue development, drug-eluting stents are often used, because they slowly release a drug that prevents the formation of scar tissue within the artery. However, the drug coating used may cause a defect in endothelial re-growth, thus increasing the risk of thrombosis (3). This problem is the focus of research today to find an alternative for the drugs currently used.

To prevent the smooth muscle proliferation induced upon stent insertion, Tang et al. examined the role of the metabolic enzyme CTP synthase (CTPS) in stent-induced inflammation (3). The researchers found that the endothelial and smooth muscle cells use different CTPS pathways to proliferate. It was also found that CTPS1, a key molecule in DNA synthesis during cellular proliferation, was induced by the growth factors produced during cardiovascular intervention. With these findings, the researchers decided to block CTPS1 function and found that smooth muscle cells reduced proliferation and therefore endothelial growth inhibiting paracrine factors, leading to increased proliferation of endothelial cells (3). A therapeutic drug that inhibits CTPS1 would allow for smooth muscle cell proliferation inhibition and improved vascular endothelial repair for patients with stents. Further research on a CTPS1 inhibitor as a therapeutic option for stent insertion following angioplasty could potentially eliminate thrombosis due to stent insertion and improve the recovery rate for stent patients.

References:

1. Campisi J. Cardiovascular system: organization & hemodynamics. Biomedical Physiology Notes, 2013.

2. Harvard Health Publications. Building a better stent. Harvard Health Letter 23(8): 3, 2013.

3. Tang R, Cui XB, Wang JN, Chen SY. CTP synthase 1, a smooth muscle-sensitive therapeutic target for effective vascular repair. Arterioscler Thromb Vasc Biol 33(10): 2336-44, 2013.

Breast Cancer, Estrogen, and HDAC inhibitors

The FDA recently designated Syndax Pharmaceutical’s lead product, entinostat, as a Breakthrough Therapy for advanced estrogen receptor (ER)-positive breast cancer (Schull).  Entinostat is considered a class I histone deacetylase inhibitor (Syndax). 

As an overview, chromatin is formed by winding double-stranded DNA around proteins called histones, which regulate transcription by providing access to certain genes.  Histones can be modified in several ways, one of which is the addition of acetyl groups, called acetylation (Horobin).  Histone acetylation induces conformational changes that increase the access of transcription factors to DNA, which allows DNA to be transcribed for protein production.  Histone deacetylases (HDACs) are enzymes that remove acetyl groups from the histones and thus prevent availability of the transcription factors (Camolotto). There are five classes of HDACs (Horobin), and alterations in these enzymes have been identified in malignant cells (Secrist).

ER+ breast cancer is a type of breast cancer that has cells sensitive to the female hormone estrogen, meaning that the growth of these malignant cells is dependent on the binding of the estrogen to their receptors (Mayo). Approximately 80% of all breast cancers are considered ER+ (Breastcancer.org).  Treatment of ER+ breast cancers often involves blocking the estrogen receptors with drugs such as tamoxifen, or utilizing aromatase inhibitors, such as exemestane, which block the enzyme aromatase from synthesizing estrogen in the ovaries (American).  Both treatments reduce the estrogen fuel source to the cancer cells, thus preventing further growth.  Unfortunately, the cells can undergo modifications, such as the histone modifications previously mentioned, and become less dependent on estrogen (Horobin).  As a result these cancer cells become resistant to the endocrine therapies like tamoxifen and exemestane.

Drugs, such as entinostat, have shown potential in reversing this resistance, by targeting HDACs, and restoring the cancer cells’ sensitivity to estrogen (Horobin).  In a recent, Phase II study, entinostat in combination with exemestane was shown to improve both progression free survival and overall survival.  The combination treatment was also well tolerated with fatigue, nausea, and neutropenia as the most frequent adverse events (Yardley).  As cancers continue to evolve, these combination therapies show promise in not only treating resistant cancers, but eliminating some of the high grade side-effects seen with chemotherapy and radiation.

REFERENCES:

American Cancer Society [2013 Jul 7]. Aromatase inhibitors: What are aromatase inhibitors? [Internet]. ACS website. [cited 2013 Nov 29]. Available from: http://www.cancer.org/cancer/breastcancer/moreinformation/medicinestoreducebreastcancer/medicines-to-reduce-breast-cancer-risk-aromatase-inhibitors.

