I recently wrote that mild cognitive impairment is one of the most feared disorders, especially as we age. One of the reasons for this is the fear of progressing to Alzheimer’s disease. The fear of developing Alzheimer’s with MCI is grounded in reality.

A recent study of patients with MCI and a protein biomarker called amyloid in the brain showed that the probability of developing Alzheimer’s disease was 50% after three years (ADI Conference 2012; Abstracts OC037 and OC035). However, those who had MCI without the amyloid proteins had a reduced one in ten chance of developing Alzheimer’s. Amyloid-beta plaques tend to accumulate in the brain and may be an early sign of Alzheimer’s. Researchers used a positron emissions tomography scan to make these assessments.

Modifiable risk factors for Alzheimer’s disease include chronic diseases, such as diabetes, high cholesterol and high blood pressure.

Where are we with medical therapies, and what can we do to possibly modify our risk for Alzheimer’s? Drug therapies in the research pipeline have had mixed results. However, one drug already on the market may be beneficial for those with diabetes: metformin.

What about diet? The answer depends on the type of diet. The standard American diet, with its high saturated fat and increased sugars, may increase the risk of Alzheimer’s, while a low-fat, nutrient-dense diet may reduce the risk of Alzheimer’s disease. Let’s review the evidence.

Future potential drug therapies

There is good news and bad news for potential Alzheimer’s drugs in development. Recently, the FDA stopped a drug trial because Phase III (the final stage) of development did not show better results than placebo in patients with Alzheimer’s (N Engl J Med. 2013;369:341-350). The drug that failed, semagacestat, was tested at two different doses and compared to a placebo. Its focus, like many Alzheimer’s drugs in development, was on reducing amyloid-beta plaques.

This was a well-designed, randomized controlled trial involving over 1,500 patients with a duration of about a year and a half. The patients on the drug actually did worse in terms of cognitive abilities and had more side effects than those on the placebo. This is disheartening.

However, don’t lose hope. There is another drug in the early stages of development, a microglial modulator. Microglia is to the brain as HDL or “good cholesterol” is to the cholesterol profile. They remove the “garbage.” Amyloid plaques interfere with microglia and ultimately cause inflammation. Microglial modulators are able to resist this process in mice, potentially reducing amyloid plaque deposits in the brain and improving memory. In a recent preliminary trial in humans, it showed promise for preventing patients with MCI from progressing to Alzheimer’s disease (AAI Conference 2013; oral presentation: O3-06-5). These were early results, and a much larger Phase III study is needed before conclusions can be drawn. But this is a potentially exciting new approach.

Dietary impact

Even mildly elevated blood glucose (sugar) levels may be a contributor to Alzheimer’s disease. In a recent study, even slightly elevated sugar levels led to increased risk (N Engl J Med. 2013;369:540-548). When a blood glucose level of 115 mg/dL, a prediabetes level, was compared to 100 mg/dL, risk increased by 18%. The risk of developing Alzheimer’s was even greater in those who were diabetic with higher sugars. Those with a blood glucose of 190 mg/dL, compared to those with a blood sugar of 160 mg/dL, had 40% greater risk for developing Alzheimer’s. This study followed over 2,000 patients for approximately seven years.

The scary aspect is that a slight rise in sugars from normal can lead to a significant rise in Alzheimer’s risk. The authors concluded that those who had slight glucose elevations should make lifestyle changes, including diet and exercise.

Metformin

It is thought that diabetes may increase the risk of Alzheimer’s by at least twofold. In a recent observational trial, involving over 14,000 patients with a follow-up of five years, they found that metformin may reduce the risk of Alzheimer’s dementia substantially (AAIC 2013. Oral Presentation: O1-05-05). There was an approximate 20% reduced Alzheimer’s risk with metformin. Other medications, when compared to metformin, increased the risk of Alzheimer’s. For example, insulin increased risk 23%. However, this was not a randomized controlled trial. So, I might lean toward using metformin in diabetes patients, but not draw dramatic conclusions about other diabetic medications.

Integrative conference

In July, I attended an integrative conference, the International Conference on Nutrition and the Brain, hosted by Physicians Committee for Responsible Medicine in Washington, D.C. Presented evidence suggested that diet has an impact on Alzheimer’s disease (medscape.com). A diet high in saturated fat may negatively affect cognition and increase the risk of Alzheimer’s. On the other hand, a high-nutrient, plant-based diet may have the opposite effect. The suggested diet consists of low saturated fat, a focus on fruits, vegetables, beans and legumes, and a small handful of nuts and seeds daily. They also stressed the importance of cardiovascular exercise, such as a walking with alacrity for 30 minutes, four times a week. You should also avoid aluminum from sources like cookware and antacids.

High saturated fat and high sugar effect

Interestingly there is a RCT that shows a high-saturated fat and high-sugar diet may increase the load of amyloid-beta protein plaques by preventing their clearance from the brain, whereas the diet with lower saturated fat and sugar had beneficial results (JAMA Neurol. 2013;70(8):972-980). According to the authors, diet may modify the risk profile for this disease, depending on the diet’s composition. Though the trial was small and short in duration, four weeks, it was still impressive.

I mentioned the word “fear” in the introduction several times. Hopefully, this article turned that fear into confidence that you can reduce the risk of developing Alzheimer’s disease. Decreasing saturated fat and sugar intake may be the first steps to reaching this goal. Whether metformin is needed by those with high blood sugar levels or not, lifestyle modifications, including a high-nutrient, plant-based diet, seems to have promise.

We hope for the best with drug therapies in the pipeline, though most have disappointed or are only in early stages of development, so it is even more imperative to utilize what may be our most powerful weapon, lifestyle changes.

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.

Mild cognitive impairment is one of the more common disorders that occur as we age. But age is not the only determinant. There are a number of modifiable risk factors. MCI is feared, not only for its own challenges, but also because it may lead to dementia, with Alzheimer’s disease and vascular dementia being the more common forms. Prevalence of MCI may be as high as 1 in 5 in those over the age of 70 (Ann Intern Med. 2008;148:427-434). It is thought that those with MCI may have a 10% chance of developing Alzheimer’s disease (uptodate.com).

Since there are very few medications presently that help prevent cognitive decline, the most compelling questions are: what increases risk and what can we do to minimize the risk of developing cognitive impairment? These are the important questions.

