What I am about to say may be hard to comprehend, especially for those who have germaphobic tendencies, which would be most of us, but we harbor microorganisms, or microbes (small organisms), in our body that outnumber our cells by a 10-to-1 ratio, even in healthy individuals. There are over one trillion microorganisms in the body.

These organisms make up what is called the microbiome. It includes bacteria, viruses and single-cell eukaryotes. Our relationship to these organisms is complex, spanning from parasitic (detrimental) to commensalistic (one benefits and the other is not affected) to mutualistic (both benefit). The microbiome is found throughout the body, including the skin, the eyes and the gut. Our focus is going to be on the gut since that is where the majority of the microbiome resides.

What is the importance of the gut microbiome? The short answer is it may have a role in diseases — preventing and promoting them. These diseases include obesity, diabetes, irritable bowel syndrome, autoimmune diseases, such as rheumatoid arthritis and Crohn’s, and infectious diseases, such as colitis.

Similar to the Human Genome Project, which mapped our genes, there is a Human Microbiome Project, launched by the National Institutes of Health in 2007, to map out the composition and diversity of these gut organisms. We are still in the early stages of understanding this vast universe of microbes, yet there are some preliminary studies.

What impacts the microbiome? It is affected by drugs, such as antibiotics that can wipe out the diversity in the microbes, at least in the short term, and by lifestyle modifications, such as diet. Microbiome diversity may be significantly different in distinct geographic locations throughout the world. Also, the birth process — vaginal compared to Cesarean section — may have a significant influence on an organisms’ composition. Let’s look at the evidence.

C-sections and reduced breast-feeding

The mode of birth delivery may be important. While C-sections have become more common, they may have a negative impact on the development of gut microbes. In a recent study, infants who were delivered by C-section had a significant reduction in Escherichia-Shigella and a lack of Bacteroides in their guts, compared to those delivered by vaginal birth (1). This effect was seen mostly in elective C-sections, since emergency C-sections may have some vaginal influence. Elective C-sections may reduce exposure to maternal microbes.

Breast-feeding may be beneficial to the gut flora. Those infants who were breastfed had a significantly lower concentration of the bacterium Clostridium difficile, which causes colitis (infection of the colon) and diarrhea. The non-breast-fed infants had higher levels of Peptostreptococcaceae, part of the family of Clostridium bacteria, which as mentioned, relates to colitis. This was a very small study involving 24 healthy infants divided equally between male and female. Of course, consult your OB/GYN before making a decision on the birth process, especially if there are extenuating circumstances that prohibit vaginal birth. Fortunately, breast-feeding is already being encouraged.

Obesity: From mice and men

Obesity can be one of the most frustrating disorders; most obese patients continually struggle to lose weight. Obese and overweight patients now outnumber malnourished individuals worldwide (2).

I know this will not come as a surprise, but we are a nation with a weight problem; about 70 percent of Americans are overweight or obese. For the longest time, the paradigm for weight loss had been that if you ate fewer calories, you would lose weight. However, extreme low-caloric diets did not seem to have a long-term impact. It turns out that our guts, dominated by bacteria, may play important roles in obesity and weight loss, determining whether we gain or lose weight. Let’s look at the data on obesity.

The results from a study involving human twins and mice are fascinating (3). In each pair of human twins, one was obese and the other was lean. Gut bacteria from obese human twins were transplanted into thin mice. The result: The thin mice became obese. However, when the lean human twins’ gut bacteria were transplanted to thin mice, the mice remained thin.

By pairing sets of human twins, one obese and one thin in each set, with mice that were identical to each other and raised in a sterile setting, researchers limited the confounding effects of environment and genetics on weight.

The most intriguing part of the study compared the effects of diet and gut bacteria. When the mice who had received gut transplants from obese twins were provided gut bacteria from thin twins and given fruit- and vegetable-rich (high in fiber), low-fat diet tablets, they lost significant weight. But they only lost weight when on a good diet; there was no impact on obesity if the diet was not high in fiber and low in saturated fat. The authors believe this suggests that an effective diet may alter the microbiome of obese patients, helping them lose weight. These are exciting, but preliminary, results. It is not clear yet which bacteria may be contributing these effects. However, the authors theorize that some gut bacteria may have a protective effect against weight gain with a high fiber, low saturated fat diet.

This suggests that the diversity of gut bacteria may be a crucial piece of the weight-loss puzzle.

Rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune disease that can be disabling, with patients typically suffering from significant morning stiffness and joint soreness. What if gut bacteria influenced RA risk? In a recent study, the gut bacteria in mice that were made susceptible to RA by deletion of certain genes (HLA-DR genes) were compared to those who were more resistant to developing RA (4). Researchers found that the RA-susceptible mice had a predominance of Clostridium bacteria and that those resistant to RA were dominated by bacteria of the Bifidobacterium genus and the Porphyromonadaceae family. The significance is that the RA-resistant mice bacteria are known for their anti-inflammatory effects.

Although nobody can say what the ideal gut bacteria should consist of, and the research is still evolving when it comes to the microbiome, there are potential ways of influencing this milieu, especially in our gut. While C-sections definitely have their place, vaginal deliveries may be more beneficial to the infants’ gut bacteria than elective C-sections.

Diet composition seems to be important to the composition and diversity of gut bacteria, impacting the development or prevention of diseases, such as obesity and rheumatoid arthritis.

References: (1) CMAJ. 2013;185:373-374. (2) “The Evolution of Obesity”; Johns Hopkins University Press; 2009. (3) Science. 2013;341:1241214. (4) PLoS One. 2012;7:e36095.

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

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

COPD is an umbrella term that includes emphysema, chronic bronchitis of more than three months for two consecutive years and/or chronic obstructive asthma. It is an obstructive lung disease that limits airflow. The three most common symptoms of the disease involve shortness of breath, especially on exertion, production of sputum and cough. This disease affects greater than 5 percent of the U.S. population (2).

