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Dr. David Dunaief

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People who are considered metabolically healthy may still have a higher risk of developing heart problems if they are obese.
Obesity still increases risks of many chronic diseases

By David Dunaief, M.D.

Have we entered a fourth dimension where it’s possible to be obese and healthy? Hold on to your seats for this wild ride. This would be a big relief, since more than one-third of Americans are obese, another third are overweight and the numbers are on the rise (1). In one analysis referenced by the Centers for Disease Control and Prevention (CDC), the average medical cost for obesity alone is 41.5 percent higher than for those of normal weight, based on 2006 numbers (2). Still, there are several studies that suggest it’s possible to be metabolically healthy and still be obese.

What does metabolically healthy mean? It is defined as having no increased risk of diabetes or cardiovascular disease (heart disease and stroke) because blood pressure, cholesterol levels and inflammatory biomarkers remain within normal limits.

However, read on before thinking that obesity can be equated with health. Though several studies may suggest metabolic health with obesity, there is a caveat: Some of these obese patients will go on to become metabolically unhealthy; but even more importantly, obesity will increase their risk significantly for a number of other chronic diseases. These include osteoarthritis, diverticulitis, rheumatoid arthritis and migraine. There is also a higher rate of premature mortality, or death, associated with obesity. In other words, the short answer is that obesity is NOT healthy.

Metabolically healthy obesity

Several published studies imply that there is such a thing as “metabolically healthy obesity,” or MHO. In the Cork and Kerry Diabetes and Heart Disease Phase 2 Study, results show that approximately one-third of obese patients may fall into the category of metabolically “healthy” (3). This means that they are not at increased risk of cardiovascular disease, based on five metabolic parameters, including LDL “bad” cholesterol, HDL “good” cholesterol, triglycerides, fasting plasma glucose and insulin resistance. The researchers compared three groups: MHO, metabolically unhealthy obese and nonobese participants. Both the MHO participants and the nonobese patients demonstrated these positive results.

There were over 2,000 participants involved in this study, with an equal proportion of men and women ranging in age from 45 to 75. The researchers believe that a beneficial inflammation profile, including a lower C-reactive protein and a lower white blood cell count, may be at the root of these results.

In the North West Adelaide Health Study, a prospective (forward-looking) study, the results show that one-third of obese patients may be metabolically healthy, but it goes further to say that this occurs in mostly younger patients, those less than 40 years old, and those with a lower waist circumference and more fat in the legs (4). The reason for the positive effects may have to do with how fat is transported through the body.

In metabolically unhealthy obese patients, fat is deposited in the organs, such as the liver and heart, potentially leading to cardiovascular disease and type 2 diabetes. A theory is that mitochondria, the cells’ energy source, are disrupted, potentially increasing inflammation.

However, the results also showed that over a 10-year period, one-third of “healthy” obese patients transitioned into the unhealthy category. Over a longer period of time, this number may increase.

Premature mortality

To hammer the nail into the coffin, so to speak, obesity may be associated with premature mortality. In one study, about 20 percent of American patient deaths were associated with being obese or overweight (5). The rates were highest among white men, white women and black women. The researchers found this statistic surprising; previous estimates were far lower. Researchers reviewed a registry of 19 consecutive National Health Interview Surveys, from 1986 to 2004, including more than 500,000 patients with ages ranging from 40 to 84.9 years old.

Interestingly, obesity seems to have more of an effect on mortality as we age: obesity raised mortality risk 100 percent in those who were 65 and over, compared to a 25 percent increased risk in those who were 45.

Osteoarthritis

It is unlikely that any group of obese patients would be able to avoid pressure on their joints. In an Australian study, those who were obese had a greater than two times increased risk of developing osteoarthritis of the hip and a greater than seven times increased risk of developing osteoarthritis of the knee (6). If this weren’t bad enough, obese patients complained of increased pain and stiffness, as well as decreased functioning, in the hip and knee joints. There were over 1,000 adults involved in this study. Patients who were 39 years or older demonstrated that obesity’s impact on osteoarthritis can affect those who are relatively young.

There is a solution to obesity and its impact on osteoarthritis of the knees and hips. In a randomized controlled trial of 454 patients over 18 months, those who lost just 10 percent of their body weight saw significant improvement in function and knee joint pain, compared to those who lost less than 10 percent of their body weight (7). So, if you are 200 pounds, this would mean you would experience benefits after losing only 20 pounds.

When diet and exercise together were utilized, patients saw the best outcomes, with reduced pain and inflammation and increased mobility, compared to diet or exercise alone. However, diet was superior to exercise in improving knee joint pressure. Also, inflammatory biomarkers were reduced significantly more in the combined diet and exercise group and in the diet alone group, compared to the exercise alone group.

The diet was composed of two shakes and a dinner that was vegetable rich and low in fat. The exercise component involved both walking with alacrity plus resistance training for a modest frequency of three times a week for one hour each time. Thus, if you were considering losing weight and did not want to start both exercise and diet regimens at once, focusing on a vegetable-rich diet may be most productive.