Many chronic diseases and disorders contribute to MCI risk. These include diabetes, heart disease, Parkinson’s disease and strokes. If we can control these maladies, we may reduce the risk of cognitive decline. This involves making lifestyle modifications such as exercise and diet. We know that we can’t stop aging, but we can age gracefully.

Heart disease

Although we have made great strides, heart disease continues to be prevalent in America. In a recent observational study, results demonstrate that those suffering from years of heart disease are at a substantial risk of developing MCI (JAMA Neurol. 2013;70:374-382). The study involved 1,450 participants who were between the ages of 70 and 89 and were not afflicted by cognitive decline at the beginning of the study. Patients with a history of cardiac disease had an almost two times greater risk of developing nonamnestic MCI, compared to those individuals without cardiac disease. Women with cardiac disease were affected even more, with a three times increased risk of cognitive impairment.

Nonamnestic MCI affects executive functioning – decision-making abilities, spatial relations, problem-solving capabilities, judgments and language. It is a more subtle form of impairment that may be more frustrating because of its subtlety. It may lead to vascular dementia and may be a result of clots. This gives us yet another reason to treat and prevent cardiac disease.

Stroke

Not surprisingly, stroke may have a role in cognitive impairment. Stroke is also referred to as a type of vascular brain injury. But what is surprising is that in a recent study, the results show that the location of the stroke was more relevant than the frequency or the multitude of strokes (JAMA Neurol. 2013;70:488-495). If strokes occurred in the cortical and subcortical grey matter regions of the brain, executive functioning and memory were affected, respectively. Thus, the location of strokes may be a better predictor of subsequent cognitive decline than the number of strokes. Clinically silent strokes that were found incidentally by MRI scans had no direct effect on cognition, according to the authors.

Exercise

Exercise may play a significant role in potentially preventing cognitive decline and possibly even improving MCI in patients who have the disorder. Interestingly, different types of exercise have different effects on the brain. Aerobic exercise may stimulate one type of neuronal development, while resistance training or weight lifting another.

In an animal study involving rats, researchers compared aerobic exercise to weight lifting (J Alzheimers Dis. 2012;32:329-339). Weightlifting was simulated by attaching weights to the tail of rats while they climbed ladders. Both groups showed improvements in memory tests, however, there was interesting divergence. With aerobic exercise, the level of the protein BDNF (brain-derived neurotrophic factor) increased significantly. This is important since BDNF is involved in neurons and the connections among them, called synapses, related mostly to the hippocampus, or memory center. The rats that “lifted weights” had an increase in another protein, IGF (insulin growth factor), that promotes the development of neurons in a different area of the brain. The authors stressed the most important thing is to exercise, regardless of the type.

In a recent study that complements the previous study, women were found to have improved spatial memory when they exercised – either aerobic or weight lifting (J Aging Res. 2013;2013:861893). Interestingly, verbal memory was improved more by aerobic exercise than by weight lifting. Spatial memory is the ability to recall where items were arranged, and verbal memory is the ability to recall words. The authors suggest that aerobic exercise and weight lifting affect different parts of the brain, which corroborates the animal study findings above.

This was a randomized controlled trial that was six months in duration and involved women, ages 70 to 80, who had MCI at the trial’s start. There were three groups in the study: aerobic, weight lifting and stretching and toning. Those who did stretches or toning alone experienced deterioration in memory skills over the same period.

Here is the catch with exercise: we know exercise is valuable in preventing disorders like cardiovascular disease and cognitive decline, but are Americans doing enough? A recent CDC report says the majority of the adult population is woefully deficient: only about 1 in 5 Americans exercise regularly doing both weights and aerobic exercise (Morb Mortal Wkly Rep. 2013;62:326-330).

Diet

Several studies show that the Mediterranean diet helps prevent MCI and possibly prevents conversion from MCI to Alzheimer’s (Neurology 2013;80:1684-1692; Arch Neurol. 2009 Feb.;66:216-225). In addition, a recent study showed that high levels of carbohydrates and sugars, when compared to lower levels, increased the risk of cognitive decline by more than three times (J Alzheimers Dis. 2012;32:329-339). The authors surmise that carbohydrates have a negative impact on insulin and glucose utilization in the brain.

Cognitive decline is a disorder that should be taken very seriously, and everything that can be done to prevent it should be utilized. Though the number of Americans exercising regularly is woefully deficient, the silver lining is that there is substantial room for improvement. Exercise has potentially positive effects on neuron growth and development. We need more campaigns like the NFL’s Play 60, which entices children to be active at least 60 minutes every day, but we need to also target adults of all ages. Let’s not squander the opportunity to reduce the risk of MCI, a potentially life-altering disorder.

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.

I thought a discussion of insomnia would be a good follow-up to my recent article on sleep deprivation. Like sleep deprivation, insomnia is an all-too-common complaint. Though the statistics vary widely, about 30 percent of Americans are affected, according to the most frequently used estimate (Sleep. 2009;32(8):1027). Women tend to be affected more than men. Insomnia is thought to have several main components: difficulty falling asleep, difficulty staying asleep, waking up before a full night’s sleep, and sleep that is not restorative or restful (American Academy of Sleep Medicine 2nd edition 2005).

Unlike sleep deprivation, patients have plenty of time for sleep. Having one or all of these components is considered insomnia. There is debate about whether or not it is actually a disease, though it certainly has a significant impact on patients’ functioning (Arch Intern Med. 1998;158(10):1099).

Insomnia is frustrating, because it does not necessarily have one cause. Causes can include aging; stress; psychiatric disorders; disease states, such as obstructive sleep apnea and thyroid dysfunction; asthma; medication; and it may even be idiopathic (of unknown cause). It can occur on an acute (short-term), intermittent, or chronic basis. Regardless of the cause, it may have a significant impact on quality of life. Insomnia also may cause comorbidities (diseases), two of which we will investigate further: heart failure and prostate cancer.

Fortunately, there are numerous treatments. These can involve medications, such as benzodiazepines like Ativan and Xanax. The downside of these medications is they may be habit-forming. Nonbenzodiazepine hypnotics (therapies) include sleep medications, such as Lunesta (eszopiclone) and Ambien (zolpidem). All of these medications have side effects. We will investigate Ambien further, because of recent warnings.

There are also natural treatments, involving supplements, cognitive behavioral therapy, and lifestyle changes.

Let’s look at the evidence.

