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David Dunaief

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We should dedicate 33 percent of our lives to sleep to improve brain health. Stock photo

By David Dunaief, M.D.

The brain is the most important and complex organ, yet what we know about the brain is inverse to its prominence. In other words, our knowledge only scratches the surface. While other organs can be transplanted readily, it is the one organ that can’t, at least not yet.

The brain also has something called the blood-brain barrier. This is an added layer of small, densely packed cells, or capillaries, that filter what substances from the blood they allow to pass through from the rest of the body (1). This is good, since it protects the brain from foreign substances; however, on the downside, it also makes it harder to treat, because many drugs and procedures have difficulty penetrating the blood-brain barrier.

Unfortunately, there are many things that negatively impact the brain, including certain drugs, head injuries and lifestyle choices. There are also numerous disorders and diseases that affect the brain, including neurological (dementia, Parkinson’s, stroke), infectious (meningitis), rheumatologic (lupus and rheumatoid arthritis), cancer (primary and secondary tumors), psychiatric mood disorders (depression, anxiety, schizophrenia), diabetes and heart disease.

These varied diseases tend to have three signs and symptoms in common: they either cause an alteration in mental status — cognitive decline, weakness or change in mood – or a combination of these.

Probably our greatest fear regarding the brain is cognitive decline. We have to ask ourselves if we are predestined to this decline, either because of the aging process alone or because of a family history, or if there is a third option, a way to alter this course. Dementia, whether mild or full-blown Alzheimer’s, is cruel; it robs us of functioning. We should be concerned about Alzheimer’s because 5.2 million Americans have the disease, and it is on the rise, especially since the population is aging (2).

Fortunately, there are several studies that show we may be able to choose the third option and prevent cognitive decline by altering modifiable risk factors. They involve rather simple lifestyle changes: sleep, exercise and possibly omega-3s. Let’s look at the evidence.

The impact of clutter

The lack of control over our mental capabilities as we age is what frightens us the most since we see friends, colleagues and relatives negatively affected by it. Those who are in their 20s seem to be much sharper and quicker. But are they really?

In a recent study, German researchers found that educated older people tend to have a larger mental database of words and phrases to pull from since they have been around longer and have more experience (3). When this is factored into the equation, the difference in terms of age-related cognitive decline becomes negligible. This study involved data mining and creating simulations. It showed that mental slowing may be at least partially related to the amount of clutter or data that we accumulate over the years. The more you know, the harder it becomes to come up with a simple answer to something. We may need a reboot just like a computer. This may be possible through sleep and exercise and omega-3s.

Sleep

I have heard people argue that sleep gets in the way of life. Why should we have to dedicate 33 percent of our lives to sleep? There are several good reasons. One involves clearing the mind, and another involves improving our economic outlook.

For the former, a study shows that sleep may help the brain remove waste, such as those all-too-dangerous beta-amyloid plaques (4). When we have excessive plaque buildup in the brain, it may be a sign of Alzheimer’s. This study was done in mice. When mice were sleeping, the interstitial space (the space between brain gyri, or structures) would increase by as much as 60 percent.

This allowed the lymphatic system, with its cerebrospinal fluid, to clear out plaques, toxins and other waste that had developed during waking hours. With the enlargement of the interstitial space during sleep, waste removal was quicker and more thorough because cerebrospinal fluid could reach much further into the spaces. When the mice were anesthetized, a similar effect was seen as with sleeping.

In a published follow-up study, the authors found that sleep position had an impact on glymphatic transport in rodents. Sleeping in a lateral position, or on their sides, was more effective at clearing waste than prone or supine positions. Of course, the authors note that for rodents a prone position is similar to their awake positions. It would be most like a human sleeping while sitting upright (5).

In another study, done in Australia, results showed that sleep deprivation may have been responsible for an almost 1 percent decline in gross domestic product for the country (6). The reason is obvious: People are not as productive at work when they don’t get enough sleep. Their attitude tends to be more irritable, and concentration may be affected. We may be able to turn on and off sleepiness on an acute, or short-term, basis, depending on the environment, but it’s not as if we can do this continually.

According to the Centers for Disease Control and Prevention, an average of 4 percent of Americans report having fallen asleep in the past month behind the wheel of a car (7). I hope this hammers home the importance of sleep.

Exercise

How can I exercise, when I can’t even get enough sleep? Well there is a study that just may inspire you to exercise.

In the study, which involved rats, those that were not allowed to exercise were found to have rewired neurons in the area of their medulla, the part of the brain involved in breathing and other involuntary activities. There was more sympathetic (excitatory) stimulus that could lead to increased risk of heart disease (8). In those rats that were allowed to exercise regularly, there was no unusual wiring, and sympathetic stimuli remained constant. This may imply that being sedentary has negative effects on both the brain and the heart.

This is intriguing since we used to think that our brain’s plasticity, or ability to grow and connect neurons, was finite and stopped after adolescence. This study’s implication is that a lack of exercise causes unwanted new connections. Of course, these results were done in rats and need to be studied in humans before we can make any definitive suggestions.

Omega-3 fatty acids

In the Women’s Health Initiative Memory Study of Magnetic Resonance Imaging Study, results showed that those postmenopausal women who were in the highest quartile of omega-3 fatty acids had significantly greater brain volume and hippocampal volume than those in the lowest quartile (9). The hippocampus is involved in memory and cognitive function.

Specifically, the researchers looked at the level of omega-3 fatty acids, called eicosapentaenoic acid and docosahexaenoic acid, in red blood cell membranes. The source of the omega-3 fatty acids could either have been from fish or supplementation. This was not delineated. The researchers suggest eating fish high in these substances, such as salmon and sardines, since it may not even be the omega-3s that are playing a role but some other substances in the fish. It’s never too late to improve brain function. You can still be sharp at a ripe old age. Although we have a lot to learn about the functioning of the brain, we know that there are relatively simple ways we can positively influence it.

