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David Dunaief

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A heart attack does not always have obvious symptoms. Stock photo
Chest pain is only one indicator

By David Dunaief, M.D.

Dr. David Dunaief

Heart disease is the most common chronic disease in America. When we refer to heart disease, it is an umbrella term; heart attacks are one component. Fortunately, the incidence of heart attacks has decreased over the last several decades, as have deaths from heart attacks. However, there are still 720,000 heart attacks every year, and more than two-thirds are first heart attacks (1).

How can we further improve these statistics and save more lives? We can do this by increasing awareness and education about heart attacks. It is a multifaceted approach: recognizing the symptoms and knowing what to do if you think you’re having a heart attack.

If you think someone is having a heart attack, call 911 as quickly as possible and have the patient chew an adult aspirin (325 mg) or four baby aspirins. Note that the Food and Drug Administration does not recommend aspirin for primary prevention of a heart attack. However, the use of aspirin here is for treatment of a potential heart attack, not prevention. It is also very important to know the risk factors and how to potentially modify them.

Heart attack symptoms

The main symptom is chest pain, which most people don’t have trouble recognizing. However, there are a number of other, more subtle, symptoms such as discomfort or pain in the jaw, neck, back, arms and epigastric, or upper abdominal, areas. Others include nausea, shortness of breath, sweating, light-headedness and tachycardia (racing heart rate). One problem is that less than one-third of people know these other major symptoms (2). About 10 percent of patients present with atypical symptoms — without chest pain — according to one study (3).

It is not only difficult for the patient but also for the medical community, especially the emergency room, to determine who is having a heart attack. Fortunately, approximately 80 to 85 percent of chest pain sufferers are not having a heart attack. More likely, they have indigestion, reflux or other non-life-threatening ailments.

There has been a raging debate about whether men and women have different symptoms when it comes to heart attacks. Several studies speak to this topic. Let’s look at the evidence.

Men vs. women

There is data showing that, although men have heart attacks more commonly, women are more likely to die from a heart attack (4). In a Swedish prospective (forward-looking) study, after having a heart attack, a significantly greater number of women died in hospital or near-term when compared to men. The women received reperfusion therapy, artery opening treatment that consisted of medications or invasive procedures less often than the men.

However, recurrent heart attacks occurred at the same rate, regardless of sex. Both men and women had similar findings on an electrocardiogram; they both had what we call ST elevations. This was a study involving approximately 54,000 heart attack patients, with one-third of them being women.

One theory about why women are treated less aggressively when first presenting in the ER is that they have different and more subtle symptoms — even chest pain symptoms may be different. Women’s symptoms may include pain in the lower portion of the chest or upper portion of the abdomen and may have significantly less severe pain that could radiate or spread to the arms. But, is this true? Not according to several studies.

In one observational study, results showed that, though there were some subtle differences in chest pain, on the whole, when men and women presented with this main symptom, it was of a similar nature (5). There were 34 chest pain characteristic questions used to determine if a difference existed. These included location, quality or type of pain and duration. Of these, there was some small amount of divergence: The duration was shorter for a man (2 to 30 minutes), and pain subsided more for men than for women. The study included approximately 2,500 patients, all of whom had chest pain. The authors concluded that determination of heart attacks with chest pain symptoms should not factor in the sex of patients.

This trial involved an older population; patients were a median age of 70 for women and 59 for men, with more men having had a prior heart attack. This was a conspicuous weakness of an otherwise mostly solid study, since age and previous heart attack history are important factors.

Therefore, I thought it apt to present another observational study with a younger population, where there was no significant difference in age; the median age of both men and women was 49. In this GENESIS-PRAXY study, results showed that chest pain remained the most prevalent presenting symptom in both men and women (6). However, of the patients who presented without distinct chest pain and with less specific EKG findings (non-ST elevations), significantly more were women than men. Those who did not have chest pain symptoms may have had some of the following symptoms: back discomfort, weakness, discomfort or pain in the throat, neck, right arm and/or shoulder, flushing, nausea, vomiting and headache.

If the patients did not have chest pain, regardless of sex, the symptoms were, unfortunately, diffuse and nonspecific. The researchers were looking at acute coronary syndrome, which encompasses heart attacks. In this case, independent risk factors for disease not related to chest pain included both tachycardia (rapid heart rate) and being female. The authors concluded that there need to be better ways to calibrate non-chest pain symptoms.Some studies imply that as much as 35 percent of patients do not present with chest pain as their primary complaint (7).

Let’s summarize

So what have we learned about heart attack symptoms? The simplest lessons are that most patients have chest pain, and that both men and women have similar types of chest pain. However, this is where the simplicity stops and the complexity begins. The percentage of patients who present without chest pain seems to vary significantly depending on the study — ranging from less than 10 percent to 35 percent.

Therefore, it is even difficult to quantify the number of non-chest pain heart attacks. This is why it is even more important to be aware of the symptoms. Non-chest pain heart attacks have a bevy of diffuse symptoms, including obscure pain, nausea, shortness of breath and light-headedness. This is seen in both men and women, although it occurs more often in women. When it comes to heart attacks, suspicion should be based on the same symptoms for both sexes. Therefore, know the symptoms, for it may be your life or a loved one’s that depends on it.

References:

(1) Circulation. 2014;128. (2) MMWR. 2008;57:175–179. (3) Chest. 2004;126:461-469. (4) Int J Cardiol. 2013;168:1041-1047. (5) JAMA Intern Med. 2014 Feb. 1;174:241-249. (6) JAMA Intern Med. 2013;173:1863-1871. (7) JAMA. 2012;307:813-822.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. 

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Overuse may lead to serious side effects

By David Dunaief, M.D.

Dr. David Dunaief

Reflux (GERD) disease, sometimes referred to as heartburn, though this is more of a symptom, is one of the most commonly treated diseases. Continuing with that theme, proton pump inhibitors (PPIs), which have become household names, are one of the top-10 drug classes prescribed or taken in the United States. In fact, Centers for Disease Control and Prevention data shows that use has grown precipitously in the 10 years ending in 2010 for those ages 55 to 64, from 9 percent of the population to 16 percent (1). This is a 78 percent increase in the number of prescriptions for these drugs.

In 2010, there were 147 million prescriptions filled for PPIs (2). The class of drugs includes Prevacid (lansoprazole), Prilosec (omeprazole), Nexium (esomeprazole), Protonix (pantoprazole) and Aciphex (rabeprazole). This growth may not capture the fact that several of these medications are now available over the counter.

I remember when PPIs were touted as having one of the cleanest side effect profiles. This may still be true, if we are using them correctly for reflux disease. They are supposed to be used for the short term. This can range from 7 to 14 days for over-the-counter PPIs to 4 to 8 weeks for prescription PPIs.

Why did we not know that this class of drugs might be associated with chronic kidney disease, dementia, bone fractures and Clostridium difficile (a bacterial infection of the gastrointestinal tract) before they were approved? Well, if you look at the manufacturers’ package inserts for these drugs, the trials, such as for Protonix, were no longer than a year (3), yet we are putting patients on these medications for decades. And the longer people are on them, the more complications arise.

Typical symptoms of reflux are heartburn and/or regurgitation. Atypical symptoms include coughing and throat clearing. But these atypical symptoms may not be as common as you might think. In fact, in one study, coughing and throat clearing taken together only resulted in a very small portion of patients having reflux disease (4). Having one of these two symptoms showed a slightly higher risk of reflux, but very modest.