While it is interesting that some obese patients are metabolically healthy, this does not necessarily last, and there are a number of chronic diseases involved with increased weight. Though we should not be prejudiced or judgmental of obese patients, this disease needs to be treated to avoid increased risk of mortality and increased risk of developing other diseases.

References: (1) CDC.gov. (2) Health Aff. September/October 2009;vol. 28 no. 5 w822-w831. (3) J Clin Endocrinol Metab online. 2013 Aug. 26. (4) Diabetes Care. 2013;36:2388-2394. (5) Am J Public Health online. 2013 Aug. 15. (6) BMC Musculoskelet Disord. 2012;13:254. (7) 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, visit www.medicalcompassmd.com or consult your personal physician.

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Stress may increase cold virus severity

By David Dunaief, M.D.

Dr. David Dunaief

September marks the beginning of the academic calendar and noticeably shorter daylight hours. The pace of life tends to become more hectic. Although some stress is valuable to help motivate us and keep our minds sharp, high levels of constant stress can have detrimental effects on the body.

It is very likely that there is a mind-body connection when it comes to stress. In other words, it may start in the mind, but it can lead to acute or chronic disease promotion. Stress can also play a role with your emotions, causing irritability and outbursts of anger and possibly leading to depression and anxiety.

Stress symptoms are hard to distinguish from other disorders, but they can include stiff neck, headaches, stomach upset and difficulty sleeping. Stress may also be associated with cardiovascular disease, with an increased susceptibility to infection from viruses causing the common cold and with cognitive decline and Alzheimer’s (1).

A stress steroid hormone called cortisol is released from the adrenal glands and can have beneficial effects in small bursts. We need cortisol in order to survive. Some of cortisol’s functions include raising glucose (sugar) levels when they are low and helping reduce inflammation and stress levels (2). However, when cortisol gets out of hand, higher chronic levels may cause inflammation, leading to disorders such as cardiovascular disease, as research suggests. Let’s look at the evidence.

Inflammation 

Inflammation may be a significant contributor to more than 80 percent of chronic diseases, so it should be no surprise that it is an important factor with stress. In a meta-analysis (a group of two observational studies), high levels of C-reactive protein (CRP), a biomarker for inflammation, were associated with increased psychological stress (3).

What is the importance of CRP? It may be related to heart disease and heart attacks. This study involved over 73,000 adults who had their CRP levels tested. The research went further to suggest that increased levels of CRP may result in more stress and also depression. With CRP higher than 3.0 there was a greater than twofold increase in depression risk. The researchers suggest that CRP may heighten stress and depression risk by increasing levels of different proinflammatory cytokines, inflammatory communicators among cells (4).

In another study, results suggested that stress may influence and increase the number of hematopoietic stem cells (those that develop all forms of blood cells), resulting specifically in an increase in inflammatory white blood cells (5). The researchers suggest that this may lead to these white blood cells accumulating in atherosclerotic plaques in the arteries, which ultimately could potentially increase the risk of heart attacks and strokes.

Chronic stress overactivates the sympathetic nervous system — our “fight or flight” response — which may alter the bone marrow where the stem cells are found. This research is preliminary and needs well-controlled trials to confirm these results.

Infection

Stress may increase the risk of colds and infection. Cortisol over the short term is important to help suppress the symptoms of colds, such as sneezing, cough and fever. These are visible signs of the immune system’s infection-fighting response.

However, the body may become resistant to the effects of cortisol, similar to how a type 2 diabetes patient becomes resistant to insulin. In one study of 296 healthy individuals, participants who had stressful events and were then exposed to viruses had a higher probability of catching a cold. It turns out that these individuals also had resistance to the effects of cortisol. This is important because those who were resistant to cortisol had more cold symptoms and more proinflammatory cytokines (6).

Diabetes and heart disease

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

Lifestyle changes can reduce effects of stress

Lifestyle plays an important role in stress at the cellular level, specifically at the level of the telomere, which determines cell survival. The telomeres are to cells what the plastic tips are to shoelaces; they prevent them from falling apart. The longer the telomere, the slower the cell ages and the longer it survives. In a study, those women who followed a healthy lifestyle — one standard deviation over the average lifestyle — were able to withstand life stressors better since they had longer telomeres (8).

This healthy lifestyle included regular exercise, a healthy diet and a sufficient amount of sleep. On the other hand, the researchers indicated that those who had poor lifestyle habits lost substantially more telomere length than the healthy lifestyle group. The study followed women 50 to 65 years old over a one-year period.

In another study, chronic stress and poor diet (high sugar and high fat) together increased metabolic risks, such as insulin resistance, oxidative stress and central obesity, more than a low-stress group eating a similar diet (9). The high-stress group members were caregivers, specifically those caring for a spouse or parent with dementia. Thus, it is especially important to eat a healthy diet when under stress.