Heart Failure

Insomnia may perpetuate heart failure, which can be a difficult disease to treat. In the HUNT analysis (Nord-Trøndelag Health Study) , an observational study, results showed insomnia patients had a dose-dependent response for increased risk of developing heart failure (Eur Heart J. online 2013;Mar 5). In other words, the more components of insomnia involved, the higher the risk of developing heart disease.

There were three components: difficulty falling asleep, difficulty maintaining sleep, and nonrestorative sleep that is not restful. If one component was involved, there was no increased risk. If two components were involved, there was a 35 percent increased risk, although not statistically-significant.

However, if all three components were involved, there was 350 percent increased risk of developing heart failure, even after adjusting for other factors. This was a large study, involving 54,000 Norwegians, with a long duration of 11 years.

Prostate Cancer

Prostate cancer has a plethora of possible causes, and insomnia may be a contributor. Having either of two components of insomnia, difficulty falling asleep or staying asleep (sleep disruption), increased the risk of prostate cancer by 1.7 and 2.1 times, respectively, according to a recent observational study (Cancer Epidemiol Biomarkers Prev; 2013;22(5):872–9).

However, when looking at a subset of data related to advanced or lethal prostate cancer, both components, difficulty falling asleep and sleep disruption, independently increased the risk even further, 2.1 and 3.2 times, respectively.

This suggests that sleep is a powerful factor in prostate cancer, and other studies have shown that it may have an impact on other cancers, as well. There were 2,102 men involved in the study with a duration of five years. While there are potentially strong associations, this and other studies have been mostly observational. Further studies are required before any definitive conclusions can be made.

What about potential treatments?

Ambien

While nonbenzodiazepine hypnotics may be beneficial, this may come at a price. In a recent report by the Drug Abuse Warning Network part of the Substance Abuse and Mental Health Services Administration, the number of reported adverse events with Ambien that perpetuated emergency department visits increased by more than two-fold over a five-year period from 2005 to 2010 (SAMSHA.gov). Insomnia patients most susceptible to having significant side effects are women and the elderly. The director of SAMHSA recommended focusing on lifestyle changes for treating insomnia: by making sure the bedroom is sufficiently dark, getting frequent exercise, and avoiding caffeine.

In reaction to this data, the FDA is requiring the manufacturer of Ambien to reduce the dose recommended for women by 50 percent (FDA.gov). Ironically, sleep medication like Ambien may cause drowsiness the next day — the FDA is investigating if it is safe to drive after taking these medications the night before.

Magnesium

The elderly population tends to suffer the most from insomnia, as well as nutrient deficiencies. In a double-blinded, randomized controlled trial, the gold standard of studies, results show that magnesium had resoundingly positive effects on elderly patients suffering from insomnia (J Res Med Sci. 2012 Dec;17(12):1161-9).

Compared to a placebo group, participants given 500 mg of magnesium daily for eight weeks had significant improvements in sleep quality, sleep duration, and time to fall asleep, as well as improvement in the body’s levels of melatonin, a hormone that helps control the circadian rhythm.

The strength of the study is that it is an RCT, however, it was small, involving 46 patients over a relatively short duration.

Cognitive Behavioral Therapy

In a recent study, just one 2½-hour session of cognitive behavioral therapy delivered to a group of twenty patients suffering from chronic insomnia saw subjective, yet dramatic, improvements in sleep duration from 5 to 6½ hours and decreases in sleep latency from 51 to 22 minutes (APSS 27th Annual Meeting 2013; Abstract 0555). The patients who were taking medication to treat insomnia experienced a 33 percent reduction in their required medication frequency per week. The topics covered in the session included relaxation techniques, sleep hygiene, sleep restriction, sleep positions, and beliefs and obsessions pertaining to sleep. These results are encouraging.

It is important to emphasize the need for sufficient and good-quality sleep to help prevent, as well as not contribute to, chronic diseases, such as cardiovascular disease and prostate cancer. While medications may be necessary in some circumstances, they should be used with the lowest possible dose for the shortest amount of time and with caution, reviewing possible drug-drug and drug-supplement interactions. Supplementation with magnesium may be a valuable step toward improving insomnia. Lifestyle changes including sleep hygiene and exercise should be sought, regardless of whether or not medications are used.

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 or consult your personal physician.

If you’ve ever felt sleep deprived, this article is for you. Fatigue is a common patient complaint, and there is a long list of maladies that may be responsible: sleep deprivation, infectious diseases (such as Lyme) and hypothyroidism (low thyroid functioning), to name a few.

We are going to focus on sleep deprivation, since it may impact our quality of life, influencing weight gain, disorders involving insulin resistance, kidney function and cognition, as well as chronic diseases, like diabetes. Even a short duration of inadequate sleep can have a surprising impact.

How much sleep do we need? Conventional wisdom has always been eight hours (Sleep. 1995;18:908). However, it varies depending on the individual. About 26% of Americans get eight or more hours of sleep per night (National Sleep Foundation, 2005). During the work week, approximately 30% of individuals in the U.S. get fewer than six hours of sleep.

The evidence suggests that, when you get to five hours or fewer per night, most people get into trouble.

Weight gain

In a recent, small prospective (forward-looking) study, results show that sleep deprivation results in weight-gain. Why is this? You actually burn more calories (about 5% more) when you sleep fewer hours, but you consume significantly more calories than you metabolize (Proc Natl Acad Sci USA. 2013;110:5695-5700). The individuals who were sleep-restricted gained about two pounds. That may not sound like much but the scary part is it occurred over a short time period — one work week, or five days.

Study participants were in a controlled setting, with half of them restricted to five hours of sleep and half of them permitted to sleep up to nine hours. Everyone was given access to ample amounts of food. Interestingly, not only did the amount of food consumed by those who were sleep deprived increase, but carbohydrate consumption became dominant. When participants who had been sleep deprived were transitioning toward adequate sleep in the second week, they began to make better food choices and started to lose weight.

In addition, researchers found that natural melatonin levels are altered by sleep deprivation, resulting in a change in our circadian rhythms or biological clocks that make it harder to fall asleep.

In another study, the results were similar (Sleep. 2013;36:981-990). This one involved 225 healthy participants. Those who were sleep restricted gained ironically about two pounds of weight over five days. Just like the previous study, participants were in a controlled laboratory where food was provided and their sleep monitored. In both studies, significant late night eating was common.

In a Nurses’ Health Study, results show that, for participants who regularly slept five hours or fewer, there was a 32% increased risk of gaining more than 30 pounds (Am. J. Epidemiol. 2006;164:947-954). This observational study involved approximately 68,000 women and was 16 years in duration.

