Archive for June, 2010

Lowering Your Blood Pressure with a DASH of Salt

by Leah Frankel, MS, RD |

With increasing numbers of Americans diagnosed with high blood pressure (also known as hypertension), it’s likely you or someone in your family is battling this disease (probably with a smattering of medications). While most people diagnosed with high blood pressure end up taking medications at some point, this can be prevented with a few minor dietary changes. You probably know a few of these tricks, for instance that a high salt intake is bad for hypertension, but that’s just the tip of the iceberg!  We’ll explore hypertension as well as what you can do to manage your high blood pressure while concurrently enjoying the food you eat.

What is hypertension?

Hypertension is defined as persistently elevated blood pressure, with a systolic blood pressure of 140 mm Hg or higher and/or a diastolic blood pressure of 90 mm Hg or higher. You’ve probably been told that your blood pressure is “something over something”; the first “something” is the systolic pressure and the second “something” is the diastolic pressure.  What the heck does that mean?  Systolic blood pressure is our blood pressure when the heart is contracting and diastolic blood pressure is the pressure when our heart is relaxed. The most common type of hypertension is known as essential (also called “primary”) hypertension.  Essential hypertension is diagnosed when the cause of the high blood pressure is unknown (yes, doctors came up with a fancy term to say, “Your blood pressure is high but we don’t know why.”); as opposed to secondary hypertension which is caused by another disease, such as chronic renal failure, endocrine disorders or certain medications.  While high blood pressure usually doesn’t present with any symptoms, uncontrolled blood pressure can lead to death or other diseases including congestive heart failure and stroke.

What’s actually happening in your body when you have high blood pressure?

Blood pressure depends on two factors, the amount of blood being pushed out of the heart and the resistance the blood feels as it moves through the blood vessels. When the diameter of the blood vessel narrows, there is more resistance and blood pressure rises. Think of it this way: your body is trying to push all this blood around but you made the opening smaller, so it has to push harder (the increased blood pressure) to get as much blood to circulate through the body. Some medications work by dilating the vessels so there is less resistance to flow and your blood pressure is lowered. There are also a few systems in the body that help regulate blood pressure: the sympathetic nervous system and the kidneys. The sympathetic nervous system regulates blood pressure in the short term by secreting norepinephrine, a stress hormone, which constricts the arteries leading to increased blood pressure (this is why your blood pressure goes up when you’re under stress). The kidneys have two mechanisms to maintain blood pressure: they control the volume of fluid in the blood (with less volume you don’t need to push as hard, therefore lowering blood pressure) and by activating the renin-angiotensin system which affects 1) how much salt or water is retained and 2) the constriction of blood vessels.  When any of these systems aren’t doing their job correctly, hypertension develops.

How diet changes can help

When most people think of dietary interventions to control high blood pressure the first thing that comes to mind is sodium intake. However, not everyone’s blood pressure is affected by salt intake. Only about 30-50% of people with hypertension are salt sensitive meaning that their blood pressure is affected the amount of salt they consume. We know what you’re thinking, “If I’m not sensitive to sodium then I’m destined to end up on medication.” Luckily, reducing your salt intake is only one approach to controlling high blood pressure.

The most common intervention for controlling hypertension is the DASH (Dietary Approaches to Stop Hypertension) diet. The DASH diet suggests consuming:

  • 7-8 servings of grains a day, primarily whole grains

  • 4-5 servings of vegetables each day

  • 4-5 servings of fruit a day

  • 2-3 servings of dairy, with an emphasis on low-fat or fat free food

  • 2 servings of meat a day, but sticking with only lean meats

  • 4-5 servings of nuts or beans a week

  • 2-3 servings of fat/oil per day with an emphasis on polyunsaturated and monounsaturated oils, and limiting sweets

So how does the DASH diet differ from a standard well balanced diet? It’s actually quite similar. The DASH diet simply puts more emphasis on lean proteins, healthy fats, a reduction in processed foods and an increase in fruits and vegetables (you can see the full DASH Diet Pyramid at the end of the article).  Studies investigating the DASH diet have proven that following the DASH guidelines can lead to significantly lower blood pressure, even when sodium intake isn’t reduced (1). However, study participants who followed the DASH diet and reduced their salt intake had an even better outcome.

Sodium in your food

If you’re already following a well-balanced diet like to the DASH diet but want to know how to reduce your sodium intake, it’s important to know what foods to look out for.  Everyone has different sodium needs/restrictions based on medical conditions including congestive heart failure and chronic kidney disease.  That being said, a typical low sodium diet should contain no more than 2 g (2000 mg) sodium per day. In order to follow a low sodium diet, you want to limit or avoid: canned foods, cured meats, salted snacks, soups, and dairy products; the more processed a food is, the more likely its high in sodium.

Sodium content in various foods (some of the numbers may surprise you):

  • 8 oz milk: 120 mg

  • 1 oz cheese: 200 mg

  • ½ cup fresh or frozen vegetables: 10 mg

  • ½ cup canned vegetables: 230 mg

  • ½ cup fresh or frozen fruit: 2 mg

  • 1 slice bread: 150 mg

  • 1 tsp salted butter or margarine: 50 mg

  • 1 tsp unsalted butter or margarine: 1 mg

  • 1 tbsp salad dressing: 350 mg

  • 1 cup soup: 900 mg

  • 1 cup low sodium soup: 25 mg

  • 1 tsp salt: 2300 mg (that’s more than your whole day’s worth!)