Interestingly, in terms of sleep, the Evolution of Pathways to Insomnia Cohort (EPIC) study shows that those who deal with stressful events directly are more likely to have good sleep quality. Using medication, alcohol or, most surprisingly, distractors to deal with stress all resulted in insomnia after being followed for one year (10). Cognitive intrusions or repeat thoughts about the stressor also resulted in insomnia.

Psychologists and other health care providers sometimes suggest distraction from a stressful event, such as television watching or other activities, according to the researchers. However, this study suggests that this may not help avert chronic insomnia induced by a stressful event. The most important message from this study is that how a person reacts to and deals with stressors may determine whether they suffer from insomnia.

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

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

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

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A gluten-free diet can significantly improve symptoms in patients with irritable bowel syndrome.
Gluten control may help with IBS

By David Dunaief, M.D.

Dr. David Dunaief

Gluten has been gaining in notoriety over the last several years. When we hear someone mention a gluten-free diet, several things tend to come to mind. One may be that this is a healthy diet. Along the same lines, we may think gluten is bad for us. However, gluten-free is not necessarily synonymous with healthy. There are many beneficial products containing gluten.

We might think that gluten-free diets are a fad, like low-fat or low-carb diets. Still, we keep hearing how more people feel better without gluten. Could this be a placebo effect? What is myth and what is reality in terms of gluten? In this article I will try to distill what we know about gluten and gluten-free diets, who may benefit and who may not.

But first, what is gluten? Most people I ask don’t know the answer, which is okay; it is part of the reason I am writing the article. Gluten is a plant protein found mainly in wheat, rye and barley.

Now to answer the question of whether going gluten-free is a fad. The answer is a resounding “no” since we know that patients who suffer from celiac disease, an autoimmune disease, benefit tremendously when gluten is removed (1). In fact, it is the main treatment.

But what about people who don’t have celiac disease? There seems to be a spectrum of physiological reaction to gluten, from intolerance to gluten (sensitivity) to gluten tolerance (insensitivity). Obviously, celiac disease is the extreme of intolerance, but even these patients may be asymptomatic. Then, there is nonceliac gluten sensitivity (NCGS), referring to those in the middle portion of the spectrum (2). The prevalence of NCGS is half that of celiac disease, according to the NHANES data from 2009-2010 (3). However, many disagree with this assessment, indicating that it is much more prevalent and that its incidence is likely to rise (4). The term was not even coined until 2011.

What is the difference between full-blown celiac disease and gluten sensitivity? They both may present with intestinal symptoms, such as bloating, gas, cramping and diarrhea, as well as extraintestinal (outside the gut) symptoms, including gait ataxia (gait disturbance), malaise, fatigue and attention deficit disorder (5). Surprisingly, they both may have the same results with serological (blood) tests, which may be positive or negative. The first line of testing includes anti-gliadin antibodies and tissue transglutaminase. These measure a reaction to gluten; however, they don’t have to be positive for there to be a reaction to gluten. HLA–DQ phenotype testing is the second line of testing and tends to be more specific for celiac disease.

What is unique to celiac disease is a histological change in the small intestine, with atrophy of the villi (small fingerlike projections) contributing to gut permeability, what might be called “leaky gut.” Biopsy of the small intestine is the most definitive way to diagnose celiac disease. Though the research has mainly focused on celiac disease, there is some evidence that shows NCGS has potential validity, especially in irritable bowel syndrome.

Before we look at the studies, what does it mean when a food says it’s “gluten-free”? Well, the FDA has weighed in by passing regulation that requires all gluten-free foods to have no more than 20 parts per million of gluten (6).

Irritable bowel syndrome

Irritable bowel syndrome (IBS) is a nebulous disease diagnosed through exclusion, and the treatments are not obvious. That is why the results from a randomized controlled trial, the gold standard of studies, showing that a gluten-free diet significantly improved symptoms in IBS patients, is so important (7). Patients were given a muffin and bread on a daily basis.

Of course, one group was given gluten-free products and the other given products with gluten, though the texture and taste were identical. In six weeks, many of those who were gluten-free saw the pain associated with bloating and gas mostly resolve; significant improvement in stool composition, such that they were not suffering from diarrhea; and their fatigue diminished. In fact, in one week, those in the gluten group were in substantially more discomfort than those in the gluten-free group. There were 34 patients involved in this study.

As part of a well-written March 4, 2013 editorial in Medscape by David Johnson, M.D., a professor of gastroenterology at Eastern Virginia Medical School, he questions whether this beneficial effect from the IBS trial was due to gluten withdrawal or to withdrawal of fermentable sugars because of the elimination of some grains, themselves (8). In other words, gluten may be just one part of the picture. He believes that nonceliac gluten sensitivity is a valid concern.

Autism

Autism is a very difficult disease to quantify, diagnose and treat. Some have suggested gluten may play a role. Unfortunately, in a study with children who had autism spectrum disorder and who were undergoing intensive behavioral therapy, removing both gluten and casein, a protein found in dairy, had no positive impact on activity or sleep patterns (9). These results were disappointing. However, this was a very small study involving 22 preschool children. Removing gluten may not be a panacea for all ailments.