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

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

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

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

Let’s look at the evidence.

Biomarkers for inflammation

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

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

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

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

Statin effect

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

Interestingly, even those who had taken the statin previously saw a significant reduction in COPD exacerbation risk. The duration of statin use was not important; a short use of statins, whether presently or previously, had substantial benefit. However, the greatest benefit was seen in those who had been on a medium to high dose or were on the drug currently. The researchers believe that the mechanism of action for statins in this setting has to do with their anti-inflammatory and immune-modulating effects. This was a retrospective (backward-looking) study with over 14,000 participants. We will need a prospective (forward-looking) study and RCT to confirm the results.

Exercise

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

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

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

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

References:

(1) Natl Vital Stat Rep. 2011 Dec.;59(10):1-126. (2) MMWR Morb Mortal Wkly Rep. 2012;61:938. (3) N Engl J Med. 2002;346:988-994. (4) www.goldcopd.org. (5) JAMA. 2013;309:2353-2361. (6) Respiratory Research. 2013;14:24. (7) Am J Med. 2013 Jul;126:598-606. (8) ATS 2013 International Conference: Abstract A1360. (9) Am J Respir Crit Care Med. 2013; online Feb. 28.

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

What is mild cognitive impairment (MCI)? It is a good question, for the parameters are fuzzy. MCI is a hodgepodge of terminology including amnestic and nonamnestic types, with the amnestic type possibly leading to dementia. It is defined as a disorder, but not a disease, that is between normal aging and dementia. As a disorder, it may be more easily reversed. The number of people affected is difficult to pin down, but estimates range from 14  to 22 percent of the U.S. population aged 70 and older (1). Risk factors for MCI include increased age; family history; chronic diseases including heart disease, high blood pressure and diabetes; drug therapies; and lifestyle (2).

So is being overweight potentially detrimental, or is it being underweight? In short, when you are obese and lose weight, it actually decreases your risk. It is not difficult to understand when you put it into context, which we will do.

Also, are there ways to decrease your risk? Well, I already mentioned one, weight loss for the obese patient. I will delineate how weight loss could be both beneficial and detrimental. Another is a twist on a Mediterranean-type diet.

So without further ado, let’s look at the research. Most of the studies refer to dementia; remember, MCI is a malady not a disease; therefore it is harder to find specific studies relating to increased risk.

Increased weight

Rarely does it seem that being overweight or obese is beneficial. Dementia is no exception. I know I am using the risk of dementia study, but I want to demonstrate that the overweight and obese individuals, who now make up at least two-thirds of the U.S. population, are jeopardizing their cognitive abilities.

In an observational study using the Swedish Twin Registry, results showed that being overweight or obese in midlife significantly increased dementia risk — a 71 percent increase in the overweight patient and an almost fourfold increase in the obese (3). This may be a powerful reason to watch your weight at any age.

Underweight

If being obese or overweight may be harmful, what about being underweight? According to the results of a retrospective (backward-looking) study from the UK Clinical Practice Research Datalink, those who are underweight have a 34 percent increased risk of dementia and are at greater risk than those who are overweight or obese (4). In fact, this study suggests that those who are overweight and obese are at lower risk for dementia than even those who are normal weight.

But wait, how can that be? Didn’t the study above suggest that being overweight was bad? First impression says that either the study focusing on overweight/obese patients was wrong or this study has a caveat. Well, the latter is the case. In fact, the researchers did not delineate among potential causes for patients to be underweight or even normal weight. Many times, patients are underweight or normal weight at middle to advanced years due to weight loss-inducing chronic diseases, such as cancer and autoimmune diseases. Underweight was defined as a BMI <20 kg/m2. Other previous studies also contradict the obesity paradox seen in this study.

Unintended weight loss

In one recent study, results demonstrated that unintended weight loss from midlife to later life is a potentially ominous sign for increased risk of mild cognitive impairment (5). There was a statistically significant difference between those who were at higher risk of developing MCI because of greater unintentional weight loss and those who did not experience as much weight loss. The absolute difference was 0.8 kg and the increased risk was 4 percent; however, in a subgroup with a 5-kg weight loss every 10 years, there was an almost 25 percent increased risk of mild cognitive impairment. At the beginning of the study, none of the patients had MCI, and the average age was 70 years. The researchers used retrospective data to compile weight loss from midlife.

Possible solutions to the rescue

What can be done about this? There are lifestyle changes, including dietary changes and weight loss that may help to reduce   the risk or even reverse MCI.

Weight loss, intentional that is!

On the flip side to unintended weight loss, there is intentional weight loss in those who are obese. In a recent randomized controlled trial (RCT), results showed that those who were treated with a calorie-restricted diet saw improvements in language, memory and executive functioning (allows one to complete tasks or reach goals) compared to those in the conventional medicine treatment group without diet counseling (6). The study population had a mean age of 68 and included 80 participants with 40 participants in each arm. It was composed of 80 percent women. Those in both groups were obese, ranging in BMI from obese to morbidly obese, 30-49.5 kg/m2.

The goal was to reach 10 percent weight loss with most of these women, though that was not achieved. This study used a calorie-restricted diet to achieve weight loss. About 40 percent of the participants did lose 5 percent of weight during the study’s one-year duration. The good news: Even with this modest 5 percent weight loss, there was improvement in cognition, especially verbal memory, which involves remembering words and utilizing language skills. The more weight they lost, the better they did cognitively (a dose-response curve). This is encouraging for a follow-up study with more significant weight loss.

Mediterranean diet with extra fat

Recently, we have been furiously debating the importance of fat in the diet. In an RCT, results showed that adding extra virgin olive oil (EVOO) or nuts to the Mediterranean-type diet increased participants’ cognitive functioning (7). There were three groups; all were on the Mediterranean diet, but the two treatment groups differed — one had added EVOO and the other had added nuts.

