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Mediterranean Diet
Can we overcome our genes?

By David Dunaief, M.D.

Dr. David Dunaief

We have made great strides in the fight against heart disease, yet it remains the number one cause of death in the United States. Approximately one-third of Americans over the age of 35 will die of heart disease (1). 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 2013 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 (2). 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 (3). 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 humans. 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.

Mediterranean-type diet

A study about the Mediterranean-type diet and its potential positive impact on cardiovascular disease risk was published in the New England Journal of Medicine (4). 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 (5, 6). Ornish actually showed a reversal of atherosclerosis in one of his studies (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.

References: (1) Circulation. 2008;117(4):e25. (2) www.uptodate.com. (3) The Lancet. 2013;Mar 11. (4) N Engl J Med. Online 2013;Feb 25. (5) J Fam Pract. 1995;41(6):560-568. (6) Am J Cardiol. 2011;108:498-507. (7) JAMA. 1998 Dec 16;280(23):2001-2007.

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

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Implications for thyroid removal are lifelong

By David Dunaief, M.D.

Dr. David Dunaief

It is very interesting that the amount of coverage by the lay press concerning thyroid nodules does not reflect the number of people who actually have them. More than 50 percent of people have thyroid nodules detectable by high-resolution ultrasound (1); however, news coverage for general, nonphysician audiences is infrequent.

You can understand how coverage should be more in the forefront. Fortunately, most nodules are benign. A small percent, 4 to 6.5 percent, are malignant, and the number varies depending on the study (2). Thyroid nodules are being diagnosed more often incidentally on radiologic exams, such as CT scans of the chest, MRI scans, PET scans and ultrasounds of the carotid arteries in the neck (3).

There is a conundrum of what to do with a thyroid nodule, especially when it is found incidentally. It depends on the size. If it is over 1 centimeter, usually it is biopsied by fine needle aspiration (FNA) (4). This is the cutoff point for thyroid nodules found with a radiologic exam. Most are asymptomatic. However, if there are symptoms, these might include difficulty swallowing, difficulty breathing, hoarseness, pain in the lower portion of the neck and a goiter (5).

FNA biopsy is becoming more common. In a study evaluating several databases, there was a greater than 100 percent increase in thyroid FNAs performed over a five-year period from 2006 to 2011 (6). This resulted in a 31 percent increase in thyroidectomies, surgeries to remove the thyroid partially or completely.

However, the number of thyroid cancers diagnosed with the surgery did not rise in this same period. To make matters even more confusing, from 2001 to 2013, the number of thyroid cancers increased by 200 percent. In the study authors call for more detailed guidelines, which are lacking for thyroid nodules. Though the number of cancers diagnosed has increased, the mortality rate has remained relatively stable over several decades at about 1,500 patients per year (7). Thyroid nodules in this study were least likely to be cancerous when the initial diagnosis was by incidental radiologic exam.

Treating borderline results

As much as 25 percent of FNA biopsies are indeterminate. We are going to look at two modalities to differentiate between benign and malignant thyroid nodules when FNA results are equivocal: a PET scan and a molecular genetics test. A meta-analysis (a group of six studies) of PET scan results showed that it was least effective in resolving an unclear FNA biopsy. The PET scan was able to rule out patients who did not have malignancies significantly but did not do a good job of identifying those who did have cancer (8).

On the other hand, a molecular-based test was able to potentially determine whether an indeterminate thyroid nodule by FNA was malignant or benign (9). This test was a combination of microRNA gene expression classifier with the genetic mutation panel. I know the test combination sounds confusing, but the important takeaway is that it was more effective than previous molecular tests in clarifying whether a patient had a benign or cancerous nodule.

Unlike in the PET scan study above, the researchers were able to not only rule out the majority of malignancies but also to rule them in. It was not perfect, but the percent of negative predictive value (ruled out) was 94 percent, and the positive predictive value (ruled in) was 74 percent. The combination test improved the predictive results of previous molecular tests by 65 to 69 percent. This is important to help decide whether or not the patient needs surgery to remove at least part of the thyroid. The trial used hospital-based patients, but follow-up studies need to include community-based practices.

Is a negative FNA definitive?

We know that FNA is the gold standard for determining whether patients have malignant or benign thyroid nodules. However, a negative result on FNA is not always definitive for a benign thyroid nodule. When this occurs, it is referred to as a false negative result. In a retrospective (looking back at events) study, from the Longitudinal Health Insurance Database in Taiwan, 62 percent of thyroid nodules that were cancerous were diagnosed with one biopsy, and 82 percent were found within the year after that biopsy (10). However, about 17 percent of patients needed more than two FNA biopsies, and 19 percent were diagnosed after one year with cancerous thyroid nodules.

Significance of calcification on ultrasound

Microcalcifications in the nodule can be detected on ultrasound. The significance of this may be that patients with microcalcifications are more likely to have malignant thyroid nodules than those without them, according to a small prospective study involving 170 patients (11). This does not mean necessarily that a patient has malignancy with calcifications, but there is a higher risk. The results demonstrated that more than half of the malignant thyroid nodules, 61 percent, had microcalcifications.

Good news

As I mentioned above, most thyroid nodules are benign. The results of one study go even further, showing that most asymptomatic benign nodules do not progress in size significantly after five years (12). This was a prospective (forward-looking) study involving 992 patients with between one and four benign thyroid nodules diagnosed cytologically (by looking at the cells) or by ultrasound. The factors that did contribute to growth of about 11 percent of the nodules were age (<45 years old had more growth than >60 years old), multiple nodules, greater nodule volume at baseline and being male.

