House Call, MD: Health Carefully Explained

by Rebecca Shatsky, MD 2011 | shatsky@myhousecallmd.com

It’s one of the great paradoxes of life: what we perceive as beautiful has a tendency to be bad for us. Tan skin, while masking cellulite and stretch marks, is quite literally a sign of skin damage. Tanning is a fashion trend. Throughout history, tan skin has fallen in and out of fashion. Unfortunately, for the past forty or fifty years, since the days of fashion icon Coco Chanel, tan skin has been a status symbol that we equate with health, happiness and the lavish life the wealthy can afford filled with luxurious vacations.  Even now in 2010, after the dangers of sun exposure have been spelled out explicitly by dermatologic research, the tanning trend is stronger than ever.  Self-proclaimed “tanorexics” from the MTV series The Jersey Shore (particularly Nicole “Snooki” Polizzi) broadcast their love of tanning beds to anyone who will listen. Last month, Polizzi even slammed president Obama for imposing a new 10% tax on tanning beds that went into effect on July 1^st. Republican political opponent, John McCain, was quick to respond to Snooki’s criticism of Obama with a tweet supporting Polizzi’s “freedom to tan,” a fairly controversial move considering McCain’s recent struggle with the deadly skin cancer, malignant melanoma. Naturally, with tanning now in the political hot seat (both literally and figuratively), we at House Call think it’s only appropriate to re-educate our readers on the process of tanning and the dangers of skin caner with scientific research and medical literature leading the debate (instead of reality TV stars and politicians).

The Science of Skin Color:

A person’s natural skin color is determined by the concentration of a pigment called melanin in the skin. Melanin is produced by skin cells called melanocytes. While the number of melanocytes in the skin is fairly similar from person to person, the activity level of these cells when it comes to producing melanin varies greatly and is determined primarily by genetics. The activity of melanocytes is partially responsible for the wide spectrum of skin color that exists among humans.  Also, melanocytes can produce several varieties of melanin, which differ in chemical properties and color. Eumelanin, the most abundant form of the compound, can be either black or brown and is associated with darker skin tones and suntans. Pheomelanin is a yellow-red pigment present in abundance in people with red hair and fair complexions. Some individuals are unable to produce melanin at all due to gene defects or enzyme deficiencies that they are born with. These defects result in very light colored skin, hair and eyes (a condition known as albinism).

Melanin absorbs light and is a natural protectant for skin cells against UV rays that damage DNA.   Pheomelanin absorbs less UV radiation than eumelanin.  Since redheaded people produce more pheomelanin and less eumelanin, red heads do not tan very well and have a much higher incidence of skin cancer (in case you hadn’t noticed). Conversely, darker individuals have continuous production of eumelanin, naturally protecting them from UV DNA damage and lowering their incidence of skin cancer.

What Happens When We Tan?

UV radiation is a carcinogen; it causes mutations in your DNA that your body has to repair before new cells are made in order to prevent cancer from developing. When the skin is exposed to excessive amounts of UV radiation (with frequent sun or tanning bed exposure), the body can’t fix the mutations fast enough and skin cancer can develop. While the production of melanin in the skin is influenced primarily by genetics, it can also be revved up temporarily in response to UV radiation. Exposure to UV light causes an increase in Melanocyte-Stimulating Hormone (MSH), a hormone released from the brain. The release of this hormone into the blood stream revs up production of melanin by melanocytes in the skin, resulting in the golden brown skin color we call a tan. The extra melanin from a suntan is supposed to protect cells from further damage via UV radiation, but the melanin producing pathway takes time (it takes at least four hours to see a tan and then 5-7 days of repeated sun exposure to get the full effect).  In addition, extra melanin does not offer complete protection from DNA damage. Basically, while you spend time building up your base tan you are concurrently building up mutations in your DNA, predisposing yourself to skin cancer.

What’s Wrong With Tanning Beds?

Most people know that sunburns are bad. A sunburn is an immediate indication that the skin has been directly damaged by UV rays and is actively trying to repair that damage by increasing blood flow to the affected area (giving you a painful red hue).  If you are a fair-skinned individual that always burns (even if the burn “turns into a tan”), you are at high risk for skin cancer and every time you get burned you increase that risk.  What we are just learning, however, is that even people who tan easily are at increased risk for skin cancer, especially with repeat long-term exposure from tanning bed use. A landmark study that was published in the June 2010 issue of Cancer Epidemiology Biomarkers and Prevention determined that tanning bed users had a 74% increased risk of developing melanoma. The use of high pressure tanning devices was reported to be particularly dangerous, increasing the risk of melanoma to four times that of people who did not use tanning beds (3). Overall, the amount of exposure is thought to be the greatest risk factor for development of cancer and the cumulative number of tanning hours logged was a significant predictor of cancer development risk. This study is the largest ever to examine the use of indoor tanning as a risk factor for melanoma.  The results have instigated considerable debate amongst the FDA and other preventative health organizations about how to limit the use of tanning beds in the future. The new federal 10% tax on tanning beds instituted on July 1^st, 2010 may be the first in a series of steps to reduce the popularity of tanning beds.  There is talk of developing new laws to restrict use among those under the age of 18.