Let’s look at some of the research.

Though PPIs may increase the risk of a number of complications, keep in mind that none of the data are from randomized controlled trials (RCTs), which are the gold standard of studies, but mostly observational studies that suggest an association, but not a link. Long-term RCTs to determine side effects are prohibitively expensive.

PPI and kidney disease

Recent research has tied proton pump inhibitors to a host of alarming health problems. Stock photo

In two separate studies, results showed that there was an increase in chronic kidney disease with prolonged PPI use (5). All of the patients started the study with normal kidney function based on glomerular filtration rate (GFR). In the Atherosclerosis Risk in Communities (ARIC) study, there was a 50 percent increased risk of chronic kidney disease, while the Geisinger Health System cohort study found there was a modest 17 percent increased risk. The first study had a 13-year duration, and the second had about a six-year duration. Both demonstrated a modest, but statistically significant, increased risk of chronic kidney disease.

 But as you can see, the medications were used on a chronic basis for years. In an accompanying editorial to these published studies, the author suggests that there is overuse of the medications or that they are used beyond the resolution of symptoms and suggests starting with diet and lifestyle modifications as well as a milder drug class, H2 blockers (6).

PPI and bone fractures

In a meta-analysis (a group of 18 observational studies), results showed that PPIs can increase the risk of hip fractures, spine fractures and any-site fractures (8). Interestingly, when it came to bone fractures, it did not make a difference whether patients were taking PPIs for more or less than a year. How much less than a year was not delineated. They found increased fracture risks of 58, 26 and 33 percent for spine, hip and any site, respectively. It is not clear what may potentially increase the risk; however, it has been proposed that it may have to do with calcium absorption through the gut. 

PPIs reduce the amount of acid, which may be needed to absorb insoluble calcium salts. In another study, seven days of PPIs were shown to lower the absorption of calcium carbonate supplements when taken without food (9).

PPI and dementia

Stock photo

A German study looked at health records from a large public insurer and found there was a 44 percent increased risk of dementia in the elderly who were using PPIs, compared to those who were not (7). These patients were at least age 75. The authors surmise that PPIs may cross the coveted blood-brain barrier and have effects by potentially increasing beta-amyloid levels, markers for dementia. With occasional use, meaning once every 18 months for a few weeks to a few months, there was a much lower increased risk of 16 percent. 

The researchers also suggested that PPIs may be significantly overprescribed in the elderly. Unfortunately, there were confounding factors that may have conflated the risk, such as multiple drug use, having diabetes, or patient also having depression or a stroke history. Researchers also did not take into account family history of dementia, high blood pressure or excessive alcohol use, all of which have effects on dementia occurrence.

Need for magnesium

PPIs may have lower absorption effects on several electrolytes including magnesium, calcium and B12. In one observational study, PPIs combined with diuretics caused a 73 percent increased risk of hospitalization due to low magnesium (10). Diuretics are water pills that are commonly used in disorders such as high blood pressure, heart failure and swelling.

Another study confirmed these results. In this second study, which was a meta-analysis (a group of nine studies), PPIs increased the risk of low magnesium in patients by 43 percent, and when researchers looked only at higher quality studies, the risk increased to 63 percent (11). The authors note that a significant reduction in magnesium could lead to cardiovascular events.

The bottom line is even though some PPIs are over-the-counter and some are prescription medications, it is best if you confer with your doctor before starting them. You may not need PPIs, but rather a milder medication referred to as H2 blockers (Zantac, Pepcid). Even better, start with lifestyle modifications including diet, not eating later at night, raising the head of the bed, losing weight and stopping smoking, if needed, and then consider medications (12). If you do need medications, know that PPIs don’t give immediate relief and should only be taken for a short duration: 7 to 14 days, according to the FDA (13), without a doctor’s consult, and 4 to 8 weeks with one. Most of the problems occur with long-term use.

References:

(1) cdc.gov. (2) PLoS Med. 2014;11(9):e1001736. (3) protonix.com. (4) J Clin Gastroenterol. Online Jul 18, 2015. (5) JAMA Intern Med. 2016;176(2). (6) JAMA Intern Med. 2016;176(2):172-174. (7) JAMA Neurol. online Feb 15, 2016. (8) Osteoporos Int. online Oct 13, 2015. (9) Am J Med. 118:778-781. (10) PLoS Med. 2014;11(9):e1001736. (11) Ren Fail. 2015;37(7):1237-1241. (12) Am J Gastroenterol 2015; 110:393–400. (13) fda.gov.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician. 

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Being a couch potato is detrimental to your health. Stock photo
Hint — it’s not only about weight

By David Dunaief, M.D.

Dr. David Dunaief

What causes Type 2 diabetes? It would seem like an obvious answer: obesity, right? Well, obesity is a contributing factor but not necessarily the only factor. This is important because the prevalence of diabetes is at epidemic levels in the United States, and it continues to grow. The latest statistics show that about 12.2 percent of the U.S. population aged 18 or older has Type 2 diabetes, and about 9.4 percent when factoring all ages (1).

Not only may obesity play a role, but sugar by itself, sedentary lifestyle and visceral (abdominal) fat may also contribute to the pandemic. These factors may not be mutually exclusive, of course.

We need to differentiate among sugars because form is important. Sugar and fruit are not the same with respect to their effects on diabetes, as the research will help clarify. Sugar, processed foods and sugary drinks, such as fruit juices and soda, have a similar effect, but fresh fruit does not.

Sugar’s impact

Sugar may be sweet, but it also may be a bitter pill to swallow when it comes to its effect on the prevalence of diabetes. In an epidemiological (population-based) study, the results show that sugar may increase the prevalence of Type 2 diabetes by 1.1 percent worldwide (2). This seems like a small percentage; however, we are talking about the overall prevalence, which is around 9.4 percent in the U.S., as we noted above.

Also, the amount of sugar needed to create this result is surprisingly low. It takes about 150 calories, or one 12-ounce can of soda per day, to potentially cause this rise in diabetes. This is looking at sugar on its own merit, irrespective of obesity, lack of physical activity or overconsumption of calories. The longer people were consuming sugary foods, the higher the incidence of diabetes. So the relationship was a dose-dependent curve. 

Interestingly, the opposite was true as well: As sugar was less available in some countries, the risk of diabetes diminished to almost the same extent that it increased in countries where it was overconsumed.

In fact, the study highlights that certain countries, such as France, Romania and the Philippines, are struggling with the diabetes pandemic, even though they don’t have significant obesity issues. The study evaluated demographics from 175 countries, looking at 10 years’ worth of data. This may give more bite to municipal efforts to limit the availability of sugary drinks. Even steps like these may not be enough, though. Before we can draw definitive conclusion from the study, however, there need to be prospective (forward-looking) studies.

The effect of fruit

The prevailing thought has been that fruit should only be consumed in very modest amounts in patients with — or at risk for — Type 2 diabetes. A new study challenges this theory. In a randomized controlled trial, newly diagnosed diabetes patients who were given either more than two pieces of fresh fruit or fewer than two pieces had the same improvement in glucose (sugar) levels (3). Yes, you read this correctly: There was a benefit, regardless of whether the participants ate more fruit or less fruit.

This was a small trial with 63 patients over a 12-week period. The average patient was 58 and obese, with a body mass index of 32 (less than 25 is normal). The researchers monitored hemoglobin A1C (HbA1C), which provides a three-month mean percentage of sugar levels. It is very important to emphasize that fruit juice and dried fruit were avoided. Both groups also lost a significant amount of weight while eating fruit. The authors, therefore, recommended that fresh fruit not be restricted in diabetes patients.