Effects on aging

In a very small, but well-designed, randomized prospective study, adipocytes (fat cells) in sleep-deprived individuals became resistant or insensitive to ever-higher levels of insulin (Ann Intern Med. 2012;157:549-557). This may be a precursor to increased risk of weight gain and diabetes. The sleep-deprived participants were allowed four-and-a-half hours of sleep per night over a period of four days compared to the control group, which was allowed eight-and-a-half hours per night. The most surprising effect found was that the fat cells of sleep deprived individuals aged approximately two decades metabolically, so that participants in their 20s had fat cells that functioned similar to those in their 40s.

Diabetes

In the Millennium Cohort Study, participants with inadequate sleep were at significantly greater risk of developing type 2 diabetes than those with sufficient sleep (Diabetes Care Online. July 2013). In fact, participants who had five hours of sleep per night were at a 28% increased risk, and those who had fewer than five hours a night had a 52% greater risk. Adequate sleep was defined as at least seven hours. This was a prospective (forward-looking) observational study involving over 47,000 military personnel. The researchers brought up a good point: while sleep is on the decline, diabetes has been on the rise over the last three decades.

Cognition

Sleep deprivation’s impact on cognition may be immediate. In a study, healthy participants were subjected to sleep deprivation that resulted in decreased neurobehavorial functioning, or cognition, when compared to controls (Sleep. 2010;33:1013-1026). Those in the sleep-deprivation group were restricted for five days to four hours per night in bed, while those in the control group were allowed 10 hours per night. The sleep-deprived group was then allowed one night of 10 hours of sleep. While they recovered some neurobehavorial functioning, they didn’t reach their previous baseline levels. This study simulated the work week followed by one day of recovery. The study was an in-laboratory, well-controlled study involving 159 healthy participants.

In the Familial Adult Children Study (FACS), presented at the prestigious 64th Annual American Academy of Neurology Meeting, participants with poor quality sleep were more likely to have high levels of amyloid beta plaques (AAN Abstract 703). The significance of these plaques is that they may be precursors to Alzheimer’s disease. The researchers discovered that participants who woke five times in each hour of sleep had a substantially greater risk of developing amyloid beta plaques. Thus, those with lesser sleep efficiency were more likely to have preclinical Alzheimer’s disease. None of the patients showed any symptomatic cognitive deficits, only early preclinical signs of Alzheimer’s. This is a very preliminary study that requires further prospective and randomized clinical trials.

At this point, we can agree that sleep deprivation is something to be taken seriously. If you are fatigued, it may not be a bad idea to have your glucose (sugars) checked. Also, getting sufficient sleep may help slow the metabolic aging of your cells — and most of us want to forestall the aging process. As we age, cognition is a central issue. If we can decrease our risk of cognitive decline while aging, this is an ideal scenario. So, make sure you are getting good quality and quantity of sleep that fits your individual needs. It is not just an inconvenience to be tired, it actually affects your health.

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.

By David Dunaief, M.D.

COPD, or chronic obstructive pulmonary disease, is the third leading cause of mortality in the United States (Natl Vital Stat Rep. 2011 Dec.;59(10):1-126), 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 greater than 5% of the U.S. population (MMWR Morb Mortal Wkly Rep. 2012;61:938).

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 risk of and treat COPD exacerbations? The most important step is to stop smoking, since 80% 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 (N Engl J Med. 2002;346:988-994).

One of the underlying components of COPD may be chronic inflammation (www.goldcopd.org). 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).

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.

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 (JAMA. 2013;309:2353-2361). In other words, the risk of frequent exacerbation increased 20%, 70% and 270% 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% 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 interleukin-6 (IL-6) was elevated at the start of the trial in stable COPD patients, the risk of mortality increased by almost 2.7-fold (Respiratory Research. 2013;14:24). 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% reduction in the risk of COPD exacerbations, with the effect based on a dose-dependent curve (Am J Med. 2013 Jul;126:598-606). 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 RCT to confirm the results.

Exercise

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 (ATS 2013 International Conference: Abstract A1360). 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.

When exercising, we are told to vary our exercise routines on regular basis. One study demonstrates that this may be especially important for COPD patients (Am J Respir Crit Care Med. 2013; online Feb. 28). Results show that nonlinear periodization exercise training is better than traditional routines of endurance and resistance training in severe COPD patients. The goal of NLPE is to regularly alter the time spent working out, the number of sets, the number of repetitions and the intensity of the workout.

This study was randomized, involved 110 patients, and was three months in duration. Significantly more severe COPD patients achieved their exercise goals using NLPE 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.

Nonspecific inflammatory biomarkers are potentially valuable for providing 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.

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.

Age-related macular degeneration (AMD) remains the leading cause of central vision loss or severe visual impairment in patients over the age of 65 (Ophthalmology. 2008;115:116–126). In fact, advanced AMD is the cause of greater than half of severe vision impairment in the U.S. (Arch Ophthalmol. 2004;122:477-485). There are several stages of the disease: early-stage, or dry; intermediate; and advanced (either geographic atrophy or wet) AMD.

Fortunately, there are drugs that help treat the vision loss, and options are expanding. These involve vascular endothelial growth factors, including ranibizumab, off-label bevacizumab and the newest, aflibercept. There is also a combination drug therapy in development that may improve vision further; it involves the current medications, plus a potential new class, a platelet-derived growth factor (PDGF) inhibitor.

However, there is no cure for AMD. In fact, there is no treatment for the early, or dry, form of AMD. Therefore, identifying factors that may help decrease the risk of progression to advanced disease should be front and center. The goal of the Age-Related Eye Disease Study 2 (AREDS2) was just this – to reduce progression by identifying the optimal supplement formulation.

Just as important is identifying factors that may increase overall risk of developing AMD. We know that smoking, family history and age are contributing factors, and potentially iron (Am J Epidemiol. 2009;169:867-876). In addition, sunlight may play a role. Also, there have been three recent studies with conflicting results regarding aspirin’s potential to raise AMD risk.

Let’s look at the evidence.

Age-Related Eye Disease Study 2

The purpose of AREDS2 was to improve a multivitamin identified in the original AREDS study that illustrated a 25 percent reduction in progression from early-stage to advanced AMD. The multivitamin was composed of zinc, copper, beta-carotene and vitamins C and E, all considered to enhance antioxidant defenses.