The authors’ suggestion is that the current paradigm might be altered and that after the follow-up scan, the next ultrasound scan might be five years later instead of three years. However, they did discover thyroid cancer in 0.3 percent after five years.

Thyroid function may contribute to risk

In considering risk factors, it’s important to note that those who had a normal thyroid stimulating hormone (TSH) were less likely to have a malignant thyroid nodule than those who had a high TSH, implying hypothyroidism. There was an almost 30 percent prevalence of cancer in the nodule if the TSH was greater than >5.5 mU/L (13).

The bottom line is that there is an urgent need for new guidelines regarding thyroid nodules. Fortunately, most nodules are benign and asymptomatic, but the number of cancerous nodules found is growing. We are getting better at diagnosing nodules. Why the death rate remains the same year over year for decades may have to do with the slow rate at which most thyroid cancers progress, especially two of the most common forms, follicular and papillary.

References: (1) AACE 2013 Abstract 1048. (2) Thyroid. 2005;15(7):708. (3) uptodate.com. (4) AACE 2013 Abstract 1048. (5) thyroid.org. (6) AAES 2013 Annual Meeting. Abstract 36. (7) AACE 2013 Abstract 1048. (8) Cancer. 2011;117(20):4582-4594. (9) J Clin Endocrinol Metab. Online May 12, 2015. (10) PLoS One. 2015;10(5):e0127354. (11) Head Neck. 2008 Sep;30(9):1206-1210. (12) JAMA. 2015;313(9):926-935. (13) J Clin Endocrinol Metab. 2006;91(11):4295.

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

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Diet choices and vitamin B3 have surprising effects

By David Dunaief

Dr. David Dunaief

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

The incidences of these skin cancers are very difficult to pin down because they are not readily reported. However, most of us either know someone who has had these types of skin cancer or have had them ourselves. There were roughly 3.5 million nonmelanoma skin cancer treatments in the U.S. in 2006, with the number of treatments increasing 77 percent from 1992 to 2006 (1). SCC and BCC outcomes diverge, with the former having a higher risk of metastases compared to the latter, which tends to grow much slower (2).

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

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

Beyond skin cancer

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

Tanning beds — No surprise

We know that tanning beds may be a cause for concern. Now the FDA has changed the classification of tanning beds from low to moderate risk and requires a warning that they should not be used by those under the age of 18 (6). The catch is that this does not have teeth; if tanning salons ignore the new rules, there is no punishment.

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

A recent study showed that drying lamps used after a manicure could lead to skin cancer.

Manicure risk, really?

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

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

Vitamin B3 to the rescue

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

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

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

NSAIDs as beneficial?

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

Diet — The good and the bad

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

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

References: (1) Arch Dermatol. 2010;146(3):283. (2) uptodate.com. (3) nih.gov. (4) Br J Cancer. 2006;94(5):743. (5) J Natl Cancer Inst. 2008;100(17):1215-1222. (6) federalregister.gov. (7) Am J Public Health. Online June 11, 2015. (8) JAMA Dermatol. 2014;150(7):775-776. (9) ASCO 2015 Annual Meeting: Abstract 9000. (10) J Invest Dermatol. 2015;135(4):975-983. (11) Am J Clin Nutr. 2007;85(5):1401.

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

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Sedentary lifestyle increases risk in the young

By David Dunaief, M.D.

Dr. David Dunaief

First, the good news: We have made great strides in reducing mortality from heart attacks. When we compare cardiovascular disease — heart disease and stroke — mortality rates from 1975 to the present, there is a substantial decline of approximately one-quarter. However, if we look at these rates since 1990, the rate of decline has slowed (1).

Plus, one in 10 visits to the emergency room are related to potential heart attack symptoms. Luckily, only 10 to 20 percent of these patients actually are having a heart attack (2). We need to reduce our risk factors to improve this scenario.

Some risk factors are obvious, while others are not. The obvious ones include age (men at least 45 years old and women at least 55 years old), family history, high cholesterol, high blood pressure, obesity, sedentary lifestyle, diabetes and smoking. Less obvious risk factors include gout, atrial fibrillation and osteoarthritis. Lifestyle modifications, including a high-fiber diet and exercise, also may help allay the risks.

Let’s look at the evidence.

Obesity

On a board exam in medicine, if smoking is one of the choices with disease risk, you can’t go wrong by choosing it. Well, it appears that the same axiom holds true for obesity. But how substantial a risk factor is obesity? In the Copenhagen General Population Study, results showed an increased heart attack risk in obese

(BMI >30 kg/m²) individuals with or without metabolic syndrome (high blood pressure, high cholesterol and high sugar) and in those who were overweight (BMI >25 kg/m²) (3). The risk of heart attack increased in direct proportion to weight. Specifically, there was a 26 percent increase in heart attack risk for those who were overweight and an 88 percent increase in risk for those who were obese without metabolic syndrome. This study had a follow-up of 3.6 years.

It is true that those with metabolic syndrome and obesity together had the highest risk. But, it is quite surprising that obesity, by itself, can increase heart attack risk when a person is “metabolically healthy.” Since this was an observational trial, we can only make an association, but if it is true, then there may not be such thing as a “metabolically healthy” obese patient. Therefore, if you are obese, it is really important to lose weight.

Lifestyle modifications such as weight loss, physical activity and diet can help decrease the risk of heart attacks.

