Authors Posts by David Dunaief

David Dunaief

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Significant improvements were seen in one month with lifestyle modifications

Chronic kidney disease is on the rise in this country. In a study that looked at data from the National Health and Nutrition Examination Survey, prevalence of chronic kidney disease (CKD) increased more than 30 percent from 1988 to 2004 (JAMA. 2007;298:2038-2047). Early-stage (mild) CKD is no exception and may not be getting enough attention. In this article, we will look beyond the more obvious causes of mild chronic kidney disease, such as diabetes, smoking, aging, obesity and high blood pressure (JAMA. 2004;291:844-850).

Why is early-stage CKD so important? It is associated with a 40 percent increased risk of developing cardiovascular events, such as heart attacks (N Engl J Med. 2004;351:1296-1305). It also significantly increases the risk of peripheral artery disease (PAD). Those with decreased kidney function have a 24 percent prevalence of PAD, compared to 3.7 percent in those with normal kidney function (Circulation. 2004;109:320–323). Of course, it can lead ultimately to end-stage renal (kidney) disease, requiring dialysis and potentially a kidney transplant.

One of the problems with early-stage CKD is that it tends to be asymptomatic. However, there are simple tests, such as a basic metabolic panel and a urinalysis, that will indicate whether a patient may have mild chronic kidney disease. These indices for kidney function include an estimated glomerular filtration rate (eGFR), creatinine level and protein in the urine. While the other two indices have varying ranges depending on the laboratory used, a patient with an eGFR of 30 to 59 mL/minute/1.73 m2 is considered to have mild disease. The eGFR and the kidney function are inversely related, meaning as eGFR declines, the more severe the chronic kidney disease.

What can be done to stem early-stage CKD, before complications occur? There are several studies that have looked at medications and lifestyle modifications and their impacts on its prevention, treatment and reversal.

Let’s look at the evidence.

 

Medications

Allopurinol is usually thought of as a medication for the prevention of gout. However, in a randomized controlled trial, the gold standard of studies, the results show that allopurinol may help to slow the progression of CKD, defined in this study as an eGFR less than 60 mL/min/1.73 m2 (Clin J Am Soc Nephrol. 2010 Aug;5:1388-1393). The group using 100 mg of allopurinol showed significant improvement in eGFR levels (a 1.3 mL/minute per 1.73 m2 increase) compared to the control group (a 3.3 mL/minute per 1.73 m2 decrease) over a two-year period. There were 113 patients involved in this study. The researchers concluded that there was a slow progression of CKD with allopurinol. Allopurinol also decreased cardiovascular risk by 71 percent.

Fibrates are a class of drug usually used to boost HDL (“good”) cholesterol levels and reduce triglyceride levels, another cholesterol marker. Fibrates have gotten negative press recently for not showing improvement in cardiovascular outcomes. However, in patients with mild to moderate CKD, a meta-analysis (a group of 10 studies) recently showed a 30 percent reduction in major cardiovascular events and a 40 percent reduction in the risk of cardiovascular mortality with the use of fibrates (J Am Coll Cardiol. 2012 Nov. 13;60:2061-2071). This is important, since patients with CKD are mostly likely to die of cardiovascular disease.

The authors concluded that fibrates seem to have a much more powerful beneficial effect in CKD patients, as opposed to the general population. So, there may be a role for fibrates after all.

 

Lifestyle modifications

Fruits and vegetables may play a role in helping patients with CKD. In a recent study, the results showed that fruits and vegetables work as well as sodium bicarbonate in improving kidney function by reducing metabolic acidosis levels (Clin J Am Soc Nephrol. 2013;8:371-381).

What is the significance of metabolic acidosis? It means that body fluids become acidic and it is associated with chronic kidney disease. The authors concluded that both sodium bicarbonate and a diet including fruits and vegetables were renoprotective, helping to protect the kidneys from further damage in patients with CKD. Alkali diets are primarily plant-based, although not necessarily vegetarian or vegan-based diets. Animal products tend to cause an acidic environment. The study was one year in duration, however, though the results were impressive, the study was small, with 77 patients.

Sodium rears its ugly head yet again. Red meat is not thought of positively, and animal fat is not far behind. In the Nurses’ Health Study, the results show that animal fat, red meat and salt all negatively impact kidney function (Clin J Am Soc Nephrol. 2010; 5:836-843). The risk of protein in the urine, a potential indicator of CKD, increased by 72 percent in those participants who consumed the highest amounts of animal fat compared to the lowest, and by 51 percent in those who ate red meat at least twice a week. With higher amounts of sodium, there was a 52 percent increased risk of having lower levels of eGFR.

The most interesting part with sodium was that the difference between higher mean consumption and the lower mean consumption was not that large, 2.4 grams compared to 1.7 grams. In other words, the difference between approximately a teaspoon of sodium and three quarters of a teaspoon was responsible for the decrease in kidney function.

In my practice, when CKD patients follow a vegetable-rich, nutrient-dense diet, there are substantial improvements in kidney functioning. For instance, for a recent patient, his baseline eGFR was 54 mL/min/1.73 m2. After one month of lifestyle modifications, his eGFR improved by 9 points to 63 mL/min/1.73 m2, which is a return to “normal” functioning of the kidney. However, this is an anecdotal story and not a study.

Therefore, it is important to have your kidney function checked with mainstream tests. If the levels are low, we should address the issue through medications and/or lifestyle modifications to manage and reverse early-stage CKD. However, lifestyle modifications don’t have the negative side effects of medications. Don’t wait until symptoms and complications occur. In my experience, it is much easier to treat and reverse a disease in its earlier stages, and CKD is no exception.