Breastcancer.org [2013 Nov 13]. How to read hormone receptor test results [Internet]. Breastcancer.org Symptoms & Diagnosis website. [cited 2013 Nov 29]. Available from: http://www.breastcancer.org/symptoms/diagnosis/hormone_status/read_results.

Camolotto SA, Racca AC, Ridano ME, Genti-Raimondi S, Panzetta-Dutari GM. 2013 Feb. PSG gene expression is up-regulated by lysine acetylation involving histone and nonhistone proteins. PLOS ONE. 8(2):1-12.

Horobin J. 2011. The case for epigenetic oncology therapy. Vital Signs. 4:18-19.

Mayo Clinic. [2013 Jul 13]. Breast cancer types: What your type means [Internet]. Mayo Clinic Diseases and Conditions website. [cited 2013 Nov 29]. Available from: http://www.mayoclinic.com/health/breast-cancer/HQ00348/NSECTIONGROUP=2.

Secrist JP, Zhou X, Richon VM. 2003 Dec. HDAC inhibitors for the treatment of cancer. Curr Opin Investig Drugs. 4(12):1422-1427.

Schull D, Middleman M. 2013 Sep 11. Syndax’s entinostat receives breakthrough therapy designation from FDA for treatment of advanced breast cancer. Syndax Pharmaceuticals [Internet]. [cited 2013 Nov 29]. Available from: http://www.syndax.com/news.aspx. Syndax Pharmaceuticals. 2013. Entinostat [Internet]. [cited 2013 Nov 29]. Available from: http://www.syndax.com/dev-entinostat.aspx.

Yardley DA, Ismail-Khan RR, Melichar B, Lichinitser M, Munster PN, Klein PM, Cruickshank S, Miller KD, Lee MJ, Trepel JB. 2013 Jun. Randomized phase II, double-blind, placebo-controlled study of exemestane with or without entinostat in postmenopausal women with locally recurrent or metastatic estrogen receptor-positive breast cancer progressing on treatment with a nonsteroidal aromatase inhibitor. J CLIN ONCOL. 31(17): 2128-2135.

Human Brain Complexity Restrained by Metabolism

From proteins all the way to entire organs, structure nearly always informs function. For example, our hearts are structured in such a way that pumping deoxygenated blood to the lungs, and pumping oxygenated blood systemically are favorable actions. Furthermore, heart size corresponds to body size (2), so that blood can be pumped appropriately. However, there are caveats to the structure dictates function rule.

So what is an exception to the rule? There is new research suggesting that the density of neurons in the human brain is not necessarily ideal for functionality. Some researchers have postulated that increased numbers of neurons would explain the complexity of the human brain, and therefore humans should have extremely dense brains – evidenced by many neurons and numerous synapses (1). As humans, we do have a lot of neurons; however, the number of neurons in a mammalian brain seems to be a product of metabolic constraint (1).

For centuries, neuroscientists have perpetuated this mythical estimate of 100 billion neurons in the human brain – although, no one actually knew where that number came from, or if it mattered relative to other species. Recently, these numbers were quantified as 86 billion neurons in a human brain compared to 33 billion neurons in a gorilla brain (1). If gorillas are larger than humans why is there such a discrepancy? The primate brains require 20% of the daily energy budget; every day each one billion neurons require 6 kcal of energy (1). Consequently, it is costly to have a lot of neurons. One of the differences between us and gorillas is that humans aren’t regularly eating raw foods. Raw foods are generally lower-calorie foods and they require a great deal of energy to find, if you’re a gorilla (1). As humans, we can cook food which means integrating higher energy foods into the diet quickly, with little energy expenditure (1).  In some sense, evolution may have influenced the “structure dictates function” rule. Whereby the “function” of energy metabolism has limited the structure, or the number of neurons we are able to have.

1. Herculano-Houzel S. The remarkable, yet not extraordinary, human brain as

a scaled-up primate brain and its associated cost. PNAs. 2012. 126: 10661-10668.

2. Seo JS, Lee SY, Won KJ, Kim DJ, Sohn DS, Yang KM, Cho SH, Park JD, Lee KH, Kim HD. Relationship between normal heart size and body indices in Korean. J Korean Med Sci. 2000 Dec;15(6):641-655.

What really induces that "turkey coma"?