Interestingly, nuts and olive oil had different effects. The group that had nuts, consisting of one ounce per day of a mixture of almonds, walnuts and hazelnuts, saw an improvement in word memory.

Meanwhile, those in the EVOO group saw more gains in thought processing, executive functioning in the frontal cortex. The EVOO group consumed five tablespoons of olive oil a day, or one liter a week. This is a large amount of olive oil. Remember, though, that the brain is made up of 70 percent fat. There were a total of 447 study participants with a mean age of 67 years, and the study duration was pretty long at approximately four years. No participant had mild cognitive impairment at the start of the trial, though they were at high risk for cardiovascular disease.

Although there was significant improvement in cognition in the treatment groups compared to the control, there was no difference in occurrence of MCI.  Overall incidence of MCI was very small across the groups. A good follow-up study might be a group eating a Mediterranean diet with olive oil plus nuts.

A diet high in “good” fats, especially a Mediterranean-type diet with either nuts or olive oil, appears to be beneficial to improve cognition in older adults.

References:

(1) Arch Neurol. 1999;56(3):303; Ann Intern Med. 2008;148(6):427. (2) uptodate.com. (3) Neurology. 2011;76(18):1568-1574. (4) Lancet Diabetes Endocrinol. 2015;3(6):431-436. (5) JAMA Neurol. online Feb. 1, 2016. (6) J Clin Endocrinol Metab. online Dec. 29, 2015. (7) JAMA Intern Med. 2015 Jul;175(7):1094-1103

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

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

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

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

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

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

Let’s look at some of the research.

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

PPI and kidney disease

In two separate studies, results showed that there was an increase in chronic kidney disease with prolonged PPI use (5). All of the patients started the study with normal kidney function based on glomerular filtration rate (GFR). In the Atherosclerosis Risk in Communities (ARIC) study, there was a 50 percent increased risk of chronic kidney disease, while the Geisinger Health System cohort study found there was a modest 17 percent increased risk. The first study had a 13-year duration, and the second had about a six-year duration. Both demonstrated a modest, but statistically significant, increased risk of chronic kidney disease. But as you can see, the medications were used on a chronic basis for years. In an accompanying editorial to these published studies, the author suggests that there is overuse of the medications or that they are used beyond the resolution of symptoms and suggests starting with diet and lifestyle modifications as well as a milder drug class, H2 blockers (6).

PPI and dementia

A recent German study looked at health records from a large public insurer and found there was a 44 percent increased risk of dementia in the elderly who were using PPIs, compared to those who were not (7). These patients were at least age 75. The authors surmise that PPIs may cross the coveted blood-brain barrier and have effects by potentially increasing beta-amyloid levels, markers for dementia. With occasional use, meaning once every 18 months for a few weeks to a few months, there was a much lower increased risk of 16 percent. The researchers also suggested that PPIs may be significantly overprescribed in the elderly. Unfortunately, there were confounding factors that may have conflated the risk, such as multiple drug use, having diabetes, or patient also having depression or a stroke history. Researchers also did not take into account family history of dementia, high blood pressure or excessive alcohol use, all of which have effects on dementia occurrence.

PPI and bone fractures

In a recent meta-analysis (a group of 18 observational studies), results showed that PPIs can increase the risk of hip fractures, spine fractures and any-site fractures (8). Interestingly, when it came to bone fractures, it did not make a difference whether patients were taking PPIs for more or less than a year. How much less than a year was not delineated. They found increased fracture risks of 58, 26 and 33 percent for spine, hip and any site, respectively. It is not clear what may potentially increase the risk; however, it has been proposed that it may have to do with calcium absorption through the gut. PPIs reduce the amount of acid, which may be needed to absorb insoluble calcium salts. In another study, seven days of PPIs were shown to lower the absorption of calcium carbonate supplements when taken without food (9).

Need for magnesium

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

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

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

References:

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

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

Cardiovascular disease is anything but boring; what we know about it is constantly evolving. New information comes along all the time, which on the whole is a good thing. Even though this disease has been on the decline, it is still the number one killer of Americans, responsible for about one million deaths per year (1). However, not all studies nor all analyses on the topic are created equal. Therefore, I thought it apropos to present a quiz on cardiovascular disease myths and truths.

Saturated fat

Most of the medical community has been under the impression that saturated fat is not good for us. We need to limit our intake to no more than 10 percent of our diet. But is this true? The results of a meta-analysis (a group of 72 randomized clinical trials and observational studies) challenge this paradigm (2). While saturated fat did not decrease the risk of cardiovascular disease, it did not significantly increase the risk either. Also, the results showed that trans fats increase the risk of this disease. Of course, trans fats are a processed fat, so this is something that most of us would agree upon. And in the clinical trials portion of the meta-analysis, omega-3 and omega-6 polyunsaturated fats did not significantly reduce the risk of cardiovascular disease.

Does this mean that we can go back to eating saturated fats with impunity? Well, there were weaknesses and flaws with this study. The authors only looked at the one dimension of fat. Their comparison was based on the upper third of intake of one type of fat versus the lower third of intake of the same type of fat (whether it was saturated fat or a type of unsaturated fat). It did not consider whether saturated fat was substituted with refined grains or unsaturated fatty acids. Also, what was the source of saturated fats, animal or plant, and did these sources also contain unsaturated fats as well, like olive oil or nuts, which contain good fats? Therefore, there are many unanswered questions and potentially several significant flaws with this study.

Mark Bittman, a popular columnist for The New York Times, referenced this meta-analysis as his justification for promoting butter and other sources of saturated animal fat, such as cheese, pork and the skin from chicken. Many of his articles in the past have contributed to the health and wellness of his readers. In this case, I think he does a disservice to his readers, making statements that are dangerous and hopefully will not result in more cardiovascular disease.