AREDS2 researchers compared multiple formulations of the original AREDS multivitamin, adding omega-3 fatty acids — fish oil including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) — and/or lutein/zeaxanthin. They also compared variations with and without beta-carotene. In this randomized controlled trial (RCT), the gold standard of studies, the results with fish oil were disappointing (JAMA. 2013;309:2005-2015). There was no risk reduction — a stark contrast to an observational study I mentioned in my May 3, 2011 article. RCTs always trump observational trials.

AREDS2 showed a modest decrease in risk with lutein/zeaxanthin in a certain population. Beta-carotene deletion decreased the risk of lung cancer, mostly in previous smokers, but it did not affect progression to late AMD. It may also have had a role in preventing the absorption of lutein/zeaxanthin.

The lutein/zeaxanthin group saw an additional 5 percent reduction in risk in the group that had the lowest levels of these compounds from their diet at the trial’s start. Those patients who ate more foods with lutein and zeaxanthin, such as green, leafy vegetables and red, orange and yellow fruits and vegetables, did not see this small but significant beneficial effect. The reason may be that the patients eating a higher nutrient-dense diet already have sufficient levels of lutein and zeaxanthin. The duration of AREDS2 was five years and involved 4203 AMD patients between 50 to 85 years of age with the possibility of progression to advanced disease.

Aspirin effect conflicting

It is essential to discuss the role of aspirin, since approximately 20 percent of patients take this drug on a chronic basis (ahrq.gov). There are three recent studies: two were observational and one meta-analysis included observational studies. As I mentioned, observational studies are not the best types of studies.

In the Beaver Dam Eye Study, results showed there was a significant, yet small, increased risk of developing advanced, but not early-stage, AMD when taking aspirin (JAMA. 2012;308:2469-2478). The data can be subdivided even further: those with advanced AMD – neovascular (wet) and geographic atrophy groups – saw vastly different results, with increased risk for the former and decreased risk for the latter. Negative effects only occurred if patients had been taking aspirin for at least 10 years. Those at the five-year mark did not see a difference compared to nonusers. Chronic use was defined as at least two times weekly. Aspirin dosage did not have any impact.

In a second study, aspirin was associated with an increased risk of early AMD (Br J Ophthalmol. 2013 June;97:785-788). However, it became nonsignificant when patients with cardiovascular disease were factored into the mix. The authors concluded that there was no association, though caution and further study may be needed of patients who have cardiovascular disease and take aspirin, which make up a substantial number of aspirin users.

In the third and most recent study, a meta-analysis (group of 10 studies), there was no association between aspirin use and AMD. Risk levels were the same in early and advanced disease. The moral of the story is to speak with your doctor when considering taking aspirin if you have AMD.

Rosemary extract

On a more upbeat note, it seems that rosemary extract or oil plus zinc decreases the risk of developing retinal damage in rats that is similar to advanced AMD (Molecular Vision. 2013;19:1433-1445).Rats were exposed to damaging lights to try to induce detrimental effects. Zinc alone and rosemary alone were not nearly as effective as the combination. These two substances together decreased the damaging effects of the green light to the retina (back of the eye). Interestingly, the current AREDS multivitamin was not found to be as beneficial as the combination of zinc and rosemary. These are encouraging possibilities for a multivitamin of the future that prevents AMD progression.

We know that aspirin’s benefit outweighs its risk in cardiovascular disease; therefore, do not consider stopping aspirin until talking to your physician. Until well-designed RCTs are done, it is not clear that aspirin elevates AMD risk.

Unfortunately, the ideal formulation for a multivitamin to prevent AMD progression has not been perfected. The AREDS2 formulation with the addition of lutein/zeaxanthin and the deletion of beta-carotene is not commercially available yet. If you don’t have a smoking history, then taking the original AREDS multivitamin formulation is beneficial, plus lutein/zeaxanthin or foods containing these substances. However, if you do smoke, you may want to talk to your doctor about using the AREDS formulation that contains lutein instead of beta-carotene.

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 www.medicalcompassmd.com and/or consult your personal physician.

Hunger is only one reason we eat. There are many psychological and physiological factors that influence our eating behavior, including addictions, lack of sleep, stress, environment, hormones and others. This can make weight management or weight loss for the majority who are overweight or obese — approximately 70 percent of the U.S. population — very difficult to achieve (www.cdc.gov).

A June 29 New York Times article, entitled “Why Healthy Eaters Fall for Fries,” reported on the effect of posting food calories in New York City chain restaurants. Unfortunately, the results were mostly abysmal, with only a few exceptions; there was either no change or even an increase in calorie intake, when researchers examined customers receipts.

Does this mean we are doomed to acquiesce to temptation? Actually, no: It is not solely about willpower. Changing diet composition is more important.

What can be done to improve the situation? In my experience in my practice, increasing the quality of food has a tremendous impact. Foods that are the most micronutrient dense, such as plant-based foods, rather than those that are solely focused on macronutrient density, such as protein, carbohydrates and fats, tend to be the most satisfying. In a week to a few months, one of the first things patients notice is a significant reduction in their cravings. But don’t take my word for it. Let’s look at the evidence.

Effect of refined carbohydrates

By this point, many of us know that refined carbohydrates are not beneficial. Well, there is a new randomized controlled trial, the gold standard of studies, with results that show refined carbohydrates may cause food addiction (Am J Clin Nutr Online 2013;Jun 26). There are certain sections of the brain involved in cravings and reward that are affected by high glycemic (sugar) foods, as shown by MRI scans of participants.

The participants consumed a 500-calorie shake with either a high glycemic index or with a low glycemic index. The participants were blinded (unaware) to which type they were drinking. The ones who drank the high glycemic shake had higher levels of glucose in their blood initially, followed by a significant decline in glucose levels and increased hunger four hours later. In fact, the region of the brain that is related to addiction, the nucleus accumbens, showed a spike in activity with the high glycemic intake.

According to the authors, this effect may occur regardless of the number or quantity of calories consumed. Granted, this was a very small study, but it was well designed. High glycemic foods include carbohydrates, such as white flour, sugar and white potatoes. The conclusion: Everyone, but especially those trying to lose weight, should avoid refined carbohydrates. The composition of calories matters.