                As we began clearing the plates it slowly started to spread around the table…the post-Thanksgiving meal sleepiness. Along with it, I began to hear mumbles of, “I feel the tryptophan kicking it,” and just then it hit me.  Could tryptophan really be responsible for the overwhelming tiredness people feel after eating a Thanksgiving meal?  Turns out the best answer is “maybe.”

            Tryptophan is an essential amino acid, meaning the human body cannot produce it and so it must come from our diets.  Tryptophan is metabolized in the body, and is used in both the production of niacin (a B vitamin essential for nerve function and digestion) and serotonin (a neurotransmitter which helps regulate mood, sleep cycles, appetite, and behavior).  Serotonin can be further metabolized to melatonin, which aids in the regulation of circadian and seasonal rhythms (Galano, Tan, and Reiter, 2011).  So, with an increase in tryptophan which is a precursor to regulators of sleep cycles and circadian rhythms it would make sense that those who overstuff themselves with turkey, which contains tryptophan, would be sleepy right?  Well, research suggests otherwise.

            Turns out, chicken and milk actually contain more tryptophan than turkey (Milagres et al, 2013).  So why do people only seem to be sleepy after eating their Thanksgiving turkey and not their regular Saturday night chicken dinner?  Research suggests it is primarily the amount of turkey and other foods consumed on Thanksgiving and not tryptophan itself, which causes the sluggishness (Zamoski, 2013).  As we know from physiology, the parasympathetic nervous system is responsible for “resting and digesting.”  Well, when people consume large amounts of calories (an average of 4,400 more on Thanksgiving Day), they activate this division of the nervous system.  In addition, digesting that many additional calories is actually a lot of work for the body.  So, you essentially are using a lot of energy just to digest all the food you ate, which tires your body out, and induces that ever infamous “turkey coma” (Park et al, 2011).

            So, next year (or later this week when you eat too many leftovers) just remember it is partially the turkey that makes you sleepy, but it’s also the large quantities of rolls, green bean casserole, mash potatoes, cranberry sauce, sweet potatoes, and of course those several slices of pie that are all going to work in combination to put you to sleep.

 

Galan A, Tan D, and Reiter R. 2011 Jul. Melatonin as a natural ally against oxidative stress: a physicochemical examination. Journal of Pineal Research 51(1): 1-16.

 

Milagres M, Minim V, Minim L, Simigueli A, Moraes L, and Martino H. 2013 Nov. Night milking adds value to cow’s milk. Journal of Science of Food and Agriculture. DOI: 10.1002/jsfa.6480

 

Zamoski L. 2013. Does tryptophan really make you sleepy—and is turkey to blame? Experts set the record straight. http://www.webmd.com/food-recipes/features/the-truth-about-tryptophan

 

Park S, Kang K, Lee SW, Ahn MJ, Bae JM, and Back K. 2010 Oct. Production of serotonin by dual expression of tryptophan decarboxylase and tryptamine 5-hydroxylase in E. coli. Applied Microbiology and Biotechnology. 89: 1387-1394.

Improved Treatment for Eating Disorders?

Eating disorders affect many women and men throughout the US and the underlying cause is still widely unknown, thus making treatment difficult. Some think eating pathologies are a result of other primary causes and cultural influences, while others believe it has to do with the appetite regulatory system.  A current study looks at the neural system involved with the emotional, reward and cognitive features of food intake, called the corticolimbic pathway.

Within the corticolimbic pathway, one study specifically looked at the involvement of the gustatory cortex and the anterior insula in recovered patients with anorexia and bulimia nervosa.  These two neural pathways are thought to be involved in responses to physical properties of food and its rewarding effects. Furthermore, they innervate the area that controls some behavioral functions called the rostral ventral-central striatum.  In order to test the brain’s involvement in eating disorder patients as compared to healthy controls, fMRI was used to look at brain activity during the administration of sucrose and sucralose.  Interestingly, it was found that the right anterior insula response was decreased in women who had anorexia and much higher for women with bulimia as compared to controls.  This may explain the decrease in perception of appetite in anorexia and increase in perception of appetite in bulimia patients when compared to controls. This finding also indicates a dysfunction in taste processing within women with eating disorders. The difference in signal strength and processing in women with anorexia and bulimia as compared to controls my provide important neural information that can lead to better treatments.

            Since anorexia and bulimia are so prevalent in today’s culture and treatment is limited to various cognitive therapies, this study provides potentially beneficial information that can lead to better treatments.  This is significant because these diseases have high morbidity, mortality, and reoccurrence rates. 