 

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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Associating calories with exercise expenditures results in better choices

When we think of losing weight, calories are usually the first thing that comes to mind. We know that the more calories we consume, the greater our risk of becoming overweight or obese and developing many chronic diseases, including top killers such as heart disease, diabetes and cancer. Despite this awareness, obesity and chronic diseases are on the rise according to the Centers for Disease Control.

How can this be the case? I am usually focused on the quality of foods, rather than calories, and I will delve into this area as well, but we suffer from misconceptions and lack of awareness when it comes to calories. The minefield of calories needs to be placed in context. In this article, we will put calories into context, as they relate to exercise, and help to elucidate the effects of mindful and distracted eating.

Let’s look at the studies.

 

Impact of energy expenditure

One of the most common misconceptions is that if we exercise, we can be more lax with what we are eating. But researchers in a recent study found that this was not the case (J Exp Biol. 2013; Abstract 367.2). The results showed that when menu items were associated with exercise expenditures, consumers tended to make better choices and ultimately eat fewer calories. In other words, including the amount of exercise needed to burn calories was paired on the menu with food options, resulting in a significant reduction in overall consumption. The example that the authors gave was that of a four-ounce cheeseburger, which required that women walk with alacrity for two hours in order to burn off the calories.

Those study participants who had menus and exercise expenditure data provided simultaneously, compared to those who did not have the exercise data, chose items that resulted in a reduction of approximately 140 calories, 763 versus 902 kcals.

Even more interestingly, study participants not only picked lower calorie items, but they ate less of those items. Although this was a small preliminary study, the results were quite impactful. The effect is that calories become a conscious decision rooted in context, rather than an abstract choice.

 

The importance of mindful eating

Most of like to think we are multitaskers. However, when eating, multitasking may be a hazard. In a meta-analysis (a group of 24 studies), researchers found that when participants were distracted while eating, they consumed significantly more calories immediately during this time period, regardless of dietary constraints (Am J Clin Nutr. 2013 April;97:728-742).

This distracted eating also had an impact on subsequent meals, increasing the amount of food eaten at a later time period, while attentive eating reduced calories eaten in subsequent meals by approximately 10 percent. Distracted eating resulted in greater than 25 percent more calories consumed for the day. When participants were cognizant of the amount of food they were consuming, and when they later summoned memories of their previous eating, there was a vast improvement in this process.

The authors concluded that reducing distracted eating may be a method to help in both weight loss and weight management, providing an approach that does not necessitate calorie counting. These results are encouraging, since calorie counting frustrates many who are watching their weight over the long term.

 

The perils of eating out

Most of us eat out at least once in a while. In many cultures, it is a way to socialize. However, as much as we would like to control what goes into our food, we lose that control when eating out. In a study that focused on children, the results showed that when they ate out, they consumed more calories, especially from fats and sugars (JAMA Pediatr. 2013;167:14-20). Of the 9,000 teenagers involved in the study, between 24 percent and 42 percent had gone to a fast food establishment and 7 to 18 percent had eaten in sit-down restaurants when asked about 24-hour recall of their diets on two separate occasions.

Researchers calculated that this resulted in increases of 310 calories and 267 calories from fast food and sit-down restaurants, respectively. This is not to say we shouldn’t eat out or that children should not eat out, but that we should have more awareness of the impact of our food choices. For example, the Bloomberg administration has required calories be displayed in many New York City chain restaurants.

 

Quality of calories

It is important to be aware of the calories we are consuming, not only from the quantitative perspective, but also from a perspective that includes the quality of those calories. In another study involving children, the results showed that those offered vegetables for snacks during the time that they were watching television needed significantly fewer calories to become satiated than when given potato chips (Pediatrics. 2013;131:22-29). The authors commented that this was true for overweight and obese children as well, however, they were more likely to be offered unhealthy snacks, like potato chips.

In a paper published in JAMA in June 2012, the authors state that we should not restrict one type of nutrient over another, but rather focus on quality of nutrients consumed (JAMA 2012; 307:2627-2634).

In my practice, I find that when my patients follow a vegetable-rich, nutrient-dense diet, one of the wonderful “side effects” they experience is a reduction or complete suppression of food cravings. As far as mindless eating goes, I suggest if you are going to snack while working, watching TV or doing some other activity, then snack on a nutrient-dense, low-calorie food, such as carrots or blackberries. If you don’t remember how many vegetables or berries that you ate, you can take heart in knowing it’s beneficial. It can also be helpful to keep a log of what you’ve eaten for the day, to increase your cognizance of distracted eating.

Therefore, rather than counting calories and becoming frustrated by the process, be aware of the impact of your food choices. Why not get the most benefit out of lifestyle modifications with the least amount of effort? Rather than having to exercise more to try to compensate, if you actively choose nutrient-dense, low-calorie foods, the goal of maintaining or losing weight, as well as preventing or potentially reversing chronic diseases, becomes attainable through a much less painful and laborious process.

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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Two studies provide seemingly conflicting information on heart disease

L-carnitine, or carnitine, has been around for a while. The people most familiar with it may be athletes, because for years it has been touted as possibly providing more energy, though the research has not borne out on this topic.

What is L-carnitine and why is it of interest? It is derived from amino acids and most healthy individuals can get sufficient amounts regardless of their type of diet. Carnitine helps in the production of energy in the cell. It is involved in bringing long-chain fatty acids to the mitochondria — “the powerhouse” of the cell — which are then utilized for energy through oxidation. It also keeps potential waste from accumulating in the mitochondria so it performs more efficiently. Thus, it may have antioxidant properties (ods.od.nih.gov/factsheets).

So why is all of this important? L-carnitine may play a role in several chronic diseases, such as heart disease, type 2 diabetes, high blood pressure and even fatty liver disease.

Let’s look at the evidence.

 

Heart disease

There are two studies with conflicting results on heart disease. In one study, the results are negative, while the other study shows beneficial results. How could that be the case?