References: (1) medicinenet.com. (2) alz.org. (3) Top Cogn Sci. 2014 Jan.;6:5-42. (4) Science. 2013 Oct. 18;342:373-377. (5) J Neurosci. 2015 Aug 5;35(31):11034-11044. (6) Sleep. 2006 Mar.;29:299-305. (7) cdc.gov. (8)J Comp Neurol. 2014 Feb. 15;522:499-513. (9) Neurology. 2014;82:435-442. 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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Hormone replacement can have serious consequences. Stock photo

By David Dunaief, M.D.

We are bombarded continually with ads suggesting that men should talk to their doctors about “Low T.” This refers to low testosterone. Is this all hype, or is this a serious malady that needs medical attention? The short answer is it depends on the candidate. The best candidates have deficient testosterone levels and are symptomatic.

Men do go through andropause or have unusually low testosterone (hypogonadism). The formal name for treatment is androgen replacement therapy.

The greatest risk factor for lower testosterone is age. As men age, the level of testosterone decreases. Respectively, 20, 30 and 50 percent of those who are in their 60s, 70s and 80s have total testosterone levels of less than 320 ng/dL (1). However, some of the pharmaceutical ads would have you think that most men over 40 should seek treatment. Treatments offered include gels, transdermal patches and injections.

While real estate is all about “location, location, location,” with testosterone “caution, caution, caution” should be used.

Who are the most appropriate candidates for therapy? Those who have symptoms including lack of sexual desire, fatigue and lack of energy. However, what is scary is that around 25 percent of patients are getting scripts for testosterone without first testing their blood levels to determine if they have a deficiency (2). A simple blood test can measure total testosterone, as well as free and weakly bound levels at mainstream labs.

The number of testosterone scripts increased threefold from 2001 to 2011 for men more than 40 years old (3). Either we have discovered vast numbers of men with low levels or, more likely, marketing has caused the number of scripts to outstrip the need.

What are the risks and benefits of treating testosterone levels? Is testosterone treatment really the fountain of youth? There are benefits reported for those who actually have significantly deficient levels. Benefits may include improvements in muscle mass, strength, mood and sexual desire (4). However, several studies have suggested that testosterone therapy may increase the risk of cardiovascular disease, including stroke, heart disease and even death. These are obviously serious side effects. It also may cause acquired hypogonadism by shrinking the testes, resulting in a dependency on exogenous, or outside, testosterone therapy.

When testosterone is given, it may be important to also test PSA levels (5). If they increase by more than 1.4 ng/ml over a three-month period, then it may be wise to have a discussion with your physician about considering discontinuing the medication. You should not stop the medication without first talking to your doctor, and then a consult with a urologist may be appropriate. If the PSA is greater than 4.0 ng/ml initially, treatment should probably not be started without a urology consult.

How can you raise testosterone levels and improve symptoms without hormone therapy? Lifestyle changes, including losing weight, exercising and altering dietary habits, have shown promising results. Let’s look at the evidence.

Cardiovascular risk

One study’s results showed that men were at significantly increased risk of experiencing a heart attack within the first three months of testosterone use (6). There was an overall 36 percent increased risk. When stratified by age, this was especially true of men who were 65 and older. This population had a greater than twofold risk of having a heart attack. This risk may have to do with an increased number of red blood cells with testosterone therapy. Those who were younger showed a trend toward increased risk but did not meet statistical significance.

When the patient was younger than 65 and had heart disease, there was a significant twofold greater risk of a heart attack; however, those without heart disease did not show risk. This does not mean there is no risk for those who are “healthy” and younger; it just means the study did not show it. This observational study compared over 50,000 men who received new testosterone scripts with over 150,000 men who received scripts for erectile dysfunction drugs: phosphodiesterase type 5 (PDE5) inhibitors, including tadalafil (Cialis) and sildenafil (Viagra). PDE5 inhibitors have not demonstrated this cardiovascular risk.

Unfortunately, this is not the only study that showed potential cardiovascular risks. A 2013 study reinforced these results, showing that there was an increased risk of stroke, heart attack and death after three years of testosterone use (7). Ultimately, it found a 30 percent greater chance of cardiovascular events. What is worse is that risk was significant in both those with a history of heart disease and those without. This was a retrospective study involving 1,200 men with a mean age of 60.

We need randomized controlled trials to make a more definitive association. Still, these are two large studies that suggest increased risk. If you already have heart disease, be especially careful when considering testosterone therapy.

FDA response

The FDA, which approved testosterone therapy originally, is now investigating the possible cardiovascular risk profile based on the above two studies (8). The FDA doesn’t suggest stopping medication if you are taking it presently, but it should be monitored closely. The agency, in the meantime, has issued an alert to doctors about the potential dangerous side effects of androgen replacement therapy. The FDA says that the use of testosterone therapy is for those with low levels and other medical issues, such as hypogonadism from either primary or secondary causes.

Conflicting data

Two newer studies contradict the previous findings and suggest that testosterone supplementation for those who are deficient may not increase the risk of cardiovascular events or death. However, both studies have their weaknesses. One found that, although the cardiovascular events and death increased over the first two months, over the medium (9 months) and long terms (35 months), the risks actually decreased (9). Weaknesses: There was an initial detrimental cardiovascular effect; the study was observational; and the population was not well-defined as to participants’ history of cardiovascular disease or not. The second study was retrospective or backward-looking in time (10). These studies may not change the FDA warnings. What we need is a large randomized controlled trial.