The meta-analysis above, which Bittman uses to buoy his arguments, does not differentiate among plant or animal saturated fat sources. But in one that does, the researchers found saturated fats from animal sources increased cholesterol and the risk of cardiovascular disease (3). In another study, specifically using unsaturated fats in place of saturated fat reduced the risk of cardiovascular disease (4, 5).

Fish oil

There is whole industry built around fish oil and reducing the risk of cardiovascular disease. Yet the data don’t seem to confirm this theory. In the latest study, the age-related eye disease study 2 (AREDS2), unfortunately, 1 gram of fish oil (long-chain omega-3 fatty acids) daily did not demonstrate any benefit in the prevention of cardiovascular disease nor its resultant mortality (6). This study was done over a five-year period in the elderly with macular degeneration. The cardiovascular primary end point was a tangential portion of the ophthalmic AREDS2. This does not mean that fish, itself, falls into that same category, but for now there does not seem to be a need to take fish oil supplements for heart disease, except potentially for those with very high triglycerides. Fish oil, at best, is controversial; at worst, it has no benefit with cardiovascular disease.

Fiber

We know that fiber tends to be important for a number of diseases, and cardiovascular disease does not appear to be an exception. In a meta-analysis, involving 22 observational studies, the results showed a linear relationship between fiber intake and decreased risk for developing cardiovascular disease (7). In other words, for every 7 grams of fiber consumed, there was 9 percent reduced risk in developing the disease. It did not matter the source of the fiber from plant foods; vegetables, grains and fruit all decreased the risk of cardiovascular disease. This did not involve supplemental fiber, like that found in Fiber One or Metamucil.

To give you an idea about how easy it is to get a significant amount of fiber, one cup of lentils has 15.6 grams of fiber, one cup of raspberries or green peas has almost 9 grams and one medium-size apple has 4.4 grams. Americans are sorely deficient in fiber (8).

We typically get between 8 to 14 grams of fiber so we have a lot of room for improvement. The American Dietetic Association recommends 25 grams of fiber for women and 40 grams for men, but I advocate 40 grams for both.

Diet soda

A 2014 presentation at the American College of Cardiology examined the Women’s Health Initiative: The study suggests that diet soda may increase the risk of heart disease (9). In those drinking two or more cans per day, defined as 12 ounces per can, there was a 30 percent increased risk of a cardiovascular event, such as a stroke or heart attack, but an even greater risk of cardiovascular mortality, 50 percent, over 10 years. These results took into account confounding factors like smoking, diabetes, high blood pressure and obesity. This study involved over 56,000 postmenopausal women for an almost nine-year duration.

Vitamin D

The results of an observational study in the elderly suggest that vitamin D deficiency may be associated with cardiovascular disease risk. The study showed that those whose vitamin D levels were low had increased inflammation, demonstrated by elevated biomarkers including C-reactive protein (CRP) (10). This biomarker is related to inflammation of the heart, though it is not as specific as one would hope.

Beware in regards to saturated fat. If a study looks like an outlier or too good to be true, then it probably is. I would not run out and get a cheeseburger just yet. However, study after study has shown benefit with fiber. So if you want to reduce the risk of cardiovascular disease, consume as much whole food fiber as possible. Also, since we live in the Northeast, consider taking at least 1000 IUs of vitamin D daily. This is a simple way to help thwart the risk of the number one killer.

References:

(1) uptodate.com. (2) Ann Intern Med. 2014;160(6):398-406. (3) JAMA 1986;256(20):2623. (4) Am J Clin Nutr. 2009;99(5):1425-1432. (5) Cochrane Database Syst Rev. 2012:5;CD002137. (6) JAMA Intern Med. Online March 17, 2014. (7) BMJ 2013; 347:f6879. (8) Am J Med. 2013 Dec;126(12):1059-1067.e1-4. (9) ACC Scientific Sessions 2014; Abstract 917-05. (10) J Clin Endocrinol Metab online February 24, 2014.

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

Not surprisingly, osteoarthritis is widespread. The more common joints affected are the knees, hips and hands. There are three types of treatment for this disease: surgery, involving joint replacements of the hips or knees; medications; and nonpharmacologic approaches. The most commonly used first-line medications are acetaminophen and nonsteroidal anti-inflammatory drugs, such as ibuprofen. Unfortunately, medications mostly treat the symptoms of pain and inflammation.

However, the primary objectives in treating osteoarthritis should also include improving quality of life, slowing progression of the disease process and reducing its disabling effects (1).

Dairy and milk

When we think of dairy, specifically milk, there are two distinct camps: One believes in the benefits, and the other thinks it may contribute to disease. In this case they both may be at least partly correct. In the Osteoarthritis Initiative study, an observational study of over 2,100 patients, results showed that low-fat (1 percent) and nonfat milk may slow the progression of osteoarthritis (2). The researchers looked specifically at joint space narrowing that occurs in those with affected knee joints. Radiographic imaging changes were used at baseline and then to follow the patients for up to 12 to 48 months for changes. Compared to those who did not drink milk, patients who did saw significantly less narrowing of knee joint space.

Was it a dose-dependent response? Not necessarily. Specifically, those who drank less than three glasses/week and those who drank four to six glasses/week both saw slower progression of joint space narrowing of 0.09 mm. Seven to 10 glasses/week resulted in a 0.12 mm preservation. However, those who drank more than 10 glasses/week saw less beneficial effect, 0.06 mm preservation compared to those who did not drink milk. Interestingly, there was no benefit seen in men or with the consumption of cheese or yogurt.