Check the labels on the foods you buy.  We guarantee that you’ll be surprised to discover how much sodium is in the food you eat each day.  Be especially careful when eating out.  New laws require restaurants to include nutritional information so you’ll be able to monitor how much salt you’re actually eating.   If you’re cooking at home, an easy trick is to substitute salt with spices that are sodium free.

Let’s not forget about exercise

As we know, exercise provides a number of benefits including 1) decreased risk of developing many diseases including diabetes and cardiovascular disease, 2) help with weight loss and/or maintenance and 3) improved energy level and mood. Numerous studies have shown that physical activity can also help improve hypertension. A meta-analysis (a study that compares the results of multiple other studies) by Kelley et al. showed that walking decreased blood pressure by an average of 2% (2).  Time to put on your walking shoes!

So when do I start?

Following the DASH diet, decreasing sodium intake and exercising can be beneficial for people with or without hypertension.  Yes, following these guidelines has been shown to reduce blood pressure even in people without high blood pressure (1). So whether you’re recently diagnosed with hypertension, have been on medications for your high blood pressure for years or would like to prevent hypertension in the future, these small changes can make a big difference.  We say you start today.

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  1. Appel LJ, Moore TJ, Obarzanek E, et al. The effect of dietary patterns on blood pressure: results from the Dietary Approaches to Stop Hypertension trial. New England Journal of Medicine 1997;336:1117-24.

  2. Kelley GA, et al. Walking and resting blood pressure in adults: a meta-analysis. Preventative Medicine 2001; 33:120-127.


06 2010

Medical Marijuana: Miracle Treatment or Abused Drug?

by Georgina Lee, PharmD 2011 |

What do the movies “Pineapple Express,” “Cheech & Chong,” Bob Marley, and the TV series “Weed” all have in common?  The answer is marijuana, also known by its many aliases as Mary Jane, hemp, pot, dope, giggle weed and grass to name a few.  Its popularity dates back as far as the third millennium B.C.  It has been used for recreational, religious, spiritual and medicinal purposes (apparently it’s not just used by experimental college students!).  Marijuana, scientifically known as “Cannabis,” is made up of dried parts of the Cannabis sativa hemp plant including its flowers, stems, leaves and seeds.   The resinous part of the plant (the concentrated secretions the plant produces) is known as hashish or “hash,” which also contains psychoactive properties.  Most people recognize marijuana by its distinct smell when smoked which can be described as a simultaneously sweet and sour odor.  Typically, marijuana is smoked as a cigarette (aka “joint”), in a pipe or is humidified in a bong.  It is also smoked in “blunts,” which are cigars that have been emptied of tobacco and refilled with marijuana (immortalized by countless reggae songs).  Since the blunt retains the tobacco leaf used to wrap the cigar, this type of delivery combines marijuana’s active ingredients with nicotine and other harmful chemicals (a double whammy).  Additionally, people mix marijuana into foods such as the case with “magic brownies.” This form of consumption produces stronger effects than when smoked (it seems like the brownies would taste better too).  The use of Marijuana has long been a source of controversy and debate in regards to its role in the medical world and it’s easy to see why.  As medical marijuana dispensaries continue to spring up on street corners across America, the medical community must take a good hard look at the need for marijuana as part of its arsenal of medicinal therapies.

How does Marijuana affect the brain?

The main active chemical in marijuana is delta-9-tetrahydrocannabinol or THC for short.  THC acts upon cannabinoid receptors in various parts of the brain including the cerebellum.  The cerebellum is responsible for balance, posture and coordination of movement after receiving input from sensory systems and the motor cortex (the area in our brain that controls our voluntary movements).  THC also acts upon the hippocampus which contains many cannabinoid receptors and is involved with memory formation.  Some studies have suggested that marijuana affects memory by decreasing the activity of neurons in this area and, because the hippocampus is involved in new memory formation, someone under the influence of marijuana may have impaired short-term memory (“hmm…what happened last night?”).  However, most studies in humans suggest that if a person stops using marijuana, their memory abilities can recover.  Marijuana also affects sensory perception in the cerebral cortex, which can lead to an altered perception of incoming sensory information (such as finding a sock or your friend’s nose extremely funny).

How is Marijuana used medically?

Marijuana is currently used for the treatment of a number of medical complaints and conditions including nausea, vomiting, lack of appetite, spasms, glaucoma and pain.  In 1992, scientists discovered a naturally produced substance called anandamide that activates THC receptors and has many of the same physiological effects as THC.  The discovery of anandamide led to the discovery of additional cannabinoid molecules and receptors including 2-arachidonoglycerol, which helps to control pain.  Oral forms of THC such as Dronabinol (Marinol) are already available to treat chemotherapy-induced nausea and vomiting in addition to treating weight loss in patients who suffer from AIDS wasting syndrome.  However, some studies have shown that Marinol lacks several of the therapeutic compounds available in natural cannabis (aka Marijuana) that has 66 naturally occurring cannabinoids.  One of these is known as cannabidol (CBD), which is a non-psychoactive cannabinoid that has been clinically demonstrated to have analgesic, anti-spasmodic, anxiolytic, anti-psychotic, anti-nausea and anti-inflammatory properties.  Other researchers found that natural extracts of CBD, when administered with THC, significantly reduced pain and other symptoms in patients suffering from multiple sclerosis (an autoimmune disease that affects the brain and spinal cord).  CBD has also demonstrated neuro-protective properties against glutamate neurotoxicity (which occurs during a stroke), cerebral infarction (localized cell death in the brain) and ethanol-induced neurotoxicity.  Some clinical trials have shown CBD to have anti-tumoral properties (via the inhibition of the growth of glioma (brain tumor) cells and selectively induction apoptosis (programmed cell death) in malignant cells…pretty cool if you ask us).  The other cannabinoids found in Marijuana have demonstrated anticonvulsant, anti-inflammatory, anti-depressant, and antioxidant activity in addition to slowing disease progression in certain autoimmune and neurologic diseases including multiple sclerosis, amyotrophic lateral sclerosis (Lou Gehrig’s disease) and Huntington’s disease.  Keep in mind, however, that some of these trials are in very early stages and more in depth research must take place to draw any concrete conclusions.