Obesity and weight loss

Not surprisingly, obesity is an important factor in testosterone levels. In a study that involved 900 men with metabolic syndrome — borderline or increased cholesterol levels, sugar levels and a waist circumference greater than 40 inches — those who lost weight were 50 percent less likely to develop testosterone deficiencies. Those who participated in lifestyle modification had a highly statistically significant 15 percent increase in testosterone (11). Also, when men increased their physical activity and made dietary changes, there was an almost 50 percent risk reduction one year out, compared to their baseline at the start of the trial.

Interestingly, metformin had no effect in preventing lower testosterone levels in patients with abnormal sugar levels, but lifestyle modifications did. These patients were relatively similar to the average American biometrics with prediabetes: HbA1c of 6 percent and glucose of 108 mg/dL; a mean of 42-inch waists; and a BMI that was obese at 32 kg/m2. The mean age was between 53 and 54.

If there is one thing that you get from this article, I hope it’s that testosterone is not something to be taken lightly. You can improve testosterone levels if you’re overweight by losing fat pounds. If you think you have symptoms and you might need testosterone, talk to your doctor about getting a blood test before you do anything. It may be preferable to try alternate medications that improve erections such as sildenafil and tadalafil.

References: (1) J Clin Endocrinol Metab. 2001 Feb;86(2):724. (2) J Clin Endocrinol Metab. Online 2014; Jan 1. (3) JAMA Intern Med. 2013 Aug 12;173(15):1465-1466. (4) J Clin Endocrinol Metab. 2000 Aug;85(8):2839. (5) UpToDate.com. (6) PLoS One. 2014 Jan 29; 9(1):e85805. (7) JAMA. 2013;310:1829-1836. (8) FDA.gov. (9) Lancet Diabetes Endocrinol. 2016;4(6):498-506. (10) Eur Heart J. 2015;36(40):2706-2715. (11) ENDO 2012; Abstract OR28-3.

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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Obesity, sugar, a sedentary lifestyle and abdominal fat contribute to the rise in type 2 diabetes.

By David Dunaief, M.D.

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 13.3 percent of the U.S. population aged 20 or older has type 2 diabetes, and about 9.3 percent when factoring all ages. For those 65 and older, the prevalence is considerably higher, at 25.9 percent (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 9.3 percent in the U.S., as noted in the introduction.

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 BMI 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 mostly 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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By David Dunaief

We know that inflammation is a critical part of many chronic diseases. Rheumatoid arthritis (RA) is no exception. With RA, inflammation is rampant throughout the body and contributes to painful joints, most commonly concentrating bilaterally in the smaller joints of the body, including the metacarpals and proximal interphalangeal joints of the hand, as well as the wrists and elbows. With time, this disease can greatly diminish our ability to function, interfering with our activities of daily living. The most basic of chores, such as opening a jar, can become a major hindrance.

In addition, RA can cause extra-articular, a fancy way of saying outside the joints, manifestations and complications. These can involve the skin, eyes, lungs, heart, kidneys, nervous system and blood vessels. This is where it gets a bit dicier. With increased complications comes an increased risk of premature mortality (1).

Four out of 10 RA patients will experience complications in at least one organ. Those who have more severe disease in their joints are also at greater risk for these extra-articular manifestations. Thus, those who are markedly seropositive for the disease, showing elevated biomarkers like rheumatoid factor (RF), are at greatest risk (2). They have an increased risk of cardiovascular disease events, such as heart attacks and pulmonary disease. Fatigue is also increased, but the cause is not well understood. We will look more closely at these complications.

Are there treatments that may increase or decrease these complications? It is a very good question, because some of the very medications used to treat RA also may increase risk for extra-articular complications, while other drugs may reduce the risks of complications. We will try to sort this out, as well. The drugs used to treat RA are disease-modifying antirheumatic drugs (DMARDs), including methotrexate; TNF inhibitors, such as Enbrel (etanercept); oral corticosteroids; and NSAIDs (non-steroidal anti-inflammatory drugs).

It is also important to note that there are modifiable risk factors. We will focus on two of these, weight and sugar. Let’s look at the evidence.

CARDIOVASCULAR DISEASE BURDEN
We know that cardiovascular disease is very common in this country for the population at large. However, the risk is even higher for RA patients; these patients are at a 50 percent higher risk of cardiovascular mortality than those without RA (3). The hypothesis is that the inflammation is responsible for the RA-cardiovascular disease connection (4). Thus, oxidative stress, cholesterol levels, endothelial dysfunction and high biomarkers for inflammation, such as ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein), play roles in fostering cardiovascular disease in RA patients (5).

THE YING AND YANG OF MEDICATIONS
Although drugs such as DMARDS (including methotrexate and TNF inhibitors, Enbrel, Remicade, Humira), NSAIDs (such as celecoxib) and corticosteroids are all used in the treatment of RA, some of these drugs increase cardiovascular events and others decrease them. In meta-analysis (a group of 28 studies), the results showed that DMARDS reduced the risk of cardiovascular events by up to 30 percent, while NSAIDs and corticosteroids increased the risk (6). The oral steroids had the highest risk of heart complications, approximately a 50 percent rise in risk. This may be one reason rheumatologists encourage their RA patients to discontinue oral steroid treatments as quickly as possible.
In an observational study, the results reaffirm that corticosteroids increased the risk of a heart attack in RA patients, this time by 68 percent (7). The study involved over 8,000 patients with a follow-up of nine years. Interestingly, there was a dose-response curve. In other words, the results also showed that for every 5 mg increase in dosage, there was a corresponding 14 percent increase in heart attack risk.

BAFFLING DISEASE COMPLICATION
Most complications seem to have a logical connection to the original disease. Well, it was a surprise to researchers when the results of the Nurses’ Health Study showed that those with RA were at increased risk of cardiovascular disease and of respiratory disease (8). In fact, the risk of dying from respiratory disease was 106 percent higher in the women with RA compared to those without, and the risk was even higher in women who were seropositive (had elevated levels of rheumatoid factor). The authors surmise that seropositive patients have greater risk of death from respiratory disease because they have increased RA severity compared to seronegative patients. The study followed approximately 120,000 women for a 34-year duration.