Sedentary lifestyle

If obesity were not enough of a wake-up call, let’s look at another aspect of lifestyle: the impact of being sedentary. A recent observational study found that activity levels had a surprisingly high impact on heart disease risk (4). Of four key factors — weight, blood pressure, smoking and physical inactivity — age was the determinant as to which one had the most negative effect on women’s heart disease risk. Those under the age of 30 saw smoking as most negatively impactful. For those over the age of 30, lack of exercise became the most dominant risk factor for heart disease, including heart attacks.

For women over the age of 70, the study found that increasing physical activity may have a greater positive impact than addressing high blood pressure, losing weight, or even quitting smoking. However, since high blood pressure was self-reported and not necessarily measured in a doctor’s office, it may have been underestimated as a risk factor. Nonetheless, the researchers indicated that women should make sure they exercise on a regular basis to most significantly reduce heart disease risk.

Osteoarthritis

The prevailing thought with osteoarthritis is that it is best to suffer with hip or knee pain as long as possible before having surgery. But when do we cross the line and potentially need joint replacement? Well, in a recent study, those with osteoarthritis of the hip or knee joints that caused difficulty walking on a flat surface were at substantially greater risk of cardiovascular events, including heart attack (5). Those who had surgery for the affected joint saw a substantially reduced heart attack risk. It is important to address the causes of osteoarthritis to improve mobility, whether with surgery or other treatments.

Gout

When we think of gout, we relate it to kidney stones. But gout increases the risk of heart attacks by 82 percent, according to an observational study (6). Gout tends to affect patients more when they are older, but the risk of heart attack with gout is greater in those who are younger, ages 45 to 69, than in those over 70. What can we do to reduce these risk factors?

There have been studies showing that fiber decreases the risk of heart attacks. However, does fiber still matter when someone has a heart attack? In a recent analysis using data from the Nurses’ Health Study and the Health Professional Follow-up Study, results showed that higher fiber plays an important role in reducing the risk of death after a heart attack (7). Those who consumed the most fiber, compared to the least, had a 25 percent reduction in post-heart attack mortality.

Even more impressive is the fact that those who increased their fiber after the cardiovascular event had a 31 percent reduction in mortality risk. In this analysis, it seemed that more of the benefit came from fiber found in cereal. The most intriguing part of the study was the dose-response. For every 10-g increase in fiber consumption, there was a 15 percent reduction in the risk of post-heart attack mortality. Since we get too little fiber anyway, this should be an easy fix.

Lifestyle modifications are so important. In the Nurses’ Health Study, which followed 120,000 women for 20 years, those who routinely exercised, ate a quality diet, did not smoke and were a healthy weight demonstrated a whopping 84 percent reduction in the risk of a cardiovascular event such as a heart attack (8).

What have we learned? We can substantially reduce the risk of heart attacks and even potentially the risk of death after sustaining a heart attack with lifestyle modifications that include weight loss, physical activity and diet — with, in this case, a focus on fiber. While there are a number of diseases that contribute to heart attack risk, most of them are modifiable. With disabling osteoarthritis, addressing the causes of difficulty with mobility may also help reduce heart attack risk.

References: (1) Heart. 1998;81(4):380. (2) JAMA Intern Med. 2014;174(2):241-249. (3) JAMA Intern Med. 2014;174(1):15-22. (4) Br J Sports Med. 2014, May 8. (5) Presented Research: World Congress on OA, 2014. (6) Rheumatology (Oxford). 2013 Dec;52(12):2251-2259. (7) BMJ. 2014;348:g2659. (8) N Engl J Med. 2000;343(1):16.

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

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Bones: What is beneficial and what is not?
Dr. David Dunaief

The prevalence of osteoporosis is increasing especially as the population ages. Why is this important? Osteoporosis may lead to increased risk of fracture due to a decrease in bone strength (1). That is what we do know. But what about what we think we know?

For decades we have been told that if we want strong bones, we need to drink milk. Advertising slogans have morphed from “Milk does a body good” to “Got Milk?” to “Milk Life.” Celebrities have worn milk mustaches to show how important it is to our diet. This has been drilled into our brains since we were toddlers. Milk has calcium and is fortified with vitamin D, so milk could only be helpful, right? Not necessarily.

The data is mixed, but studies indicate that milk may not be as beneficial as we have been led to believe. Even worse, it may be harmful. The operative word here is “may.” We will investigate this further. Vitamin D and calcium are good for us. But do supplements help prevent osteoporosis and subsequent fractures? Again the data is mixed, but supplements may not be the answer for those who are not deficient.

Of course, we know which drugs are potentially beneficial for osteoporosis; however, which one works the best for whom may be unclear. There are minimal head-to-head trials comparing different drugs (2). They all have beneficial reductions in fracture risk in patients with osteoporosis, but they also have side effects.

What do the guidelines tell us about those who are at potential risk for osteoporosis and fracture? A study looked at the predictability, or reliability, of the United States Preventive Services Task Force (USPSTF) recommendations for screening patients for osteoporosis. Unfortunately, the study showed that USPSTF guidelines were a nominal improvement over chance (3). In other words, the guidelines were able to predict only 24 percent of patients who ended up developing osteoporosis between the ages of 50 and 64.

Milk — it’s not what you think

Recent studies involving men and women in Sweden showed that milk may be harmful.

The results of a large, observational study involving men and women in Sweden showed that milk may be harmful (4). When comparing those who consumed three or more cups of milk daily to those who consumed less than one, there was a 93 percent increased risk of mortality in women between the ages of 39 and 74. There was also an indication of increased mortality based on dosage.

