Bee Sting Therapy

Bee Sting Therapy

            Last night I was speaking with a young lady about her aunt who had the relapsing form of Multiple Sclerosis (MS) who is trying bee sting therapy, also known as apitherapy. This technique has been used as a treatment for many diseases in Egypt, Greece, and China for the last 3-5000 years. The main component of bee venom that is usually looked at as the source of the therapy derived benefits is melittin. This chemical exerts strong anti-inflammatory properties and also prompts the body to produce increased levels of cortisol. Apamin, another component of the venom, also induced increased cortisol levels by stimulating the adrenal gland. Now to perform a name drop from our physiology class, I would also like to mention that adolapin (yet another peptide component of bee venom) blocks cyclooxygenase, which you will remember can decrease production of prostaglandins and thus exude an anti-inflammatory response.

The young said her aunt had a great response to bee sting therapy, which constituted an apitherapist (not a doctor) administering about 15 stings per week. Excited and confused at how this therapy was supposed to work, I researched a bit today and found that this individual’s results are very rare. And most studies find no improvement in disease activity in patients utilizing bee sting therapy vs. control patients.

I then looked at other diseases that do have studies that show a significant improvement with the introduction of bee venom. The most common of which was rheumatoid arthritis. In one particularly study I looked at, those with the treatment showed significantly improved mobility and decreased pain levels.

What really strikes me about bee sting therapy is the voluntary willingness to be stung, sometimes up to 20 times per week. I recently was stung a few times and was reminded how truly annoying a bee sting can be. Though if I did have a debilitating disease and multiple bee stings were suggested as a treatment option, I am sure I would explore that route.

References:

1.     Al-Samie MA, Ali M. Studies on bee venom and its medical uses. Int J Adv Res Tech. 2012. 1(2):1-15.

2.

Wesselius T, Heersema DJ, Mostert JP, Heerings M, Admiraal-Behloul F, Talebian A, van Buchem MA, De Keyser J. A randomized crossover study of bee sting therapy for multiple sclerosis. Nuerology. 65(11):1764-1768, 2005.

Liu XD, Zhang JL, Zheng HG, Liu FY, Chen Y. Clinical randomized study of bee-sting therapy for rheumatoid arthritis. Zhen Ci Yan Jiu. 2008; 33: 197-200.

What myelination has to do with schizophrenia

As we all learned in physiology class, many of us may not yet have a fully myelinated prefrontal cortex.  Phylogenetically, the prefrontal cortex was one of the most recent regions of the brain to develop, and consequently one of the last to mature in all of us (Fuster, 2002). This area of our brain has been found to be involved in social behavior, decision-making, cognition, judgement and personality. When we are in our teens and very early twenties, we experience a large decrease in the grey matter in our prefrontal cortex. This late decrease in grey matter is unique to only the prefrontal cortex. According to Arnsten & Shansky (2004) and Lewis (1997), many risky behaviors such as alcohol, drug, and nicotine abuse, as well as psychiatric disorders, such as depression, bipolar disorder, and schizophrenia can develop during this prefrontal cortex developmental stage.

This is an image of the brain with the prefrontal cortex shown and labeled in purple, just anterior to the basal forebrain. 

Harris et al. (2009) performed a study in which they looked at the difference in gene expression in the prefrontal cortex of 48 subjects from ages 0 to 49 who had already passed away. The researchers specifically looked at late adolescents in order to determine the difference in susceptibility to psychiatric disorders, such as schizophrenia. According to Castle and Murray (1993), schizophrenia is usually seen in the age range of 15-25, precisely when myelination of the prefrontal cortex is occurring. The gene, NRG1 (specifically increased isoform 1, and potentially isoform 4) seems to be linked with schizophrenia (Harris et al. 2009). Harris et al. found that gene expression for oxidative phosphorylation and glycolysis, transcription and translation are at their highest during this important adolescent stage. The researchers hypothesized that this may be due to the increased need for energy by the prefrontal cortex because of the ATP-dependent myelin synthesis occurring. The researchers found a similarity between gene regulations during late adolescence and genes that are not functioning correctly in schizophrenia patients. Based on their data, Harris et al. hypothesize that the schizophrenic brain is affected because of the lack of energy (ATP) provided to complete the process of myelination in the prefrontal cortex.