What about cinnamon?

It turns out that cinnamon, a spice many people love, may help to prevent, improve and reduce sugars in diabetes. In a review article, the authors discuss the importance of cinnamon as an insulin sensitizer (making the body more responsive to insulin) in animal models that have Type 2 diabetes (4).

Cinnamon may work much the same way as some medications used to treat Type 2 diabetes, such as GLP-1 (glucagon-like peptide-1) agonists. The drugs that raise GLP-1 levels are also known as incretin mimetics and include injectable drugs such as Byetta (exenatide) and Victoza (liraglutide). In a study with healthy volunteers, cinnamon raised the level of GLP-1 (5). Also, in a randomized control trial with 100 participants, 1 gram of cassia cinnamon reduced sugars significantly more than medication alone (6). The data is far too preliminary to make any comparison with FDA-approved medications. However it would not hurt, and may even be beneficial, to consume cinnamon on a regular basis.

Sedentary lifestyle

What impact does lying down or sitting have on diabetes? Here, the risks of a sedentary lifestyle may outweigh the benefits of even vigorous exercise. In fact, in a recent study, the authors emphasize that the two are not mutually exclusive in that people, especially those at high risk for the disease, should be active throughout the day as well as exercise (7).

So in other words, the couch is “the worst deep-fried food,” as I once heard it said, but sitting at your desk all day and lying down also have negative effects. This coincides with articles I’ve written on exercise and weight loss, where I noted that people who moderately exercise and also move around much of the day are likely to lose the greatest amount of weight.

Thus, diabetes is most likely a disease caused by a multitude of factors, including obesity, sedentary lifestyle and visceral fat. The good news is that many of these factors are modifiable. Cinnamon and fruit seem to be two factors that help decrease this risk, as does exercise, of course.

As a medical community, it is imperative that we reduce the trend of increasing prevalence by educating the population, but the onus is also on the community at large to make at least some lifestyle modifications. So America, take an active role.

References:

(1) www.cdc.gov/diabetes. (2) PLoS One. 2013;8(2):e57873. (3) Nutr J. published online March 5, 2013. (4) Am J Lifestyle Med. 2013;7(1):23-26. (5) Am J Clin Nutr. 2007;85:1552–1556. (6) J Am Board Fam Med. 2009;22:507–512. (7) Diabetologia online March 1, 2013.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician. 

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Some seemingly innocent activities can increase risk

By David Dunaief, M.D.

Dr. David Dunaief

Warmer weather is finally upon us, and we now have long, sunny days. However, longer sun exposure does increase the risk of skin cancer. Melanoma is the most serious skin cancer, but fortunately it is not the most common. Basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (SCC) are more prevalent, in that order. Here, we will focus on these two types.

The incidences of these skin cancers are very difficult to pin down because they are not always reported. However, most of us either know someone who has had these types of skin cancer or have had them ourselves. There were roughly three million people diagnosed with nonmelanoma skin cancer in the U.S. in 2012, with the number of treatments increasing 77 percent from 1994 to 2014 (1). SCC and BCC outcomes diverge, with the former having a higher risk of metastases compared to the latter, which tends to grow much slower (2).

These skin cancers may present in different ways. BCC may have a bump that is pearly, waxy, light-colored or pink or flesh-colored or brown. It may bleed, ooze and crust, but may not heal, and can be sunken in the middle (3). SCC has the appearance of a growing nodule. It may also be scaly or crusty and may have flat reddish patches. It may be a sore that also may not heal. It is found on sun-exposed areas, more commonly the forehead, hands, lower lip and nose (3). Interestingly, SCC develops over years of gradual ultraviolet sun exposure, while BCC develops more like melanoma through intense multiple sporadic burns (4).

The more well-known risks for these types of skin cancer include sun exposure (UV radiation), light skin, age, ethnicity and tanning beds (2). But there are other risk factors, such as manicures. There are also ways to reduce risk with sunscreen reapplied every two hours, depending on what you are doing, but also NSAIDs (nonsteroidal anti-inflammatory drugs) and even vitamin B3. Let’s look at the research.

Ultraviolet radiation from the sun or tanning beds can cause skin cancer. Stock photo

 

Risks of other cancers

Though nonmelanoma skin cancers (NMSCs) have far less potential to be deadly, compared to melanoma, there are other risks associated with them. In the CLUE II cohort study of over 19,000 participants, results show something very disturbing: A personal history of NMSC can lead to other types of cancer throughout the body (5). The increased risk of another type of cancer beyond NMSC is 103 percent in those with BCC and 97 percent in those with SCC, both compared to those who did not have a personal history of NMSC.

Tanning beds — No surprise

We know that tanning beds may be a cause for concern. Now the FDA has changed the classification of tanning beds from low to moderate risk and requires a warning that they should not be used by those under the age of 18 (6). Some states have more restrictive laws, banning tanning bed use or requiring parental consent when teens are below certain ages. Compliance with these laws varies.

However, in a prospective (forward-looking) study, results show that people’s responses to warnings depended on how the warnings were framed (7). Compared to the text-only FDA warning requirement, graphic warnings that emphasized the risks of skin cancer were more likely to help people stop using tanning beds, whereas graphic warnings that demonstrated the positive benefits of not using these devices had no effects. So you may have to scare the daylights out of those in their teens and early twenties.

Manicure risk, really?

I am told women and some men love manicures. Manicures cannot possibly be dangerous, right? Not so fast. It is not the actual manicure itself, but rather the drying process that poses a risk. In a prospective study, results show that drying lamps used after a manicure may increase the risk of DNA damage to the skin, which could lead to skin cancer, though the risk is small per visit (8).

There were a lot of variables. The shortest number of visits to increase the risk of skin cancer was eight, but the intensity of the UVA irradiance varied considerably in 17 different salons. The median number of months it took to have carcinogenic potential with exposure was around 35, or roughly three years. The authors recommend either gloves or suntan lotion when using these devices, although both seem to be somewhat impractical with wet nails. It’s best to let your nails dry naturally.

Vitamin B3 to the rescue

Many vitamins tend to disappoint when it comes to prevention. Well, hold on to your hat. This may not be the case for vitamin B3. In the Australian ONTRAC study, the results showed that vitamin B3 reduced the risk of developing NMSC by 23 percent, compared to those who took a placebo (9). Even better was the fact that SCC was reduced by 30 percent.

The most interesting part about this study is that these results were in high-risk individuals who had a personal history of NMSC. The participants were given B3 (nicotinamide 500 mg) twice daily for one year.

After the patients discontinued taking B3, the benefits dissipated within six months. The study was on the small side, including 386 patients with two or more skin cancer lesions in the last five years, with a mean of eight lesions. The side effects were minimal and did not include the flushing (usually neck and facial redness) or headaches seen with higher levels of niacin, another derivative. The caveat is that this study was done in Australia, which has more intense sunlight. We need to repeat the study in the U.S. Nicotinamide is not expensive, and it has few side effects.

NSAIDs as beneficial?

Results have been mixed previously in terms of NSAIDs and skin cancer prevention. However, a more recent meta-analysis (nine studies of varying quality, with six studies considered higher quality) showed that especially nonaspirin NSAIDs reduced the risk of SCC by 15 percent compared to those who did not use them (10).