References:

Oberndorfer, TA, Frank GKW, Simmons AN, Wagner A, McCurdy D, Fudge JL,Yang TT, Paulus MP, Kaye WH. 2013. Altered insula response to sweet taste processing after recovery from Anorexia and Bulimia Nervosa.  Am J Psychiatry. 170: 1143-1151.

THC and Painkillers: A recipe for symptom relief without memory loss

With laws being passed in Colorado recently to make the personal use of marijuana legal, it made me think about uses for symptom relief for conditions such as glaucoma, cancer, and multiple sclerosis. The active ingredient, THC, is what helps to provide this major benefit for those suffering from chronic pain, weight loss, and other symptoms. Recently, however, THC has been shown to be involved in memory disturbance that some patients report while using medical marijuana. For some patients, the symptoms of memory loss can be more difficult to manage than the symptoms of their condition (2). It was previously thought that marijuana worked to relieve symptoms through inhibiting the COX-2 pathway, which is the same way that painkillers such as aspirin and ibuprofen work to decrease pain (2). However, recent research using mice has found that this is not that case and rather addition of pain killers to use of medical marijuana may actually decrease the memory disturbance experienced by these patients.

A study published in the science journal Cell this month investigated the mechanism of THC and found that it surprisingly works to increase the activity of the COX-2 pathway (1). Repeated exposure to this increase in the products of this pathway were shown to be involved in decreases in long-term synaptic plasticity, the mechanism for formation and recall of memories. When mice being given THC were also treated with a COX-2 inhibitor, memory impairments were either significantly reduced or removed entirely (1). Although this study is preliminary and the topic definitely requires more research, the ability to relieve the disabling side-effects associated with medical marijuana may help improve quality of life for many patients. Additionally, the researchers suggest that this could provide relief for non-medical abusers of marijuana (1). With the new law going into effect, this research may help bolster support for the safe, legal, and beneficial use of marijuana.

References

1. Chen R, Zhiang J, Fan N, Teng Z, Wu Y, Yang H, Tang Y, Sun H, Song Y, Chen C. 2013 Nov. D9-THC-Caused synaptic and memory impairments are mediated through COX-2 Signaling. Cell. 155: 1154-1165.

2. Painkillers may curb memory loss from medical marijuana. Science Magazine. http://news.sciencemag.org/brain-behavior/2013/11/painkillers-may-curb-memory-loss-medical-marijuana

Listening with our teeth: SoundBite technology

Currently, there are several options available for those who have from hearing loss such as hearing aids to amplify sound, bone-anchored hearing aids for those who have conductive, mixed or unilateral hearing loss, or the cochlear implant for those who have profound or total hearing loss. Aside from the current options available aimed at improving communication for individuals who have hearing loss, there is currently a newer sate-of-the-art technology on the market that aims at improving hearing levels through bone conduction. 

For those who have conductive hearing loss or single-sided deafness, you might consider trying the SoundBite. Conventional hearing aids use air conduction to simply turn up the volume of sound traveling into the ear and require a functional ear. The SoundBite is a bone-conduction device that does not require a functional middle or outer ear to deliver sound (Miller 2010). 

SoundBite technology allows people with unilateral deafness, conductive or mixed hearing loss, to wear an intraoral device and a small microphone in the deaf ear to regain lost hearing.  The SoundBite is a bone conduction prosthetic hearing device that produces the perception of sound by replacing the function of the middle and inner ear. SoundBite technology allows sound to travel through the teeth, through the bones, to the cochlea, while bypassing the middle and inner ear completely (SoundBite Medical 2013). 

The SoundBite hearing system consists of a behind-the-ear microphone unit, which houses the receiver, wireless transmitter, and attached microphone as well as a discrete removable in-the-mouth hearing device (SoundBite Medical 2013). Once sound is captured by the microphone, the digital audio device behind the ear processes the sound and transmits the sound to the removal custom made in-the-mouth hearing device. The mouth piece produces vibrations that are conducted through teeth, through bone, to both cochlea (SoundBiteMedical 2013). 

(SoundBite Medical (2013)

(SoundBite Medical 2013)

In recent studies to determine patient safety and satisfaction with the SoundBite, patients who completed the study reported high rates of auditory benefit in a variety of listening situations, high overall rates of satisfaction with the device, and an overall improvement in communication (Gurgel & Shelton 2013). In one patient, there was a small amount of dental-related soreness, but resolved after a routine dental visit. Another study found that hearing levels improved about 3dB in comparison to not wearing a hearing device (Murray et al. 2011). 