For every one glass of milk consumed there was a 15 percent increased risk of death in these women. There was a much smaller, but significant, 3 percent per glass increased risk of death in men. Women experienced a small, but significant, increased risk of hip fracture, but no increased risk in overall fracture risk. There was no increased risk of fracture in men, but there was no benefit either. There were higher levels of biomarkers that indicate oxidative stress and inflammation found in the urine.

This study was 20 years in duration and is eye-opening. We cannot make any decisive conclusions, only associations, since it is not a randomized controlled trial. But it does get you thinking. The researchers surmise that milk has high levels of D-galactose, a simple sugar that may increase inflammation and ultimately contribute to this potentially negative effect, whereas other foods have many-fold lower levels of this substance.

Ironically, the USDA recommends that, from 9 years of age through adulthood, we consume three cups of dairy per day (5). This is interesting, since the results from the previous study showed the negative effects at this recommended level of milk consumption. The USDA may want to rethink these guidelines.

Prior studies show milk may not be beneficial for preventing osteoporotic fractures. Specifically, in a meta-analysis that used data from the Nurses’ Health Study for women and the Health Professionals Follow-up Study for men, for each additional glass of milk per day during the teenage years there was a 9 percent increased risk of hip fracture in men only (6). However, this effect was negated when height was taken into account. Neither men nor women saw any benefit from milk consumption in preventing hip fractures. In other words, the milk you drank during your teenage years might not reduce hip fractures later in life.

Calcium disappointments

Unfortunately, it is not only milk that may not be beneficial. There was a meta-analysis that included observational studies and clinical trials. In the meta-analysis involving a group of observational studies, there was no statistically significant improvement in hip fracture risk in those men or women ingesting at least 300 mg of calcium from supplements and/or food on a daily basis (7).

The researchers did not differentiate the types of foods containing calcium. In a group of randomized controlled trials analyzed in the same study, those taking 800 to 1,600 mg of calcium supplements per day also saw no increased benefit in reducing nonvertebral fractures. In fact, in four clinical trials the researchers actually saw an increase in hip fractures among those who took calcium supplements. A weakness of the large multivaried meta-analyses is that vitamin D baseline levels, exercise and phosphate levels were not taken into account.

Vitamin D benefit

Finally, though the data is not always consistent for vitamin D, when it comes to fracture prevention, it appears it may be valuable. In a meta-analysis (involving 11 randomized controlled trials), vitamin D supplementation resulted in a reduction in fractures (8). When patients were given a median dose of 800 IUs (ranging from 792 to 2,000 IUs) of vitamin D daily, there was a significant 14 percent reduction in nonvertebral fractures and an even greater 30 percent reduction in hip fractures in those 65 years and over. However, vitamin D in lower levels showed no significant ability to reduce fracture risk.

Just because something in medicine is a paradigm does not mean it’s correct. Milk may be an example of this. Also, ironically, the “Milk Life” slogan may need an overhaul, especially in women between the ages of 39 and 74 years old, where there is a potential increased risk of mortality. No definitive statement can be made about calcium, although even in randomized controlled trials with supplements there seemed to be no significant benefit. Of course, the patients in these trials were not necessarily deficient in calcium or vitamin D.

In order to get benefit from vitamin D supplementation to prevent fracture, patients may need at least 800 IUs per day, which is the Institute of Medicine’s recommended amount for a relatively similar population as in the study. Also, different drugs have different benefits and side effect profiles.

Remember that studies, though imperfect, are better than tradition alone. Prevention and treatment therefore should be individualized, and deficiency in vitamin D or calcium should usually be treated, of course. Please, talk to your doctor before adding or changing any supplements.

References: (1) JAMA. 2001;285:785-795. (2) Ann Intern Med. 2014;161(10):711-723. (3) NAMS 2014 Meeting: Abstract S-13. Oct. 16, 2014. (4) BMJ 2014;349:g6015. (5) choosemyplate.gov. (6) JAMA Pediatr. 2014;168(1):54-60. (7) Am J Clin Nutr. 2007 Dec;86(6):1780-1790. (8) N Engl J Med. 2012 Aug. 2;367(5):481.

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

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In recent studies, whole fruit was shown to actually reduce the risk of type 2 diabetes.
Some surprising results about lifestyle

By David Dunaief, M.D.

Most of us know that type 2 diabetes is an epidemic in America and continues to grow. Type 2 diabetes was thought to be an adult-onset disease, but more and more children and adolescents are affected as well. The most recent statistics show that 50 percent of teens with diabetes between the ages of 15 and 19 have type 2 (1). Thus, this disease is pervasive throughout the population.

Let’s test our diabetes IQ. See if you can determine whether the following items are true or false.

•Whole fruit should be limited or avoided.

•Soy has detrimental effects with diabetes.

•Plant fiber provides too many carbohydrates.

•Coffee consumption contributes to diabetes.

•Bariatric surgery is an alternative to lifestyle changes.

My goal is to help debunk type 2 diabetes myths. All of these statements are false. Let’s look at the evidence.

Fruit

Fruit, whether whole fruit or fruit juice, has always been thought of as taboo for those with diabetes. This is only partially true. Yes, fruit juice should be avoided because it does raise or spike glucose (sugar) levels. The same does not hold true for whole fruit. Studies have demonstrated that patients with diabetes don’t experience a spike in sugar levels whether they limit the number of fruits consumed or have an abundance of fruit (2). In another study, whole fruit actually was shown to reduce the risk of type 2 diabetes (3).

