Type 2 Diabetes and Victoza

Type 2 diabetes is also known as noninsulin-dependent or adult onset diabetes.  Currently, adult onset diabetes represents 90% of all newly diagnosed cases of diabetes.  Type 2 diabetes is a disease of concern in the United States because more than 1/3 of the population is considered obese.  The populations with the highest rates of type 2 diabetes are the overweight and the elderly.

In contrast with type 1 diabetes, type 2 is a disease of insulin resistance.  This means that the beta cells of the pancreas continue to secrete insulin, but the cells in the body are unable to respond to insulin and take up glucose from the blood.  The three main cell types affected by insulin resistance are liver, muscle and fat cells.  As the demand for insulin increases, the beta cells in the pancreas eventually are unable to keep up with body's increasing insulin demands.  As a result of the impaired glucose uptake, individuals diagnosed with type 2 diabetes are hyperglycemic; meaning that they have high blood sugar levels.

Due to the insulin resistance, most diagnosed patients must take exogenous insulin or other medications aimed at lowering their hemoglobin A1C levels.  One of the newer medications aimed at controlling hemoglobin A1C levels is Victoza.  Victoza is a non-insulin injection that allows for tighter control of blood sugar levels by increasing insulin secretion from beta cells in the pancreas, reducing glucagon secretion and by delaying gastric emptying.  The delayed gastric emptying can lead to weight loss in patients because they will feel full for a longer period of time and are likely to eat less.

Another benefit of Victoza compared to other medications is that it acts in a glucose dependent manner.  This means that Victoza will only work properly if blood glucose levels are sufficiently high.  The glucose dependency of Victoza results in reduced risk for hypoglycemia and allows for much tighter blood glucose control.











References:
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001356/
http://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes-report-web.pdf
http://www.cdc.gov/obesity/data/adult.html
http://www.mayoclinic.org/diseases-conditions/type-2-diabetes/expert-answers/byetta/faq-20057955

Should doctors go to clown school?

Growing up I learned that laughing makes you live longer, it is great in theory but I assumed it was always just an old wives tale. However it turns out that there are many medical practices which use laughter as a preventive medicine or a treatment. The doctors I have met tend to make corny jokes before a patient goes through a surgery or other nerve racking procedure. This makes sense when a person laughs they cause the amount of stress hormones being released to reduce so before surgery the quickest way for a doctor to relieve a patient of some stress is to help them laugh.
Some studies have found that laughter helps to reduce anxiety, increase the quality of sleep, and in some studies laughter increased immunity levels. Laughter is very hard to monitor because there are many other factors which are actually causing the increased immunity.  There is also the problem with the placebo affect in patients who are being treated by laughter, it is unclear if a patient is having reduced levels of stressed because they think they should be or because the laughter is chemically causing a change.  I can't imagine that there are many complications which come with laughing so I think it is a great way to help alleviate stress and depression at a very low cost.

Do you think that is important for the doctor to make there patient laugh and feel less stressed?

Sources:

Bennett, P. N., Parsons, T., Ben‐Moshe, R., Weinberg, M., Neal, M., Gilbert, K., ... & Hutchinson, A. (2014). Laughter and Humor Therapy in Dialysis. In Seminars in dialysis.

How Does Smoking Increase the Risk of Heart Attacks?

Smoking cigarettes has been proven to be deleterious to one’s health in numerous ways. One harmful side effect of smoking is the increased risk of having a heart attack. A recent paper published in the International Journal of Basic and Applied Physiology sought to answer why chronic cigarette smokers have a threefold higher risk of heart attacks than non-smokers. The researchers discovered two key indicators of increased heart attack prevalence in smokers, which were elevated levels of C-reactive protein and increased platelet aggregability in smokers compared to non-smokers.