Antibiotics

The microbiome in the gut may play a pivotal role as to whether a person develops celiac disease. In an observational study using data from the Swedish Prescribed Drug Register, results indicate that those who were given antibiotics within the last year had a 40 percent greater chance of developing celiac disease and a 90 percent greater risk of developing inflammation in the gut (10). The researchers believe that this has to do with dysbiosis, a misbalance in the microbiota, or flora, of the gastrointestinal tract. It is interesting that celiac disease may be propagated by change in bacteria in the gut from the use of antibiotics.

Not everyone will benefit from a gluten-free diet. In fact, most of us will not. Ultimately, people who may benefit from this type of diet are those patients who have celiac disease and those who have symptomatic gluten sensitivity. Also, patients who have positive serological tests, including tissue transglutaminase or anti-gliadin antibodies are good candidates for gluten-free diets.

There is a downside to a gluten-free diet: potential development of macronutrient and micronutrient deficiencies. Therefore, it would be wise to ask your doctor before starting gluten withdrawal. The research in patients with gluten sensitivity is relatively recent, and most gluten research has to do with celiac disease. Hopefully, we will see intriguing studies in the near future, since the U.S. market for gluten-free packaged products has grown to over $1.5 billion.

References: (1) Am J Gastroenterol. 2013;108:656-676. (2) Gut 2013;62:43–52. (3) Scand J Gastroenterol. (4) Neurogastroenterol Motil. 2013 Nov;25(11):864-871. (5) medscape.com. (6) fda.gov. (7) Am J Gastroenterol. 2011; 106(3):508-514. (8) medscape.com. (9) 9th annual AIM for Autism Research 2010; abstract 140.007. (10) BMC Gastroenterol. 2013:13(109).

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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Studies have shown that eating grapefruit reduces your risk of developing diabetes.
Be wary of ‘no sugar added’ labels

By David Dunaief, M.D.

Dr. David Dunaif

We should all reduce the amount of added sugar we consume because of its negative effects on our health. It is recommended that we get no more than 10 percent of our diet from added sugars (1). However, we are consuming at least 30 percent more added sugar than is recommended (2).

Is all sugar bad for us? The answer is not straightforward. It really depends on the source, and when I mention “source,” my meaning may surprise you.

We know that white, processed sugar is bad. But, I am constantly asked which sugar source is better: honey, agave, raw sugar, brown sugar or maple syrup. None are really good for us; they all raise the level of glucose (a type of sugar) in our blood.

Two-thirds of our sugar intake comes from processed food, while one-third comes from sweetened beverages, according to the most recent report from the Centers for Disease Control and Prevention. (2) Sweetened beverages are defined as sodas, sports drinks, energy drinks and fruit juices. That’s right: Even 100 percent fruit juice can raise glucose levels. Don’t be deceived by “no added sugar” labels.

These sugars increase the risk of, and may exacerbate, chronic diseases, such as diabetes, heart disease, high blood pressure, cancer and obesity. This is such a significant problem that several legislative initiatives have been introduced that would require a warning label on sweetened drinks (3).

However, I did say that sugar’s source impacts its effect. Most fruits have beneficial effects in preventing disease, including diabetes, and do not raise sugar levels, even in patients with diabetes. It is a myth that whole fruit raises your sugar levels. However, dried fruits, fruit juice and fruit juice concentrate do raise your sugar levels. Note that sugar extracted from fruit has an effect similar to that of sugar added to foods and sweetened beverages. Let’s look at the evidence.

Heart disease

When we think of sugar’s effects, heart disease is not usually the first disease that comes to mind. However, results from a 20-year study of 31,000 U.S. adults showed that, when comparing those who consumed the least amount of added sugar (less than 10 percent of calories daily) with those who consumed 10 to 25 percent and those who consumed more than 25 percent of daily calories from sugar, there were significant increases in risk of death from heart disease (4). The added sugar was from foods and sweetened beverages, not from fruit and fruit juices. This was not just an increased risk of heart disease, but an increased risk of cardiovascular death. This is a wake-up call to rein in our sugar consumption.

Obesity and weight gain

Does soda increase obesity risk? An assessment published in PLoS One, a highly respected, peer-reviewed journal, showed that it depends on whether studies were funded by the beverage industry or had no ties to any lobbying groups (5). Study results were mirror images of each other: Studies not affiliated with the industry show that soda may increase obesity risk, while studies funded by the beverage industry show there may not be any association.

In studies without beverage industry funding, greater than 80 percent (10 of 12) showed associations between sugary drinks and increased weight or obesity, whereas with the beverage industry-funded studies, greater than 80 percent of them did not show this result (5 of 6). The moral of the story is that patients must be diligent in understanding how studies are funded; and if the results sound odd, they probably are. If this is the case, make sure to ask your doctor about the studies’ findings. Not all studies are equally well designed.