I very highly suggest reading the the journal article: Gene expression in the prefrontal cortex during adolescence: implications for the onset of schizophrenia, as it highlights many physiological processes that we have discussed in class and that may be a major factor in the onset of schizophrenia.

http://www.biomedcentral.com/1755-8794/2/28/#B34

References:
1. Fuster JM. Frontal lobe and cognitive development. 2002. J Neurocytol. 31(3-5):373-385
2. Arnsten AF, Shansky RM. 2004. Adolescence: vulnerable period for stress-induced prefrontal cortical function? Introduction to part IV. Ann N Y Acad Sci. 1021:143-147.
3. Lewis DA. 1997. Development of the prefrontal cortex during adolescence: insights into vulnerable neural circuits in schizophrenia. 16(6):385-398.
4. Harris LW, Lockstone HE, Khaitovich P, Weickert CS, Webster MJ, Bahn S. 2009. Gene expression in the prefrontal cortex during adolescence: implications for the onset of schizophrenia. BMC Medical Genomics. 2:28.  

Prune Belly Babies

When I worked in the Emergency Department I used to encounter a lot of new syndromes, and diseases that would leave me wondering what was going on with those patients. More often than not, I would go home after my shift, and research the patient. One of the patients that I remember doing the most research for was this baby with Prune Belly Syndrome (PBS).

Prune-Belly Syndrome is a rare congenital anomaly with an incidence of 1 per 30,000–50, 000 live births and it is characterized by poor development of the abdominal muscles, causing the skin of the belly area to wrinkle like a prune, undescended testicles, and urinary tract problems (Papantoniou 2007).

Diagnosis of PBS is usually confirmed with an ultrasound which demonstrates an abdominal cavity filled with fluid. While in the womb, the developing baby's abdomen swells with fluid. That fluid disappears after birth, leading to a wrinkled abdomen that looks like a prune. The appearance is more noticeable due to the lack of abdominal muscles.

Many women are advised to terminate their pregnancy if the fetus has other congenital defects. PBS is a syndrome that is more often than not accompanied by pulmonary hypoplasia, heart defects, and muscle/skeletal problems leading to a short life span.

However, many treatments are available such as surgery to help strengthen the abdominal muscles, antibiotics to treat the various respiratory and urinary tract infections. Most recently in Chicago there was a five year old patient who received a surgery to improve liquid containment of the bladder reducing urinary tract infections. The appendix was detached  from the cecum and joined to one end of the bladder, bringing the other end through an opening, or stoma, in the abdominal wall. This conduit is supported by the bladder muscle so when the bladder is full, there is no leakage.

Finally, PBS has no known cause, and further research is needed to expand the knowledge on this syndrome to expand the life spans and improve the lives of the children affected by it.  

Prenatal diagnosis of prune-belly syndrome at 13 weeks of gestation: case report and review of literature. Papantoniou, N., et al. Journal Of Maternal-Fetal & Neonatal Medicine. 2010 23: 1263-1267.

 Information about the surgery can be found at: http://www.uchicagokidshospital.org/specialties/urology/stories/graham.html

Pre-workout? What's the point?

 A former roommate of mine was very into lifting weights.  He would lift weights several times each week and before every workout I always saw him drinking a pre-workout mix.  I never understood the logic behind pre-workout formulas.  My roommate claimed he used it to “wake him up” before every workout.  This made sense because just about every pre-workout mix contains some amount of caffeine.  However, this seemed counterintuitive to me.  I would never drink a soda or a cup of coffee before working out so why would I want to drink a pre-workout mix that had caffeine?  Certainly there had to be other ingredients in the supplement besides caffeine. 

Glycine Propionyl-L-Carnitine (GPLC), the active ingredient in many pre-workout formulas, has been found to increase nitric oxide metabolites at rest.  Several studies have been done assessing the effect increased nitric oxide metabolites have on exercise performance.  One such study assessed the effect GPLC by having subjects perform five 10-second Wingate sprints, with a one-minute recovery time between each sprint. The experiment recorded peak power, mean power, decrement in power output, lactate levels, and heart rate.    GPLC was found to increase peak power, while also decreasing lactate levels four and fourteen minutes post exercise.  The proposed mechanism by which GPLC works is that increasing NO synthesis results in vasodilation.  Vasodilation causes capillary beds to swell increasing the interface with skeletal muscle. 

I admit that while I never understood why my roommate always drank pre-workout, I still tried it several times.  I liked that I seemed more awake after taking it, and I felt as though I was able to lift more weight for longer periods of time.  I suppose now that I have found actual evidence showing pre-workout has beneficial effects on exercise I will have to quit giving my former roommate a hard time for always taking it before he works out. 

Jacobs, P., Goldstein, E., Blackburn, W., Orem, I., & Hughes, J. (2009). Glycine propionyl-l-carnitine

produces enhanced anaerobic work capacity with reduced lactate accumulation in resistance trained males. Journal of the International Society of Sports Nutrition, 6(9).