It is clear that there are many options available to those who have hearing loss. The more commonly used devices require surgery and are more expensive. The SoundBite system is a safe and effective, way to improve hearing levels in those who have unilateral deafness, conductive, or mixed hearing loss. 

References:
SoundBite Hearing System Technology for Single Sided Deafness and Conductive Hearing Loss. 2013. Sonitus Medical. Retrieved from: http://www.sonitusmedical.com/product/technology.cfm

Gurkel RK, Shelton C. Nov 2013. The SoundBite hearing system: Patient-assessed safety and benefit study. Division of Otolaryngology. 123(11):2807-12. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/23856912

Murray M, Popelka GR, Miller R. Apr 2011. Efficacy and safety of an in-the-mouth bone conduction device for single-sided deafness. Ear Nose and Throat. 32(3):437-43. Retrieved from: 
 http://www.ncbi.nlm.nih.gov/pubmed/21221045

Miller RJ. It's time we listened with our teeth: the SoundBite hearing system. Nov 2010. Sonitus Medical. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/21055609

Pain? Block it out!

Imagine this: your 12-year-old child broke his foot and needs surgery to fix it. You are against the typical pain medications like Morphine and Fentanyl because of their systemic effects, so what can you do? Thankfully there is a developing method of pain management that is relatively easy and very effective: continuous peripheral nerve blocks. Nerve blocks have been used for a long time for such operations as minor dental work but in the recent years (2000 and on) continuous nerve blocks have been used for war injuries/amputations and post surgery pain management. When an injury or surgery takes place, pain receptors called nociceptors depolarize in response to the stimuli and send action potentials up their associated nerve, through the body and to the appropriate brain areas and pain is felt (Vas 2005). Continuous peripheral nerve blocks are a relatively simple idea where the sensory nerve sending signals from the injury site to the brain is isolated using imaging techniques and continuously infused with local anesthetics. These local anesthetics such as Bupivacaine or other –caine drugs, are continuously pumped near or sometimes into the nerve and work to block the action potential coming from the injury site. Bupivacaine does so by binding the intracellular portion of sodium channels, blocking sodium influx and therefore propagation of the action potential. This is hugely beneficial to the world of pain management because drugs like Morphine work to dumb the pain down once the brain receives the signal but nerve blocks stop the signal from ever reaching the brain. Imagine a road between your house and McDonalds. You want McDonalds but its bad for you, just like you want pain signals but they hurt and are not comfortable. A continuous peripheral nerve block is like a drawbridge that is raised on that road, not allowing you to get McDonalds. Once McDonalds is closed for good (i.e. your pain is gone) the nerve block is lifted and the drawbridge is put back down and you can drive like normal to Whole Foods. A study done on battlefield injuries found that continuous nerve blocks contributed to better pain outcomes, even while the patient was transported in a huge plane for 13 hours (Buckenmaier et. al 2009). This procedure has been vastly improved thanks to the War on Terror and the sacrifices made by the soldiers and we now have many practical uses in the US. Nerve blocks are now used for helping patients with hip fractures by blocking the femoral nerve (Layzell 2013). This is hugely important because hip fractures are usually in elderly patients who are extremely sensitive to narcotic pain medicines like Morphine. We will be seeing a lot more of this procedure in the near future, the localized effects are much greater than systemic effects caused by Morphine.

Buckenmaier CC, Rupprecht C, McKnight G, McMillan B, White R, Gallagher RM and Polomano R. Nov 2009. Pain following battlefield injury and evacuation: a survey of 110 casualties from the wars in Iraq and Afghanistan. Pain Medicine. 10(8):1487-1496

Layzell MJ. Aug 2013. Use of femoral nerve blocks in adults with hip fractures. Nursing Standard. 27(52):49-56.

Vas L. 2005. Continuous sciatic block for leg and foot surgery in 160 children. Pediatric Anesthesia. 15:971-978

http://www.news-medical.net/health/Morphine-Pharmacology.aspx

http://www.drugs.com/pro/bupivacaine.html

Be Thankful That Our Ancestors Weren't Vegetarians

I was reading my October issue of Scientific American [yes, I am somewhat behind], and I came across an article explaining a fairly new hypothesis regarding the longevity of humans in relation to other primates (Pringle, 2013). The widespread belief is that modern medicine, sanitation systems, and food availability have allowed humans to live so much longer – and this is true over the past 200 years. However, extension of human lifespan began long before these lifestyle modifications were implemented.