Diabetes and the benefits of fruit

Diabetes requires the patient to limit or avoid fruit altogether. Correct? This may not be true. Several studies may help change the long-standing, commonly held paradigm that fruit should be restricted in patients with diabetes and to prevent development of diabetes.

One study found that whole fruit may reduce the risk of diabetes by reducing inflammation and reducing insulin resistance (6). Specifically, results demonstrated a reduction in the inflammatory biomarker hsCRP. Ultimately, this may result in better glucose control. A potential reason for these impressive results may be the high levels of flavonoids, specifically anthocyanins and flavones.

Flavonoids, as a class, are phytochemicals (plant nutrients) that provide pigment to fruits and vegetables and may have substantial antioxidant activities. Substances that are high in these two flavonoids include red grapes, berries, tea and wine.

Another study, a meta-analysis that looked at three large studies, including the Nurses’ Health Study, NHS II, and the Health Professionals Follow-up Study, showed that those who consumed the highest amount of anthocyanins were likely to experience a 15 percent reduction in the development of type 2 diabetes (7). Researchers compared those in the highest quintile of anthocyanin consumption with those in the lowest quintile.

Specifically, at least two servings of blueberries per week were shown to reduce the risk of diabetes by 23 percent, and at least five servings of apples and pears per week were also shown to reduce the risk by 23 percent. These were compared to those who consumed less than one serving per month. This is a small amount of fruit for a significant reduction.

From the same three studies, it was also shown that grapes, bananas and grapefruit reduce the risk of diabetes, while fruit juice and cantaloupe may increase risk (8).

In still another diabetes study, involving those who were newly diagnosed with type 2 diabetes, the risk of increasing glucose levels was no greater in those who consumed more than two servings of fruit per day, when compared to those who consumed fewer than two servings per day (9).

The properties of flavonoids, which are found in whole fruit, may also result in anticancer and anticardiovascular disease properties, the opposite effect of added sugars (10).

Chronic disease incidence and complications from these diseases have skyrocketed in the last several decades. Therefore, any modifiable risk factor should be utilized to decrease our risk. By keeping added sugar to a minimum in our diets, we could make great strides in the fight to maintain our quality of life as we age.

We don’t have to avoid sugar completely; we still can satiate a sweet tooth by eating ripe fruits. Our access to fruit, even off-season, has expanded considerably. The most amazing thing is that fruit may actually reduce the risk of diabetes, something we thought for years might exacerbate it.

References: (1) health.gov: Dietary Guidelines for Americans 2015-2020, eighth edition. (2) cdc.gov. (3) reuters.com. (4) JAMA Intern Med. online Feb 3, 2014. (5) PLoS Med. 2013 Dec;10(12):e1001578. (6) J Nutr. 2014 Feb;144(2):202-208. (7) Am J Clin Nutr. 2012 Apr;95(4):925-933. (8) BMJ. online Aug 29, 2013. (9) Nutr J. published online March 5, 2013. (10) Plant Foods Hum Nutr. 2004 Summer;59(3):113-122.

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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Coffee may decrease levothyroxine absorption

By David Dunaief, M.D.

Dr. David Dunaief

It seems like everyone has heard of hypothyroidism. But do we really know what it is and why it is important? The thyroid is a butterfly-shaped organ responsible for maintaining our metabolism. It sits at the base of the neck, just below the laryngeal prominence, or Adam’s apple. The prefix “hypo,” derived from Greek, means “under” (1). Therefore, hypothyroidism indicates an underactive thyroid and results in slowing of the metabolism.

Many people get hypo- and hyperthyroidism confused, but they are really complete opposites. Blood tests determine if a person has hypothyroidism. Items that are tested include thyroid stimulating hormone (TSH), which is usually increased, thyroxine (free T4) and triiodothyronine (free T3 or T3 uptake). Both of these last two may be suppressed (2).

The thyroid sits at the base of the neck, just below the Adam’s apple and is responsible for maintaining metabolism.

There are two types of primary hypothyroidism: subclinical and overt. In the overt (more obvious) type, classic symptoms include weight gain, fatigue, thinning hair, cold intolerance, dry skin and depression, as well as the changes in all three thyroid hormones on blood tests mentioned above. In the subclinical, there may be less obvious or vague symptoms and only changes in the TSH. The subclinical can progress to the overt stage rapidly in some cases (3). Subclinical is substantially more common than overt; its prevalence may be as high as 10 percent of the U.S. population (4).

What are potential causes or risk factors for hypothyroidism? There are numerous factors, such as medications, including lithium; autoimmune diseases, whether personal or in the family history; pregnancy, though it tends to be transient; and treatments for hyperthyroidism (overactive thyroid), including surgery and radiation.

The most common type of hypothyroidism is Hashimoto’s thyroiditis (5). This is where antibodies attack thyroid gland tissues. Several blood tests are useful to determine if a patient has Hashimoto’s: thyroid peroxidase (TPO) antibodies and antithyroglobulin antibodies.