Comparing macronutrients

We tend to focus on macronutrients when looking at diets. These include protein, carbohydrates and fats, but are these the elements that have the most impact on weight loss? In a RCT, when comparing different macronutrient combinations, there was very little difference among groups, nor was there much success in helping obese patients reduce their weight (N Engl J Med 2009 Feb 26;360:859; N Engl J Med 2009 Feb 26; 360:923). In fact, only 15 percent of patients achieved a 10 percent reduction in weight after two years.

The four different macronutrient diet combinations involved an overall calorie restriction. In addition, each combination had either high protein, high fat; average protein, high fat; high protein, low fat; or low protein, low fat. Carbohydrates ranged from low to moderate (35 percent) in the first group to high (65 percent) in the last group. This was another relatively well-designed study, involving 811 participants with an average BMI of 33 kg/m2, which is defined as obesity (at least 30 kg/m2). Again, focusing primarily on macronutrient levels and calorie counts did very little to improve results.

Impact of obesity

In an epidemiological study looking at National Health and Nutrition Examination Survey data, results demonstrate that those who are overweight and obese tend to be lacking in micronutrients (Medscape General Medicine. 2006;8(4):59). The authors surmise that it may have to do with the change in metabolic activity associated with more fat tissue. These micronutrients include carotenoids, such as lutein, zeaxanthin, beta-carotene, alpha-carotene and beta-cryptoxanthin, as well as vitamin B12, folate and vitamins C, E and D.

However, it does not mean this population should take supplements to make up for the lack of micronutrients. Quite the contrary, micronutrients from supplements are not the same as those from foods. Overweight and obese patients may need some supplements, but first find out if your levels are low, and then see if changing your diet might raise these levels. With a few exceptions, such as vitamin D and potentially B12, most micronutrient levels can be raised without supplementation. Please ask your doctor.

Steroid levels

It may seem like there are numerous factors influencing weight loss, but the good news is that once people lose the weight, they may be able to continue to keep the weight off. In a recent prospective (forward-looking) study, results show that once obese patients lose the weight, the levels of cortisol metabolite excretion decreases significantly (Clin Endocrinol. 2013;78(5):700-705).

Why is this important? Cortisol is a glucocorticoid, which means it raises the level of glucose and is involved in mediating visceral or belly fat. This type of fat has been thought to coat internal organs, such as the liver, and result in nonalcoholic fatty liver disease. To learn more about this, please read my May 2 article. Decreasing the level of cortisol metabolite may also result in a lower propensity toward insulin resistance and may decrease the risk of cardiovascular mortality. This is an encouraging preliminary, yet small, study involving women.

Therefore, controlling or losing weight is not solely about willpower. Don’t use the calories on a menu as your sole criteria to determine what to eat; even if you choose lower calories, it may not get you to your goal. While calories may have an impact, the nutrient density of the food may be more important. Thus, those foods high in micronutrients may also play a significant role in reducing cravings, ultimately helping to manage weight.

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.

While obesity has been thought of as a chronic disease by some, until recently, it was not officially recognized as such. Obesity impairs body function, with potentially negative impacts on physical activity and psychological well-being. It lines internal organs with fat, putting stress on the body; fat tissue may cause dysfunctional cell-signaling, potentially increasing inflammation in the body (Front Endocrinol (Lausanne). 2013 Jun 12;4:71).

The American Medical Association has taken an important step forward, declaring obesity a disease, unto itself. Obesity’s prevalence in the U.S. has increased by more than two-fold in the last two decades (JAMA 2010, 303(3):235-24). More than one-third of Americans are obese, defined as a body mass index of great than 30 kg/m2, according to the CDC.

The AMA’s move is a wake-up call that should be taken very seriously. They recognize that the first step to reversing this trend is increasing awareness among the medical community of its independent detrimental effects. This decision may impact government policy, medical reimbursement rates, and the social stigma patients have to withstand.

Unfortunately, obesity is also associated with many other chronic diseases. Integrative medicine physician Mark Hyman, M.D. entitled his book “Diabesity” to emphasize the association between diabetes and obesity. Other diseases associated with obesity include rheumatoid arthritis, cardiovascular disease, nonalcoholic fatty liver disease, osteoarthritis, and infection. I will discuss the RA association in more detail, since obesity was shown to potentially affect RA treatment.

Obesity treatment options include surgery, medications and lifestyle modifications. While it’s important for obese patients to lose weight, we have to be conscious about the way we do this. The drug Fen-phen, for instance, caused pulmonary hypertension and valvular heart disease. Surgery can potentially result in side effects, such as dumping syndrome and malabsorption. Even lifestyle modifications, including exercise and diet, need to be evaluated.

New launching of weight-loss drug

There are now two drugs approved by the FDA for weight-loss: Qsymia (phentermine hydrochloride/topiramate) and Belviq (lorcaserin). Both drugs have extensive side effects. Belviq was just recently launched in the United States (Medscape.com); however, it has not been approved by the European Union for fear of side effects, including tumors, disease of the heart valves and depression. It was also rejected by the FDA the first time because of its side-effect profile.

Effect on rheumatoid arthritis

On June 27 I wrote an article about RA, so I thought it appropriate to write about how RA is intertwined with obesity. A recent study found that greater than 50 percent of women who have RA are also obese (Arthritis Care Res (Hoboken). 2013;65(1):71-7). This was a cohort (those with disease compared to those without) study, involving over 1,400 participants. The reasons for this association may be underlying inflammation, greater amounts of estrogen or vitamin D deficiency. Obese men and women had a 24 percent increased risk of developing RA. The researchers are worried, since the prevalence of obesity in the general population continues to rise. This is not good news on the whole; women are more likely than men to develop RA, in general, according to a separate study (Ann Rheum Dis. 2007;66:1491-1496).

Obesity results in less robust outcomes when it comes to RA treatment. In an abstract presented at the European League Against Rheumatism Congress 2013, those who were obese had a two-fold greater risk of being on TNF (tumor necrosis factor) alpha inhibitors, compared to those who were of normal weight (BMI <25 kg/m2) (EULAR Congress 2013 Abstract OP0178). The researchers treated 346 RA patients with methotrexate plus or minus prednisone, but if they did not respond sufficiently, a TNF alpha inhibitor was added.

This occurred significantly more frequently with obese patients. Those who were obese had a less-than-ideal response to methotrexate plus or minus prednisone at a rate that was more than two times greater at 12 months than those of normal weight. Again, inflammation was postulated as the potential cause of poor response to the initial treatment in obese patients.