However, there are significant flaws with this study. First, the patients were only asked about their dietary intake of milk at baseline; therefore their consumption could have changed during the study. Second, there was a recall bias; patients were asked to recall their weekly milk consumption for the previous 12 months before the study began. I don’t know about you, but I can’t recall my intake of specific foods for the last week, let alone for the past year. Third, there could have been confounding factors, such as orange consumption.

Oddly, this was not a dose-response curve, since the most milk consumption had less beneficial effect than lower amounts. Also, why were these effects only seen in women? Finally, researchers could not explain why low-fat or nonfat milk had this potential benefit, but cheese was detrimental and yogurt did not show benefit. We are left with more questions than answers.

Would I recommend consuming low-fat or nonfat milk? Not necessarily, but I may not dissuade osteoarthritis patients from drinking it. There are very few approaches that slow the progression of joint space narrowing.

Vitamin D

Over the last five years or so, the medical community has gone from believing that vitamin D was potentially the solution to many diseases to wondering whether, in some cases, low levels were indicative of disease, but repletion was not a change-maker. Well, in a recent randomized controlled trial, the gold standard of studies, vitamin D had no beneficial symptom relief, nor any disease-modifying effects (3). This two-year study of almost 150 men and women raised blood levels of vitamin D on average to 36 ng/ml, which is considered respectable. Researchers used MRI and X-rays to track their results.

Glucosamine

There is raging debate about whether glucosamine is an effective treatment for osteoarthritis. In the latest installment, there was a RCT, the results of which showed that glucosamine hydrochloride was not effective in treating osteoarthritis (4). In the trial, 201 patients with either mild or moderate knee pain drank diet lemonade with or without 1500 mg of glucosamine hydrochloride.

There was no difference in cartilage changes in the knee nor in pain relief in those in the placebo or treatment groups over a six-month duration. Bone marrow lesions also did not improve with the glucosamine group. The researchers used 3T MRI scans (an advanced radiologic imaging technique) to follow the patients’ disease progression. This does not mean that glucosamine does not work for some patients. Different formulations, such as glucosamine sulfate, were not used in this study.

Weight

This could not be an article on osteoarthritis if I did not talk about weight. Do you remember analogies from the SATs? Well here is one for you: Weight loss, weight loss, weight loss is to osteoarthritis as location, location, location is to real estate. In a recent study involving 112 obese patients, there was not only a reduction of knee symptoms in those who lost weight, but there was also disease modification, with reduction in the loss of cartilage volume around the medial tibia (5).

On the other hand, those who gained weight saw the inverse effect. A reduction of tibial cartilage is potentially associated with the need for knee replacement. The relationship was almost one-to-one; for every 1 percent of weight lost, there was a 1.2 mm3 preservation of medial tibial cartilage volume, while the exact opposite was true with weight gain.

Exercise and diet

In a recent study, diet and exercise trumped the effects of diet or exercise alone (6). Patients with osteoarthritis of the knee who lost at least 10 percent of their body weight experienced significant improvements in function and a 50 percent reduction in pain, as well as reduction in inflammation, compared to those who lost 5 to 10 percent and those who lost less than 5 percent. This study was a well-designed, randomized controlled single-blinded study with a duration of 18 months.

Researchers used a biomarker — IL6 — to measure inflammation. The diet and exercise group and the diet-only group lost significantly more weight than the exercise-only group, 23.3 pounds and 19.6 pounds versus 4 pounds. The diet portion consisted of a meal replacement shake for breakfast and lunch and then a vegetable-rich, low-fat dinner. Low-calorie meals replaced the shakes after six months. The exercise regimen included one hour of a combination of weight training and walking with alacrity three times per week.

Therefore, concentrate on lifestyle modifications if you want to see potentially disease-modifying effects. These include both exercise and diet. In terms of low-fat or nonfat milk, while the study had numerous flaws, if you drink milk, you might continue for the sake of osteoarthritis, but stay on the low end of consumption. And remember, the best potential effects shown are with weight loss and with a vegetable-rich diet.

References:

(1) uptodate.com. (2) Arthritis Care Res online. 2014 April 6. (3) JAMA. 2013;309:155-162. (4) Arthritis Rheum online. 2014 March 10. (5) Ann Rheum Dis online. 2014 Feb. 11. (6) JAMA. 2013;310:1263-1273.

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

Last week, I wrote about factors that increase the risk of gallstones, an all-too-common gastrointestinal problem. Many of these factors are modifiable. Continuing on the topic, this week I will discuss complications and prevention techniques.

Complications include cardiovascular disease, psoriasis and pancreatitis. I’ve written in the past about the gallstone-pancreatitis association. Here, I will focus on other complications.

Cardiovascular complications

Cardiovascular disease, comprised of heart disease and stroke, is responsible for about 45 percent of deaths in the United States. In a recent observational, prospective (forward-looking) study, the results show an overall 32 percent increased risk of cardiovascular disease in patients with gallstones (1). When these results are further broken out, there was a 42 percent increased risk of heart disease, a 15 percent increased risk of stroke and a 31 percent increased risk of heart failure. These results are scary.

Interestingly, those who were younger, 18 to 40 years old, were at the highest risk of developing cardiovascular disease. And those who had mild gallstone disease were at higher risk, as well. This study was six years in duration and involved more than 34,000 patients. The authors hypothesized that the possible reason for this association between gallstones and cardiovascular disease may have to do with an abundance of cholesterol, inflammation and oxidative stress.

Psoriasis and psoriatic arthritis

In the Nurses’ Health Study II, a prospective observational trial, results show that there is a 70 percent increased risk of developing psoriasis and a 196 percent increased risk of developing psoriatic arthritis in women who have a personal history of gallstone disease (2). These results were segregated from obesity. In fact, this association between gallstones and psoriasis was greatest in those who had a body mass index of <30 — a threefold increased risk.