Wow this sounds like a great plant.  What’s the hold up?

According to the National Institute on Drug Abuse (NIDA), 25.8 million Americans aged 12 and older had abused Marijuana at least once a year.  The NIDA-funded 2008 Monitoring the Future Study showed that 10.9% of 8th graders, 23.9% of 10th graders, and 32.4% of 12th graders had abused marijuana at least once a year prior to being surveyed.  That’s a lot of young people getting high!

Short-term side effects of Marijuana include cough, increased heart rate, dizziness, silliness (“the giggles”), sleepiness, hunger (better known as the “munchies”), confusion, memory impairment, bloodshot eyes and changes in eating and sleeping habits.  NIDA researchers rank peer pressure and curiosity as the leading reasons for this drug abuse.  They also note that users can become heavily dependent on “pot” as a way to cope with anxiety, anger, depression and boredom because of its relaxing properties.  In one study conducted in Memphis, Tennessee, researchers found that out of 150 reckless drivers, 33% tested positive for marijuana and 12% tested positive for both marijuana and cocaine.  That means 45% of “bad drivers” in Memphis are driving around under the influence of Marijuana!  Many anti-Marijuana ads and commercials have surfaced over the years as a result of these statistics in order to educate and prevent people from abusing the drug.  Long-term concerns about smoking Marijuana include dependency, increased risk of cough, bronchitis and emphysema (a progressive disease of the lung that causes shortness of breath) as well as increased risk of cancer of the head, neck and lungs due to the smoke inhalation (Google Image search “oral cancer” for some exquisite photos to scare your kids straight).  The moral of the story is that Marijuana, when used inappropriately or unnecessarily, can be a very dangerous drug.

Hmm, this sounds like a tricky situation…

Essentially, legalizing medical Marijuana is a tug of war between parents, patients, medical professionals, pro- and anti-activist groups, city and state, state and federal, so on and so forth (you get the idea). Currently, the talk of the town surrounds Marijuana dispensaries and their growing locales around the nation.   Many anti-Marijuana activists want to shut down these dispensaries while owners and pro-Marijuana activists fight to keep them open.  A New York Times article stated in its June 24, 2005 editorial “When Medical Marijuana is Misused” that “Those who believe, as we do, that marijuana should be legally available for medical treatments have to be concerned about abuses in California’s pioneering medical marijuana program.  If the abuses cannot be curbed, a political backlash could undermine the ability of thousands of patients to get marijuana to treat the nausea of chemotherapy, loss of appetite that accompanies AIDS and other medical problems…Public officials would be wise to clean up their programs lest flagrant abuses by a few bad actors bring about destruction of a program that benefits many…”  In other words, Marijuana should be treated just like any other controlled substance in the medical world, meaning its abuse needs to be monitored through government regulations and its therapeutic benefits researched and developed for those who qualify after failing other therapies.  An example of such is Sativex, which was approved and launched in the UK on June 21, 2010 (only a few days ago!), making it the first cannabis-based (taken directly from the plant) prescription medication in the world (vs. Marinol, a synthetic version of a chemical in the plant).    It can be prescribed for the treatment of neuropathic pain and spasticity in patients with multiple sclerosis as well as pain relief in adult patients with advanced cancer who experience moderate to severe pain.  In October 2009, the Obama Administration Department of Justice announced an end to federal raids by the Drug Enforcement Administration of medical Marijuana dispensaries that are operating in “clear and unambiguous compliance with existing state laws.”  At the same time, the battle for legalizing medical Marijuana is far from over (get the popcorn ready).

What does the future hold for medical Marijuana?

The 2010 Congressional Research Service states that, “With strong opinions being expressed on all sides of this complex issue, the debate over medical marijuana does not appear to be approaching resolution.”  So does that mean you should run out and purchase a bong at the nearest dispensary?  Using our most sound medical judgment, we would recommend against it due to the potential risks and side effects of Marijuana contrasted with your “medical need” for treatment.  As more research is unveiled in the upcoming years, perhaps the role for medical Marijuana will be more defined.  The take home message: Seek professional medical advice before starting any new treatments!

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  1. National Academy of Sciences, Institute of Medicine. 1999. Marijuana and Medicine: Assessing the Science Base. National Academy Press: Washington, DC. p. 25: Table 1.5: Cannabinoids Identified in Marijuana.

  2. R. Mechoulam et al. 2003. Cannabidiol: an overview of some pharmacological aspects. Neuroscience Letters 346: 61-64; J. McPartland and E. Russo. 2002. Cannabis and cannabis extracts: greater than the sum of their parts. Journal of Cannabis Therapeutics 1: 103-132; A. Zuardi and F Guimaraes. Cannabidiol as an anxiolytic and antipsychotic. In: M. Mathre (Ed):Cannabis in medical practice: a legal, historical and pharmacological overview of therapeutic use of marijuana. McFarland Press: 1997: 133-141.