In the first study, L-carnitine appears to increase the risk of heart disease through the development of atherosclerosis, or plaque deposits, in the arteries (Nat Med Online. 2013 April 7). L-carnitine is found in foods such as red meat. In this study, mice and healthy human volunteers who regularly ate red meat were observed. Interestingly, the bacteria in the gastrointestinal tract, or gut, in those who consumed red meat were such that L-carnitine was broken down into a metabolite called trimethylamine-N-oxide (TMAO).

This metabolite was then found to increase cholesterol deposits in the arterial walls of mice. In other words, TMAO may promote the development of atherosclerosis. In humans, there was a predicted elevated risk of developing cardiovascular disease and cardiac events, such as heart attacks, strokes and death after three years, but like the mice, only in those that had elevated TMAO levels.

Also of interest, the researchers demonstrated that vegetarians and vegans, when given carnitine supplements, did not produce TMAO. Thus, TMAO production may have to do with microbes that populate the gut of those who consume red meat. This is a preliminary study, mind you, but it makes you wonder if it is the carnitine or the red meat that may be promoting the development of TMAO and the potential for increased atherosclerosis. Carnitine by itself did not cause increased risk of heart disease, but rather the metabolite TMAO did.

In the second study, a meta-analysis (a group of studies) showed those patients given L-carnitine supplements after a heart attack had a statistically significant reduced risk of death from all-causes by 22 percent in 11 trials, ventricular arrhythmias by 65 percent in five trials and chest pain (angina) by 40 percent in two trials (Mayo Clin Proc Online. 2013 April 15).

These were randomized controlled trials (RCTs), the gold standard of studies. The benefits may have been derived from containing the amount of infarct, or dead tissue, in the heart, as well as by increasing the amount of energy in cardiomyocytes (the muscle cells of the heart). In some of the studies, L-carnitine supplements were given for as long as six to 12 months.

Thus, the authors concluded that L-carnitine may be important for those suffering a heart attack, but also in the secondary prevention of a recurrent heart attack. The authors postulated that the mechanism by which L-carnitine derived its beneficial effects was through the improvement in glucose (sugar) utilization in the mitochondria. However, even though it was a meta-analysis, the population size was not large. According to the authors, the patients who might be candidates for carnitine supplementation are those who have had a heart attack and can’t take beta blockers or ACE inhibitors.

 

Type 2 diabetes

In a meta-analysis (a group of four studies), those given L-carnitine saw an improvement in parameters associated with type 2 diabetes (Exp Clin Endocrinol Diabetes Online. 2013 Feb. 2). There was a significant decrease in fasting glucose (sugar) levels of 14.3 mg/dL and in LDL “bad” cholesterol levels of 8.8 mg/dL. The patients who received L-carnitine were those who were deficient. These studies were RCTs, though they were not large in size.

 

Role in high blood pressure

In a study involving rats, the results ultimately showed that L-carnitine reduced oxidative stress on the kidneys and helped reverse hypertension-induced kidney damage (Eur J Nutr Online. 2012 Dec. 6). The impact is most likely from the downregulation, or decrease, in inflammatory factors, such as NF-kB, and the upregulation of anti-inflammatory factors, such as NRF2 and PPAR alpha. Thus, L-carnitine may have antioxidant properties that help protect the kidney against damage produced by high blood pressure. These results are exciting, but they are preclinical, or animal-based, and need studies in humans to confirm the results.

 

Fatty liver disease

As I discussed in last week’s article, fatty liver is a pervasive disease that is benign most of the time, but not always. In a RCT, L-carnitine reduced the liver enzymes significantly (Am J Gastroenterol. 2010;105:1338-1345). These patients had the complication of hepatitis, which was induced by non-alcoholic fatty liver disease. So these were patients on a potentially dangerous road to cirrhosis and, ultimately, to hepatocellular carcinoma (cancer of the liver). In 24 weeks, L-carnitine supplementation not only decreased the liver enzymes, but also cholesterol, glucose and insulin levels. Thus, as the authors concluded, L-carnitine supplementation seemed to improve the overall liver functioning in patients with complications of fatty liver disease.

Though these studies are early or small and more study is warranted, this may be a valuable substance. Thus, it may be worth having your L-carnitine blood levels checked if you have a chronic disease where there might be a deficiency, such as in type 2 diabetes. Check with your physician first, but patients could take L-carnitine supplements if their levels were low or for a protective effect. In cases of heart attacks, high blood pressure and fatty liver disease, carnitine supplementation may decrease organ damage, regardless of your levels.

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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The disease is much more common than you might expect; lifestyle modifications help

When we think of the most prevalent chronic diseases, heart disease, stroke, cancer, diabetes and others come to mind. However, there is also a chronic liver disease — nonalcoholic fatty liver disease — a conglomeration of fats, including triglycerides.

The problem with this disease is that it could lead to nonalcoholic steatohepatitis (fatty liver hepatitis), fibrosis (too much connective tissue due to repair) and eventually cirrhosis, which might ultimately result in cancer (hepatocellular carcinoma).

Fortunately, the risk of going down this dangerous path is relatively small. Most of the time, it remains a mild fatty liver disease.

Although it is rare, a study presentation in 2012 at the American Association for the Study of Liver Diseases suggested that NAFLD was the third most common risk for hepatocellular carcinoma behind infection and alcohol abuse (AASLD. 2012 Nov. 11; Abstract 97). Some study patients with hepatocellular carcinoma progressed to this level without first having cirrhosis. Those patients who developed liver cancer but did not have cirrhosis were more likely to have diabetes, obesity, high blood pressure and/or a high cholesterol profile. NAFLD occurs more frequently in males than females, and it needs to be taken very seriously.