The researchers determined that C-reactive protein (CRP) levels were a good predictor of coronary artery disease, which is narrowing of the arteries. The levels CRP directly correlate with inflammation, and levels are typically high after events like surgery, injury, or infection. CRP is a protein that can easily be detected by a routine blood analysis test. When macrophages secrete a specific signaling molecule, CRP is produced in the liver and released into the blood. From there its role is to function in an immune response by binding to damaged cells, which promotes phagocytosis and apoptosis of the injured cells. Inflammation and damaged epithelium in the bronchioles due to smoking increases the level of CRP. 78% of smokers in the study had increased CRP levels in their blood compared to just 8% of non-smokers.

In addition, researchers found that smoking increases the ability for platelets in the blood to aggregate. With increased platelet aggregability, there is a greater chance for a thrombotic episode, which is a blood clot in an artery or vein. Normally we want our platelets to function by aggregating and binding fibrinogen and Von Willebrand factor to form a clot when bleeding occurs. However, when this platelet aggregation pathway is improperly triggered, it can result in potentially deadly blood clots like coronary thrombosis, a pulmonary embolism, or deep vein thrombosis. While the researchers did not determine the exact mechanism how chronic cigarette smoking leads to platelet aggregation, they did find that smoking increased platelet aggregability 4 times as compared to non-smokers.

Overall, the study found that people who have smoked 5 or more cigarettes per day for 3 years, are three times more likely to have a heart attack than non-smokers. The researchers concluded that this increased risk of heart attacks in smokers is partially due to elevated CRP levels and increased ability for platelets to aggregate and form clots.

Sources

http://ijbap.weebly.com/uploads/1/3/1/4/13145127/21final_ijbap_2013_-_copy_.pdf

http://www.nlm.nih.gov/medlineplus/ency/article/003356.htm

Statins Reduce Inflammation from Air Pollution

Retrieved from: livinginatoxicworld.wordpress.com

Every day we breathe in all sorts of different particles that are floating in our air. Some of those particles can be quite hazardous in the short term and we are quickly made aware of it. There are particles, however, that we are potentially breathing in that can cause long term hazardous effects as well. One is increased risk for cardiovascular disease.

Retrieved from: murrayvillechiropractic.com

New research is showing an additional benefit to patients who are prescribed statins. Statins are generally prescribed to lower patient cholesterol levels and reduce the risk for cardiovascular events such as heart attack and stroke. In the United States, approximately 1 in 4 Americans age 45 and older is currently on a statin such as Lipitor (Bienkowski, 2014). Studies have found that statins may also reduce inflammation caused by breathing in airborne particles that can increase the risk for cardiovascular disease.

A study conducted by O'Neill et al. at the University of Michigan (2006) found that statins may have additional beneficial effects. The study suggested that airborne particles 2.5 micrometers and smaller, due to the burning of fossil fuels, can lead to an increased risk for cardiovascular disease. It is the inflammation from breathing these particles in that is the major contributing factor. The study found that participants on statins had reduced inflammation compared to participants that were not and that statins reduced the effects of air pollution on cardiac function (O'Neill et al., 2006).

Another study conducted by Ostro et al. (2014) examined nearly 2,000 women in the United States and monitored their exposure to particles in the air also measured as any particulate matter smaller than 2.5 micrometers. The study found that chronic exposure led to an increase in the presence of C-reactive protein (CRP), an inflammatory marker for cardiovascular disease. Interestingly, there was no correlation between chronic airborne particle exposure and increased presence of CRP in patients who were taking statins (Ostro et al., 2014).

This is however not enough evidence for statins to be prescribed as an anti-inflammatory, cardiovascular disease, “cure all” for patients exposed to chronic airborne particles. More research is needed but it is enough evidence to begin developing studies specially designed around this instead of finding a correlation in an existing study. It is also not clear however, if other anti-inflammatory drugs may have similar effects and thus needs to be investigated further (Bienkowski, 2014).