  3. P. Consroe and S. Snider. Therapeutic Potential of Cannabinoids in Neurological Disorders. In: R. Mechoulam (Ed):Cannabinoids as Therapeutic Agents. CRC Press: 1986 21-51; E. Carlini and J. Cunha. 1981. Hypnotic and antiepileptic effects of cannabidiol. Journal of Clinical Pharmacology. 21: 417S-427S; J. Cunha et al. 1980. Chronic administration of cannabidiol to healthy volunteers and epileptic patients. Pharmacology 21: 175-185.

  4. D. Wade et al. 2004. Do cannabis-based medicinal extracts have general or specific effects on symptoms in multiple sclerosis? A double-blind, randomized, placebo-controlled study on 160 patients. Multiple Sclerosis 10: 339-340; D. Wade et al. 2003. A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms. Journal of Clinical Rehabilitation 17: 21-29.

  5. A. Hampson et al. 1998. Cannabidiol and THC are neuroprotective antioxidants. Proceedings of the National Academy of Sciences 95: 8268-8273.

  6. K. Mishima et al. 2005. Cannabidiol Prevents Cerebral Infarction. Stroke 36: 1077-1082.

  7. C. Hamelink et al. 2005. Comparison of cannabidiol, antioxidants, and diuretics in reversing binge ethanol-induced neurotoxicity. Journal of Pharmacology and Experimental Therapeutics (electronically published May 5, 2005, ahead of printing).

  8. H. Patsos et al. 2005. Cannabinoids and cancer: potential for colorectal cancer therapy. Biochemical Society Transactions. 33: 712-714; M. Guzman. 2003. Cannabinoids: potential anticancer agents. Nature Reviews Cancer 3: 745-755.

  9. P. Massi et al. 2004. Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines.Journal of Pharmacology and Experimental Therapeutics 308: 838-845; G. Carter et al. 2004. Medical marijuana: emerging applications for the management of neurologic disorders. Physical Medicine and Rehabilitation Clinics of North America 15: 943-954.

  10. C. Turner et al. 1980. Constituents of Cannabis sativa L.: A review of the natural constituents. Journal of Natural Products 43: 169-304.

  11. F. Evans. 1991. Cannabinoids; the separation of central from peripheral effects on a structural basis. Planta Medica 57: S60-S67.

  12. P. Wirth et al. 1980. Anti-inflammatory properties of cannabichromene. Life Science 26: 1991-1995.

  13. R. Deyo and R. Musty. A cannabichromene (CBC) extract alters behavioral despair on the mouse tail suspension test of depression. In: International Cannabinoid Research Society (Ed.) 2003 Symposium on the Cannabinoids. ICRS: 2003.

  14. S. Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research 21: 353-356.

  15. J. McPartland and E. Russo. 2002. Cannabis and cannabis extracts: greater than the sum of their parts. Journal of Cannabis Therapeutics.

  16. Society for Neuroscience. “Marijuana-like compound may aid array of debilitating conditions ranging from Parkinson’s Disease to pain.” October 26, 2004.

  17. G. Pryce et al. 2003. Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain. 126: 2191-2202.

  18. C. Raman et al. 2004. Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. Amyotrophic Lateral Sclerosis & Other Motor Neuron Disorders 5: 33-39.

  19. I. Lastres-Becker et al. 2003. Effects of cannabinoids in the rat model of Huntington’s disease generated by an intrastraital injection of malonate. Neuroreport 14: 813-816.

  20. Marijuana Law Reform – NORML. Web. 25 June 2010. <>.

  21. Medical Marijuana Web. 25 June 2010. <>.

  22. Eddy, Mark. “Medical Marijuana: Review and Analysis of Federal and State Policies.” Congressional Research Service. 2 Apr. 2010. Web. 25 June 2010.

  23. “Medical Cannabis Dispensing Collectives and Local Regulation.” Americans for Safe Access(2006). Print.

  24. Volkow, Nora D. “Research Report Series: Marijuana Abuse.” National Institute on Drug Abuse(2005). Print.


06 2010

Seeing Through Pink Eye

by Marissa Camilon, MD 2011 |

While it may be better to see life through rose-colored glasses, acquiring pink eye is not the recommended approach. Anyone who has suffered through this highly contagious and (usually) brief condition can testify to the suffering it causes. You’re itchy, you’re watery and you’re incontestably uncomfortable. Your eyes are your window to the world and, as such, you can’t give them a rest for several days at a time while they heal.  In a nutshell, pink eye sucks.  Luckily, it’s pretty easy to treat and usually lasts for a short amount of time.  What you may not know, however, is that the conventional ways to treat it, the ones passed down from your grandma’s aunt’s nanny, may not be what is the best treatment for your eyes.

What it Pink Eye?

“Pink eye” is more commonly known in the medical world as conjunctivitis, or inflammation of your conjunctiva (the moist layer of tissue that covers most of your eye and the inside of your eyelids). There are many causes for inflammation in this area that are broken down into two major categories: infectious and non-infectious causes. Under the infectious category we have conjunctivitis caused by viruses or bacteria.  Under the non-infectious category we have allergic and non-allergic causes (an example of a non-allergic cause is spilling chemicals in your eyes). While studies show mixed results, most physicians in the trenches will tell you that the most common cause of conjunctivitis is viral.  This makes sense since viral conjunctivitis is extremely infectious (it spreads like fires in the Hollywood Hills in the late summer), spread through any type of bodily secretions, especially secretions from the eye.  That’s where those darn bugs have it figured all out, right?  They make our eyes insanely itchy causing us to rub them all day typically right before we touch phones, doorknobs, and other people’s hands.  That’s also the reason that most of viral outbreaks occur in schools or daycare centers (i.e. places where objects can easily go from eye to hand to mouth to who knows where else).