WHY AM I SO TIRED?
While we have tactics for treating joint inflammation, we have yet to figure out how to treat the fatigue associated with RA. In a recently published Dutch study, the results showed that while the inflammation improved significantly, fatigue only changed minimally (9). The consequences of fatigue can have a negative impact on both the mental and physical qualities of life. There were 626 patients involved in this study for eight years of follow-up data. This study involved two-thirds women, which is significant; women in this and in previous studies tended to score fatigue as more of a problem.

LIFESTYLES OF THE MORE PAINFUL AND DEBILITATING
We all want a piece of the American dream. To some that means eating like kings of past times. Well, it turns out that body mass index plays a role in the likelihood of developing RA. According to the Nurses’ Health Study, those who are overweight or obese and are ages 55 and younger have an increased risk of RA, 45 percent and 65 percent, respectively (10). There is higher risk with increased weight because fat has pro-inflammatory factors, such as adipokines, that may contribute to the increased risk. Weight did not influence whether they became seropositive or seronegative RA patients.
With a vegetable-rich, plant-based diet you can reduce inflammation and thus reduce the risk of RA by 61 percent (11). In my clinical practice, I have seen numerous patients able to reduce their seropositive loads to normal or near-normal levels by following this type of diet.

SUGAR, SUGAR!
At this point, we know that sugar is bad for us. But just how bad is it? When it comes to RA, results of the Nurses’ Health Study showed that sugary sodas increased the risk of developing seropositive disease by 63 percent (12). In subset data of those over age 55, the risk was even higher, 164 percent. This study involved over 100,000 women followed for 18 years.

THE JUST PLAIN WEIRD – INFECTION FOR THE BETTER
Every so often we come across the surprising and the interesting. I would call it a Ripley’s Believe It or Not moment. In a recent study, those who had urinary tract infections, gastroenteritis or genital infections were less likely to develop RA than those who did not (13). The study did not indicate a time period or potential reasons for this decreased risk. However, I don’t think I want an infection to avoid another disease. When it comes to RA, prevention with diet is your best ally. Barring that, disease-modifying anti-rheumatic medications are important for keeping inflammation and its progression in check. However, oral steroids and NSAIDs should generally be reserved for short-term use. Before considering changing any medications, discuss it with your physician.

REFERENCES
(1) J Rheumatol 2002;29(1):62. (2) uptodate.com. (3) Ann Rheum Dis 2010;69:325–31. (4) Rheumatology 2014;53(12):2143-2154. (5) Arthritis Res Ther 2011;13:R131. (6) Ann Rheum Dis 2015;74(3):480-489. (7) Rheumatology 2013;52:68-75. (8) ACR 2014: Abstract 818. (9) RMD Open 2015.  (10) Ann Rheum Dis. 2014;73(11):1914-1922. (11) Am J Clin Nutr 1999;70(6),1077–1082. (12) Am J Clin Nutr 2014;100(3):959-67. (13) Ann Rheum Dis 2015;74:904-907.

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, go to the website www.medicalcompassmd.com and/or consult your personal physician.

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By David Dunaief

Now that spring has sprung, the pace of life tends become more hectic. Although some stress is valuable to help motivate us and keep our minds sharp, high levels of constant stress can have detrimental effects on the body.
It is very likely that there is a mind-body connection when it comes to stress. In other words, it may start in the mind, but it can lead to acute or chronic disease promotion. Stress can also play a role with your emotions, causing irritability and outbursts of anger, and possibly leading to depression and anxiety. Stress symptoms are hard to distinguish from other disorders but can include stiff neck, headaches, stomach upset and difficulty sleeping. Stress may also be associated with cardiovascular disease, with an increased susceptibility to infection from viruses causing the common cold and with cognitive decline and Alzheimer’s (1).
A stress steroid hormone called cortisol is released from the adrenal glands and can have beneficial effects in small bursts. We need cortisol in order to survive. Some of cortisol’s functions include raising the glucose (sugar) levels when they are low and helping reduce inflammation and stress levels (2). However, when cortisol gets out of hand, higher chronic levels may cause inflammation, leading to disorders such as cardiovascular disease, as recent research suggests. Let’s look at the evidence.

Inflammation
Inflammation may be a significant contributor to more than 80 percent of chronic diseases, so it should be no surprise that inflammation is an important factor with stress. In a recent meta-analysis (a group of two observational studies), high levels of C-reactive protein, a biomarker for inflammation, were associated with increased psychological stress (3).
What is the importance of CRP? It may be related to heart disease and heart attacks. This study involved over 73,000 adults who had their CRP levels tested. The research went further to suggest that increased levels of CRP may result in more stress and also depression. With CRP higher than 3.0 there was a greater than twofold increase depression risk. The researchers suggest that CRP may heighten stress and depression risk by increasing levels of different proinflammatory cytokines, inflammatory communicators among cells (4).
In one recent study, results suggested that stress may influence and increase the number of hematopoietic stem cells (those that develop of all forms of blood cells), resulting in specifically an increase in inflammatory white blood cells (5). The researchers suggest that this may lead to these white blood cells accumulating in atherosclerotic plaques in the arteries, which ultimately could potentially increase the risk of heart attacks and strokes. Chronic stress overactivates the sympathetic nervous system — our “fight or flight” response — which may alter the bone marrow where the stem cells are found. This research is preliminary and needs well-controlled trials to confirm these results.