In yet another study, researchers looked at different whole fruits to determine their impacts on glucose levels. They found that berries reduced glucose levels the most, but even bananas and grapes reduced these levels (4) — that’s right, bananas and grapes, two fruits people associate with spiking sugar levels and increasing carbohydrate load. The only fruit that seemed to have a mildly negative impact on sugars was cantaloupe. Fruit is not synonymous with sugar. One of the reasons for the beneficial effect is the flavonoids, or plant micronutrients, but another is the fiber.

Fiber

We know fiber is important in a host of diseases, and it is not any different in diabetes. In the Nurses’ Health Study and NHS II, two very large prospective (forward-looking) observational studies, plant fiber was shown to help reduce the risk of type 2 diabetes (5). Researchers looked at lignans, a type of plant fiber, specifically examining the metabolites enterodiol and enterolactone. They found that patients with type 2 diabetes have substantially lower levels of these metabolites in their urine, compared to the control group without diabetes. There was a linear, or direct, relationship between the amount of metabolites and the reduction in risk for diabetes. The authors therefore encourage patients to eat more of a plant-based diet to get this benefit.

Foods with lignans include: flaxseed; sesame seeds; cruciferous vegetables, such as broccoli and cauliflower; and an assortment of fruits and grains (6). The researchers could not determine which plants contributed the most benefit. They believe the effect is from antioxidant activity.

Soy and kidney function

Soy sometimes has a negative association. However, in diabetes patients with nephropathy (kidney damage or disease), soy consumption showed improvements in kidney function (7). There were significant reductions in urinary creatinine levels and reductions of proteinuria (protein in the urine), both signs that the kidneys are beginning to function better.

This was a small but randomized controlled trial, considered the gold standard of studies, over a four-year period with 41 participants. The control group’s diet consisted of 70 percent animal protein and 30 percent vegetable protein, while the treatment group’s consisted of 35 percent animal protein, 35 percent textured soy protein and 30 percent vegetable protein.

This is very important since diabetes patient are 20 to 40 times more likely to develop nephropathy than those without diabetes (8). It appears that soy protein may put substantially less stress on the kidneys than animal protein. This negative effect with animal protein may be due to higher levels of phosphorus. However, those who have hypothyroidism should be cautious or avoid soy since it may suppress thyroid functioning.

Coffee

Coffee is a staple in America and in my household. It is one thing my wife would never let me consider taking away. Well, she and the rest of the coffee-drinking portion of the country can breathe a big sigh of relief when it comes to diabetes.

There is a meta-analysis (involving 28 prospective studies) that shows coffee decreases the risk of developing diabetes (9). It was a dose-dependent effect; two cups decreased the risk more than one cup. Interestingly, it did not matter whether it contained caffeine or was decaffeinated. This suggests that caffeine is not necessarily the driving force behind the effect of coffee on diabetes.

The authors surmise that other compounds, including lignans, which have antioxidant effects, may play an important role. The duration of the studies ranged from 10 months to 20 years, and the database was searched from 1966 to 2013, with over one million participants.

Bariatric surgery

In recent years, bariatric surgery has grown in prevalence for treating severely obese (BMI>35 kg/m²) and obese (BMI >30 kg/m²) diabetes patients. In a meta-analysis of bariatric surgery (involving 16 RCTs and observational studies), the procedure illustrated better results than conventional medicines over a 17-month follow-up period in treating HbA1C (three-month blood glucose measure), fasting blood glucose and weight loss (10). During this time period, 72 percent of those patients treated with bariatric surgery went into diabetes remission and had significant weight loss.

However, after 10 years without proper management involving lifestyle changes, only 36 percent remained in remission with diabetes, and a significant number regained weight. Thus, whether one chooses bariatric surgery or not, altering diet and exercise are critical to maintain long-term benefits.

There is still a lot to be learned with diabetes, but our understanding of how to manage lifestyle modifications, specifically diet, is becoming clearer. The take-home messages are: Don’t avoid whole fruit; soy is potentially valuable; fiber from plants may play a very powerful role in preventing and treating diabetes; and coffee may help prevent diabetes.

Thus, the overarching theme is that you can’t necessarily go wrong with a plant-based diet focused on fruits, vegetables, beans and legumes. And if you choose a medical approach, bariatric surgery is a viable option, but don’t forget that you need to make significant lifestyle changes to increase the likely durability over 10 or more years.

References: (1) JAMA. 2007;297:2716-2724. (2) Nutr J. 2013 Mar. 5;12:29. (3) Am J Clin Nutr. 2012 Apr.;95:925-933. (4) BMJ online 2013 Aug. 29. (5) Diabetes Care. online 2014 Feb. 18. (6) Br J Nutr. 2005;93:393–402. (7) Diabetes Care. 2008;31:648-654. (8) N Engl J Med. 1993;328:1676–1685. (9) Diabetes Care. 2014;37:569-586. (10) Obes Surg. 2014;24:437-455.

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

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By David Dunaief, M.D.

 

Dr. David Dunaief

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

Why is chronic kidney disease (CKD) a tricky disease?

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

What are the stages?

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

March is National Kidney Month

Why is CKD important?

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

Who should be screened?

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

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

The fix!

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

Why exercise?

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

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

Protein is important, right?