How do you know if it’s serious?

Historically, you decide to visit the doctor (or more commonly you take your child to the doctor) when you notice the tell-tale pink eyes, complete with extra discharge and dried mucus crusting your eye lid closed in the morning (that seems to be the standard diagnostic criteria in town).  Before you completely write it off as “just another episode of pink eye,” there are a couple of things you should keep in mind. First, there can be more serious causes of pink eye than a simple virus so let your doctor know if you:

  • wear contacts

  • have concurrent headaches and nausea

  • have suddenly blurry vision

  • have a very, very strong feeling that there is something inside your eye

Any of these signs can indicate that something more serious is going on and is worthy of sharing with your doctor during your appointment.

How to Treat Pink Eye

Now we return to your doctor’s appointment.  While we all want the “magic bullet” to cure our medical ails, pink eye is another case where this just doesn’t work.  Since most cases of pink eye are viral in origin, antibiotics (i.e. medications that kill bacteria) won’t do anything for it (this little tidbit of information may not be what you have heard in the past).  Previously, antibiotics were generally given to those with pink eye, even when they were suspected to be viral, to prevent any bacterial infection that could occur on top of the viral infection.  Even as late as 1994, treatment guidelines stated that antibiotic treatment was always necessary for that exact reason (the prevention of a bacterial “super-infection”…not as cool as it sounds).  Since then, new research has shown that these bacterial super-infections rarely occur and that antibiotic treatment may actually be harmful. Giving someone antibiotics without any infectious bacteria means exposing normal, “naïve” bacteria to antibiotics that they can build resistance to.  The result is the evolution of stronger, antibiotic resistant bacteria that are harder to treat in the future. In the words of Homer Simpson, “Doh!”

This strategic change in our approach to treating pink eye is still slowly making its way through American society.  One major issue is the long-standing rule at schools and nurseries stating that children should be treated with antibiotics before returning to school.  Their goal is to decrease the number of children who can potentially become infected. Remember that we are most likely dealing with a viral infection that will not be killed by antibiotics.  The only real way to control the spread of viral conjunctivitis is to not share napkins, utensils or cups and, like we’ve heard so many times, by washing your hands!  The second major battle takes place with people who have heard or seen the previous use of antibiotics during cases of “pink eye.”  These people will go to the doctor expecting to be handed antibiotic eye drops and put pressure on their doctor to prescribe them as they did in the past.  Luckily, these two issues can be rectified with education about the self-limiting, viral nature of this disease.

For those sitting in the waiting room, here’s some good news: in the majority of cases, this is a self-limited condition that can be treated symptomatically. That means using over the counter antihistamines, decongestants or lubricating agents to relieve the dryness and discomfort in your eyes.  So while you may not get the “cure” to pink eye at the doctor’s office, you can definitely get some help with the real troublesome stuff so that you can live your life while your body’s immune system does exactly what it was designed to do.

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  1. Azar MJ, Dhaliwal DK, Bower KS, Kowalksi RP, Gordon YJ. “Possible consequences of shaking hands with your patients with epidemic keratoconjunctivitis.” Am J Ophthalmol 1996, June; 121 (6): 711-2.

  2. Bennett C, David S. “Treatment of viral conjunctivitis in children/in reply.” American Academy of Family Physicians 2003; 67 (9): 1873-5.

  3. O’Brien T, Jeng B, McDonald M, Raizman M. “Acute conjunctivitis: truth and misconceptions.” Current Medical Research and Opinion 2009; 25 (8): 1953-61.

  4. Rose P, Harnden A, Brueggemann A, Perera R, Sheikh A, Crook D, Mant D. “Chloramphenicol treatment for acute infective conjunctivitis in children in primary care: a randomized double-blind placebo-controlled trial.” Lancet 2005; 366: 37-43.

  5. Weiss A. “Acute Conjunctivitis in Childhood.” Current Problems in Pediatrics 1994; 4-11.


06 2010

Type II Diabetes: A Beginner’s Guide

by Rebecca Shatsky, MD 2011 |

According to commercials for the OneTouch glucose monitoring device, rock and roll legend B.B. King hasn’t let Type II diabetes give him the blues. In commercials, little computerized finger stick devices might even look kind of fun, a sentiment we would guess that few diabetics probably share. But, while drug companies and the popular media may try to downplay the gravity and life-altering nature of this chronic disease, few physicians see diabetes as something to be taken lightly.

If you live in America these days, chances are you know someone who either has or has been affected by Type II diabetes. The disease has ravaged the country leaving no stone unturned. Recently rising to epidemic proportions, diabetes has become the leading cause of kidney failure, amputations and blindness in the US. It is also a major contributor to the number one cause of death in the industrialized world: heart disease.

Unfortunately, even though diabetes has become exceedingly common, few doctors really take the time to explain the disease to their patients. This lack of education has led to widespread confusion amongst patients and poor compliance with treatment regimes, a vicious cycle that benefits no one. So, on that account, we want to take this opportunity to summarize things and simplify, providing the basics without all the confusing medical jargon.

What is Type II Diabetes??

Diabetes is a disease of metabolism (the breakdown of sugar for energy) so to understand diabetes, we have to first look at what normally happens in the body after we eat a meal.