Myths versus realities

I would like to separate the myths from the realities with hypothyroidism. Does treating hypothyroidism help with weight loss? Not necessarily. Is soy potentially bad for the thyroid? Yes. Does coffee affect thyroid medication? Maybe. And finally, do vegetables, specifically cruciferous vegetables, negatively impact the thyroid? Probably not. Let’s look at the evidence.

Treatments: medications and supplements

When it comes to hypothyroidism, there are two main medications: levothyroxine and Armour Thyroid. The difference is that Armour Thyroid converts T4 into T3, while levothyroxine does not. Therefore, one medication may be more appropriate than the other, depending on the circumstance. However, T3 can be given with levothyroxine, which is similar to using Armour Thyroid.

What about supplements?

A recent study tested 10 different thyroid support supplements; the results were downright disappointing, if not a bit scary (6). Of the supplements tested, 90 percent contained actual medication, some to levels higher than what are found in prescription medications. This means that the supplements could cause toxic effects on the thyroid, called thyrotoxicosis. Supplements are not FDA-regulated, therefore, they are not held to the same standards as medications. There is a narrow therapeutic window when it comes to the appropriate medication dosage for treating hypothyroidism, and it is sensitive. Therefore, if you are going to consider using supplements, check with your doctor and tread very lightly.

Soy impact

What role does soy play with the thyroid? In a randomized controlled trial, the gold standard of studies, the treatment group that received higher amounts of soy supplementation had a threefold greater risk of conversion from subclinical hypothyroidism to overt hypothyroidism than those who received considerably less supplementation (7). Thus, it seems that in this small, yet well-designed, study, soy has a negative impact on the thyroid. Therefore, those with hypothyroidism may want to minimize or avoid soy. Interestingly, those who received more soy supplementation did see improvements in blood pressure and inflammation and a reduction in insulin resistance, but, ultimately, a negative impact on the thyroid.

The reason that soy may have this negative impact was illustrated in a study involving rat thyrocytes (thyroid cells) (8). Researchers found that soy isoflavones, especially genistein, which are usually beneficial, may contribute to autoimmune thyroid disease, such as Hashimoto’s thyroiditis. They also found that soy may inhibit the absorption of iodide in the thyroid.

Weight loss

Since being overweight and obese is a growing epidemic, wouldn’t it be nice if the silver lining of hypothyroidism is that, with medication to treat the disease, we were guaranteed to lose weight? In a recent retrospective (looking in the past) study, results showed that only about half of those treated with medication for hypothyroidism lost weight (9). This has to be disappointing to patients. However, this was a small study, and we need a large randomized controlled trial to test it further.

WARNING: The FDA has a black box warning on thyroid medications — they should never be used as weight loss drugs (10). They could put a patient in a hyperthyroid state or worse, having potentially catastrophic results.

Coffee

I am not allowed to take away my wife’s coffee; she draws the line here with lifestyle modifications. So I don’t even attempt to with my patients, since coffee may have some beneficial effects. But when it comes to hypothyroidism, taking levothyroxine and coffee together may decrease the absorption of levothyroxine significantly, according to one study (11). It did not seem to matter whether they were taken together or an hour apart. This was a very small study involving only eight patients. Still, I recommend avoiding coffee for several hours after taking the medication. This should be okay, since the medication must be taken on an empty stomach.

Vegetables

There is a theory that vegetables, specifically cruciferous ones such as cauliflower, cabbage and broccoli, may exacerbate hypothyroidism. In one animal study, results suggested that very high intake of these vegetables reduces thyroid functioning (12). This study was done over 30 years ago, and it has not been replicated.

Importantly, this may not be the case in humans. In the recently published Adventist Health Study-2, results showed that those who had a vegan-based diet were less likely to develop hypothyroidism than those who ate an omnivore diet (13). And those who added lactose and eggs to the vegan diet also had a small increased risk of developing hypothyroidism. However, this trial did not focus on raw cruciferous vegetables, where additional study is much needed.

There are two take-home points, if you have hypothyroid issues: Try to avoid soy products, and don’t think supplements that claim to be thyroid support and good for you are harmless because they are over the counter and “natural.” In my clinical experience, an anti-inflammatory, vegetable-rich diet helps improve quality of life issues, especially fatigue and weight gain, for those with Hashimoto’s thyroiditis.

References: (1) dictionary.com. (2) nlm.nih.gov. (3) Endocr Pract. 2005;11:115-119. (4) Arch Intern Med. 2000;160:526-534. (5) mayoclinic.org. (6) Thyroid. 2013;23:1233-1237. (7) J Clin Endocrinol Metab. 2011 May;96:1442-1449. (8) Exp Biol Med (Maywood). 2013;238:623-630. (9) American Thyroid Association. 2013;Abstract 185. (10) FDA.gov. (11) Thyroid. 2008;18:293-301. (12) Crit Rev Food Sci Nutr. 1983;18:123-201. (13) Nutrients. 2013 Nov. 20;5:4642-4652.