References:

Bienkowski, B. (2014, November 24). Statins may protect people from air pollution. Retrieved

November 30, 2014, from http://www.scientificamerican.com/article/statins-may-protect-people-from-air-pollution/?WT.mc_id=SA_Twitter

O'Neill, M.S., et al., (2007). Air pollution and inflammation in type 2 diabetes: A mechanism for susceptibility. Occupational and Environmental Medicine, 64(6), 373-379. Retrieved from http://ezproxy.msu.edu/login?url=http://search.proquest.com/docview/19525147?accountid=12598

Ostro, B., et al. (2014). Chronic PM2.5 exposure and inflammation: Determining sensitive

subgroups in mid-life women. Environmental Research, 132, 168-175. Retrieved November 30, 2014, from http://www.sciencedirect.com/science/article/pii/S0013935114000899

Cold Medications Part II

I had so much fun with my last post about Tylenol and alcohol that I decided to write this second one. I suppose that part of the fun was that I basically just told a story, but I also liked it because I learned something from it and I think that talking about decongestants and antihistamines will be similarly helpful. I think these things are particularly important to keep in mind as students all around the country prepare for finals week.

Finals week usually means a lot of late nights, lots of coffee, and at least a little bit of extra stress and possibly even a great deal of extra stress. In addition, I think there are an awful lot of people who don’t manage to eat particularly well. Basically, finals week is prime time to catch a cold because our immune systems tend to be rather weakened as a result of the poor eating, late nights, and excess stress. This means that it is not uncommon for people to face taking an exam with a cold.

My personal experience divides colds into two states: the congested stage along with that irritating headache and the runny nose stage. Usually, people will take decongestants for the headache and antihistamines to manage the runny nose. Let’s think about the decongestants first.

It might be your first instinct to reach for the decongestants if you wake up the day of the final with one of those horribly uncomfortable plugged noses. You can feel the pressure building up as a result and it gives you one of those headaches that it’s exactly painful, but does make it terribly difficult to concentrate. Decongestants could be the answer because you want to be able to think at your optimum levels for the exam. It’s completely understandable, but decongestants are vasoconstrictors. That is, they narrow your blood vessels and this is what helps to reduce inflammation. So far, so good. Things are looking good. The targeted vasoconstriction around the nose is successful, but decongestants are not localized exclusively to the nose, meaning that blood vessels throughout your body are being narrowed to some extent. Vasoconstriction increases your blood pressure and can also increase your heart rate. Seeing as your heart rate and blood pressure have probably already gone up on account of your excessive coffee consumption and your stress levels, it might not be the best idea to take a decongestant which will only exacerbate this problem. Additionally, decongestants may cause anxiety and, again, because of finals, you are probably plenty anxious as it is. Basically, it might seem like the logical choice to pop some decongestants, but it might not actually be a good way to improve your performance on that final.

Oaky, now let’s think about antihistamines. Like decongestants, it makes perfect sense to take an antihistamine if you wake up the morning of a final and find that your nose is running uncontrollably. For one thing, it’s uncomfortable, but for another, you don’t want to be that guy during your final. We all know the guy I’m talking about: the guy who sniffles/snarks/whatever throughout the entire exam. It’s distracting and it’s pretty gross and it grates and grates on your concentration when someone else do it, so you’re probably determined not to be that guy. It’s very admirable. The problem is that antihistamine decrease histamine production. Histamines are part of the immune system and they contribute to inflammation, so it’s pretty easy to see who decreasing histamine production will decrease your symptoms. The problem is that antihistamines also tend to have a sedative effect, making you drowsy and impairing your ability to concentrate. While it makes sense to not want to be Mr. Sniffles during your whole exam, it might not be worth the detrimental effects to your concentration and critical thinking. Additionally, antihistamines tend to accumulate, so if you take them for a couple of days, you could be looking at increased drowsiness as a result.

By now, you’re probably wondering why I have a vendetta against cold remedies. It’s a fair point. While I can understand wanting to relieve your cold symptoms, I think it’s important to know that you are usually trading one set of symptoms for another set. Furthermore, the second set might not be particularly pleasant for students trying to perform well on their finals. Basically, the take-home is to think critically about your reasons for taking cold medications in light of the stresses already on your body and the tasks that are before you.