Diet — The good and the bad

In terms of diet studies, there have been mixed positive and neutral results, especially when it comes to low-fat diets. These are notoriously difficult to run because the low-fat group rarely remains low fat. However, in a prospective dietary study, results showed that effects on skin cancer varied depending on the foods. For those who were in the highest tertile of meat and fat consumption, compared to those in the lowest tertile, there was a threefold increased risk of a squamous cell cancer in those who had a personal history of SCC (11). But what is even more interesting is that those who were in the highest tertile of vegetable consumption, especially green leafy vegetables, experienced a 54 percent reduction in skin cancer, compared to those in the lowest consumption tertile.

Thus, know that there are modifiable risk factors that reduce the risk of nonmelanoma skin cancer and don’t negatively impact your enjoyment of summer. There may be easy solutions to help prevent recurrent skin cancer, as well, that involve both medication and lifestyle modifications.

References:

(1) skincancer.org. (2) uptodate.com. (3) nih.gov. (4) Br J Cancer. 2006;94(5):743. (5) J Natl Cancer Inst. 2008;100(17):1215-1222. (6) federalregister.gov. (7) Am J Public Health. Online June 11, 2015. (8) JAMA Dermatol. 2014;150(7):775-776. (9) ASCO 2015 Annual Meeting: Abstract 9000. (10) J Invest Dermatol. 2015;135(4):975-983. (11) Am J Clin Nutr. 2007;85(5):1401.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician. 

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TIAs are a serious warning sign of stroke and should not be ignored.
Ministrokes are not inconsequential

By David Dunaief, M.D.

Dr. David Dunaief

A TIA (transient ischemic attack) is sometimes referred to as a ministroke. This is a disservice since it makes a TIA sound like something that should be taken lightly. Ischemia is reduced or blocked blood flow to the tissue, due to a clot or narrowing of the arteries. Symptoms may last less than five minutes. However, a TIA is a warning shot across the bow that needs to be taken very seriously on its own merit. It may portend life-threatening or debilitating complications that can be prevented with a combination of medications and lifestyle modifications.

Is TIA common?

It is diagnosed in anywhere from 200,000 to 500,000 Americans each year (1). The operative word is “diagnosed,” because it is considered to be significantly underdiagnosed. I have helped manage patients with symptoms as understated as the onset of double vision. Other symptoms may include facial or limb weakness on one side, slurred speech or problems comprehending others, dizziness or difficulty balancing or blindness in one or both eyes (2). TIA incidence increases with age (3).

What is a TIA?

TIAs are a serious warning sign of stroke and should not be ignored.

The definition has changed over time from one purely based on time (less than one hour), to differentiate it from a stroke, to one that is tissue based. It is a brief episode of neurological dysfunction caused by focal brain ischemia or retinal ischemia (low blood flow in the back of the eye) without evidence of acute infarction (tissue death) (4). In other words, TIA has a rapid onset with potential to cause temporary muscle weakness, creating difficulty in activities such as walking, speaking and swallowing, as well as dizziness and double vision.

Why take a TIA seriously if its debilitating effects are temporary? 

Though they are temporary, TIAs have potential complications, from increased risk of stroke to heightened depressive risk to even death. Despite the seriousness of TIAs, patients or caregivers often delay receiving treatment.

Stroke risk

After a TIA, stroke risk goes up dramatically. Even within the first 24 hours, stroke risk can be 5 percent (5). According to one study, the incidence of stroke is 11 percent after seven days, which means that almost one in 10 people will experience a stroke after a TIA (6). Even worse, over the long term, the probability that a patient will experience a stroke reaches approximately 30 percent, one in three, after five years (7).

To go even further, there was a study that looked at the immediacy of treatment. The EXPRESS study, a population-based study that considered the effect of urgent treatment of TIA and minor stroke on recurrent stroke, evaluated 1,287 patients, comparing their initial treatment times after experiencing a TIA or minor stroke and their subsequent outcomes (8).

The Phase 1 cohort was assessed within a median of three days of symptoms and received a first prescription within 20 days. In Phase 2, median delays for assessment and first prescription were less than one day. All patients were followed for two years after treatment. Phase 2 patients had significantly improved outcomes over the Phase 1 patients. Ninety-day stroke risk was reduced from 10 to 2 percent, an 80 percent improvement.

The study’s authors advocate for the creation of TIA clinics that are equipped to diagnose and treat TIA patients to increase the likelihood of early evaluation and treatment and decrease the likelihood of a stroke within 90 days. The moral of the story is: Treat a TIA as a stroke should be treated, the faster the diagnosis and treatment, the lower the likelihood of sequela, or complications.

Predicting the risk of stroke complications

Both DWI (diffusion weighted imaging) and ABCD2 are potentially valuable predictors of stroke after TIA. The ABCD2 is a clinical tool used by physicians. ABCD2 stands for Age, Blood pressure, Clinical features and Diabetes, and it uses a scoring system from 0 to 7 to predict the risk of a stroke within the first two days of a TIA (9).

Heart attack

In one epidemiological study, the incidence of a heart attack after a TIA increased by 200 percent (10). These were patients without known heart disease. Interestingly, the risk of heart attacks was much higher in those over 60 years of age and continued for years after the event. Just because you may not have had a heart attack within three months after a TIA, this is an insidious effect; the average time frame for patients was five years from TIA to heart attack. Even patients taking statins to lower cholesterol were at higher risk of heart attack after a TIA.

Mortality

If stroke and heart attack were not enough, TIAs decrease overall survival by 4 percent after one year, by 13 percent after five years and by 20 percent after nine years, especially in those over age 65, according to a study published in Stroke (11). The reason younger patients had a better survival rate, the authors surmise, is that their comorbidity (additional diseases) profile was more favorable.

Depression

In a cohort (particular group of patients) study that involved over 5,000 participants, TIA was associated with an almost 2.5-times increased risk of depressive disorder (12). Those who had multiple TIAs had a higher likelihood of depressive disorder. Unlike with stroke, in TIA it takes much longer to diagnose depression, about three years after the event.

What can you do?

Awareness and education are important. While 67 percent of stroke patients receive education about their condition, only 35 percent of TIA patients do (13). Many risk factors are potentially modifiable, with high blood pressure being at the top of the list, as well as high cholesterol, increasing age (over 55) and diabetes.

Secondary prevention (preventing recurrence) and prevention of complications are similar to those of stroke protocols. Medications may include aspirin, antiplatelets and anticoagulants. Lifestyle modifications include a Mediterranean and DASH diet combination. Patients should not start an aspirin regimen for chronic preventive use without the guidance of a physician.

In researching information for this article, I realized that there are not many separate studies for TIA; they are usually clumped with stroke studies. This underscores the seriousness of this malady. If you or someone you know has TIA symptoms, the patient needs to see a neurologist and a primary care physician and/or a cardiologist immediately for assessment and treatment to reduce risk of stroke and other long-term effects.

References:

(1) Stroke. Apr 2005;36(4):720-723; Neurology. May 13 2003;60(9):1429-1434. (2) mayoclinic.org. (3) Stroke. Apr 2005;36(4):720-723. (4) N Engl J Med. Nov 21 2002;347(21):1713-1716. (5) Neurology. 2011 Sept 27; 77:1222. (6) Lancet Neurol. Dec 2007;6(12):1063-1072. (7) Albers et al., 1999. (8) Stroke. 2008;39:2400-2401. (9) Lancet. 2007;9558;398:283-292. (10) Stroke. 2011; 42:935-940. (11) Stroke. 2012 Jan;43(1):79-85. (12) Stroke. 2011 Jul;42(7):1857-1861. (13) JAMA. 2005 Mar 23;293(12):1435.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician. 