Yes, protein is important for tissue and muscle health. But when it comes to CKD, more is not necessarily better, and may even be harmful. In a meta-analysis (a group of 10 randomized controlled trials, the gold standard of studies), results showed that the risk of death or treatment with dialysis or kidney transplant was reduced by 32 percent in those who consumed less protein compared to unrestricted protein (6). This meta-analysis used the Cochrane database to search for studies. According to the authors, as few as two patients would need to be treated for a year in order to prevent one from either dying or reaching the need for dialysis or transplant. Unfortunately, the specific quantity of protein consumption that is ideal in CKD patients could not be ascertained since the study was a meta-analysis.

Sodium: How much?

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

Of course medications have a place

We routinely give certain medications, ACE inhibitors or ARBs, to patients who have diabetes to protect their kidneys. What about patients who do not have diabetes? ACEs and ARBs are two classes of anti-hypertensives — high blood pressure medications — that work on the RAAS system of the kidneys, responsible for blood pressure and water balance (8).

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

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

References: (1) Am J Kidney Dis. 2015;65(3):403-411. (2) Am J Kidney Dis. 2013;62(2):245-252. (3) Ann Int. Med. 2012;157(8):567-570. (4) www.Medscape.com. (5) Clin J Am Soc Nephrol. 2014;9(7):1183-1189. (6) Cochrane Database Syst Rev. 2009;(3):CD001892. (7) Curr Opin Nephrol Hypertens. 2014;23(6):533-540. (8) J Am Coll Cardiol. 2014;63(7):650-658.

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

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In Europe, lipoic acid is classified as a drug, unlike in the United States, where it is a supplement.
Lipoic acid may have a significant effect on multiple chronic diseases

By David Dunaief, M.D.

Lipoic acid, also known as alpha lipoic acid and thioctic acid, is a noteworthy supplement. I am not a big believer in lots of supplements for several reasons: Diet contributes thousands more nutrients that work symbiotically; in the United States, supplements are not regulated by the FDA, thus there is no official oversight; and research tends to be scant and not well-controlled.

Dr. David Dunaief

So why would I write about lipoic acid? It is a supplement that has scientific data available from randomized controlled trials, which are the gold standard of studies. In Europe, lipoic acid is classified as a drug, unlike the United States, where it is a supplement (1).

Lipoic acid is an antioxidant, helping to prevent free radical damage to cells and tissues, but also is a chelating agent, potentially removing heavy metals from the body. Lipoic acid is involved in generating energy for cells; it is an important cofactor for the mitochondria, the cell’s powerhouse. It may also boost glutathione production, a powerful antioxidant in the liver (1). We produce small amounts of lipoic acid in our bodies naturally. Lipoic acid may be important in chronic diseases, including Alzheimer’s, multiple sclerosis and diabetic peripheral neuropathy. Let’s look at the evidence.

Diabetic peripheral neuropathy

Diabetic peripheral neuropathy, or diabetic neuropathy, involves oxidative stress and occurs in up to half the population with diabetes. One in five patients, when diagnosed, will already have peripheral neuropathy. The most common type is distal symmetric polyneuropathy — damage to nerves on both sides of the body in similar locations. It causes burning pain, numbness, weakness and pins and needles in the extremities (2).

The best studies with lipoic acid focus on peripheral neuropathy with diabetes. In a double-blinded, randomized controlled trial (SYDNEY I), results showed that the total treatment score had improved significantly more for those receiving 600 mg lipoic acid by intravenous therapy compared to the placebo group (3). Also, individual symptoms of numbness, burning pain and prickling significantly improved in the group treated with lipoic acid compared to placebo.

The study involved 120 diabetes patients with stage 2 neuropathy. Its weakness was its duration; it was a very short trial, about three weeks. The author concluded that this therapy would be a good adjunct for those suffering diabetic neuropathy.

In a follow-up to this study (SYDNEY II), the design and the results were the same (4). In other words, in a second double-blinded, placebo-controlled trial, the lipoic acid treatment group showed significantly better results than the placebo group. There were 180 patients with a similarly short duration of five weeks.

Why include this study? There were several important differences. One was that lipoic acid was given in oral supplements, rather than intravenously. Thus, this is a more practical approach. Another difference is that there were three doses tested for lipoic acid: 600, 1,200 and 1,800 mg. Interestingly, all of them had similar efficacy. However, the higher doses had more side effects of nausea, vomiting and vertigo, again without increased effectiveness. This suggests that an oral dose of 600 mg lipoic acid may help treat diabetic peripheral neuropathy.

Dementia and Alzheimer’s

In a recent randomized, placebo-controlled trial involving Alzheimer’s patients, results were significantly better for lipoic acid (600-mg oral dose) in combination with fish oil, compared to fish oil alone or to placebo (5). The amount of fish oil used was 3 grams daily containing 675 mg docosahexaenoic acid and 975 mg eicosapentaenoic acid of the triglyceride formulation.

The duration of this pilot study was 12 months with 39 patients, and the primary end point was a change in an oxidative stress biomarker, which did not show statistical significance. However, and very importantly, the secondary end point was significant: slowing the progression of cognitive and functional decline with the combination of fish oil and lipoic acid. Minimental status and instrumental activities of daily living declined less in the combination treatment group. This was encouraging, although we need larger trials.

However, another study showed 900 mg lipoic acid in combination with 800 IU daily of vitamin E (alpha tocopherol strain) and 500 mg vitamin C actually mildly reduced an oxidative stress biomarker but had a negative impact on Alzheimer’s disease by increasing cognitive decline on a minimental status exam (6). What we don’t know is whether the combination of supplements in this study produced the disappointing effects or if an individual supplement was the cause. It is unclear since the supplements were tested in combination. The study duration was 16 weeks and involved 78 moderate to severe Alzheimer’s patients.