Infection
Stress may increase the risk of colds and infection. Cortisol over the short term is important to help suppress the symptoms of colds, such as sneezing, cough and fever. These are visible signs of the immune system’s infection-fighting response. However, the body may become resistant to the effects of cortisol, similar to how a type 2 diabetes patient becomes resistant to insulin. In one study of 296 healthy individuals, participants who had stressful events and were then exposed to viruses had a higher probability of catching a cold. It turns out that these individuals also had resistance to the effects of cortisol. This is important because those who were resistant to cortisol had more cold symptoms and more proinflammatory cytokines (6).

Cortisol
When we measure cortisol levels, we tend to test the saliva or the blood. However, these laboratory findings only give one point in time. Thus, when trying to determine if raised cortisol may increase cardiovascular risk, the results are mixed. However, in a recent study, measuring cortisol levels from scalp hair was far more effective (7). The reason for this is that scalp hair grows slowly, and therefore it may contain three months’ worth of cortisol levels. The study showed that those in the highest quartile of cortisol levels were at a three-times increased risk of developing diabetes and/or heart disease compared to those in the lowest quartile. This study involved older patients between the ages of 65 and 85.

Lifestyle and the Cellular Level
Lifestyle plays an important role in stress at the cellular level, specifically at the level of the telomere, which determines cell survival. The telomeres are to cells as the plastic tips are to shoelaces; they prevent them from falling apart. The longer the telomere, the slower the cell ages and the longer it survives. In a recent study, those women who followed a healthy lifestyle — one standard deviation over the average lifestyle — were able to withstand life stressors better since they had longer telomeres (8).
This healthy lifestyle included regular exercise, a healthy diet and a sufficient amount of sleep. On the other hand, the researchers indicated that those who had poor lifestyle habits lost substantially more telomere length than the healthy lifestyle group. The study followed women 50 to 65 years old over a one-year period.
In another study, chronic stress and poor diet (high sugar and high fat) together increased metabolic risks, such as insulin resistance, oxidative stress and central obesity, more than a low-stress group eating a similar diet (9). The high-stress group was caregivers, specifically those caring for a spouse or parent with dementia. Thus, it is especially important to eat a healthy diet when under stress.
Interestingly, in terms of sleep, the Evolution of Pathways to Insomnia Cohort study shows that those who deal with stressful events directly are more likely to have good sleep quality. Using medication, alcohol or, most surprisingly, distractors to address stress all resulted in insomnia after being followed for one year (10). Cognitive intrusions or repeat thoughts about the stressor also resulted in insomnia.
Psychologists and other health care providers sometimes suggest distraction from a stressful event, such as television watching or other activities, according to the researchers. However, this study suggests that this may not help avert chronic insomnia induced by a stressful event. The most important message from this study is that how a person reacts and deals with a stressors may determine whether they suffer from insomnia.

Constant stress is something that needs to be recognized. If not addressed, it can lead to suppressed immune response or increased levels of inflammation. CRP is an example of an inflammatory biomarker that may actually increase stress. In order to address chronic stress and lower CRP, it is important to adopt a healthy lifestyle that includes sleep, exercise and diet modifications. A good lifestyle may be protective against cell aging when exposed to stressors.

References:
(1) Curr Top Behav Neurosci. 2014 Aug. 29. (2) Am J Physiol. 1991;260(6 Part 1):E927-E932. (3) JAMA Psychiatry. 2013;70:176-184. (4) Chest. 2000;118:503-508. (5) Nat Med. 2014;20:754-758. (6) Proc Natl Acad Sci U S A. 2012;109:5995-5999. (7) J Clin Endocrinol Metab. 2013;98:2078-2083. (8) Mol Psychiatry Online. 2014 July 29. (9) Psychoneuroendocrinol Online. 2014 April 12. (10) Sleep. 2014;37:1199-1208.

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, go to the website www.medicalcompassmd.com and/or consult your personal physician.

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By David Dunaief

Steroids have been in the news with headlines about sports figures like Alex Rodriguez, the NY Yankees baseball player notorious for their illegal use. However, if we look beyond the flashy headlines to rudimentary use, we see that corticosteroids, or steroids, play an important role in medicine. This is a commonly prescribed class of medications. In fact, our bodies make corticosteroids, the indigenous form of steroids, in the cortex of the adrenals, glands that sit on top of the kidneys. Here, we are going to concentrate on the exogenous form, meaning from the outside as medication.

The use or benefit
Steroids have an anti-inflammatory effect. This is critical since many acute and chronic diseases are based at least partially on inflammation. Chronic diseases that benefit include allergic, inflammatory and immunological diseases (1). These types of diseases touch on almost every area of the body from osteoarthritis and  autoimmune diseases — rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, lupus, psoriasis and eczema — to asthma, COPD (emphysema and chronic bronchitis) and eye disorders. This type of medication is pervasive.

The delivery
Steroids are delivered via the oral route, as topical creams, lotions and eye drops or via injections, intravenous solutions and inhaled formulations. The most commonly known medication is prednisone, but there is a plethora of others, including prednisolone, methylprednisolone, cortisone, hydrocortisone and dexamethasone.
Their benefits can be tremendous, improving functionality and reducing pain or improving breathing. You could say they are lifesaving in some instances, and with rescue inhalers they may just be that.

The bad
However, there is a very big caveat: they come at a price. Steroids have lots and lots of adverse events associated with them. This is where the bad part comes in and keeps on coming. Steroids cause weight gain, increased glucose (sugars), high blood pressure, cardiovascular events, osteoporosis, change in mood (psychoses), cataracts, glaucoma, infection, peptic ulcers, Cushing’s syndrome and the list goes on. Ironically, steroids help with breathing; however, as I’ve seen in my clinical experience, they can cause shortness of breath when weaned from a longer-use high dose too quickly.

The upshot
The good news is that a plant-based diet may have similar beneficial effects in chronic diseases as steroids without all the downsides. Let’s look at the evidence.