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It is very important to take white-coat hypertension seriously. Stock photo
As many as 30 percent of patients experience this phenomenon

By David Dunaief, M.D.

Dr. David Dunaief

White-coat hypertension (high blood pressure) is defined as blood pressure that is elevated to at least 140/90 mm Hg at a physician’s office, but “normal” when measured at home. The blood pressure considered normal at home for most Americans is less than 135/85 mm Hg. This is a real phenomenon caused by the anxiety or stress of being in a doctor’s office. It is also known as “isolated office hypertension.”

About 15 to 30 percent of patients experience white-coat hypertension (1). However, when the diastolic (bottom number) blood pressure is greater than 105 mm Hg, it is unlikely to be simply caused by doctor’s office-related stress (2).

Consequences

What are the consequences of white-coat hypertension? The first challenge is that physicians may overtreat it, prescribing medications that lead to low blood pressure when not in the office. Alternately, we sometimes discount it because it seems benign or harmless. However, some studies show that it may increase the risk of sustained hypertension, which is a major contributor to developing cardiovascular disease — heart disease and stroke.

It is very important to take white-coat hypertension seriously because Centers for Disease Control and Prevention data show that the percentage of adults age 20 and over with hypertension reached 33.5 percent in the 2013-14 period (3).

What can be done?

What can be done about white-coat hypertension? Well, it does not need to be treated with medication, except potentially in elderly patients (over 80 years of age) but should involve lifestyle modifications, including dietary changes, stress reduction and exercise. In terms of diet, increased beet juice, green leafy vegetables and potassium, as well as decreased sodium intake may be important. You should monitor the blood pressure at home, taking multiple readings during the day, or by 24-hour ambulatory blood pressure readings, which require wearing a monitor. The latter provides the additional advantage of blood pressure readings during your sleep.

If you do monitor your blood pressure at home, the American Heart Association has suggestions on how to get the most accurate readings, such as measurements early in the morning before exercising and eating, as well as in the evening (4). You should also be comfortably seated, don’t cross your legs, and sit/relax for a few minutes before taking a reading. Let’s look at the evidence.

Risk of sustained high blood pressure

There were no substantial studies demonstrating any consequences from white-coat hypertension until 2005. Most previous studies on white-coat hypertension were not of long enough duration.

In the 2005 population-based Ohasama study, results showed that the participants who had white-coat hypertension were 2.9 times more likely to develop sustained hypertension, compared to those who had normal blood pressure in the doctor’s office (5). There were almost 800 participants involved in this study, with a mean age at the start of 56. What was really impressive about the study was its duration, with an eight-year follow-up. This gives a better sense of whether white-coat hypertension may develop into sustained hypertension. The researchers concluded that it may lead to a less than stellar outlook for cardiovascular prognosis.

Another study, published in 2009, reinforced these results. The PAMELA study showed that those with white-coat hypertension had about a 2.5-times increased risk of developing sustained high blood pressure, compared to those who had normal readings in all environments (6). There were 1,412 participants involved in the study, ranging in age from 25 to 74. Just like the previous study, an impressive aspect was the fact that there was a long follow-up period of 10 years. Thus, this was a substantial study, applicable to the general population over a significant duration.

Prevention of sustained hypertension

In a small, randomized controlled trial, beet juice was shown to reduce blood pressure significantly (7). Patients either were given 250 ml (about 8 ounces) of beet juice or comparable amounts of water. The patients who drank the beet juice saw an 11.2 mm Hg decrease in blood pressure, while those who drank water saw a 0.7 mm Hg reduction. This effect with the beet juice continued to remain significant. Even after 24 hours, there was a sustainable 7.2 mm Hg drop in blood pressure, compared to readings taken prior to drinking the juice. Although these results are encouraging, we need to study whether these effects can be sustained over the long term. Also, this study was done in patients with high blood pressure. I don’t know of any prevention studies done in patients with white-coat hypertension.

The researchers believe the effect is caused by high nitrate levels in beet juice that are converted to nitrite when it comes in contact with human saliva. Nitrite helps to vasodilate, or enlarge blood vessels, and thus helps to decrease blood pressure in a similar way as some antihypertensive (blood pressure) medications. The authors go on to surmise that green leafy vegetables offer protection from cardiovascular disease in part due to increased nitrite levels, similar to those in beet juice. 

A subsequent double-blind, placebo-controlled clinical trial with 68 hypertensive patients found that blood pressure was significantly reduced in the clinic and in home readings over a four-week period, when compared to nitrate-free beet juice (8).

If you have diabetes, prediabetes, a family history or a high risk for diabetes, I recommend eating beets instead, since drinking beet juice will raise your sugar levels.

Increasing potassium levels significantly through food sources, not supplements, has a profound effect in reducing blood pressure. In a study where 3,500 to 4,700 mg of potassium were consumed through foods, the systolic (top number) blood pressure was reduced by 7.1 mm Hg (9). We should be getting 4,700 mg of potassium daily, which equates to about 10 bananas daily. Almonds, raisins and green leafy vegetables, such as Swiss chard, also have significant amounts of potassium.

White-coat hypertension should not be neglected. It is important to monitor blood pressure at home for at least three days with multiple readings, and then send them to your physician for review. Though patients don’t need to be on blood pressure medications at this stage, it does not mean you should be passive about the process. Make lifestyle modifications to reduce your risk of developing sustained hypertension.

References:

(1) Hypertension. 2013;62:982-987, originally published Nov 13, 2013. (2) J Hypertens. 2001;19(6):1015. (3) cdc.gov. (4) Am Fam Physician. 2005 Oct 1;72(7):1391-1398. (5) Arch Intern Med. 2005 Jul 11;165(13):1541-1546. (6) Hypertension. 2009; 54: 226-232. (7) Hypertension. Online 2013; April 15. (8) Hypertension. 2015 Feb; 65(2): 320–327. (9) BMJ. 2013 Apr 3;346:f1378. 

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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Lifestyle modifications play a role in reducing the risk of developing dementia. Stock photo
Managing biological age through diet can reduce risk

By David Dunaief, M.D.

Dr. David Dunaief

Dementia may be diagnosed when someone experiences loss of memory plus loss of another faculty, such as executive functioning (decision-making) or language abilities (speaking, writing or reading). The latter is known as aphasia. Alzheimer’s disease is responsible for approximately 60 to 80 percent of dementia cases (1).

Unfortunately, there are no definitive studies that show reversal or a cure for Alzheimer’s disease. This is why prevention is central to Alzheimer’s — and dementia in general.

In terms of dementia, there is good news and some disappointing news.

We will start with the good news. Though chronological age is a risk factor that cannot be changed, biological age may be adjustable. There are studies that suggest we may be able to prevent dementia through the use of both lifestyle modifications and medications.

Telomeres’ length and biological age

Biological age may be different from chronological age, depending on a host of environmental factors that include diet, exercise and smoking. There are substances called telomeres that are found at the ends of our chromosomes. They provide stability to this genetic material. As our telomeres get shorter and shorter, our cellular aging and, ultimately, biological aging, increases.