In yet another study, obese patients’ response to TNF alpha inhibitors was less robust compared to those who were not obese (Arthritis Care Res (Hoboken). 2013 Jan;65(1):94-100). At the end of the first year, remission rates of RA in obese patients were less than half those of normal patients. However, when the researchers analyzed the individual TNF alpha inhibitors, only Remicade’s (infliximab) poor response reached statistical significance, while the others were trending toward significance. This study involved 641 patients, but only 66 who were obese.

Let’s recap: patients with a history of obesity are twice as likely to develop RA and require TNF alpha inhibitors, but the effectiveness of these TNF inhibitors is reduced for them.

Lifestyle modifications

Lifestyle changes are critical to treating obesity; however, not all lifestyle modifications, including diet and exercise, are created equal. A recent study showed that those on a very low-calorie diet, or “crash diet,” were three times more likely to develop gallstones than those on a low-calorie diet (Int J Obes (Lond). Online 2013;May 22). The participants on the very low-calorie approach consumed liquid meals for 6 to 10 weeks, ingesting 500 calories per day, and then switched to a maintenance diet. The low-calorie group consumed liquid meals and solid foods totaling 1,200 to 1,500 calories per day for 12 weeks and then switched to a maintenance diet.

The reason for increased gallstones may be the impact of a very low-calorie diet on the bile’s composition and the gallbladder’s ability to discharge it. There were over 6,000 participants involved in the study. Thus, losing weight too rapidly is probably not the best approach.

In my experience, a high-nutrient, plant-based diet is one effective method for losing weight. I wrote about the quality of calories consumed, mindful eating and exercise in two articles published on Aug. 2, 2012 and April 30, 2013. I encourage you to read them, if you want to learn more about this topic.

Whether or not you agree with the AMA’s decision to elevate obesity to a chronic disease, it needs to be treated. Lifestyle modifications should be included in every paradigm, regardless of whether surgery or drugs are used as well. Some people may benefit from drug therapy, and some may benefit from surgery, but all will benefit from appropriate lifestyle modifications.

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 or consult your personal physician.

Rheumatoid arthritis is a complicated autoimmune disease to manage, especially in the more advanced stages. It is important that we stay abreast of the latest research, since RA is becoming more common (Arthritis Rheum. 2010 June;62(6):1576-1582). Recently, the prestigious European League Against Rheumatism (EULAR) Congress 2013 had its annual conference, so I thought it appropriate to discuss some of the findings. Most of the data is in abstract form and considered preliminary until the papers are fully published.

RA can be one of the most disabling diseases, with symptoms such as morning stiffness, diffuse joint pain and swelling that can affect multiple joints, with the proximal joints in the hands, wrists and feet most commonly affected bilaterally (Lancet. 2001;358(9285):903-911). It is not uncommon for RA patients also to be depressed, which can take its toll on productivity.

Treatment options

Medications used to treat RA involve disease-modifying antirheumatic drugs. One of the most common drugs used is methotrexate, which is frequently combined with tumor necrosis factors alpha inhibitors, such as Remicade (infliximab), Enbrel (etanercept), Humira (adalimumab) and other DMARDs. We will discuss the benefits and drawbacks of TNF inhibitors, which have anti-inflammatory effects, but also suppress the immune system.

The goal of these drugs is to reduce synovitis, or inflammation in the joints, helping to lessen joint damage. They can be quite effective. Unfortunately, compliance can be an issue. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also used for treatment, however, they should not be combined with methotrexate or at least caution should be advised when doing so.

Lifestyle modifications may also play a role in ameliorating RA, including helping with fall risk.

Compliance

Even though there are a number of drug therapy options, compliance is an issue. In a recent study, approximately 33 percent of patients stopped or switched their RA medication within the first year, and by year two, the number increased to approximately half of patients (EULAR, Abstract OP0064). Patients on TNF inhibitors discontinued slightly less.

The main reason for discontinuation was a perceived lack of drug effectiveness, followed by side effects and therapy preferences. For those on TNF inhibitors, adverse reactions or safety were the main concerns. The greater the symptoms and progression of the disease, and the higher the psychological toll of the disease, such as depression and anxiety, the higher the probability that medication would be discontinued.

There were over 6,000 RA patients involved in this study, with disease duration averaging 11 years. The researchers used the Consortium of Rheumatology Researchers of North America registry to make this assessment.

FDA warning

Why might side effects be a concern for TNF inhibitors? In 2011, the FDA found there were 100 cases of Listeria and Legionella pneumonia infections associated with these drugs. Therefore, a warning was placed on all TNF inhibitors. The median duration that patients were on the drugs when they experienced infections was about 10 months. However, most patients were also on methotrexate and steroids at the time of infection.

While there were infections that took place during these drugs’ clinical trials, the absolute number was small. There was a large, though retrospective, study suggesting that the risk of serious infections requiring hospitalization is not greater than with other RA medications (JAMA. 2011;306:2331-2339).

Head-to-head trial of DMARDs or biologics

There was a recent head-to-head, blinded, randomized controlled trial, called the AMPLE trial, comparing two different types of DMARDs, Humira (adalimumab), a TNF inhibitor, and Orencia (abatacept), a non-TNF inhibitor (EULAR: Abstract OP0044). Both medications showed equivalent results in RA and are popular therapies for patients who have moderate to severe disease. Radiographic tests showed no joint damage progression in 85 percent of patients. However, there were fewer side effects with Orencia. Why is this important? Because if a patient can’t tolerate one drug, or if it does not work for them, then they can be confident that there are other, equally effective, options. This trial was two years in duration and involved 643 patients.

Depression

In one study, results showed that patients with early RA were more likely to apply for disability and subsequent early retirement due to depression than from symptoms of the disease, the level of work stress, other disease in combination with RA or the perceived effectiveness of drug therapy (EULAR: Abstract OP0092). Within the first year of being diagnosed with RA, depression outweighed other factors as a reason for disability by more than threefold.

The authors suggest that a questionnaire could help identify depressed patients so they could be treated appropriately, potentially preventing disability and early retirement. There were 563 patients involved in this study.

Falls

In a recent study involving 535 patients, results showed that RA patients have a greater probability of repeat falls (Arthritis Care Res. Online 2013 Feb. 22). This may not be surprising, considering the symptoms of joint stiffness, pain and swelling. The greatest predictor of future falls was a fall history. Therefore, patients with RA need to be asked about their tendency to fall. After the first fall, patients were three times as likely to fall again. Though history of fall was most valuable, symptoms of the disease, such as swollen joints and pain were also important. Interestingly, medications for treating depression contribute to fall risk. As we mentioned, RA patients have a higher tendency to be depressed. So what can be done to reduce fall risk? Lifestyle modifications with tai chi may be one option.