So What Can I Do to Prevent Skin Cancer?

If you are currently frequenting your local tanning salon or laying out and lathering yourself in baby oil, the best thing you can do is stop cold turkey.  Not only is frequent tanning quadrupling your risk of melanoma, it causes premature skin aging (i.e. wrinkles, sagging skin, and brown spots) and cumulative skin damage.  For serious “tanorexics” who still feel they need a golden glow to feel beautiful, the switch to spray tanning can be quite easy and painless.  More and more salons are offering spray tanning as a healthy alternative to UV beds and the array of self-tanning products in drugstores is mind-boggling. The quality of self-tanning products has also significantly improved in recent years.  If you’ve tried self-tanning in the past without success, you may just want to give lotions and sprays another go.  We bet that you will be pleasantly surprised with the results.

Unfortunately, despite the nonsensical banter from politicians and TV personalities, skin cancer remains a formidable enemy in the US, affecting over 2 million people each year (4). Research estimates that one in five Americans will develop skin cancer in their lifetime and, on average, twenty Americans die of skin cancer every day (1,6).  Don’t believe the myth that most skin damage happens during your teens.  Many people in their 20’s and 30’s who tanned in their teens continue to tan because they believe the damage has already been done. According to new data, every time you tan you put yourself at increased risk, no matter how old you are (7).

The Take Home Message:

• Wear sunscreen when you’re outdoors
• Leave the tanning beds to the cast of Jersey Shore (hopefully they save some of their new-found income for health care)
• See your primary care doctor or dermatologist once a year for your annual skin exam as well as your regular skin care.

• If you’re craving a summer glow, try tanning lotions or spray tans

Skin cancer is the most common form of cancer but it is also highly preventable.  We’ll leave you with a few words of wisdom from The Skin Cancer Foundation: “Tanning’s 15 minutes are over. Go with your own glow!”

Questions? E-mail the Author: shatsky@myhousecallmd.com

References

1. American Cancer Society. Cancer Facts & Figures 2009. Atlanta: American Cancer Society; 2009.
2. Kwon HT, Mayer JA, Walker KK, Yu H, Lewis EC, Belch GE. Promotion of frequent tanning sessions by indoor tanning facilities: two studies. J Am Acad Dermatol 2003; 46:700-5.
3. Lazovich, DeAnn, Rachel Vogel, Marianne Berwick, Martin A. Weinstock, Kristin E. Anderson, and Erin M. Warshaw. “Indoor Tanning and Risk of Melanoma: A Case-Control Study in a Highly Exposed Population.” Cancer, Epidemiology, Biomarkers & Prevention 19.6 (2010): 1557-568.
4. Melanoma of the Skin, Cancer Fact Sheets, National Cancer Institute, SEER Database, 2008
5. SEER Cancer Statistics Review, 1975-2004 (NCI)
6. Robinson JK. Sun Exposure, Sun Protection, and Vitamin D. JAMA 2005; 294: 1541-43.
7. Skin Cancer Facts. The Skin Cancer Foundation. July 15, 2010.
8. The Burden of Skin Cancer. National Center for Chronic Disease Prevention and Health Promotion. May 13, 2008.

PharmD 2011 | houspian@myhousecallmd.com

You’ve may have noticed that your grandmother takes an aspirin everyday as part of her arsenal of medications. You may wonder why she’s taking aspirin when she’s in no apparent pain.  When you asked grandma she replied with her sagely tone, “The doctor said its good for my heart.” You nodded, pretending to understand, and wrote the answer off as another one of grandma’s “senior moments.” Well, it turns out that this time grandma is right. Although her answer is a simplified version of the truth, it is the truth nonetheless. Before you start popping aspirin yourself, read on to find out who should take daily aspirin and how it works to help your heart.

Read the rest of this entry →

by Georgina Lee, PharmD 2011 | lee@myhousecallmd.com

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 8^th graders, 23.9% of 10^th graders, and 32.4% of 12^th 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!

Questions? E-mail the Author: lee@myhousecallmd.com

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References:

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. http://apu.sfn.org/content/AboutSFN1/NewsReleases/am2004_cannabinoids.html

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. <http://norml.org/index.cfm>.

21. Medical Marijuana ProCon.org. Web. 25 June 2010. <http://medicalmarijuana.procon.org/>.

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.

by Rebecca Shatsky, MD 2011 | shatsky@myhousecallmd.com

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: shatsky@myhousecallmd.com

Like the article? Sign up for your free Healthy Dose newsletter here.

References:

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: http://www.accessmedicine.com/content.aspx?aID=2891108.

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.

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: houspian@myhousecallmd.com

References:

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.