According to Caleb E Finch (2010), as humans began trading their plant-based diet for more meaty alternatives sometime between 3.4 and 2.5 million years ago, the extra calories and protein not only supplied the brain with extra fuel to grow but also increased pathogen exposure. This risk of infection placed selective pressure on host-defense adaptations to better fight off disease. As Finch began to examine changes to immunological genes specific to humans, the apolipoprotein E (ApoE) gene drew his attention. ApoE functions in lipid transport and metabolism, brain development, and immune defense. The gene contains three alleles, of which ApoE3 and ApoE4 are the most prevalent. ApoE4 closely resembles chimpanzee ApoE, suggesting that it is one of the first ancestral variants to arise in the Homo genus and first to have an effect on human longevity. Notably, ApoE4 greatly enhances the acute phase of inflammation, with heightened production of pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha. With the ApoE4 allele boosting immunity, humans living two million years ago had a higher chance of surviving infection. Early humans also benefited from ApoE4 during periods of starvation, since the allele aids in absorption and storage of lipids that can be drawn on when food is scarce.

Based on its function, one would think that the ApoE4 allele would remain at a high frequency in most populations. This is not the case, however. While ApoE4 confers advantages early in life, as human lifespan extended those possessing the allele developed increased risk for chronic diseases of aging such as heart attacks, strokes, atherosclerosis, and Alzheimer’s disease. This explains the surprising findings of Randall Thompson and his team (2013) upon observing CT scans of 137 mummies spanning over 4,000 years. Thompson et al. found that atherosclerosis was common in the four preindustrial populations examined, including preagricultural hunter-gatherers. These results challenged the assumption that atherosclerosis is a modern disease, and point to a more fundamental predisposition for the illness.

The acquisition of the ApoE4 allele presents an interesting trade-off, and is a textbook example of antagonistic pleiotropy, where a gene affects the young positively and the old negatively. The fading of ApoE4 from a major allele in the population to a minor allele, replaced by the milder ApoE3 allele, makes sense in this context. It is astounding to me that a simple change in diet millions of years ago allowed us to not only increase our brain volume and gain the prefrontal cortex that makes us what we are today, but also played a role in augmenting lifespan and immunity. As a vegetarian, I can’t help but be thankful to my ancestors for eating meat – and grateful that now I don’t have to!

Finch CE. 2010. Evolution of the human lifespan and diseases of aging: Roles of infection, inflammation, and nutrition. Proc Natl Acad Sci U S A. [Internet]. [cited 2013 Nov 26]. 107(Suppl 1): 1718-1724. DOI: 10.1073/pnas.0909606106 Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2868286/

Pringle, H. 2013. Long live the humans: Modern genomes and ancient mummies are yielding clues to why the lifespan of Homo sapiens far exceeds that of other primates. Sci Am [Print]. [cited 2013 Nov 26]. 309(4): 48-55.

Thompson RC, Allam AH, Lombardi GP, Wann LS, Sutherland ML, Sutherland JD, Soliman MAT, Frohlich B, Mininberg DT, Monge JM, Vallodolid CM, Cox SL, el-Maksoud GA, Badr I, Miyamoto MI, Nur el-din AH, Narula J, Finch CE, and Thomas GS. 2013. Atherosclerosis across 4000 years of human history: The Horus study of four ancient populations. The Lancet [Internet]. [cited 2013 Nov 26]. 381(9873): 1211-1222. DOI: http://dx.doi.org/10.1016/S0140-6736(13)60598-X Available at: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)60598-X/fulltext

Can You Really Substitute Breast Milk?

In 2011, two-thirds of all infants born in the United States were ever breastfed. However, by the time these infants were three months old, only one-third were still being breastfed. The World Health Organization (WHO) recommends that infants be exclusively breastfed for the first six months, and then introduced to nutritionally adequate and safe food along with breast feeding until 12 months of age. As this data implies, the majority of the infants in the United States are being raised on either cow’s milk formula or soy formula before they reach six months of age, and this made me wonder what these formula-fed infants are missing out on nutritionally.