In a preliminary case-control study, dementia patients were shown to have significantly shorter telomere length than healthy patients (2). Interestingly, according to the authors, men have shorter telomere length and may be biologically older by four years than women of the same chronological age. The researchers caution that this is a preliminary finding and may not have clinical implications.

What I find most intriguing is that intensive lifestyle modifications increased telomere length in a small three-month study with patients who had low-risk prostate cancer (3). By adjusting their lifestyles, study participants were potentially able to decrease their biological ages.

Diet’s effect

Lifestyle modifications play a role in many chronic diseases and disorders. Dementia is no exception. In a prospective observational study, involving 3,790 participants, those who had the greatest compliance with a Mediterranean-type diet demonstrated a significant reduction in the risk of Alzheimer’s disease, compared to the least compliant (4). Participants were over the age of 65, demographics included substantial numbers of both black and white participants, and there was a mean follow-up of 7.6 years. Impressively, those who adhered more strictly to the diet performed cognitively as if they were three years younger, according to the authors.

Beta-carotene and vitamin C effect

In a small, preliminary case-control study (disease vs. healthy patients), higher blood levels of vitamin C and beta-carotene significantly reduced the risk of dementia, by 71  and 87 percent, respectively (5). The blood levels were dramatically different in those with the highest and lowest blood levels of vitamin C (74.4 vs. 28.9 µmol/L) and beta-carotene (0.8 vs. 0.2 µmol/L).

The reason for this effect may be that these nutrients help reduce oxidative stress and thus have neuroprotective effects, preventing the breakdown of neurons. This study was done in the elderly, average 78.9 years old, which is a plus, since as we age we’re more likely to be afflicted by dementia.

It is critically important to delineate the sources of vitamin C and beta-carotene in this study. These numbers came from food, not supplements. Why is this important? First, beta-carotene is part of a family of nutrients called carotenoids. There are at least 600 carotenoids in food, all of which may have benefits that are not achieved when taking beta-carotene supplements. Second of all, beta-carotene in supplement form may increase the risk of small-cell lung cancer in smokers (6).

Foods that contain beta-carotene include fruits and vegetables such as berries; green leafy vegetables; and orange, red or yellow vegetables like peppers, carrots and sweet potato. It may surprise you, but fish also contains carotenoids. In my practice, I test for beta-carotene and vitamin C as a way to measure nutrient levels and track patients’ progress when they are eating a nutrient-dense diet. Interestingly, many patients achieve more than three times higher than the highest beta-carotene blood levels seen in this small study.

Impact of high blood pressure medications

For those patients who have high blood pressure, it is important to know that not all blood pressure medications are created equal. When comparing blood pressure medications in an observational study, two classes of these medications stood out. Angiotensin II receptor blockers (known as ARBs) and angiotensin-converting enzyme inhibitors (known as ACE inhibitors) reduce the risk of dementia by 53 and 24 percent respectively, when used in combination with other blood pressure medications.

Interestingly, when ARBs were used alone, there was still a 47 percent reduction in risk; however, ACE inhibitors lost their prevention advantage. High blood pressure is a likely risk factor for dementia and can also be treated with lifestyle modifications (7). Otherwise, ARBs or ACE inhibitors may be the best choices for reducing dementia risk.

Ginkgo biloba disappoints

Ginkgo biloba, a common herbal supplement taken to help prevent dementia, may have no benefit. In the GuidAge study, ginkgo biloba was shown to be no more effective than placebo in preventing patients from progressing to Alzheimer’s disease (8). This randomized controlled trial, considered the gold standard of study designs, was done in elderly patients over a five-year period with almost 3,000 participants. There was no difference seen between the treatment and placebo groups. This reinforces the results of an earlier study, Ginkgo Evaluation of Memory trial (9). Longer studies may be warranted. The authors stressed the importance of preventive measures with dementia.

Fish oil: not the last word

Many of us take fish oil supplements in the hope of preventing dementia. However, in a meta-analysis (a group of three randomized controlled trials), the results did not show a difference between treatment groups and placebo in older patients taking fish oil with omega-3 fatty acids (10). The authors stress that this is not the final word since studies have been mixed. 

The longest of the three studies was 40 months, yet may not have been long enough to see a beneficial effect. Also participants in the meta-analysis did not necessarily have low omega-3 levels at the beginning of the studies. This doesn’t necessarily mean fish oil doesn’t work for dementia prevention, it is just discouraging, as the authors emphasize. Fish consumption, however, has shown an inverse association with Alzheimer’s and dementia overall (11).

There may be ways to prevent dementia from occurring, whether through lifestyle modifications or through the selection of medications, if they are necessary.

References:

(1) www.uptodate.com. (2) Arch Neurol. 2012 Jul 23:1-8. (3) Lancet Oncol. 2008;9(11):1048-1057. (4) Am J Clin Nutr. 2011;93:601-607. (5) J Alzheimers Dis. 2012;31:717-724. (6) Am. J. Epidemiol. 2009; 169(7):815-828. (7) Neurology. 2005;64(2):277. (8) Lancet Neurol. 2012;11(10):851-859. (9) JAMA. 2008;300(19):2253-2262. (10) Cochrane Summaries online June 13, 2012. (11) Neurology. 2007;69(20):1921.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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Accumulating evidence supports an association between depression and inflammation. Stock photo
C-reactive protein is an important biomarker

By David Dunaief, M.D.

Dr. David Dunaief

Many of us have inflammation in our bodies, inflammation that is a potential underlying cause for a great number of diseases. Can we demonstrate the level of inflammation by measuring it? The answer is yes.

One of the most widely studied biomarkers for inflammation is high-sensitivity C-reactive protein (hsCRP), also referred to as CRP. High sensitivity means that we can measure levels as low as 0.3 mg/L more accurately.

What is the significance of the different levels? In heart disease, individuals who have levels lower than 1.0 mg/L are in the optimal range for low risk of inflammation. Levels of 1 to 3 mg/L represent the average risk range, and greater than 3.0 mg/L is a higher risk profile. Above 10.0 mg/L is less specific to heart disease, although still related, but more likely associated with other causes, such as infection and autoimmune diseases (1, 2). This biomarker is derived from the liver.

CRP is not specific to heart disease, nor is it definitive for risk of the disease. However, the upside is that it may be helpful with risk stratification, which helps us understand where we sit on a heart disease risk spectrum and with progression in other diseases, such as age-related macular degeneration, diabetic retinopathy, depression and autoimmune diseases. Let’s look at the evidence.

Age-related macular degeneration

Age-related macular degeneration (AMD) is the leading cause of blindness in patients over the age of 65 (3). Therefore, it is very important to help define risk stratification for this disease. In a prospective study, results showed that hsCRP levels were inversely associated with the risk of developing AMD. The group with an hsCRP greater than 3.0 mg/L had a 50 percent increased risk of developing overall AMD compared to the optimal group with hsCRP lower than 1.0 mg/L. But even more interestingly, the risk of developing neovascular, or wet, AMD increased to 89 percent in this high-risk group.

The significance of wet AMD is that it is one type of advanced-stage AMD that results in blindness. This study involved five studies where the researchers thawed baseline blood samples from middle-aged participants who had hsCRP levels measured. There were more than 2,000 participants with a follow-up as long as 20 years. According to the study’s authors, annual eye exams and lifestyle modifications, including supplements, may be able to stem this risk by reducing hsCRP.