The prevalence of NAFLD, which is benign in most cases, is relatively high, with estimates ranging from 10 to 46 percent (Gastroenterology. 2011; 140:124-131). In fact, a recent study shows that adolescents between the ages of 12 and 18 have seen a threefold increase in NAFLD, from 3.3 percent to almost 10 percent, in the last 20 years, according to data from the National Health and Nutrition Examination Survey (DDW. 2012 May 18; Abstract 705). This correlated primarily with obesity, but the rise outstrips the rate of increase in obesity in this adolescent population.

 

How is it diagnosed?

When liver enzymes are elevated, usually two to five times normal, then it tends to be more commonly diagnosed (Hepatology. 2003; 37:1286-1292). These liver enzymes include aspartate aminotransferase and alanine aminotransferase. What makes this disease diagnosis more difficult is that patients without elevated liver enzymes may have the disease and, in most cases, they have no symptoms.

The gold standard of diagnosis is through a liver biopsy, though this is invasive and thus has its dangers. Another method is through ultrasound, a first-line diagnosis method. Ultrasound is 60 to 94 percent sensitive and 66 to 95 percent specific (J Hepatol. 2009; 51:433–445). Though it is not the most accurate, it has the fewest side effects. Ultrasound is also technician-dependent in terms of grading the amount of fatty infiltrates in the liver — mild, moderate and severe. Unfortunately, the milder the amount of fatty infiltrates, the less accurate the reading. Other methods for diagnosis include transient elastography, computed tomography and magnetic resonance.

 

What might be the cause?

What is the potential cause? One theory is that intraperitoneal fat (visceral fat or central obesity) infiltrates the liver through the portal vein, resulting in insulin resistance and fatty liver (Arterioscler Thromb Vasc Biol. 1990; 10:493-496). Therefore, it is not surprising that, along with insulin resistance, there is glucose intolerance. High triglycerides and low HDL (“good”) cholesterol are also commonly associated with the disease (Gastroenterology. 1999; 116:1413–1419).

 

How can we alter this disease?

The good news is that NAFLD is potentially reversible through lifestyle modifications, including changes in diet and an increase in exercise.

With exercise, the premise is that the more activity a patient gets, the higher the probability of metabolizing the liver fat.

In an epidemiologic study of over 3,000 patients using data from NHANES, results showed that those with NAFLD are significantly less active than those without the disease. It did not matter the type of activity, NAFLD patients did less of it. In fact, patients who had both diabetes and NAFLD were found to do the least amount of physical activity (Aliment Pharmacol Ther. 2012; 36:772-781). The scary aspect is that patients with NAFLD have a significant eight times increased risk of cardiovascular death between the ages of 45 and 54 (Am J Gastroenterol. 2008; 103:2263–2271). And we know activity improves cardiovascular results.

In a meta-analysis (a group of 23 studies ranging from one to six months in duration) that used the Cochrane database, the results showed a significant reduction in fat content in the liver and a decrease in liver enzymes when lifestyle modifications were employed (J Hepatol. 2012 Jan.; 56:255-266). Reduction in weight had the most substantial correlation with the results. Of the 23 studies, five that looked at liver cells on a microscopic level showed a reduction in inflammation that occurred with lifestyle changes. In addition, there were also improved glucose levels and sensitivity to insulin after the modifications.

Benefits of coffee

In yet another study, coffee was shown to reduce the risk of NAFLD developing into fibrosis, a more advanced stage liver disease, by a substantial 36 percent (AASLD. 2012 Nov. 11; Abstract 99). However, weaknesses in this trial were that it was unclear how many cups of coffee were needed to have this effect and whether the coffee needed to include caffeine. The researchers theorize that there are hundreds of compounds in coffee, such as vitamins, minerals, phenolic compounds, lignans and quinides that may have this effect, not just caffeine.

In my practice, I have seen several patients with liver enzymes elevated to at least twice normal levels. After following a nutrient-dense, plant-rich diet, they saw their liver enzymes significantly reduced or returned to normal levels within a few months. One patient’s liver enzymes had been raised for 20 years without a known cause, and a first-line relative had recently been diagnosed with liver cancer.

If you have risk factors for nonalcoholic fatty liver disease, such as obesity, diabetes, high blood pressure and high cholesterol, I recommend having your liver enzymes checked on a regular basis. Those with family histories of elevated liver enzymes and hepatocellular carcinoma (liver cancer) may also want to get a scan, at least with ultrasound.

The best way to treat NAFLD is with lifestyle modifications, and while it is never too late to treat NAFLD, it is better to discover the disease earlier to reduce your risk of complications. If you are obese, NAFLD is one more important reason to transform your body composition by reducing fat mass.

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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Salt is also necessary, but most people consume far too much sodium

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

More than 90 percent of people consume far too much sodium, with salt being the primary culprit (Am J Clin Nutr. 2012 Sep;96(3):647-57). Sodium is found in foods that don’t even taste salty.

Bread and rolls are the No. 1 offenders, since we eat so much of them. Other foods with substantial amounts of sodium are cold cuts and cured meats, cheeses, pizza (which has both bread and cheese), fresh and processed poultry, soups, meat dishes, pastas and snack foods. Foods that are processed and those prepared by restaurants are where most of our consumption occurs (www.cdc.gov).

By contrast, only about 2 percent of people get enough potassium from their diets (Am J Clin Nutr. 2012 Sep;96(3):647-57). According to the authors of the study, we would need to consume about eight sweet potatoes or 10 bananas each day to reach appropriate levels.

Why is it important to reduce sodium and increase potassium? A high sodium-to-potassium ratio increases the risk of cardiovascular disease by 46 percent, according to a study looking at over 12,000 Americans over almost 15 years (Arch Intern Med. 2011;171(13):1183-1191). In addition, both may have significant impacts on blood pressure and cardiovascular disease, while sodium may also impact multiple sclerosis and potentially other autoimmune diseases.