Usually, when we eat a meal rich in carbohydrates (sugar), the sugar that we eat enters our blood steam and causes blood sugar levels to rise. When blood sugar levels rise, the body responds by secreting a hormone from the pancreas, called insulin, which allows the sugar floating around in the blood to be used for energy. When the pancreas releases insulin into the blood, blood sugar levels go back down to their normal pre-meal values. The picture below shows how this occurs in your body.  Simple, right?

In diabetes, however, something in this sequence of events goes haywire and the body either doesn’t respond to the insulin in your blood or doesn’t secrete enough insulin to lower blood sugar levels to a healthy range. When blood sugar levels no longer decrease appropriately in response to insulin, we call this “insulin resistance.”

The idea of insulin resistance is central to the development of Type II diabetes. Most studies suggest that in the early stages of the disease, the body’s response to insulin becomes progressively worse over time (4). With increasing insulin resistance we become more and more unresponsive to the normal (life-sustaining) effects of insulin. It’s a little bit like alcoholism, where the body needs greater and greater amounts of alcohol to get drunk; when we become insensitive to insulin, the pancreas needs to produce and release more and more insulin just to keep the body’s blood sugars in a healthy range.

During the disease development period, the body’s blood sugar levels are normal or mildly elevated before meals and then high directly after. If you are screened for diabetes at this stage, blood glucose levels will be higher than normal, but not quite high enough to be classified as “diabetes.” We call this stage “prediabetes.” Clever, we know (we are a bunch of nerdy doctors after all).

Eventually, the pancreas can no longer produce enough insulin to keep up with your body’s increasing insulin requirements. When this happens blood sugar levels soar out of control, both before and after meals. Blood sugar levels that remain high first thing in the morning (after not eating for hours!) are a true indication that diabetes has developed and that treatment is necessary.  The diagram to the right compares the blood sugar levels of a healthy individual with that of an individual with diabetes after having a drink containing 75g of glucose (called a Glucose Tolerance Test).  As you can see, the blood glucose levels soar out of control in the individual with diabetes.

What’s wrong with a little extra sugar?

While it might not sound so bad to have a little extra sugar floating around in your blood, having poorly controlled blood sugar is actually incredibly damaging to your organs, especially your blood vessels. When the cells in your blood are exposed to high levels of sugar for long periods of time, the sugar attaches to the blood cells making them sticky and less flexible. We can measure the percentage of blood cells that have been affected by high sugar levels with a blood test called the hemoglobin A1C level. The hemoglobin A1C level gives doctors a good estimate of how high blood sugar levels have been for the past three months and can be useful in predicting how much damage may be occurring to various tissues in the body.

The best way to explain the complications of diabetes is to look at the different parts of the body the disease affects. The most pervasive and significant complication of diabetes is damage to blood vessels. Damage to large blood vessel results in an increased risk of heart attack and stroke in diabetics, while injury to small blood vessels damages the kidneys (causing kidney failure) and the eyes (leading to blindness). Damage to small blood vessels can also affect the peripheral nervous system (i.e. all nerves not in your brain or spine) and may cause pain, tingling and numbness in your arms and legs, particularly the feet. Finally diabetes has some dangerous effects on the immune system, which puts diabetics at increased risk of infection and increases the time it takes to heal from injuries and surgeries (4). While some of these adverse effects may occur in all diabetics, it is important to remember that the severity of complications is directly related to the length of time a person has had the disease as well as how well blood sugars are controlled.

Who gets diabetes and why?

There are many different theories as to why things go haywire with the body’s insulin response, but what we do know is that the greatest contributing factors to the development of the disease are obesity, physical inactivity and genetics (1).

The importance of obesity in the development of type II diabetes is demonstrated by the tremendous increase in children and adolescents diagnosed with type II diabetes (2).  Once upon a time, Type II diabetes was unheard of in children; so much so that we used to called it “Adult Onset Diabetes.” However, since the obesity crisis swept the nation, the number of children diagnosed with Type II diabetes has increased dramatically and virtually all childhood cases occur in children who are overweight or overtly obese.

The role of genetics in diabetes is well documented but still poorly understood. Certain ethnic populations are at increased risk for Type II diabetes. Those at highest risk include African Americans, Latinos and American Indians (2). We also now know that having a family history of Type II diabetes markedly increases your risk of developing the disease (so if Grandma Mildred had Type II diabetes, you are at an increased risk of developing it). The exact extent to which having a family history of diabetes increases your risk is still hard to predict since the disease is caused by both environmental factors(obesity), as well as genetics. The take home message: If you do have a family history, it’s essential to tell your doctor so they can screen you sooner rather than later.

What does this mean for me?

The most important thing to keep in mind with diabetes, whether the disease has affected you or your loved ones, is that aggressive treatment makes a difference. The surge in Type II diabetes that has occurred over the past 20 years is, without a doubt, intimately related to the obesity epidemic. And, just like obesity, the first weapon in our arsenal against diabetes is diet and exercise. If diet and exercise are not enough, then the key to staving off complications is strict blood sugar control. We cannot emphasize this point enough. It is absolutely essential to take prescribed diabetes medications every single day and to check and record blood sugar levels on a regular basis. If the medications you are taking aren’t doing the trick, make an appointment to see your doctor so that you can find the right combination of medications for you.

Lastly, although discussion of the prevention and treatment of diabetes could be an entire article in itself, it’s important to be aware of the various resources out there available to diabetics. Most insurance plans have good coverage for diabetes medications and many give out free or low cost glucose monitoring devices. The American Diabetes Association is a great resource for information. There are even health care professionals called “diabetes educators” specifically trained to help diabetics learn to live with their disease and make specific lifestyle changes to decrease their risk of complications (nobody wants to go blind as a result of poor glucose control). Ultimately, the best way to manage this disease is to be proactive and take charge of your own health. Successful control of diabetes isn’t just luck, it’s all about lifestyle.