This is not an excuse to be obese, however, because there was still a significantly increased risk, 1.71-fold, in the obese group. There were 89,234 women involved in this study over a 14-year follow-up period. As with cardiovascular disease’s association with gallstones, inflammation also may play a role with gallstones and psoriasis and psoriatic arthritis. Therefore, it may be important to reduce inflammation in the body to prevent gallstones and their complications.

Prevention

Fortunately, there are several ways to reduce the occurrence of gallstones, including lifestyle changes with exercise and diet, such as coffee, more fiber, statins and unsaturated nontrans fats (3).

Physical activity

In last week’s article on risk factors for gallstones, low physical activity increased the risk of this disease. It turns out that the opposite is also true. In the Physicians’ Health Study, results showed a significant reduction in the risk of gallstones in those in the highest quintile of activity compared to those in the lowest quintile (4). In fact, men who were in the highest quintile and under 64 years old saw the greatest reduction — 42 percent — in the risk of gallstones. However, those over the age of 65 and in the highest quintile of activity also had substantial reductions in risk — 25 percent. There were 45,813 men involved in this study over an eight-year duration. The authors concluded that, overall, 34 percent of symptomatic gallstones could be avoided if men did aerobic training for an average of 30 minutes per day, five days a week.

Fruits and vegetables

If you ever needed another reason to consume more fruits and vegetables, reducing the risk of gallstones may motivate you.

In the Nurses’ Health Study, the results showed that those in the highest quintile of fruit and vegetable intake had a 21 percent reduction in the need for a cholecystectomy (surgery to remove the gallbladder, usually due to symptomatic gallstones) compared to those in the lowest quintile (5). Interestingly, fruits and vegetables looked at separately had the same significant reduction as fruits and vegetables taken together. There were 77,090 women involved in the study with a 16-year duration.

The fruits and vegetables consumed in the study were common; they included citrus fruits, green leafy vegetables, cruciferous vegetables and other vitamin C-rich fruits and vegetables. The authors surmise that the effect may be due to antioxidants, vitamin C, dietary fiber and minerals like magnesium — and to the interactions among these different components.

This was not just a reduction in gallstones, but a reduction in the actual number of surgical procedures. This makes it a very powerful study. To give perspective, there are around 800,000 cholecystectomies done each year in the United States (6).

Rapid weight loss diets

I mentioned in last week’s article that rapid weight loss increases the risk of gallstone formation. However, if you were going to attempt a rapid weight loss diet, which is better: high fiber or high animal protein? Well, in a small, randomized controlled study, the gold standard of studies, results show that a high-fiber, very low calorie diet had one-third the number of patients with gallstone formation compared to a high-protein, very low calorie diet (7).

Although it is better not to lose weight rapidly, as far as gallstones are concerned, there may be lower risk with a high-fiber diet rather than with an animal-protein-dominant diet. It is important to note that this study considered rapid weight loss to be more than 20 pounds in a month. Both groups lost about the same amount of weight. However, the high-fiber diet resulted in less biliary sludge. The study included 68 patients with a mean BMI of 35 kg/m2, severely obese, at the start of the trial.

Coffee effect

Coffee must be one of the more controversial beverages. Using the Swedish Mammography Cohort and the Cohort of Swedish Men studies, a meta-analysis of two studies, the results show that only women, not men, had a significantly reduced risk of undergoing cholecystectomies in those who drank at least six cups of coffee a day, versus those who drank fewer than two cups (8). And this effect was not seen in all women, but only in those women who were premenopausal or on hormone replacement therapy. A cup was considered eight ounces. Does this mean these specific women should drink more coffee? Not necessarily, for it seems as if every good result is balanced out with a bad result when it comes to coffee and gallstones.

In conclusion, it is important to prevent gallstones since this disorder can lead to significant complications, including cardiovascular disease and death. Lifestyle modifications and even some medications may reduce the risk of gallstones, which in turn could have a beneficial impact on reducing heart disease and strokes, as well as autoimmune diseases, such as psoriasis and psoriatic arthritis. Inflammation seems to be the common denominator when it comes to gallstones, their complications and the ways to prevent them.

References:

(1) PLoS One. 2013 Oct 3;8(10):e76448. (2) Br J Dermatol. online Oct 11, 2014. (3) uptodate.com. (4) Ann Intern Med. 1998;128(6):417. (5) Am J Med. 2006;119(9):760. (6) AdvData. 2002;(329):1-19. (7) Georgian Med News. 2014;(231):95-99. (8) Clin Gastroenterol Hepatol. online Sep 19, 2014.

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

Have you ever heard the paradox, the more I know, the more I realize how much I don’t know? I think this statement can be aptly applied to our knowledge of hypertension, better known as high blood pressure. When it comes to high blood pressure, it is not clear if it is a disease, in itself, or a condition that may contribute to diseases such as heart disease, heart attacks, stroke, kidney failure and even death (1). Or high blood pressure may be an indicator of blood vessel disease. And if this is not confusing enough, no matter how you want to classify high blood pressure, what is the best way to control it, and what levels are ideal?

Another frightening fact is that high blood pressure has a very high prevalence in the United States. The lifetime risk of having this disorder is 90 percent for those who are 55 and older. Thus, we need to be able to effectively reverse or prevent high blood pressure.

Upheaval among the ranks in terms of blood pressure levels

What are the goals for those patients with high blood pressure? The Joint National Committee is the most recognized organization to provide evidence-based guidelines to the medical community for blood pressure. This committee’s latest iteration, referred to as JNC 8, actually relaxed the levels to control blood pressure in those 60 years and older to less than 150/90 mmHg. For everyone below the age of 60, it should be less than 140/90, even for those who have diabetes (2). Interestingly, there is insufficient evidence on the systolic (top) number for those 30-59 years old and on the diastolic (bottom) number for those under 30 years old. Therefore, the recommendations for those under 60 are based on expert consensus. Of course, these levels are based on the assumption that we are treating with blood pressure medication.