These results reinforce those of a previous prospective study that showed that elevated hsCRP increased the risk of AMD threefold (4). This study utilized data from the Women’s Health Study, which involved over 27,000 participants. Like the study mentioned above, this one also defrosted blood samples from baseline and looked at follow-up incidence of developing AMD in initially healthy women.

The highest group had hsCRP levels over 5.2 mg/L. Additionally, when analyzing   similar cutoffs for high- and low-level hsCRP, as the above trial used, those with hsCRP over 3.0 had an 82 percent increased risk of AMD compared to those with an hsCRP of lower than 1.0 mg/L.

Diabetic retinopathy — a complication of diabetes

We know that diabetes affects approximately 10 percent of the U.S. population and is continuing to rise at a rapid rate. One of the complications of diabetes affects the retina (back of the eye) and is called diabetic retinopathy. This is a leading cause of vision loss (5). One of the reasons for the vision loss is macular edema, or swelling, usually due to rupture of tiny blood vessels below the macula, a portion of the back of the eye responsible for central vision.

The Diabetes Control and Complications Trial (DCCT), a prospective study involving over 1,400 Type 1 diabetes patients, showed an 83 percent increased risk of developing clinically significant macular edema in the group with the highest hsCRP levels compared to those with the lowest (6). Although these results were with Type 1 diabetes, patients with Type 2 diabetes are at equal risk of diabetic retinopathy if glucose levels, or sugars, are not well controlled.

Depression

Depression is a very difficult disease to control and is a tremendous cause of disability. If we can minimize the risk of complications and hospitalizations, this is probably the most effective approach.

Well, it turns out that inflammation is associated with depression. Specifically, in a prospective observational trial, rising levels of CRP had a linear relationship with increased risk of hospitalization due to psychological distress and depression (7).

In other words, compared to levels of less than 1 mg/L, those who were 1 to 3 mg/L, 3 to 10 mg/L and greater than 10 mg/L had increased risk from 30 to 84 to 127 percent, respectively. This study involved over 70,000 patients.

What can be done to reduce inflammation?

This is the key question, since we now know that hsCRP is associated with systemic inflammation. In the Nurses’ Health Study, a very large, prospective observational study, the Dietary Approaches to Stop Hypertension (DASH) diet decreased the risk of both heart disease and stroke, which is impressive. The DASH diet also decreases the levels of hsCRP significantly, which was associated with a decrease in clinically meaningful end  points of stroke and heart disease (8).

The DASH diet is nutrient dense with an emphasis on fruits, vegetables, nuts, seeds, legumes and whole grains and a de-emphasis on processed foods, red meats, sodium and sweet beverages.

Conclusion

As the evidence shows with multiple diseases, hsCRP is a very valuable nonspecific biomarker for inflammation in the body.

To stem the effects of inflammation, reducing hsCRP through lifestyle modifications and drug therapy may be a productive way of reducing risk, slowing progression and even potentially reversing some disease processes.

The DASH diet is a very powerful approach to achieving optimal levels of hsCRP without incurring potential side effects. This is a call to arms to have your levels measured, especially if you are at high risk or have chronic diseases such as heart disease, diabetes, depression and autoimmune diseases. HsCRP is a simple blood test with easy-to-obtain results.

References:

(1) uptodate.com. (2) Diabetes Technol Ther. 2006;8(1):28-36. (3) Prog Retin Eye Res. 2007 Nov;26(6):649-673. (4) Arch Ophthalmol. 2007;125(3):300-305. (5) Am J Ophthalmol. 2003;136(1):122-135. (6) JAMA Ophthalmol. 2013 Feb 7;131:1-8. (7) JAMA Psychiatry. 2013;70(2):176-184. (8) Arch Intern Med. 2008;168(7):713-720.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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Pedometers can be the first step to helping those with mild COPD. Stock photo
Lifestyle changes can reduce COPD exacerbations

By David Dunaief, M.D.

Dr. David Dunaief

COPD, or chronic obstructive pulmonary disease, is the third leading cause of mortality in the United States (1), although it’s not highlighted much in the layman’s press.

COPD is an umbrella term that includes emphysema, chronic bronchitis of more than three months for two consecutive years and/or chronic obstructive asthma. It is an obstructive lung disease that limits airflow. The three most common symptoms of the disease involve shortness of breath, especially on exertion, production of sputum and cough. This disease affects 6.7 percent of the U.S. population (2).

It tends to be progressive, meaning more frequent and severe exacerbations over time. Since it is a devastating and debilitating chronic disease with no cure, anything that can identify and prevent COPD exacerbations, as well as comorbidities (associated diseases), is critically important.

What are the traditional ways to reduce the risk of and treat COPD exacerbations? The most important step is to stop smoking, since 80 percent of COPD is related to smoking. Supplemental oxygen therapy and medications, such as corticosteroids, bronchodilators (beta-adrenergic agonists and anticholinergics) and antibiotics help to alleviate symptoms (3).

One of the underlying components of COPD may be chronic inflammation (4). Therefore, reducing inflammation may help to stem COPD exacerbations. There are several inflammatory biomarkers that could potentially help predict exacerbations and mortality associated with this disease, such as interleukin-6 (IL-6), C-reactive protein (CRP), leukocyte (white blood cell) count and fibrinogen (a clotting factor of the blood).

How do we reduce inflammation, which may contribute to exacerbations of this disease? Some drugs, such as statins, work partially by reducing inflammation. They may have a role in COPD. Lifestyle changes that include a high-nutrient, anti-inflammatory diet and exercise may also be beneficial. Let’s look at the evidence.

Biomarkers for inflammation

In a recent population-based study with over 60,000 participants, results show that as three biomarkers (CRP, leukocyte count and fibrinogen) were elevated, the risk of COPD exacerbation increased in a linear manner (5). In other words, the risk of frequent exacerbation increased 20, 70 and 270 percent within the first year as the number of elevated biomarkers increased from one to three, compared to patients who did not have biomarker elevations.

As time progressed beyond the first year of follow-up, risk exacerbation continued to stay high. Patients with all three biomarkers elevated for longer periods had a 150 percent increased risk of frequent exacerbations. These predictions were applicable to patients with stable and with mild COPD.

In an observational study, results showed that when the biomarker IL-6 was elevated at the start of the trial in stable COPD patients, the risk of mortality increased almost 2.7-fold (6). Also, after three years, IL-6 increased significantly. Elevated IL-6 was associated with a worsening of six-minute walking distance, a parameter tied to poor physical performance in COPD patients. However, unlike the previous study, CRP did not show correlation with increased COPD exacerbation risk. This was a small trial, only involving 53 patients. Therefore, the results are preliminary.

These biomarker trials are exciting for their potential to shape treatments based on level of exacerbation risk and mortality, creating more individualized therapies. Their results need to be confirmed in a randomized controlled trial (RCT). Many of these biomarkers mentioned in the two trials are identifiable with simple blood tests at major labs.

Statin effect

Statins have been maligned for their side effects, but their efficacy has been their strong suit. An observational trial showed that statins led to at least a 30 percent reduction in the risk of COPD exacerbations, with the effect based on a dose-dependent curve (7). In other words, as the dose increased, so did the benefit.

Interestingly, even those who had taken the statin previously saw a significant reduction in COPD exacerbation risk. The duration of statin use was not important; a short use of statins, whether presently or previously, had substantial benefit. 

However, the greatest benefit was seen in those who had been on a medium to high dose or were on the drug currently. The researchers believe that the mechanism of action for statins in this setting has to do with their anti-inflammatory and immune-modulating effects. This was a retrospective (backward-looking) study with over 14,000 participants. We will need a prospective (forward-looking) study and an RCT to confirm the results.