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

 

Reduced sodium

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

The first study used the prestigious Cochrane review to demonstrate that blood pressure is reduced by a significant mean of -4.18 mm Hg systolic (top number) and -2.06 mm Hg diastolic (bottom number) involving both normotensive and hypertensive participants (BMJ. 2013 Apr 3;346:f1325). When looking solely at hypertensive patients, the reduction was even greater with a systolic blood pressure reduction of -5.39 mm Hg and a diastolic blood pressure reduction of -2.82 mm Hg.

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

In the second study, a meta-analysis of 42 clinical trials, there was a similarly significant reduction in both systolic and diastolic blood pressures (BMJ. 2013 Apr 3;346:f1326). This meta-analysis included adults and children. Both demographics saw a reduction in blood pressure, though the effect, not surprisingly was greater in adults. Interestingly, an increase in sodium caused a 24 percent increased risk of stroke incidence, but more importantly, a 63 percent increased risk of stroke mortality. The risk of mortality from heart disease was increased as well, by 32 percent.

In an epidemiology modeling study, the researchers projected that either a gradual or instantaneous reduction in sodium would save lives (Hypertension. 2013; 61: 564-570). For instance, a modest 40 percent reduction over 10 years in sodium consumed could prevent 280,000 premature deaths. These are only projections, but in combination with the above studies may be telling.

 

Potassium’s positive effects

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

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

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

Multiple sclerosis

There are several recent, very preliminary studies that suggest higher levels of salt may increase the risk of multiple sclerosis.

One study showed that salt seems to increase the levels of interleukin-17-producing CD4 helper T cells(Th17) that are potentially implicated in autoimmune diseases, such as multiple sclerosis (Nature. 2013 Mar 6). The researchers used mice to show feeding them high levels of salt resulted high levels of Th17 cells and, as a result, a severe form of multiple sclerosis.

Lowering sodium intake may have far-reaching benefits, and it is certainly achievable.

Dr. Kirsten Bibbins-Domingo, associate professor of Medicine at UCSF, who is published extensively on heart disease, commented in Jane Brody’s New York Times article dated April 1 that once we lower sodium intake, our taste buds tend to adapt to the change in about six weeks by expecting less salty foods.

We need to reduce our intake and give ourselves a brief period to adapt. We can also improve our odds by increasing our potassium intake, which also has a substantial beneficial effect, striking a better sodium-to-potassium balance.

 

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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The Mediterranean diet reduces cardiovascular disease significantly

We have made great strides in the fight against heart disease, yet it remains the No. 1 cause of death in the United States. Approximately one-third of Americans over the age of 35 will die of heart disease (Circulation. 2008;117(4):e25). I hope this statistic has captured your attention, because it should.

What is causing or contributing to such high numbers of heart disease deaths: genetics, environment or both? Many of us have the propensity toward heart disease. Can we alter this course or is it our destiny?

A recent study, involving the Paleo-type diet and other ancient diets, suggests that there is a significant genetic component to cardiovascular disease, while another study looking at the Mediterranean-type diet implies that we may be able to reduce risk factors greatly. Most of the risk factors for heart disease, such as high blood pressure, high cholesterol, sedentary lifestyle, diabetes, smoking and obesity are modifiable (see www.uptodate.com). Let’s look at the evidence.

 

Genetic components

In a study published online in The Lancet, researchers used computed tomography scans to look at 137 mummies from ancient times across the world, including Egypt, Peru, the Aleutian Islands and Southwestern America (The Lancet. 2013;Mar 11). The cultures were diverse, including hunter-gatherers (consumers of a Paleo-type diet), farmer-gatherers and solely farmers. Their diets were not vegetarian, but rather involved significant amounts of animal protein: fish and/or cattle.

Researchers found that one-third of these mummies had atherosclerosis (plaques in the arteries), which is a precursor to heart disease. The ratio should sound familiar. It seems to coordinate with modern times.

Interestingly, but not surprisingly, the average age of death was 43. The authors concluded that atherosclerosis could be part of the aging process in mankind. In other words, it may be a result of our genes. Being human, we all have a genetic propensity toward atherosclerosis and heart disease — some more than others — but many of us can reduce our risk factors significantly.

I am not saying that the Paleo-type diet specifically is not beneficial compared to the standard American diet. Rather, that we do not know it based on this study, which was not meant to provide the validity of the Paleo-type diet but whether atherosclerosis is part of the normal aging process. However, other studies demonstrate that we can reduce our chances of getting heart disease with lifestyle changes, potentially by following a Mediterranean-type diet with an emphasis on a plant-rich approach (see my article, “Seven highly effective habits for preventing heart disease,” March 15, 2012).

 

Mediterranean-type diet

A study about the Mediterranean-type diet and its potential positive impact on cardiovascular disease risk was recently published in the New England Journal of Medicine (N Engl J Med. Online 2013;Feb 25). Here, two variations on the Mediterranean-type diet were compared to a low-fat diet. People were randomly assigned to three different groups. The two Mediterranean-type diet groups both showed about a 30 percent reduction in the risk of cardiovascular disease, with end points including heart attacks, strokes and mortality, compared to the low-fat diet. This improvement in risk profile occurred even though there was no significant weight loss.

The Mediterranean-type diets both consisted of significant amounts of fruits, vegetables, nuts, beans, fish, olive oil and potentially wine. I call them “the Mediterranean diet with opulence,” because both groups consuming this diet had either significant amount of nuts or olive oil and/or wine. If the participants in the Mediterranean diet groups drank wine, they were encouraged to drink at least one glass a day.

The study included three groups: a Mediterranean diet supplemented with mixed nuts (almonds, hazelnuts or walnuts); a Mediterranean diet supplemented with extra virgin olive oil (at least four tablespoons a day); and a low-fat control diet. The patient population included over 7,000 participants in Spain at high risk for cardiovascular disease. The high-risk population included those with high blood pressure (80 percent of the population), diabetes and those who were overweight and/or were smokers.