The role in pneumonia
Pneumonia is among the top-10 leading causes of death in the world (2). It can be a most painful and debilitating disease. I know, for I experienced it personally while I was in my medical training. Every time I coughed, it felt like there was a fire in my chest.
In a meta-analysis (a group of nine studies), there was no overall effect of corticosteroids in reducing the risk of mortality in community-acquired pneumonia (3). However, don’t fret; when the data was broken into subsets, the findings were different. In subset data of those who had severe pneumonia, there was a statistically significant 74 percent reduction in mortality. And when duration was the main focus in subgroup analysis, those who received prolonged use of steroids reduced their risk of mortality by half. Unfortunately, with the benefit comes an increased risk of adverse events, and this meta-analysis was no exception. There was a greater than two times increased risk of abnormally high glucose levels with prolonged use. Thus, when giving steroids, especially for a prolonged use, it may be wise to check glucose levels.
In a more recent randomized controlled trial (RCT), the gold standard of studies, the results reinforced the beneficial effects of steroids on pneumonia. They showed that in those with both severe pneumonia and high inflammation, there was a two-thirds reduction in treatment failures when corticosteroids were added to the regimen (4). There were 120 patients involved in the study. They received antibiotics plus either methylprednisolone or placebo for five days.

Osteoarthritis: surprising results
As we know, osteoarthritis specifically of the knee is very common, especially as the population continues to age. Intra-articular (in the joint) injections directly into the knee are becoming routine treatment. A recent study compared injectable hyaluronic acid to injectable corticosteroid (5). The results showed that over three months, the corticosteroid was superior to hyaluronic acid in terms of reducing pain, 66 percent versus 43.8 percent, respectively. Interestingly, over the longer term, 12 months, hyaluronic acid reduced the pain and maintained its effect significantly longer than the steroid, 33 percent versus a meager 8.2 percent, respectively. Study groups received five injections of either steroid or of hyaluronic acid directly to the knee over a five-week period. Thus, steroids may not always be the most effective choice when it comes to pain reduction. Hyaluronic acid may have caused this beneficial effect by reducing inflammation, protecting cartilage and preventing cell death, according to the authors.

COPD: length may not matter
It is not unusual to treat COPD patients with oral steroids. But what is the proper duration? The treatment paradigm has been two weeks with 40 mg of corticosteroids daily. However, results in an RCT showed that five days with 40 mg of corticosteroid was noninferior (equivalent) to 14 days of the same dosage and frequency (6). About one-third of patients in each group experienced a COPD exacerbation within the six-month duration of the trial. The hope is that the shorter use of steroids will mean fewer side effects. There were over 600 patients in this trial. We have come a long way; prior to 1999, eight weeks of steroids was a more commonplace approach to treating acute COPD exacerbations.

Topical steroid risk
Even topical creams and lotions are not immune to risk. For example, potent topical creams and lotions placed around the orbit of the eye with prolonged use may negatively affect vision (7). However, the evidence is based mostly on case reporting, which is a low level of evidence.

Dietary effect
One of the great things about steroids is that they reduce inflammation, and we know that the basis of greater than 80 percent of chronic disease is inflammation. A plant-based diet involving lots of vegetables and fruits and some grains may have a similar effect as steroids. The effect of diet on chronic disease may be to modify the immune system and reduce inflammation (8). The bioactive substances from plants thought to be involved in this process are predominantly the carotenoids and the flavonoids. Thus, those patients who respond even minimally to steroids are likely to respond to a plant-based diet in much the same beneficial way without the downsides of a significant number of side effects. Diet, unlike steroids, can be used for a long duration and a high intake, with a direct relationship to improving disease outcomes.
In conclusion, it is always better to treat with the lowest effective dose for the shortest effective period when it comes to steroids. The complications of these drugs are enumerable and must always be weighed against the benefits. Sometimes, other drugs may have more beneficial effects over the long term such as hyaluronic acid injections for knee osteoarthritis. A plant-based diet, with anti-inflammatory properties similar to steroids, may be a useful alternative for chronic disease or may be used alongside these drugs, possibly reducing their dosage and duration.

REFERENCES
(1) uptodate.com. (2) N Engl J Med. 1995;333(24):1618-24. (3) PLoS One. 2012;7(10):e47926. (4) JAMA. 2015;313(7):677-686. (5) Open Access Rheum 2015;7:9-18. (6) JAMA. 2013;309(21):2223-31. (7) Australas J Dermatol. Mar 5, 2015. (8) Int J Vitam Nutr Res. 2008 Dec;78(6):293-8.

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, go to the website www.medicalcompassmd.com and/or consult your personal physician.

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By David Dunaief

As the population ages, we see more and more osteoarthritis (OA); but as the population gets heavier, we see more; and as people become more active, we see more; and as the population becomes more sedentary (weakened muscles), we see more. The point is that age, although a strong factor, may not be the only one, and while there are conflicting contributors, there are many, nonetheless.

Over 27 million people in the U.S. suffer from OA (1). Osteoarthritis is insidious, developing over a long period of time, and is chronic by nature. It is a top cause of disability (2). What can we do about it?

It turns out that OA is not just caused by friction or mechanical breakdown based on age but rather on a multitude of factors including friction but also local inflammation, genes and metabolic processes at the cellular level (3). Being a more complicated process means that we may be able to prevent and treat it better than we thought through exercise, diet, medication, injections and possibly even with supplements.

Let’s look at some of the research.

Don’t wait to lose weight!
In an older study, results showed that even a small 10-pound weight loss could result in an impressive 50 percent reduction of symptomatic knee OA over a 10-year period (4).

How can exercise be beneficial?
One of the exercises that most of us either can tolerate or actually enjoy is walking. We have heard that walking can be dangerous for exacerbating OA symptoms; the pounding can be harsh on our joints, especially our knees. Well, maybe not. Walking may have benefits. And once we figure out what exercise might be useful, in this case walking, how much should we do? In the Multicenter Osteoarthritis Study (MOST), results showed that walking may indeed be useful to prevent functional decline (5). But certainly not in overweight or obese patients and not older patients, right?