Multiple sclerosis

In a study involving rats, giving them high doses of lipoic acid resulted in slowing of the progression of multiple sclerosis-type disease (7). The mechanism by which this may have occurred involved blocking the number of inflammatory white blood cells allowed to enter the cerebrospinal fluid in the brain and spinal cord by reducing the enzymatic activity of factors such as matrix metalloproteinases.

I know this sounds confusing, but the important point is that this may relate to a human trial with 30 patients that showed reduction in the enzyme MMP (8). Thus, it could potentially slow the progression of multiple sclerosis. This is purely connecting the dots. We need a large-scale trial that looks at clinical outcomes of progression in MS, not just enzyme levels. The oral dose used in this study was 1,200 to 2,400 mg lipoic acid per day.

Interestingly, the 1,200-mg dose used in the human trial was comparable to the high dose that showed slowed progression in the rat study (9). This only whets the appetite and suggests potential. So, we have lots of data. What do we know? In diabetic neuropathy, 600 mg oral lipoic acid may be beneficial. However, in Alzheimer’s the jury is still out, although 600 mg lipoic acid in combination with fish oil has potential to slow the cognitive decline in Alzheimer’s disease. It also may have a role in multiple sclerosis with an oral dose of 1,200 mg, though this is early data.

Always discuss the options with your physician before taking a supplement; in the wrong combinations and doses, supplements potentially may be harmful. The good news is that it has a relatively clean safety profile. If you do take lipoic acid, know that food interferes with its absorption, so it should be taken on an empty stomach (1).

References: (1) lpi.oregonstate.edu. (2) emedicine.medscape.com. (3) Diabetes Care. 2003;26:770-776. (4) Diabetes Care. 2006;29:2365-2370. (5) J Alzheimer’s Dis. 2014;38:111-120. (6) Arch Neurol. 2012;69:836-841. (7) J Neuroimmunol. 2002;131:104-114. (8) Mult Scler. 2005;11:159-165. (9) Mult Scler. 2010;16:387-397.

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

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CoQ10 is the first new ‘drug’ in over a decade to show survival benefits in heart failure.
A supplement reduces the risk of cardiovascular events

By David Dunaief, M.D.

Heart attacks and heart disease get a lot of attention, but chronic heart failure is something that tends to be overlooked by the press. The reason may be that heart failure is not acute like a heart attack.

Dr. David Dunaief

To clarify by using an analogy, a heart attack is like a tidal wave whereas heart failure is like a tsunami. You don’t know it is coming until it may be too late. Heart failure is an insidious (slowly developing) disease and thus may take years before it becomes symptomatic. It also increases the risk of heart attack and death.

Heart failure occurs in about 20 percent of the population over the age of 40 (1). There are about 5.8 million Americans with heart failure (2). Not surprisingly, incidence of heart failure increases with age (3).

Heart failure (HF) 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, the 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 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 (4). 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 Q10 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 (5). 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, although the next study would suggest 300 mg was the appropriate dose.

CoQ10 — a well-run study

Results of the Q-SYMBIO study, a randomized controlled trial, the gold standard of studies, showed an almost 50 percent reduction in the risk of all-cause mortality and 50 percent fewer cardiac events with CoQ10 supplementation (6). This one randomized controlled trial followed 420 patients for two years who had severe heart failure. This involved using 100 mg of CoQ10 three times a day compared to placebo.

The lead author goes as far as to suggest that CoQ10 should be part of the paradigm of treatment. This the first new “drug” in over a decade to show survival benefits in heart failure. Thus, if you have heart failure, you may want to discuss CoQ10 with your doctor.

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 (7).

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 and iron 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.

References: (1) Circulation. 2002;106(24):3068. (2) Circulation. 2010;121(7):e46. (3) J Am Coll Cardiol. 2003;41(2):21. (4) Am J Med. 2013 Jun:126(6):494-500. (5) Am J Clin Nutr. 2013 Feb;97(2):268-275. (6) JACC Heart Fail. 2014 Dec;2(6):641-649. (7) Am Heart J. 2013;165(4):575-582.

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

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A nutrient-dense, plant-based diet that intensively controls blood sugar is likely to decrease the risk of diabetic retinopathy complication. Stock photo
Diabetic retinopathy is a leading cause of blindness.

By David Dunaief, M.D.

Dr. David Dunaief

With diabetes, we tend to concentrate on stabilization of the disease as a whole. This is a good thing. However, there is not enough attention spent on microvascular (small vessel disease) complications of diabetes, specifically diabetic retinopathy (negativity affecting blood vessels in the back of the eye), which is an umbrella term.

This disease, a complication of diabetes that is related to sugar control, can lead to blurred vision and blindness. There are at least three different disorders that make up diabetic retinopathy. These are dot and blot hemorrhages, proliferative diabetic retinopathy and diabetic macular edema. The latter two are the most likely disorders to cause vision loss. Our focus for this article will be on diabetic retinopathy as a whole and on diabetic macular edema.

Diabetic retinopathy is the No. 1 cause of vision loss in those who are of working age, 25 to 74 years old (1). Risk factors include duration of diabetes, glucose (sugars) that is not well-controlled, smoking, high blood pressure, kidney disease, pregnancy and high cholesterol (2).