The strength of this study, beyond its high-risk population and its large size, was that it was a randomized clinical trial, the gold standard of trials. However, there was a significant flaw, and the results need to be tempered. The group assigned to the low-fat diet was not, in fact, able to maintain this diet throughout the study. Therefore, it really became a comparison between variations on the Mediterranean diet and the standard American diet.

What do the leaders in the field of cardiovascular disease and integrative medicine think of the Mediterranean diet study? Interestingly there are two diametrically opposed opinions, split by field. You may be surprised by which group liked it and which did not. Cardiologists hailed the study as a great achievement. They included Henry Black, M.D., who specializes in high blood pressure, and Eric Topol, M.D. They emphasized that now there is a large RCT measuring clinical outcomes, such as heart attacks, stroke and death.

On the other hand, the integrative medicine physicians, Caldwell Esselstyn, M.D., and Dean Ornish, M.D., both of whom stress a plant-rich diet that may be significantly more nutrient dense than the Mediterranean diet in the study, expressed disappointment with the results. They feel that heart disease and its risk factors can be reversed, not just reduced. Both clinicians have published small, well-designed studies showing significant benefits from plant-based diets (J Fam Pract. 1995;41(6):560-8; Am J Cardiol. 2011;108:498-507). Dr. Ornish actually showed a reversal of atherosclerosis in one of his studies (JAMA. 1998 Dec 16;280(23):2001-7).

So which group of physicians is correct about the Mediterranean diet? Each opinion has its merits. The cardiologists’ enthusiasm is warranted, because a Mediterranean diet, even one of “opulence,” will appeal to more participants, who will then realize the benefits. However, those who follow a more strict diet, with greater amounts of nutrient-dense foods, will potentially see a reversal in heart disease, minimizing risk — and not just reducing it.

Thus, even with a genetic proclivity toward cardiovascular disease, we can very much alter our destinies. The degree depends on the willingness of the participants. Potentially, we can have an impact that ranges from reduction to reversal.

 

 

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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Sugar consumption may increase diabetes prevalence

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 diabetes prevalence is at epidemic levels in the United States, and it continues to grow. The latest statistics show that about 8 percent of the U.S. population has type 2 diabetes. For those 65 and older, the prevalence is considerably higher, at 26.9 percent (https://diabetes.niddk.nih.gov).

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 effect 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 comes to its effect on diabetes’ prevalence. In an epidemiological (population-based) study published in the journal PLoS One in February, the results show that sugar may increase the prevalence of type 2 diabetes by 1.1 percent worldwide (PLoS One. 2013;8(2):e57873). This seems like a small percentage, however, we are talking about the overall prevalence, which is around 8 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 New York City Mayor Michael Bloomberg’s drive 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 (Nutr J. published online March 5, 2013). 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 (Am J Lifestyle Med. 2013;7(1):23-26).

Cinnamon may work much the same way as some medications used to treat type 2 diabetes, such as GLP-1 agonists. In a study with healthy volunteers, cinnamon raised the level of GLP-1 (Am J Clin Nutr. 2007;85:1552–1556). Also, in a RCT with 100 participants, 1 gram of cassia cinnamon reduced sugars significantly more than medication alone (J Am Board Fam Med. 2009;22:507–512). 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 (Diabetologia online March 1, 2013).

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 my Jan. 31 article 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 and get off your butt.

 

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.

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A growing number of studies show increased calcium to be dangerous

I just realized that February is American Heart Disease Awareness Month. My wife pointed out that this is also International Typewriter Appreciation Month, whatever that means. When was the last time that you used a typewriter? Therefore, I thought that my last article for the month of February should focus on this most prevalent disease and the dangers of calcium in increasing the risk of heart attacks and all-cause mortality.

I wrote about a very similar topic on April 26, 2011. First, let me summarize what we knew then. At that time, a study called the Women’s Health Initiative showed that calcium supplements may cause a 20 percent rise in the risk of heart attack (BMJ. 2011 April 19;342:d2040). There were 17,000 women involved in this study with calcium. The participants who saw this modest rise in risk were taking 1000 mg of calcium supplementation. In the same paper, there was also a meta-analysis (group of three studies) that showed increases of 20 percent in both heart attacks and strokes with calcium. It did not matter whether participants were taking vitamin D or not. At the time, I hedged my bets by saying it was only one paper. The results were intriguing, though — the risk of a heart attack surpassed the benefits of reducing fracture.

Recently, several large studies reinforced the negative effects of calcium as related to the heart, and the impact seems to be even greater. Let’s examine these studies and their implications in more detail.

Calcium’s impact on women

In the Swedish Mammography Cohort, published in the same medical journal as the aforementioned study, the results showed an almost 50 percent increased risk of cardiovascular disease deaths in women who consumed more than 1400 mg of calcium from their diet, which included calcium supplements, compared to those who consumed 600 to 1000 mg (BMJ. 2013 Feb. 13;346:f228). Cardiovascular disease risk in this study included heart disease and stroke combined. The participants who consumed less than 600 mg of calcium also had an increase in mortality, but not nearly as significant as the high calcium intake group.

When you break down the percentages, the data are even more interesting. In this study, heart disease deaths increased by 114 percent. However, unlike the previous study, there was no significant increase in stroke deaths.

All-cause mortality, which means from any source, not just cardiovascular, was increased by 40 percent. Also, those women in the high calcium group had a two-and-a-half times greater risk of all-cause death when they were taking calcium supplements, while those in the same group who were not taking supplements had a much less significant (17 percent) increased risk.

Not to worry. As the authors point out, those who consume calcium without supplements are most likely to be in the ideal range. This was a large observational prospective (forward-looking) study involving over 60,000 women. The duration of the study was 19 years. However, a weakness of the study is that the overall event rate was small. The authors’ conclusion was that women should avoid calcium supplementation and get their calcium from dietary sources.