Source: http://www.health.harvard.edu/newsletters/Harvard_Health_Letter/2014/November/could-a-cold-remedy-make-you-sicker?utm_source=twitter&utm_medium=socialmedia&utm_campaign=112314kr1&utm_content=healthrelease

Are You Sexually Active??? You Should Tell Your Dentist.

Shockingly, recent surveys suggest that fifty percent of sexually active adults in the United States have been infected with two or more of seven genital HPV strains.

Unfortunately for sexually active adults, HPV is readily transmissible. HPV transmission does not necessarily require penetrative acts and thereby can be transmitted via any form of genital contact including vaginal, anal, and oral sex.

Beyond transmission via genital contact, HPV can target almost any basal epithelial cell on your skin. In this way, HPV may be transmitted through a number of less obvious routes. Since HPV can persist in a wide range of temperatures and is resistant to desiccation, nonsexual transmission via fomites can also occur, such as by prolonged exposure to a contaminated object (ie: dirty sheets or clothes). This means HPV can be transmitted through seemingly harmless acts, such as open-mouthed kissing and even shared drinks.

During HPV transmission, HPV’s L1 protein binds to heparan sulfate proteoglycans (HSPGs) found in the lamina densa of the basal lamina (a part of the basement membrane) of the epidermis.

Although not all HPV strains are “dangerous”, at least three of the seven genital strains of HPV have been found to be oncogenic. In the case of cervical cancer, oncogenic HPV substrains 16, 18, and 33 have been found in 99% of cervical cancers worldwide. To make the connection to oral health, genomic DNA of oncogenic HPV (subtypes 16, 18, and 33) has been detected in approximately 26% of all head and neck squamous-cell carcinomas (HNSCC). Although the means by which oncogenic HPV subtypes become associated with the stratified squamous epithelium of the head and neck region is not well understood, emerging research suggests sexual behaviors may influence the transition from the genital region to the head and neck region, due to the efficacy of HPV transmission.

As a subclass of head and neck squamous-cell carcinomas, oral and oropharyngeal cancers also have a frequent association with HPV 16 (one of the oncogenic strains). One case study suggests that a high lifetime number of oral-sex or vaginal-sex partners, engagement in casual sex, early age at first intercourse, and infrequent use of condoms are all associated with HPV-16–positive oropharyngeal cancer. Another case study found that the odds of oral HPV infection increased with the number of oral sex partners or open-mouthed kissing partners, indicating that oral HPV infection is sexually acquired and is transmitted by behaviors as common as open-mouthed kissing.

Since dentists usually only screen for oral cancer in at-risk patients (usually frequent smokers), informing your dentist about your sexual habits will enable them to perform more thorough oral / oropharyngeal cancer screenings, thus possibly saving your life!

Sources: 

1) Workowski K. 2010. Sexually Transmitted Diseases Treatment Guidelines – 2010. Morbidity and Mortality Weekly Report Recommendations and Reports.

2) Burd E. 2003. Human Papillomavirus and cervical cancer. Clinical Microbiology Reviews. 16(1): 1–17.

3) Schiller J, Day P, Kines C. 2010. Understanding of the mechanism of HPV infection. Gynecologic Oncology. 118(1): S12-S17.

4) D’Souza G, Agrawal Y, Halpern J, Bodison S, Gillison M. 2009. Oral sexual behaviors associated with prevalent oral human papillomavirus infection. Journal of Infectious Diseases.  199(9): 1263-1269.

5) D’Souza G, Kreimer A, Viscidi R, Pawlita M, Fakhry C, Koch W, Westra W, Gillison M. 2007. Case–control study of human papillomavirus and oropharyngeal cancer. New England Journal of Medicine. 356(19): 1944-1956.