Questions? E-mail the Author:

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1. Braunstein, Glenn D. “Diabetes Mellitus.” Andreoli and Carpenter’s Cecil Essentials of Medicine. By Philip S. Barnett. Philadelphia: Saunders, 2007. 676-95. Print.

2. “Diabetes Research and Statistics.” Centers for Disease Control and Prevention. Web. 18 June 2010. .

3. Ligaray, Kenneth Patrick L., and William L. Isley10. “Diabetes Mellitus, Type 2: EMedicine Endocrinology.” EMedicine – Medical Reference. 10 June 2010. Web. 18 June 2010. .

4 .Powers Alvin C, “Chapter 338. Diabetes Mellitus” (Chapter). Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J: Harrison’s Principles of Internal Medicine, 17e:

5. Steppan, CM, ST Bailey, EJ Brown, RR Banerjee, and CM Wright. “The Hormone Resistin Links Obesity to Diabetes.” Nature 409.6818 (2001): 307-12. Print.


06 2010

Would you like some beer with your prescription?

by Tania Houspian, PharmD 2011

It’s inevitable and happens at least twice a month.  Plans will be made to go out to a bar with friends and, as the first cocktail is being ordered, someone remembers that they’re on antibiotics for an infection they’d rather not talk about. The question is raised about whether or not it’s OK to drink alcohol with that particular medication.  At that point, everyone turns to the friend with some form of medical training and asks, “So can I drink or what?” Members of the House Call, MD staff have experienced this so often we’ve started to avoid going out for drinks with infection-prone friends.  What a loaded question!  If the answer is, “No”, then the friend will spend the rest of the night pouting about not being able to drink and secretly blame the messenger for it.  To avoid those awkward conversations, we’d like to take a moment and explain why sometimes it better to put the drinks aside when on certain medications.  We apologize in advance for your drink-less night out.

Why does alcohol interact with certain medications?

Alcohol is broken down by two parts of your body: your stomach and your liver. When that shot of whiskey reaches the stomach some of the alcohol is broken down and the rest is absorbed into your blood stream. From your bloodstream, the alcohol is delivered to your liver via the portal vein.  In the liver, about 10% of the remaining alcohol is broken down. The remaining alcohol is passed back into your bloodstream and is free to create all those magical affects alcohol has on your brain (i.e. thinking you’re a better dancer than you really are, being exceedingly friendly with strangers, etc.).  At any of those stops that alcohol makes in your system (stomach, liver or brain) there is a possibility for it to interact with any medications that may possibly be taking the same path (1).  Below we’ll go through different classes of medications, covering specific medications from each class and how they interact with alcohol.

Class: Antibiotics/Antifungals

Medications: Metronidazole, Nitrofurantoin, Tinidazole, Ketoconazole, Cycloserine, Cefoperazone, Cefotetan, and Griseofulvin

Just a shot of vodka along with any of these medications and you may be hugging the porcelain throne earlier in the night than you had planned. When mixed with alcohol, these medications can cause a violent reaction in your stomach called a “disulfiram-like reaction.” This reaction results in a sudden increase in heart rate, turning beet red, upset stomach, nausea, vomiting and, in worst case scenarios, death (2).  Antabuse is the name of a medication whose main component is disulfram. When people want to quit drinking they are prescribed Antabuse so that if they do give in to their urge to drink they’ll have a violent reaction to the alcohol.  The smart alecks in the crowd are now thinking, “Well I’ll just make sure to separate my antibiotic and alcohol by a long enough interval so that they’ll never meet in my stomach! I win!”  We hope you can define a “long enough interval” (and if so, let us know) because everyone’s stomach empties these medications at different rates.  As such, we can’t even being to make recommendations as to how much time you should allow for so that none of the antibiotic will meet the alcohol.  The bottom line is that if you mix the above medications with alcohol, you’re asking for some serious punishment.  You can’t say we didn’t warn you.

Class: Antihistamines

Medications: Loratadine, Fexofenadine, Diphenhydramine, Desloratadine, Loratadine, Brompheniramine, and Cetirizine

Having read Attack of the Common Cold, you know that antihistamines can help with a lot of cold symptoms.  Since they’re available to buy at the pharmacy without a prescription, some people make the mistake of assuming they’re completely safe and won’t interact with other medications or alcohol.  We are sorry to say that this assumption is wrong.  On their own, antihistamines can cause some drowsiness.  When mixed with alcohol, you might as well tuck yourself in for the night.  Aside from making you drowsier, it’s also possible to become dizzy from a drop in your blood pressure.  Dizziness can lead to falling and falling leads to all sorts of serious injuries (i.e. broken bones, concussions, etc.)(2).  Antihistamines are found in all sorts of cough, cold, and allergy combination drugs like Nyquil so read the back of the label and see if any of the above medications are in there.  We don’t recommend that you take antihistamines and drive until you know their affect on your level of alertness.  If you’re going to drink and take antihistamines, absolutely do not drive (not that you need to be reminded that you should not drink and drive!).

Class: Cough Medications

Medication: Dextromethorphan (Robitussin)

If you’ve ever had a cough and taken Robitussin, you know how sedating it is.  Imagine mixing alcohol with that.  Two words: lights out.  Mixing the two can lead to hallucinations and strange behavior (more so than alcohol alone).  While this may sound like fun to some people, believe us when we tell you that it is dangerous and harmful to your brain (2).  Don’t do it.