Calcium’s impact on men

Not to be left out, men also seem to be negatively affected by high calcium. The National Institutes of Health-AARP Diet and Health Study, published a week earlier than the women’s study mentioned above, showed that there was a 20 percent increased risk of cardiovascular disease death in those men who took at least 1000 mg of calcium on a daily basis compared to those who did not (JAMA Intern Med. Online Feb. 4). Again, the predominant effect was seen with death from heart disease. This was a prospective study, involving 388,000 men and women who were followed for over 12 years.

To make the data slightly more obtuse, this effect was only seen in men, not in the women involved in the study. The authors cannot explain why there was this difference in gender. However, when the data was analyzed further, and multivitamins were eliminated from the equation as a contributing source of calcium, those men taking calcium supplements of at least 1000 mg were even more likely to suffer heart disease deaths, with a 37 percent increased risk.

In my own practice, having seen several hundred patients in the last few years, it seems none of them have been deficient in calcium. Yet when many patients come for an initial visit, they are taking varying amounts of calcium supplements. One of the first things I usually do is either reduce or discontinue the dose. I then follow up with a laboratory test to make sure they are not deficient after changing their supplements.

I also educate them about foods that are good sources of calcium and explain why. Believe it or not, we absorb calcium best from plant-based sources in our diet, such as kale, almonds, tofu and unhulled sesame seeds. In an article entitled, “Do calcium supplements increase cardiovascular mortality?“ published on Feb. 21, the author, after reviewing much of the pertinent data, suggests that calcium-rich foods are the wisest and safest of choices, rather than supplementation (www.medscape.com).

Finally, in the EPIC trial, there was a decrease in the risk of a heart attack from dietary calcium (Heart. 2012; 98(12):920-925). Unfortunately, there was no effect, beneficial or not, on the number of deaths from all-cause mortality or cardiovascular disease. However, there was a noticeable 139 percent increased risk of heart attacks in calcium supplement users.

Therefore, the best way to avoid this conundrum of making sure your bones are strong and getting enough calcium, while not increasing your risk of mortality is to do several things. Make sure your vitamin D levels are sufficient, for vitamin D helps with the absorption of calcium into the bones. Most people are deficient or insufficient (a milder form) in vitamin D, so if you want to take a supplement, start here. The other is to have a well-balanced diet that includes calcium-rich foods, ensuring you are in the optimal range of daily intake and getting very little or no calcium from supplements. Lastly, don’t begin using calcium supplements before consulting with your physician.

 

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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Numerous diseases may have increased C-reactive protein

Many of us have inflammation in our bodies, inflammation that is a potential underlying cause for a great number of diseases. Can we demonstrate the level of inflammation by measuring it? The answer is yes, otherwise I would not be writing this article.

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

What is the significance of the different levels? In heart disease, individuals who have levels less than 1.0 mg/L are in the optimal range for low risk of inflammation. Levels of 1-3 mg/L is the average risk range and greater than 3.0 mg/L is the higher risk profile. Above 10.0 mg/L is less specific to heart disease, although still related, but more likely associated with other causes, such as infection and autoimmune diseases (uptodate.com; Diabetes Technol Ther. 2006;8(1):28-36). This biomarker is derived from the liver.

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

Let’s look at the evidence.

 

Age-related macular degeneration (AMD)

AMD is the leading cause of blindness in patients over the age of 65 (Prog Retin Eye Res. 2007 Nov;26(6):649-673). Therefore, it is very important to help define risk stratification for this disease. In a prospective study, the results showed that hsCRP levels were inversely associated with the risk of developing AMD. The group with an hsCRP more than 3.0 mg/L had a 50 percent increased risk of developing overall AMD compared to the optimal group with less than 1.0 mg/L. But even more interestingly, the risk of developing neovascular or wet AMD increased to 89 percent in this high-risk group.

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

These results reinforce those of a previous prospective study that showed that elevated hsCRP increased the risk of AMD by threefold (Arch Ophthalmol. 2007;125(3):300-305). This study utilized data from the Women’s Health Study, which involved over 27,000 participants. Like the study mentioned above, this one also defrosted blood samples from baseline and looked at follow-up incidence of developing AMD in initially healthy women.

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

Diabetic retinopathy —
a complication of diabetes

We know that diabetes affects significantly more than 10 percent of the population and is continuing to rise at a rapid rate. One of the complications of diabetes affects the retina (back of the eye) and is called diabetic retinopathy. This is a leading cause of vision loss (Am J Ophthalmol. 2003;136(1):122-135). One of the reasons for the vision loss is macular edema, or swelling, usually due to rupture of tiny blood vessels below the macula, a portion of the back of the eye responsible for central vision.

The DCCT trial, a prospective study involving over 1,400 type-1 diabetes patients, showed an 83 percent increased risk of developing clinically significant macular edema in the group with the highest hsCRP levels compared to those with the lowest (JAMA Ophthalmol. 2013 Feb 7;131:1-8). Although these results were with type-1 diabetes, patients with type-2 diabetes are at equal risk of diabetic retinopathy if glucose levels or sugars are not well-controlled.

 

Depression

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

Well, it turns out that inflammation is associated with depression. Specifically, in a recent prospective observational trial, rising levels of CRP had a linear relationship with increased risk of hospitalization due to psychological distress and depression (JAMA Psychiatry. 2013;70(2):176-184).

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

 

What can be done to reduce
inflammation?

This is the key question, since we now know that hsCRP is associated with systemic inflammation. In the Nurses’ Health Study, a very large, prospective observational study, the DASH diet decreased the risk of both heart disease and stroke, which is impressive. But for this article, in regards to hsCRP, the DASH diet decreased the levels significantly, which also was associated with a decrease in clinically meaningful endpoints of stroke and heart disease (Arch Intern Med. 2008;168(7):713-720).