Exercise

Pedometers can be the first step to helping those with mild COPD. Stock photo

Exercise is beneficial for almost every circumstance, and COPD is no exception. But did you know that a pedometer might improve results? In a three-month study, those with mild COPD were much more successful at achieving exercise goals and reducing exacerbations and symptoms when they used pedometers, compared to the group given advice alone (8). Pedometers gave patients objective feedback on their level of physical activity, which helped motivate them to achieve the goal of walking 9,000 steps daily. This is a relatively easy way to achieve exercise goals and reduce the risk of COPD exacerbations.

When exercising, we are told to vary our exercise routines on a regular basis. One study demonstrates that this may be especially important for COPD patients (9). Results show that nonlinear periodization exercise (NLPE) training is better than traditional routines of endurance and resistance training in severe COPD patients. The goal of NLPE is to alter the time spent working out, the number of sets, the number of repetitions and the intensity of the workout on a regular basis.

This study was randomized, involved 110 patients and was three months in duration. Significantly more severe COPD patients achieved their exercise goals using NLPE rather than the traditional approach. The group that used NLPE also had an improved quality of life response. The researchers believe that compliance with an NLPE-type program is mostly likely going to be greater because patients seem to enjoy it more.

Chronic inflammation may play a central role in COPD exacerbation. Nonspecific inflammatory biomarkers are potentially valuable for providing a more personalized approach to therapy. Drugs that can control inflammation, such as statins, show promise. But don’t forget the importance of lifestyle changes, such as quitting smoking and committing to an exercise regimen that is varied and/or involves the use of a pedometer. And potentially a high-nutrient, anti-inflammatory diet will also contribute positively to reducing the frequency and severity of COPD exacerbations.

References:

(1) Natl Vital Stat Rep. 2011 Dec.;59(10):1-126. (2) cdc.gov. (3) N Engl J Med. 2002;346:988-994. (4) www.goldcopd.org. (5) JAMA. 2013;309:2353-2361. (6) Respiratory Research. 2013;14:24. (7) Am J Med. 2013 Jul;126:598-606. (8) ATS 2013 International Conference: Abstract A1360. (9) Am J Respir Crit Care Med. 2013; online Feb. 28.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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In addition to bananas, plenty of other foods are high in potassium. Above are just a few examples. Stock photo
Most Americans don’t consume enough potassium

By David Dunaief M.D.

Dr. David Dunaief

One of the most popular food additives is also one of the most dangerous: salt. We need salt, but not in excess. On the other hand, potassium is beneficial in our diet. However, we have the opposite problem with potassium: It is under-consumed.

More than 90 percent of people consume far too much sodium, with salt being the primary culprit (1). Sodium is found in foods that don’t even taste salty. Bread and rolls are the primary offenders, since we eat so much of them. Other foods with substantial amounts of sodium are cold cuts and cured meats, cheeses, pizza (which has both bread and cheese), fresh and processed poultry, soups, meat dishes, pastas and snack foods. Foods that are processed and those prepared by restaurants are where most of our consumption occurs (2).

By contrast, only about 2 percent of people get enough potassium from their diets (3). According to one study, we would need to consume about eight sweet potatoes or 10 bananas each day to reach appropriate levels. Why is it important to reduce sodium and increase potassium? A high sodium-to-potassium ratio increases the risk of cardiovascular disease by 46 percent, according to the study, which looked at more than 12,000 Americans over almost 15 years (4). In addition, both may have significant impacts on blood pressure and cardiovascular disease.

To improve our overall health, we need to tip the sodium-to-potassium scales, consuming less sodium and more potassium. Let’s look at the evidence.

Reduced sodium

There are two studies that illustrate the benefits of reducing sodium in high blood pressure and normotensive (normal blood pressure) patients, ultimately preventing cardiovascular disease, including heart disease and stroke.

The first study used the prestigious Cochrane review to demonstrate that blood pressure is reduced by a significant mean of −4.18 mm Hg systolic (top number) and −2.06 mm Hg diastolic (bottom number) involving both normotensive and hypertensive participants (5). When looking solely at hypertensive patients, the reduction was even greater, with a systolic blood pressure reduction of −5.39 mm Hg and a diastolic blood pressure reduction of −2.82 mm Hg.

This was a meta-analysis (a group of studies) that evaluated data from randomized clinical trials, the gold standard of studies. There were 34 trials reviewed with more than 3,200 participants. Salt was reduced from 9 to 12 grams per day to 5 to 6 grams per day. These levels were determined using 24-hour urine tests. The researchers believe there is a direct linear effect with salt reduction. In other words, the more we reduce the salt intake, the greater the effect of reducing blood pressure. The authors concluded that these effects on blood pressure will most likely result in a decrease in cardiovascular disease.

In the second study, a meta-analysis of 42 clinical trials, there was a similarly significant reduction in both systolic and diastolic blood pressures (6). This meta-analysis included adults and children. Both demographics saw a reduction in blood pressure, though the effect, not surprisingly, was greater in adults. Interestingly, an increase in sodium caused a 24 percent increased risk of stroke incidence but, more importantly, a 63 percent increased risk of stroke mortality. The risk of mortality from heart disease was increased as well, by 32 percent.

In an epidemiology modeling study, the researchers projected that either a gradual or instantaneous reduction in sodium would save lives (7). For instance, a modest 40 percent reduction over 10 years in sodium consumed could prevent 280,000 premature deaths. These are only projections, but in combination with the above studies may be telling. The bottom line is: decrease sodium intake by almost half and increase potassium intake from foods.

Potassium’s positive effects

When we think of blood pressure, sodium comes to mind, but not enough attention is given to potassium. The typical American diet doesn’t contain enough of this mineral.

In a meta-analysis involving 32 studies, results showed that as the amount of potassium was increased, systolic blood pressure decreased significantly (8). When foods containing 3.5 to 4.7 grams of potassium were consumed, there was an impressive −7.16 mm Hg reduction in systolic blood pressure with high blood pressure patients. Anything more than this amount of potassium did not have any additional benefit. Increased potassium intake also reduced the risk of stroke by 24 percent. This effect was important. If this does not sound like a large reduction, consider that, by comparison, aspirin has been shown to reduce the risk of stroke by 20 percent.

The reduction in blood pressure was greater with increased potassium consumption than with sodium restriction, although there was no head-to-head comparison done. The good news is that potassium is easily attainable in the diet. Foods that are potassium rich include bananas, sweet potatoes, almonds, raisins and green leafy vegetables such as Swiss chard.

Lowering sodium intake may have far-reaching benefits, and it is certainly achievable. We need to reduce our intake and give ourselves a brief period to adapt — it takes about six weeks to retrain our taste buds, once we reduce our sodium intake. We can also improve our odds by increasing our dietary potassium intake, which also has a substantial beneficial effect, striking a better sodium-to-potassium balance.

References:

(1) Am J Clin Nutr. 2012 Sep;96(3):647-657. (2) www.cdc.gov. (3) Am J Clin Nutr. 2012 Sep;96(3):647-657. (4) Arch Intern Med. 2011;171(13):1183-1191. (5) BMJ. 2013 Apr 3;346:f1325. (6) BMJ. 2013 Apr 3;346:f1326. (7) Hypertension. 2013; 61: 564-570. (8) BMJ. 2013; 346:f1378.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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