Actually, the patients in this study were a mean age of 67 and were obese, with a mean body mass index (BMI) of 31 kg/m2, and either had or were at risk of knee arthritis. In fact, the most interesting part of this study was that the researchers quantified the amount of walking needed to see a positive effect. The least amount to see a benefit was between 3250 and 3750 steps per day, measured by an ankle pedometer. The best results were seen in those walking >6000 steps per day, a relatively modest amount. This was random, unstructured exercise. In addition, for every 1000 extra steps per day, there was a 16 to 18 percent reduced risk of functional decline two years later.

Where does vitamin D fit in?
For the last decade or so, we thought vitamin D was the potential elixir for chronic diseases. If it were low, that meant higher risk for disease, and we needed to replete the levels. Well, a recent randomized controlled trial (RCT), the gold standard of studies, has shown that low vitamin D levels may indeed contribute to knee osteoarthritis (6). However, repleting levels of vitamin D did not seem to stem disease progression. In fact, it had no effect on the disease, to the bewilderment of the researchers. There was no change in joint space, knee pain, mobility or cartilage loss slowing. Hmm. The patients were supplemented with vitamin D 2000 IU for two years. There were 146 patients involved in the study. Blood levels of vitamin D were raised by 16.1 ng/ml in the treatment group to >36 ng/ml, which was significantly greater than the 2.1 ng/ml increase in the placebo group. Since the reasons for the results are unclear, work to maintain normal levels of vitamin D to possibly prevent OA, rather than wait to treat it later.

Acetaminophen may not live up to its popularity
Acetaminophen is a popular initial go-to drug for the treatment of osteoarthritis, but what does the research say about its effectiveness? The answer might surprise you. Although acetaminophen doesn’t have anti-inflammatory properties, it does have analgesic properties. However, in a recent meta-analysis (involving 137 studies), acetaminophen did not reduce the pain for OA patients (7). In this study, all other oral treatments were significantly better than acetaminophen including diclofenac, naproxen and ibuprofen as well as intra-articular (in the joint) injectables, such as hyaluronic acid and corticosteroids, except for an oral cox-2 inhibitor, celecoxib, which was only marginally better.

What about NSAIDs?
NSAIDs (nonsteroidal anti-inflammatory drugs) by definition help to reduce inflammation. However, they have side effects that may include gastrointestinal bleed and have a black box warning for heart attacks. Risk tends to escalate with a rise in dose. But now there is a new twist; the FDA has approved a new formulation of an NSAID, diclofenac (Zorvolex) (8). This formulation uses submicron particles, which are roughly 20 times smaller than the older version; since they provide a greater surface area that helps the drug to dissolve faster, they require less dosage.

The approved dosage for OA treatment is 35 mg, three times a day. In a 602-patient, one-year duration, open-label randomized controlled trial, the new formulation of diclofenac demonstrated improvement in pain, functionality and quality of life (9). The adverse effects, or side effects, were similar to the placebo. The only caveat is that there was a high dropout rate in the treatment group; only 40 percent completed the trial when they were dosed three times daily.

Don’t forget about glucosamine and chondroitin
Study results for this supplement combination or its individual components for the treatment of OA have been mixed. In a double-blind RCTß, the combination supplement improved joint space, narrowing and reducing the pain of knee OA over two years. However, the pain was reduced no more than was seen in the placebo group (10). In a Cochrane meta-analysis review study (involving 43 RCTs) results showed that chondroitin with or without glucosamine reduced the symptom of pain modestly compared to placebo in short-term studies (11). However, the researchers stipulate that most of the studies were of low quality.

So, think twice before reaching for the Tylenol. If you are having symptomatic OA pain, NSAIDs such as diclofenac may be a better choice, especially with SoluMatrix fine-particle technology that uses a lower dose and thus hopefully means fewer side effects. Even though results are mixed, there is no significant downside to giving glucosamine-chondroitin supplements a chance. However, if it does not work after 12 weeks, it is unlikely to have a significant effect. And above all else, if you need to lose weight and do, it would reduce your risk of OA significantly.

REFERENCES
(1) Arthritis Rheum. 2008;58:26-35. (2) Popul Health Metr. 2006;4:11. (3) Lancet. 1997;350(9076):503. (4) Ann Intern Med.1992;116:535-539. (5) Arthritis Care Res (Hoboken). 2014;66(9):1328-36. (6) JAMA. 2013;309:155-162. (7) Ann Intern Med. 2015;162:46-54. (8) FDA.gov. (9) ACR 2014 Annual Meeting: Abstract 249. (10) Ann Rheum Dis. Online Jan 6, 2014. (11) Cochrane Database Syst Rev. 2015 Jan 28;1:CD005614.

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, go to the website www.medicalcompassmd.com and/or consult your personal physician.

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By David Dunaief

Chronic kidney disease is much more common than you think. Those at highest risk for CKD include patients with diabetes, hypertension (high blood pressure) and those with first degree relatives who have advanced disease. But those are only the ones at highest risk. This brings me to my first question.

Why is CKD a tricky disease?
Unfortunately, similar to high blood pressure and dyslipidemia (high cholesterol), the disease tends to be asymptomatic, at least initially. Only in the advanced stages do symptoms become distinct, though there can be vague symptoms such as fatigue, malaise and loss of appetite in moderate stages.

What are the stages?
CKD is classified into five stages based on the estimated glomerular filtration rate (eGFR), a way to determine kidney function. Stages 1 and 2 are the early stages, while stages 3a and 3b are the moderate stages, and finally stages 4 and 5 are the advanced stages. This demarcation is based on an eGFR of >60 ml/min for early, 30-59 ml/min for moderate and <30 ml/min for advanced. Stage 5 is end-stage kidney disease or failure.