Class: Heartburn Medications

Medications:  Nizatidine, Metoclopramide, Cimetidine, and Ranitidine

Heartburn is very unpleasant and we completely understand your need to alleviate that toxic feeling with medications. You pop a Zantac (Ranitidine) and start to feel better so you decide you will join your friends at the pub.  What can you expect to happen after your second vodka tonic?  Nothing good.  Your heart rate will increase suddenly and so will your blood pressure.  Imagine how the heartburn made you feel and amplify that ten-fold. In addition mixing alcohol with these medications can increase the affect alcohol has on you. If you’re someone who usually feels tipsy after six drinks you may start feeling not so great after two.  This happens because the heartburn medications decrease the breakdown of alcohol in your stomach so your body is exposed to more alcohol than it normally would be. In turn, alcohol inhibits the metabolism of the heartburn medications so you experience more severe side affects from those medications (the increased heart rate and blood pressure) (2).

Class: Pain Relief

Medications: Ibuprofen, Naproxen, and Aspirin

Whatever the source of pain (cramps, muscle pain, hangover, headache, etc.) most people reach for one of these trusty painkillers.  Aspirin has lost some of its popularity as a painkiller but Ibuprofen and Naproxen are gaining in popularity due to their anti-inflammatory properties that help with lots of different sources of pain.  How do these trusty pain-alleviating friends of ours interact with alcohol?  Ibuprofen, Naproxen, and Aspirin all disrupt the lining of your stomach and add to the erosive affects of alcohol.  Combine the two and you asking for some serious stomach pain. Together they can completely disrupt the lining of your stomach and allow the acidic contents of your stomach to reach the stomach tissue.  Long-term combination of alcohol and these agents can lead to bleeding in your stomach (a.k.a. gastrointestinal bleeding). Not fun and filled with long-term consequences.  It’s generally recommended that you separate these agents and alcohol by 8-10 hours or play it safe and don’t combine them in the same day (1).

Class: Antipyretic (Anti-Fever)

Medication: Acetaminophen (Tylenol)

Tylenol can be used for both pain relief and to reduce fever. It gets its own separate section from the other pain relievers because it comes with an entirely different risk when combined with alcohol. Tylenol, like alcohol, is broken down by the liver. When Tylenol and alcohol meet in the liver, the alcohol causes Tylenol to be broken down into a toxic compound.  This toxic compound causes the death of liver cells!  Did your liver just quiver out of fear? We don’t blame it.  Long-term combination of alcohol and Tylenol can cause liver failure, meaning that you’ll ultimately need a liver transplant.  Not good.  Avoid taking more than 4 grams of Tylenol a day and absolutely do not drink when taking Tylenol (1).

Class: Antidepressants

Medications: Phenelzine, Isocarboxazid, and Tranylcypromine

The antidepressants listed above are from the Monoamine Oxidase Inhibitor class (MAOI’s for short, we love acronyms in the medical world).  They have lost popularity in recent years because of the many interactions they can have with food and alcohol.  Aged foods (think salami, aged cheeses, etc.) and aged drinks (wine is the main culprit here) contain a compound called tyramine.  The metabolism of tyramine is prevented when someone is taking MAOI’s so the tyramine builds up in your body.  When tyramine builds up, it causes a sudden increase in heart rate and blood pressure that we call a hypertensive emergency (1). Yes, the kind of emergency people end up in the hospital for.  So if you are taking any of these antidepressants, do not drink aged alcoholic beverages.

Class: Sedatives

Medications: Diazepam, Lorazepam, Zolpidem, Eszopiclone, Estazolam, Ramelteon, Phenobarbital and Temazepam

The entire point of these medications is to help people fall asleep. Add on the sedating affects of alcohol and you’ll have an extremely un-alert person. This might not sound like reason enough not mix them with alcohol since being extra sleepy is something an insomniac may want.  However, the downside is that you may become completely unaware of your actions and experience amnesia. On the other hand some people become aggressive and anxious due to combining these medications with alcohol (2).  The reaction can vary from person to person.  Even with the variance among individuals, all the manufacturers of these medications clearly warn against taking these medications with excessive amounts of alcohol.

Class: Opioid Pain Killers

Medications: Morphine, Oxymorphone, Meperidine, Methadone, Propoxyphene, Oxycodone, Hydromorphone, and Codeine

Generally prescribed for serious pain, the consequences of mixing these medications with alcohol are serious.  Like with the sedatives, mixing these medications with alcohol can cause increased sedation, amnesia and loss of control.  If that’s not enough to scare you then maybe the fact that you may stop breathing will.  Opioid painkillers cause respiratory depression (decreased breathing) and alcohol adds to that affect (1).  It is this combination of painkillers and alcohol that has claimed the lives of several celebrities in the past.

There are a lot of other medications that interact with alcohol but the medications above are the most commonly used in our society.  Never assume it’s safe to combine medications or take medications with alcohol until you check with your pharmacist or doctor.  One night of fun is not worth any long-term damage you may cause your self.  The next time the answer is, “It’s probably best not to drink while on that medication,” trust us…we’re on your team.  We’ll even take you out for a drink when you’re medication-free.

Questions? E-mail the Author:


1.    Alcohol Related Drug Interactions. Pharmacist’s Letter/Prescriber’s Letter. Jan 2008. Vol 24.

2.    Harmful Interactions: Mixing Alcohol with Medicines. National Institute of Alcohol Abuse and Alcoholism. 2007.


06 2010

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