Lifestyle modifications

Lifestyle modifications include tai chi, diet, fish oil and aerobic exercise. I wrote about fish oil and aerobic exercise in my April 19, 2012, article entitled, “Rheumatoid arthritis effective management options.”

There was an extensive systematic review of the literature, which demonstrated that tai chi may have a role in reducing the risk of falls in RA by strengthening muscles and increasing flexibility (Br J Sports Med. 2012 Aug.;46(10):713-718). Unfortunately, tai chi did not have any effect on RA patients’ symptoms.

Since rheumatoid arthritis can be such a debilitating disease, both physically and mentally, it requires a significant partnership by the patient and doctor to treat it with medication and lifestyle modifications.

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 consult your personal physician.

Heart attacks and heart disease get a lot of attention, but chronic heart failure is something that tends to be overlooked by the press. Heart failure occurs in about 20 percent of the population over the age of 40 (Circulation. 2002;106(24):3068). There are about 5.8 million Americans with HF (Circulation. 2010;121(7):e46). Not surprisingly, incidence of heart failure increases with age (J Am Coll Cardiol. 2003;41(2):21).

Heart failure occurs when the heart’s pumping is not able to keep up with the body’s demands and may decompensate. It is a complicated topic, for there are two types, systolic heart failure and diastolic heart failure. The basic difference is that the ejection fraction (output of blood with each contraction of the left ventricle of the heart) is more or less preserved in diastolic HF, while it can be significantly reduced in systolic HF.

We have more evidence-based medicine, or medical research, on systolic heart failure. Fortunately, both types can be diagnosed with the help of an echocardiogram, an ultrasound of the heart. The signs and symptoms may be similar, as well, and include shortness of breath on exertion or when lying down; edema or swelling; reduced exercise tolerance; weakness and fatigue. The risk factors for heart failure include diabetes, coronary artery disease, high blood pressure, obesity, smoking, heart attacks and valvular disease.

Typically, heart failure is treated with blood pressure medications, such as beta blockers, ACE inhibitors and angiotensin receptor blockers.

We are going to look at how diet, iron and the supplement CoQ10 impact heart failure.

Effect of diet

If we look beyond the usual risk factors mentioned above, oxidative stress may play an important role as a contributor to HF. Oxidative stress is thought to potentially result in damage to the inner lining of the blood vessels, or endothelium, oxidation of cholesterol molecules, and a decrease in nitric oxide, which helps vasodilate blood vessels.

In a newly published population-based, prospective (forward-looking) study, called the Swedish Mammography Cohort, results show that a diet rich in antioxidants reduces the risk of developing HF (Am J Med. 2013 Jun:126(6):494-500) In the group that consumed the most nutrient-dense foods, there was a significant 42 percent (p<0.001) reduction in the development of HF, compared to the group that consumed the least. According to the authors, the antioxidants were derived mainly from fruits, vegetables, whole grains, coffee and chocolate. Fruits and vegetables were responsible for the majority of the effect.

This nutrient-dense approach to diet increased oxygen radical absorption capacity. Oxygen radicals have been implicated in cellular damage and DNA damage, potentially as a result of increasing chronic inflammation. What makes this study so impressive is that it is the first of its kind to investigate antioxidants from the diet and their impacts on heart failure prevention. This was a large study, involving 33,713 women, with good duration — follow-up was 11.3 years. There are limitations to this study, since it is an observational study, and the population involved only women. Still, the results are very exciting, and it is unlikely there is a downside to applying this approach to the population at large.

CoQ10 supplementation

Coenzyme Q 10 is a substance produced by the body that helps the mitochondria (the powerhouse of the cell) produce energy. It is thought of as an antioxidant. In a meta-analysis (group of 13 studies), the results showed that supplementation with CoQ10 may help improve functioning in patients with heart failure (Am J Clin Nutr. 2013 Feb;97(2):268-75). This may occur because of a modest rise in ejection fraction functioning. It seems to be important in systolic heart failure. Supplementation with CoQ10 may help to reduce its severity.

The doses used in the meta-analysis ranged from 60 mg to 300 mg. Interestingly, those that were less than or equal to 100 mg showed statistical significance, while higher doses did not reach statistical significance. This CoQ10 meta-analysis was small. It covered 13 studies and fewer than 300 patients.

Like some other supplements, CoQ10 has potential benefits, but more study is needed. Because there are no studies showing significant deleterious effects, which doesn’t mean there won’t be, it is worth starting HF patients with comprised ejection fractions on 100 mg CoQ10 and titrating up, as long as patients can tolerate it.

Preliminary results of the new Q-SYMBIO study showed an almost 50 percent reduction in the risk of all-cause mortality and 50 percent fewer cardiac events with CoQ10 supplementation. This one randomized controlled trial followed 420 patients for two years who had severe heart failure.

The lead author goes as far as to suggest that CoQ10 should be part of the paradigm of treatment. He may be a bit enthusiastic, but this is the first new “drug” in over a decade to show survival benefits. The caveat is that these results were only recently presented at the prestigious Heart Failure 2013 Congress May 25 to 28, and they still need to be published in a peer-reviewed journal.

Iron Deficiency

Anemia and iron deficiency are not synonymous, since iron deficiency can occur without anemia. A recent observational study that followed 753 heart failure patients for almost two years showed that iron deficiency without anemia increased the risk of mortality in heart failure patients by 42 percent (Am Heart J. 2013;165(4):575-582).

In this study, iron deficiency was defined as a ferritin level less than 100 ug/L (the storage of iron) or, alternately, transferrin saturation less than 20 percent (the transport of iron) with a ferritin level in the range 100-299 ug/L.

The authors conclude that iron deficiency is potentially more predictive of clinical outcomes than anemia, contributes to the severity of HF, and is common in these patients.

Thus, it behooves us to try to prevent heart failure through dietary changes, including high levels of antioxidants, because it is not easy to reverse the disease. Those with HF should have their ferritin levels checked, for these are correctable. I am not typically a supplement advocate; however, based on the latest results, CoQ10 seems like a compelling therapy to reduce risk of further complications and potentially death. Consult with your doctor before taking CoQ10 or any other supplements, especially if you have heart failure.

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 or consult your personal physician.