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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Adding cruciferous vegetables to your diet significantly decreases the risk of developing multiple cancers. Stock photo
Small studies show diet may affect gene expression

By David Dunaief, M.D.

Dr. David Dunaief

Cancer, a word that for decades was whispered as taboo, has become front and center in the medical community. Cancer is the number one killer of Americans, at least those less than 85 years old, even ahead of cardiovascular disease (1). We have thought that diet may be an important component in preventing cancer. Is diet a plausible approach?

An April 24, 2014, article published in the New York Times, entitled “An Apple a Day and Other Myths,” questioned the validity of diet in the prevention of cancer. This article covered cancer in general, which is a huge and daunting topic.

The article’s author referenced a comment by Walter Willet, M.D., a professor at the Harvard School of Public Health’s Epidemiology and Nutrition Department, as indicating that the research is inconsistent when it comes to fruits and vegetables. The article went on to state that even fiber and fats may not play significant roles in cancer.

I don’t necessarily disagree with this assessment. However, I would like to emphasize that Willet also commented that there are no large, well-controlled diet studies. This leaves the door open for the possibility that diet does have an impact on cancer prevention. I would like to respond.

As Willet hinted, the problem with answering this question may lie with the studies themselves. The problem with diet studies in cancer, in particular, is that they rely mainly on either retrospective (backward-looking) or prospective (forward-looking) observational studies.

Observational studies have many weaknesses. Among them is recall bias, or the ability of subjects to remember what they did. Durability is also a problem; the studies are not long enough, especially with cancer, which may take decades to develop. Confounding factors and patient adherence are other challenges, as are the designs and end points of the studies (2). Plus, randomized controlled trials are very difficult and expensive to do since it’s difficult and much less effective to reduce the thousands of compounds in food into a focus on one nutrient. Let’s look at the evidence.

The EPIC trial

Considered the largest of the nutrition studies is the European Prospective Investigation into Cancer and Nutrition (EPIC). It is part of what the author was using to demonstrate his point that fruits and vegetables may not be effective, at least in breast cancer. This portion of the study involved almost 300,000 women from eight different European nations (3). Results showed that there was no significant difference in breast cancer occurrence between the highest quintile of fruit and vegetable consumption group compared to the lowest. The median duration was 5.4 years.

Does this study place doubt in the dietary approach to cancer? Possibly, but read on. The most significant strength was its size. However, there were also many weaknesses. The researchers were trying to minimize confounding factors, but there were eight countries involved, with many different cultures, making it almost impossible to control. It is not clear if participants were asked what they were eating more often than at the study’s start. Risk stratification was also not clear; which women, for example, might have had a family history of the disease?

Beneficial studies with fruits and vegetables

Also, using the same EPIC study, results showed that fruit may have a statistically significant impact on lung cancer (4). Results showed that there was a 40 percent decrease in the risk of developing lung cancer in those that were in the highest quintile of fruit consumption, compared to those in the lowest quintile. However, vegetables did not have an impact. The results were most pronounced in the northern European region. I did say the answer was complex.

Ironically, it seems that some other studies, mostly smaller studies, show potentially beneficial effects from fruits and vegetables. This may be because it is very difficult to run an intensive, well-controlled, large study.

Prostate cancer

Dean Ornish, M.D., a professor of medicine at UC San Francisco Medical School, has done several well-designed pilot studies with prostate cancer. His research has a focus on how lifestyle affects genes. In one of the studies, results of lifestyle modifications showed a significant increase in telomere length over a five-year period (5).

Telomeres are found on the end of our chromosomes; they help prevent the cell from aging, becoming unstable and dying. Shorter telomeres may have an association with diseases, such as cancer and aging and morbidity (sickness). Interestingly, the better patients adhered to the lifestyle modifications, the more telomere growth they experienced. However, in the control group, telomeres decreased in size over time. There were 10 patients in the lifestyle (treatment) group and 25 patients in the control group — those who followed an active surveillance-only approach.

In an earlier study with 30 patients, there were over 500 changes in gene expression in the treatment group. Of these, 453 genes were down-regulated, or turned off, and 48 genes were up-regulated, or turned on (6). The most interesting part is that these changes occurred over just a three-month period with lifestyle modifications.

In both studies, the patients had prostate cancer that was deemed at low risk of progressing into advanced or malignant prostate cancer. These patients had refused immediate conventional therapy including hormones, radiation and surgery. In both studies, the results were determined by prostate biopsy. These studies involved intensive lifestyle modifications that included a low-fat, plant-based, vegetable-rich diet. But as the researchers pointed out, there is a need for larger randomized controlled trials to confirm these results.

Cruciferous vegetables

A meta-analysis involving a group of 24 case-control studies and 11 observational studies, both types of observational trials, showed a significant reduction in colorectal cancer (7). This meta-analysis looked at the effects of cruciferous vegetables, also sometimes referred to as dark-green, leafy vegetables.