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

 

Conclusion

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

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

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

 

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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The effect is based on flavonoids in cocoa and chocolate

Valentine’s Day is one of the wonderful things about winter. For many, it lifts the mood and spirit. A traditional gift is chocolate. But do the benefits of chocolate go beyond Valentine’s Day? The short answer is yes, which is good news for chocolate lovers. However, we are not talking about filled chocolates, but primarily dark chocolate and cocoa powder.

The health benefits of chocolate are derived in large part from its flavonoid content — compounds that are produced by plants. These health benefits are seen in cardiovascular disease, including stroke, heart disease and blood pressure. This is ironic, since many chocolate boxes are shaped as hearts. Unfortunately, it is not necessarily the chocolates that come in these boxes that are beneficial.

Let’s look at the evidence.

 

Effect on heart failure

Heart failure is very difficult to reverse. Therefore, the best approach is prevention, and dark chocolate may be one weapon in this crusade. In the Swedish Mammography Cohort study, those women who consumed dark chocolate saw a reduction in heart failure (Circ Heart Fail. 2010;3(5):612-6). The results were on a dose response curve, but only to a point. Those women who consumed two to three servings of dark chocolate a month had a 26 percent reduction in the risk of heart failure.

For the dark chocolate lovers, it gets even better. Women who consumed one to two servings per week had an even greater reduction of 32 percent. However, those who ate more than these amounts actually lost the benefit in heart failure reduction and may have increased risk. With a serving (1 ounce) a day, there was actually a 23 percent increased risk.

This study was a prospective (forward-looking) observational study that involved more than 30,000 women over a long duration, nine years. The authors comment that chocolate has a downside of too much fat and calories and, if eaten in large quantities, it may interfere with eating other beneficial foods, such as fruits and vegetables. The positive effects are most likely from the flavonols, a subset of flavonoids, which come from the cocoa solids — the chocolate minus the cocoa butter.

 

Impact on mortality from heart attacks

In a two-year observational study, results showed that chocolate seemed to reduce the risk of cardiac death after a first heart attack (J Intern Med. 2009;266(3):248-57). Again, the effects were based on a dose-response curve, but unlike the previous study, there was no increased risk beyond a certain modest frequency.

Those who consumed chocolate up to once a week saw a 44 percent reduction in risk of death, and those who ate the most chocolate — two or more times per week — saw the most effect, with 66 percent reduced risk. And finally, even those who consumed one serving of chocolate less than once per month saw a 27 percent reduction in death, compared to those who consumed no chocolate.

The study did not mention dark or milk chocolate, however this was another study that took place in Sweden. In Sweden, their milk chocolate has substantially more cocoa solids, and thus flavonols, than that manufactured for the U.S. There were over 1,100 patients involved in this study, and none of them had a history of diabetes, which is important to emphasize.

 

Stroke reduction

I don’t know anyone who does not want to reduce the risk of stroke. We tell patients to avoid sodium in order to control blood pressure and reduce their risk. Initially, sodium reduction is a difficult thing to acclimate to — and one that people fear. However, it turns out that eating chocolate may reduce the risk of stroke, so this is something you can use to balance out the lifestyle changes.

In yet another study, the Cohort of Swedish Men, which involved over 37,000 men, there was an inverse relationship between chocolate consumption in men and the risk of stroke (Neurology. 2012;79:1223-1229).Those who ate at least two servings of chocolate a week benefited the most with a 17 percent reduction in both major types of stroke — ischemic and hemorrhagic — compared to those who consumed the least amount chocolate. Although the reduction does not sound tremendous, aspirin reduces stroke risk by 20 percent. However, this study was observational, not the gold-standard randomized controlled trial, like the aspirin studies.

 

Blood pressure

One of the most common maladies, especially in people over 50, is high blood pressure. So, whatever we can do to lower blood pressure levels is important, including decreasing sodium levels, exercising and even eating flavonoid-rich cocoa.

In a meta-analysis (a group of 20 RCTs), flavonoid-rich cocoa reduced both systolic (top number) and diastolic (bottom number) blood pressure significantly: -2.77 mm Hg and -2.20 mm Hg, respectively (Cochrane Database Syst Rev. 2012:15;8:CD008893).These studies involved healthy participants, who are sometimes the most difficult in which to show a significant reduction, since their blood pressure is not high initially. One of the weaknesses of this meta-analysis is that the trials were short, between two and 18 weeks.

 

Why chocolate has an effect

Chocolate has compounds called flavonoids. The darker the chocolate, the more flavonoids there are. These flavonoids have potential antioxidant, antiplatelet and anti-inflammatory effects.

In a small randomized controlled trial comparing 22 heart transplant patients, those who received dark flavonoid-rich chocolate, compared to a cocoa-free control group, had greater vasodilation (enlargement) of coronary arteries two hours after consumption (Circulation. 2007 Nov 20;116(21):2376-82). There was also a decrease in the aggregation, or adhesion, of platelets, one of the primary substances in forming clots. The authors concluded that dark chocolate may also cause a reduction in oxidative stress.

It’s great that chocolate, mainly dark, and cocoa powder have such substantial effects in cardiovascular disease. However, certain patients should avoid chocolate such as those with reflux disease, allergies to chocolate and diabetes. Be aware that Dutch-processed, or alkalized, cocoa powder may have lower flavonoid levels and is best avoided. Also, the darker the chocolate is, the higher the flavonoid levels. I suggest that the chocolate be at least 60 to 70 percent dark.

Moderation is the key, for all chocolate contains a lot of calories and fat. Based on the studies, two servings a week are probably where you will see the most cardiovascular benefits. Happy Valentine’s Day!

 

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.