Within the first week of birth, breastfeeding produces colostrum—a liquid high in protein, fat-soluble vitamins, minerals and immunoglobins (antibodies from the mother that help to immunize the infant). For the next two-weeks transitional milk is produced—a milk high in fat, lactose, water-soluble vitamins. For the remainder of the time that the infant breastfeeds, mature milk is produced which is mostly water along with carbohydrates, proteins, and fats. Additionally, breast milk produces various trophic hormones that are essential for the maturation of the digestive tract, and peptides that aid in the development of the immune system (Al-Farsi et al., 2012). Breastfeeding itself stimulates the release of the hormone oxytocin within the mother. Oxytocin can enhance feelings of affection and emotional bonding between the mother and infant; this something that cannot be substituted by formula-feeding.

 
A study focused on the antioxidant power of breast milk compared to formula by evaluating the total antioxidant capacity (TAC), total peroxide (TP) level and oxidative stress index (OSI) of plasma in 3 to 6 month old infants. These researchers determined that breastfed infants had significantly higher TAC and vitamin C concentrations of the plasma than the formula-fed group. Additionally, the TP levels and OSI were higher in the formula-fed infants compared to the breastfed group (Aycicek et al., 2006). This information indicates that breastfed infants have lower oxidative stress than formula-fed infants.

Although there are baby formulas out there, such as Similac®, that claim to be very similar to actual breast milk with the nutrient and immune benefits include, I find it difficult to believe that they cover all the bases that breastfeeding provides.

 

References

Al-Farsi, Y. M., Al-Sharbati, M. M., Waly, M. I., Al-Farsi, O. A., Al-Shafaee, M. A., Al-Khaduri, M. M., Trivedi, M. S., & Deth, R. C. (2012). Effect of suboptimal breast-feeding on occurrence of autism: A case-control study. Nutrition,  28, e27-e32. doi:10.1016/j.nut.2012.01.007

 

Aycicek, A., Erel, O., Kocyigit, A., Selek, S., & Demirkol, M. R. (2006). Breast milk provides better antioxidant power than does formula. Nutrition, 22, 616-619. doi: 10.1016/j.nut.2005.12.011

 

 

The role of the Pill in increasing the risk of Primary Open-Angle Glaucoma

The U.S. Food and Drug Administration approved the use of oral contraception (OC) other wise known as "The Pill" contains the hormones progesterone and estrogen in 1960. By 1962 more than one million Americans were using the pill with the numbers rising from this time (Natalie, 2013). The body uses the hormones ingested through the pill for various physiological processes and regulation. Temporal studies of the effects of the pill are now being conducted to draw any conclusions on the long-term effects of ingesting synthetically made hormones that are normally used to conduct homeostasis within the body. What are the effects of ingesting an exceedingly high amount of hormones used to regulate bodily processes over time?

 One such study suggests that the use of oral contraceptives for five or more years modestly increases a woman’s risk by 5% for Primary Open Angle Glaucoma (POAG), which is a degenerative eye disease (Pasquale & Kang, 2011). Estrogen receptors can be found on retinal ganglion cells, which displays that the cells need estrogen for regulation or process of the eye (Pasquale & Kang, 2011). Although POAG is a degenerative disease and that the increase of estrogen from OC’s would decrease the degeneration of the ganglion cells, the cycle of hormonal release is dramatically disrupted through the continual use of OC’s (Pasquale & Kang, 2011). Perhaps there could be a correlation between the constant ingestion of estrogen that cause these receptors on the cells to become insensitive just as insulin receptors become desensitized and are not able to work with a high sugar and fat diet of a patient that develops Type II diabetes. There are many other factors that can be playing a role in this connection between OC use and a woman’s risk of POAG, which the authors had tried to address using a multiple regression model that included many different factors (Pasquale & Kang, 2011). This is one simple study that looks at the effects of ingesting regulatory hormones over time since there was no way to conduct temporal studies of these synthetic hormones. Although OC’s work fairly well by altering the physiological process of reproduction, what other affects does the high intake of these hormones have on physiological processes over time?

Bibliography:

Pascual, L. & Kang, J. (2011)Female reproductive factors and primary open-angle glaucoma in 

the Nurses' Health Study. Eye (Lond). 2011 May; 25(5): 633–641

Angler, N. (2013). THE PILL. Smithsonian, 41(7), 103.