The new evidence, but buyer beware

However, in a recent randomized controlled trial (SPRINT trial), results showed that when systolic blood pressure was reduced to below 120 mmHg, compared to the previous standard of 140 mmHg, there was a significant 30 percent reduction in the primary composite end point in the intensive vs. standard treatment groups (3). The composite end point involved nonfatal heart attack, nonfatal stroke, acute coronary syndrome, heart failure, or cardiovascular death. There was also a 25 percent reduction in all-cause mortality in the intensive treatment group. This trial involved 9,361 patients followed over 3.2 years. The trial was stopped early because of these positive results.

Does this mean we should treat aggressively with medication?

The caveats to this trial are several. One, the population was very specific. It involved patients who were at high risk of cardiovascular disease. The Framingham coronary heart disease risk score was at least 15 percent but with a mean of 20 percent. Two, the trial excluded diabetes patients and those with previous strokes. Considering these two factors, it means that one in six patients with high blood pressure would be appropriate for intensive blood pressure treatment with medication to a target systolic blood pressure of less than 120 mmHg.

Three, this study, does not take into account lifestyle modifications, which are very important to controlling and possibly reversing high blood pressure. Four, there was a significant increased risk of adverse events, such as hypotension (low blood pressure). If someone were to change their lifestyle, it might exacerbate this problem even more.

How can we better control blood pressure?

Office readings are not enough to know if blood pressure is controlled. Home readings are very important as well, although they are not always the most accurate. So, how do we determine what the home readings mean? A recent study tries to shed light on this issue. In the study of 286 patients, results showed that those who had at least three out of 10 systolic readings of >135 mmHg were likely to have uncontrolled high blood pressure confirmed using the gold standard of testing, 24-hour ambulatory blood pressure monitoring (4). Those who had these elevated readings were at higher risk for end organ damage affecting the heart and surrounding blood vessels. This isn’t a perfect system, but it is better than using clinic blood pressures readings alone.

What about sodium?

The recommended levels for daily sodium vary from organization to organization and depending on whether or not you have high blood pressure. The most lenient recommendation, from the 2015 U.S. Dietary Guidelines, is 2300 mg per day (5), and the most stringent, by the American Heart Association, is 1500 mg per day for everyone, though there seems to be a general consensus for targeting less than 1500 mg per day for those with high blood pressure. Whatever level you may deem appropriate, a recent study shows that about 90 percent of adult Americans are consuming more than 2300 mg per day and 86 percent of high blood pressure patients are not maintaining appropriate levels (6).

So, should we lay off the salt shaker? Not necessarily. We are getting 75 percent of our intake from restaurants and from processed foods, those that come in a box (7). In fact, small amounts of iodized salt may be beneficial. However, fancy salts such as Himalayan Pink, sea salt, kosher and others may not be iodized.

These guidelines don’t seem to differentiate between added sodium and sodium that occurs naturally in foods. In fact, if you eat a diet rich in dark leafy green vegetables, there is about 700-800 mg of naturally occurring sodium in these foods. What is great about this is that these vegetables also contain nutrients that help counterbalance the effects of sodium, such as potassium and nitrates. They also have an anti-inflammatory effect that benefits the endothelial layer, or the inner lining, of your blood vessels.

My recommendation is to avoid salt from processed foods by reading labels, although meats such as chicken can be injected with sodium without labeling. And if you do eat out, request that the chef not salt the food. If you use salt at home, use only iodized salt.

Added sugar – not so sweet

Dentists are right when they say don’t eat sugar. Their reasons are to protect to protect your teeth from decay. Well, there are many other reasons not to eat sugar. The recent REGARDS study found that a high-sugar (Southern or sweets/fat) diet may be associated with the risk of high blood pressure, whereas a plant-based diet was not (8). The mechanisms for this effect may have to do with the fact that added sugar raises insulin levels, which may raise the levels of aldosterone, the hormone responsible for the reabsorption of sodium from the kidneys. Those with the highest amount of insulin were found to have a greater than three times increased risk of high blood pressure.

When treating high blood pressure with medications, we need to individualize treatment. However, lifestyle modifications can be applied to everyone, regardless of age or risk of heart disease. If you have high blood pressure, you should take home readings and show them to your doctor for review.

References:

(1) J of Hypertension 2011:29:896-905. (2) JAMA. 2014;311(5):507-520. (3) N Engl J Med 2015; 373:2103-2116. (4) Ann Fam Med. 2016;14:63-69. (5) U.S. Department of Health and Human Services and U.S. Department of Agriculture. 2015 – 2020 Dietary Guidelines for Americans. 8th Edition. December 2015. (6) Morb Mortal Wkly Rep. 2016;64:1393-1397. (7) cdc.org. (8) Obesity Week 2015 Abstract T-OR-2108.

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

Triglycerides is a term that most of us recognize. This substance is part of the lipid (cholesterol) profile. However, this may be the extent of our understanding. Compared to the other substances, HDL (“good” cholesterol) and LDL (“bad” cholesterol), triglycerides are not covered much in the lay press, and medical research tends to be less robust than for the other components. If I were to use a baseball analogy, triglycerides are the Mets, who get far less attention than their crosstown rivals, the Yankees. Although last year, the Mets received the attention they deserved, so let’s see if this year we can get triglycerides the attention they deserve.

But are triglycerides any less important than other parts of the cholesterol profile? It is unclear whether a high triglyceride level is a biomarker for cardiovascular disease — heart disease and stroke — or an independent risk in its own right (1, 2). This debate has been going on for over 30 years. Either way, it still means triglycerides are important.

What are triglycerides? The most rudimentary explanation is that they are a kind of fat in the blood. Triglycerides are composed of sugar alcohol and three fatty acids.  Thus, it is no surprise that alcohol, sugars and excess calorie consumption may be converted into triglycerides.