A Heart for Sports

As a Colorado native and fanatic Denver Broncos fan, I have been going to NFL games since I was old enough to wear a jersey. However, there was one preseason Broncos game that I will never forget.  I remember in 2005 when the Broncos were playing the San Francisco 49ers at home. While the game was not particularly remarkable, what happened after certainly was. The starting offensive guard for the 49ers, a relatively young player named Thomas Herrion, passed away in the locker room after the game. It was later determined that Herrion died as a result of a condition called hypertrophic cardiomyopathy (HCD). HCD is a condition in which the muscles in the bottom half of the heart become significantly larger than normal. As a result of the muscles getting so large, the chamber of the heart that hold oxygen rich blood becomes much smaller and much less capable of pumping blood to the rest of the body. The current theory is that this condition is caused by some sort of genetic mutation. As a result of the large number of high profile athletes that have either died or been forced to retire as a result of this condition, a lot of research has been done in an attempt to identify the genetic cause. Recent studies have demonstrated that a mutation in the genes that are responsible for making cardiac Troponin C (cTNC) are somehow involved (Parvatiyar et al., 2012). Troponin C is an important protein involved in muscle movement. When cTNC binds to calcium floating around the muscle, it changes shape and allows other proteins to function and the muscle to contract. This action is kind of like a hand deactivating an emergency brake in a car allowing the accelerator to move the car. Recent studies have found that a mutation in region of the protein that actually binds to calcium can lead to HCD. This mutation causes the protein to be extra sensitive to calcium levels which in turn makes the heart muscles extremely excitable. This increase in activity leads to a buildup of muscle over time, especially in the regions of the heart related to HCD. Though this mutation is not the only cause of HCD, it is a new and exciting discovery that could lead to a better understanding of how the disease progresses.

References:

Parvatiyar, M.S., Landstrom  A.P., Figueiredo-Freitas, C., Potter, J.D., Ackerman, M.J., Piimto, J.R.. (2012). A mutation in TNNC1-encoded cardiac troponin C, TNNC1-A31S, predisposes to. Journal of Biologic Chemistry, 1-24.

Time for Sunny D

Ahhh… a beautiful Colorado Fall is upon us.  The leaves are beginning to change color, farmers are harvesting the fields, the air is become crisper, and most importantly, vitamin D production from sunlight is going away.

Most Americans do not realizes the global Vitamin D deficiency epidemic. Vitamin deficiency contributes to obesity, depression, heart disease and cancer.  To prevent Vitamin D deficiency an individual must simple get 15 minutes of sunlight exposure a day, or a little longer for darker skin.  But, the catch is getting the right sunlight.

UV rays, that give us wonderful sunburns, are the key ingredients in sun light for Vitamin D production. There are three types of UV rays that make it the surface: UV-A, UV-B, UV-C.  UV-B rays are stronger of the UV-A while weaker than UV-C. UV-B is also the radiation required for Vitamin D synthesis in the skin.  

However, several factors filter or block UV-B rays,  which reduce or inhibit Vitamin D synthesis.  This includes sunscreen, clothing, windows, cloud cover, time of day, time of year, altitude, and latitude. Sunscreen and clothing simple blocks UV –B thus prevent sunburns.  Windows let UV-A through, but not UV-B. The time of day is critical because of where the Sun sits in the horizon changes thought the day.  At “high noon” the sun sits high in the sky and the sunrays travel through less atmosphere.  Compared to dawn and dusk when the sun is low the sun rays travel through more atmosphere filtering out more UV-B. As result, optimal Vitamin D synthesis is from 10am and 3pm.  Similarly, the time of year also effects where the sun sits.  As we move closer to winter the sun sits lower and lower in the sky. Likewise, at higher latitudes the sun sits lower in the sky. Those who live at latitudes south of Atlanta, GA receive UV-B rays year round. Latitudes North of Atlanta, UV-B rays only make it to the surface from March to October. One saving grace for Colorado is higher altitudes reduce the amount of atmosphere that filters UV-B, thus increasing the window of UV-B exposure.  

The simple way to know how to get vitamin D is watch the foliage. Vitamin D synthesis coincides with photosynthesis.  The leaves on trees change color in order to harness a reduced sunlight radiation caused by the increased atmospheric filtering. So, when the leaves change color and the growing season stops so, too, does natural Vitamin D production until the trees bloom again in the spring. From now to then,  look for alternatives to way to get at least a 1000IU of Vitamin D per day, whether it is from diet or supplement.

References:

Michael F Holick and Tai C Chen, “Vitamin D Deficiency: a Worldwide Problem with Health Consequences.,” American Journal of Clinical Nutrition 87, no. 4 (April 2008): 1080S–6S.

O Engelsen et al., “Daily Duration of Vitamin D Synthesis in Human Skin with Relation to Latitude, Total Ozone, Altitude, Ground Cover, Aerosols and Cloud Thickness,” Photochemistry and Photobiology 81, no. 6 (2007): 1287–1290.