Why is CKD important?
The prevalence of the disease is predicted to grow by leaps and bounds in the next 15 years. Presently, approximately 13 percent of those over age 30 in the U.S. population are affected by CKD. In a new simulation model, it is expected to reach 16.7 percent prevalence in the year 2030. Currently, those who are ages 30 to 49 have a 54 percent chance of having CKD in their lifetimes; those 50 to 64 years of age, a slightly lower risk of 52 percent; and those 65 years and older, a 42 percent risk (1). Thus, a broad spectrum of people are affected. Another study’s results corroborate these numbers, suggesting almost a 60 percent lifetime risk of at least moderate stage 3a to advanced stage 5 CKD (2). If these numbers are correct, they are impressive, and the disease needs to be addressed. We need to take precautions to prevent the disease and its progression.

Who should be screened?
According to the U.S. Preventive Services Task Force, screening for CKD may not be warranted in the asymptomatic “healthy” population (3). This means people without chronic diseases. The studies are inconclusive in terms of benefits and harms. In order to qualify as CKD, there has to be a minimum of three months of decreased kidney function. This appears to be a paradox: remember, CKD is asymptomatic generally until the advanced stages. However, there are a number of caveats in the report.

Those who are at highest risk should be screened, including, as I mentioned above, patients with diabetes or hypertension. In an interview on www.Medscape.com entitled “Proteinuria: A Cheaper and Better Cholesterol?” two high-ranking nephrologists suggest that first-degree relatives to advanced CKD patients should also be screened and that those with vague symptoms of fatigue, malaise and/or decreased appetite may also be potential candidates (4). This broadens the asymptomatic population that may benefit from screening.

The fix!
Fortunately, there are several options available, ranging from preventing CKD with specific exercise to slowing the progression with lifestyle changes and medications.

Why exercise?
Here we go again, preaching the benefits of exercise. But what if you don’t really like exercise? It turns out that the results of a study show that walking reduces the risk of death and the need for dialysis by 33 percent and 21 percent respectively (5). And although some don’t like formal exercise programs, most people agree that walking is enticing.

The most prevalent form of exercise in this study was walking. The results are even more intriguing; they are based on a dose-response curve. In other words, those who walk more often see greater results. So, the participants who walked one-to-two times per week had a significant 17 percent reduction in death and a 19 percent reduction in kidney replacement therapy, whereas those who walked at least seven times per week experienced a more impressive 59 percent reduction in death and a 44 percent reduction in the risk of dialysis. Those who were in between saw a graded response. There were 6,363 participants for an average duration of 1.3 years.

Protein is important! Right?
Yes, protein is important for tissue and muscle health. But when it comes to CKD, more is not necessarily better, and may even be harmful. In a meta-analysis (a group of 10 randomized controlled trials, the gold standard of studies), results showed that the risk of death or treatment with dialysis or kidney transplant was reduced by 32 percent in those who consumed less protein compared to unrestricted protein (6). This meta-analysis used the Cochrane database to search for studies.

According to the authors, as few as two patients would need to be treated for a year in order to prevent one from either dying or reaching the need for dialysis or transplant. Unfortunately, the specific quantity of protein consumption that is ideal in CKD patients could not be ascertained since the study was a meta-analysis.

Sodium: How much?
The debate roils on: how much do we need to reduce sodium in order to see an effect? Well, the good news is that in a recent study, results showed that a modest sodium reduction in our diet may be sufficient to help prevent proteinuria (protein in the urine) (7). Different guidelines recommend sodium intake ranging from fewer than 1500 mg to 2300 mg daily. This particular study says that less than 2000 mg is beneficial, something all of us can achieve.

Of course medications have a place
We routinely give certain medications, ACE inhibitors or ARBs, to patients who have diabetes to protect their kidneys. What about patients who do not have diabetes? ACEs and ARBs are two classes of anti-hypertensives — high blood pressure medications — that work on the RAAS system of the kidneys, responsible for blood pressure and water balance (8). Results of a recent study show that these medications reduced the risk of death significantly in patients with moderate CKD. Most of the patients were considered hypertensive.

However, there was a high discontinuation rate among those taking the medication. If you include the discontinuations and regard them as failures, then all who participated showed a 19 percent reduction in risk of death, which was significant. However, if you exclude discontinuations, the results are much more robust with a 63 percent reduction. To get a more realistic picture, the intention-to-treat result (those that include both participants and drop outs) is probably the response that will occur in clinical practice unless the physician is a really good motivator or has very highly motivated patients.

While these two classes of medications, ACE inhibitors and ARBs, are good potential options for protecting the kidneys, they are not the only options. You don’t necessarily have to rely on drug therapies, and there is no downside to lifestyle modifications. Lowering sodium modestly, walking frequently, and lowering your protein consumption may all be viable options, with or without medication, since medication compliance was woeful. Screening for asymptomatic, moderate CKD may lack conclusive studies, but screening should occur in high-risk patients and possibly be on the radar for those with vague symptoms of lethargy as well as aches and pains. Of course, this is a discussion to have with your physician.

REFERENCES:
(1) Am J Kidney Dis. 2015;65(3):403-11. (2) Am J Kidney Dis. 2013;62(2):245-52. (3) Ann Int. Med. 2012;157(8):567-570. (4) www.Medscape.com. (5) Clin J Am Soc Nephrol. 2014;9(7):1183-9. (6) Cochrane Database Syst Rev. 2009;(3):CD001892. (7) Curr Opin Nephrol Hypertens. 2014;23(6):533-540. (8) J Am Coll Cardiol. 2014;63(7):650-658.

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, go to the website www.medicalcompassmd.com and/or consult your personal physician.

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