Risk factors for high triglycerides include obesity, smoking, a high carbohydrate diet, uncontrolled diabetes, hypothyroidism (underactive thyroid), cirrhosis (liver disease), excessive alcohol consumption and some medications (3).

What levels are normal and what are considered elevated? According to the American Heart Association, optimal levels are <100 mg/dL; however, less than 150 mg/dL is considered within normal range. Borderline triglycerides are 150-199 mg/dL, high levels are 200-499 mg/dL and very high are >500 mg/dL (3).

While medicines that focus on triglycerides, fibrates and niacin, have the ability to lower them significantly, it is questionable whether this reduction results in clinical benefits, such as reducing the risk of cardiovascular events. The ACCORD Study, a randomized controlled trial, questioned the effectiveness of medication; when these therapies were added to statins in type 2 diabetes patients, they did not further reduce the risk of cardiovascular disease and events (4). Instead, it seems that lifestyle modifications may be the best way to control triglyceride levels. Let’s look at the evidence.

Exercise — timing and intensity

If you need a reason to exercise, here is really good one. I frequently see questions pertaining to optimal exercise timing and intensity. Most of the answers are vague, and the research is not specific. However, hold on to your hats because a recent study may give the timing and intensity answer, at least in terms of triglycerides.

Study results showed that walking a modest distance with alacrity and light weight training approximately an hour after eating (postprandial) reduced triglyceride levels by 72 percent (5). However, if patients did the same workout prior to eating, postprandial triglycerides were reduced by 25 percent. This is still good, but not as impressive. Participants walked a modest distance of just over one mile (2 kilometers). This was a small pilot study of 10 young healthy adults for a very short duration. The results are intriguing nonetheless, since there are few data that give specifics on the optimal amount and timing of exercise.

Exercise trumps calorie restriction

There is good news for those who want to lower their triglycerides: calorie restriction may not be the best answer. In other words, you don’t have to torture yourself by cutting calories down to some ridiculously low level to get an effect. We probably should be looking at exercise and carbohydrate intake instead.

In a well-controlled trial, results showed that those who walked and maintained 60 percent of their maximum heart rate, which is a modest level, showed an almost one-third reduction in triglycerides compared to the control group (maintain caloric intake and no exercise expenditure) (6). Those who restricted their calorie intake saw no difference compared to the control. This was a small study of 11 young adult women. Thus, calorie restriction was trumped by exercise as a way to potentially reduce triglyceride levels.

Carbohydrate reduction not calorie restriction

In addition, when calorie restriction was compared to carbohydrate reduction, results showed that carbohydrate reduction was more effective at lowering triglycerides (7). In this small but well-designed study, patients with nonalcoholic fatty liver disease were randomized to one of two diets, lower calorie (1200-1500 kcal/day) or lower carbohydrate (20 g/day). Both groups significantly reduced triglycerides, but the lower carbohydrate group reduced triglycerides by 55 percent versus 28 percent for the lower calorie group. The reason for this difference may have to do with oxidation in the liver and the body as a whole. Both groups lost similar amounts of weight, so weight could not be considered a confounding or complicating factor. However, the weakness of this study was its duration of only two weeks.

Fasting versus nonfasting blood tests

The paradigm has been that, when cholesterol levels are drawn, fasting levels provide a more accurate reading. Except this may not be true.

In a new analysis, fasting may not be necessary when it comes to cholesterol levels. NHANES III data suggest that nonfasting and fasting levels yield similar results related to all-cause mortality and cardiovascular mortality risk. The LDL levels were similarly predictive regardless of whether a patient had fasted or not. The researchers used 4,299 pairs of fasting and nonfasting cholesterol levels. The duration of follow-up was strong, with a mean of 14 years (8).

Why is this relevant? Triglycerides are an intricate part of a cholesterol profile. With regards to stroke risk assessment, nonfasting triglycerides possibly may be more valuable than fasting. In a study involving 13,596 participants, results showed that as nonfasting triglycerides rose, the risk of stroke also rose significantly (9). Compared to those who had levels below 89 mg/dL (the control), those with 89-176 mg/dL had a 1.3-fold increased risk of cardiovascular events, whereas those within the range of 177-265 mg/dL had a twofold increase, and women in the highest group (>443 mg/dL) had an almost fourfold increase. The results were similar for men, but not quite as robust at the higher end, with a threefold increase.

The benefit of nonfasting is that it is more realistic and, according to the authors, also involves remnants of VLDL and chylomicrons, other components of the cholesterol profile that interact with triglycerides and may affect the inner part (endothelium) of the arteries.

What have we learned? Triglycerides need to be discussed, just as we review HDL and LDL levels regularly. Elevated triglycerides may result in heart disease or stroke. The higher the levels, the more likely there will be increased risk of mortality — both all-cause and cardiovascular. Therefore, we ideally should reduce levels to less than 100 mg/dL.

Lifestyle modifications using carbohydrate restriction and modest levels of exercise after a meal may be the way to go to achieve the best results, though the studies are small and need more research. Nonfasting levels may be as important as fasting levels when it comes to triglycerides and the cholesterol profile as a whole; they potentially give a more realistic view of cardiovascular risk, since we don’t live in a vacuum and fast all day.

References:

(1) Circulation. 2011;123:2292-2333. (2) N Engl J Med. 1980;302:1383–1389. (3) nlm.nih.gov. (4) N Engl J Med. 2010;362:1563-1574. (5) Med Sci Sports Exerc. 2013;45(2):245-252. (6) Med Sci Sports Exerc. 2013;45(3):455-461. (7) Am J Clin Nutr. 2011;93(5):1048-1052. (8) Circulation Online. 2014 July 11. (9) JAMA 2008;300:2142-2152.

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