What is diabetic macula edema, also referred to as DME? This disorder is edema, or swelling, due to extracellular fluid accumulating in the macula (3). The macula is a yellowish oval spot in the central portion of the retina — in the inner segment of the back of the eye — and it is sensitive to light. The macula is the region with greatest visual acuity. Hence, when fluid builds up from blood vessels leaking, there is potential loss of vision.

Whew! Did you get all that? If not, to summarize: Diabetic macula edema is fluid in the back of the eye that may cause vision loss. The highest risk factor for DME was for those with the longest duration of diabetes (4). Ironically, an oral class of drugs, thiazolidinediones, which includes rosiglitazone (Avandia) and pioglitazone (Actos), used to treat type 2 diabetes may actually increase the risk of DME. However, the results on this are conflicting.

DME is traditionally treated with lasers. But intravitreal (intraocular — within the eye) injections of a medication known as ranibizumab (Lucentis) may be as effective as laser. Studies suggest that injections alone may be as effective as injections plus laser treatments, though the studies are in no way definitive. Unfortunately, many patients are diagnosed with DME after it has already caused vision loss. If not treated after having DME for a year or more, patients can experience permanent loss of vision (5).

In a cross-sectional study (a type of observational study) using NHANES data from 2005-2008, among patients with DME, only 45 percent were told by a physician that the diabetes had affected their eyes (6). Approximately 46 percent of patients reported that they had not been to a diabetic nurse educator, nutritionist or dietician in more than a year — or never.

The problem is that the symptoms of vision loss don’t necessarily occur until the latter stages of the disorder. According to the authors, there needs to be an awareness campaign about the importance of getting your eyes examined on an annual basis if you have diabetes. Many patients are unaware of the association between vision loss and diabetes.

According to a study, there is good news in that the percentage of patients reporting visual impairment from 1997 to 2010 decreased (7). However, the absolute number of patients with vision loss has actually continued to grow, but at a lesser rate than diabetes as a disease has grown.

Treatment options: lasers and injections

There seems to be a potential paradigm shift in the making for the treatment of DME. Traditionally, patients had been treated with lasers. The results from a randomized controlled trial, the gold standard of studies, showed that intravitreal (delivery directly into the eye) injections with ranibizumab, whether given prompt laser treatments or treatments delayed for at least 24 weeks, were equally effective in treating DME (8).

In fact, some in the delayed group, 56 patients or about half, never even required laser treatments at all. Unfortunately, intravitreal injections may be used as frequently as every four weeks. Though in practice, ophthalmologists generally are able to inject patients with the drug less frequently. However, the advantage of receiving prompt laser treatments along with the injections was a reduction in the median number of injections.

Increased risk with diabetes drugs

You would think that drugs to treat type 2 diabetes would prevent DME from occurring as well. However, in the THIN trial, a retrospective (backward-looking) study, a class of diabetes drugs, thiazolidinediones, which includes Avandia and Actos, actually increased the occurrence of DME compared to those who did not use these oral medications (9). Those receiving these drugs had a 1.3 percent incidence of DME at year 1, whereas those who did not had a 0.2 percent incidence. This incidence was persistent through the 10 years of follow-up.

To make matters worse, those who received both thiazolidinediones and insulin had an even greater incidence of DME. There were 103,000 diabetes patients reviewed in this trial. It was unclear whether the drugs, because they were second-line treatments, or the severity of the diabetes itself may have caused these findings.

This is in contrast to a previous ACCORD eye substudy, a cross-sectional analysis, which did not show an association between thiazolidinediones and DME (10). This study involved review of 3,473 participants who had photographs taken of the fundus (the back of the eye).

What does this ultimately mean? Both of these studies were not without weaknesses. It was not clear how long the patients had been using the thiazolidinediones in either study or whether their sugars were controlled and to what degree. The researchers were also unable to control for all other possible confounding factors (11). Thus, there needs to be a prospective (forward-looking) trial done to sort out these results.

Diet

The risk of progression of diabetic retinopathy was significantly lower with intensive blood sugar controls using medications, one of the few positive highlights of the ACCORD trial (12). Medication-induced intensive blood sugar control also resulted in more increased mortality and no significant change in cardiovascular events. But an inference can be made: A nutrient-dense, plant-based diet that intensively controls blood sugar is likely to decrease the risk of diabetic retinopathy complications (13, 14).

The best way to avoid diabetic retinopathy is obviously to prevent diabetes. Barring that, it’s to have sugars well controlled. If you or someone you know has diabetes, it is imperative that they get a yearly eye exam from an ophthalmologist so that DME and diabetic retinopathy, in general, is detected as early as possible, before permanent vision loss can occur. It is especially important for those diabetes patients who are taking the oral diabetes class thiazolidinediones, which include rosiglitazone (Avandia) and pioglitazone (Actos).

References: (1) Diabetes Care. 2014;37 (Supplement 1):S14-S80. (2) JAMA. 2010;304:649-656. (3) www.uptodate.com. (4) JAMA Ophthalmol online. 2014 Aug. 14. (5) www.aao.org/ppp. (6) JAMA Ophthalmol. 2014;132:168-173. (7) Morb Mortal Wkly Rep. 2011;60:1549-1553. (8) ASRS. Presented 2014 Aug. 11. (9) Arch Intern Med. 2012;172:1005-1011. (10) Arch Ophthalmol. 2010 March;128:312-318. (11) Arch Intern Med. 2012;172:1011-1013. (12) www.nei.nih.gov. (13) OJPM. 2012;2:364-371. (14) Am J Clin Nutr. 2009;89:1588S-1596S.

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

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