In another study that involved a case-control observational design, cruciferous vegetables were shown to significantly decrease the risk of developing multiple cancers, including esophageal, oral cavity/pharynx, breast, kidney and colorectal cancers (8). There was also a trend that did not reach statistical significance for preventing endometrial, prostate, liver, ovarian and pancreatic cancers. The most interesting part is that the comparison was modest, contrasting consumption of at least one cruciferous vegetable a week with none or less than one a month. However, we need large, randomized trials using cruciferous vegetables to confirm these results.

In conclusion, it would appear that the data are mixed in terms of the effectiveness of fruits and vegetables in preventing cancer or its progression. The large studies have flaws, and pilot studies require larger studies to validate them. However, imperfect as they are, there are results that indicate that diet modification may be effective in preventing cancer. I don’t think we should throw out the baby with the bath water. There is no reason not to consume significant amounts of fruits and vegetables in the hopes that it will have positive effects on preventing cancer and its progression. There is no downside, especially if the small studies are correct.

References: (1) CA Cancer J Clin. 2011;61(4):212. (2) Nat Rev Cancer. 2008;8(9):694. (3) JAMA. 2005;293(2):183-193. (4) Int J Cancer. 2004 Jan 10;108(2):269-276. (5) Lancet Oncol. 2013 Oct;14(11):1112-1120. (6) Proc Natl Acad Sci U S A. 2008 Jun 17;105(24):8369-8374. (7) Ann Oncol. 2013 Apr;24(4):1079-1087. (8) Ann Oncol. 2012 Aug;23(8):2198-2203.

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.

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‘Why’ is as important as ‘how’

By David Dunaief, M.D.

Dr. David Dunaief

Weight loss should be a rather simple concept. It should be solely dependent on energy balance: the energy (kilocalories) we take in minus the energy (kilocalories) we burn should result in weight loss, if we burn more calories than we consume. However, it is much more complicated. Frankly, there are numerous factors that contribute to whether people who want or need to lose weight can.

The factors that contribute to weight loss may depend on stress levels. High stress levels can contribute to metabolic risk factors such as central obesity with the release of cortisol, the stress hormone (1). Therefore, hormones contribute to weight gain.

Another factor in losing weight may have to do with our motivators. We will investigate this further. And we need successful weight management, especially when approximately 70 percent of the American population is overweight or obese and more than one-third is obese (2).

Focus on improving your health by making lifestyle modifications like walking your dog.

Obesity, in and of itself, was proclaimed a disease by the American Medical Association. Even if you don’t agree with this statement, excess weight has consequences, including chronic diseases such as cardiovascular disease, diabetes, osteoarthritis, autoimmune diseases and a host of others. Weight has an impact on all-cause mortality and longevity.

It is hotly debated as to which approach is best for weight loss. Is it lifestyle change with diet and exercise, medical management with weight loss drugs, surgical procedures or even supplements? The data show that, while medication and surgery may have their places, they are not replacements for lifestyle modifications; these modifications are needed no matter what route is followed.

But the debate continues as to which diet is best. We would hope patients would not only achieve weight loss but also overall health. Let’s look at the evidence.

Low-carbohydrate vs. low-fat diets

Is a low-carbohydrate, high-fat diet a fad? It may depend on diet composition. In the publication of a randomized controlled trial (RCT), the gold standard of studies, results showed that a low-carbohydrate diet was significantly better at reducing weight than low-fat diet, by a mean difference of 3.5 kg lost (7.7 lb), even though calories were similar and exercise did not change (3).

The authors also note that the low-carbohydrate diet reduced cardiovascular disease risk factors in the lipid (cholesterol) profile, such as decreasing triglycerides (mean difference 14.1 mg/dl) and increasing HDL (good cholesterol). Patients lost 1.5 percent more body fat on the low-carbohydrate diet, and there was a significant reduction in an inflammation biomarker, C-reactive protein (CRP). There was also a reduction in the 10-year Framingham risk score. However, there was no change in LDL (bad cholesterol) levels or in truncal obesity in either group.

This study was 12 months in duration with 148 participants, predominantly women with a mean age of 47, none of whom had cardiovascular disease or diabetes, but all of whom were obese or morbidly obese (BMI 30-45 kg/m²). Although there were changes in biomarkers, there was a dearth of cardiovascular disease clinical end points. This begs the question: Does a low-carbohydrate diet really reduce the risk of developing cardiovascular disease (CVD) or its subsequent complications? The authors indicated this was a weakness since it was not investigated.

Digging deeper into the diets used, it’s interesting to note that the low-fat diet was remarkably similar to the standard American diet; it allowed 30 percent fat, only 5 percent less than the 35 percent baseline for the same group. In addition, it replaced the fat with mostly refined carbohydrates, including only 15 to 16 g/day of fiber.

The low-carbohydrate diet participants took in an average of 100 fewer calories per day than participants on the low-fat diet, so it’s no surprise that they lost a few more pounds over a year’s time. Patients in both groups were encouraged to eat mostly unsaturated fats, such as fish, nuts, avocado and olive oil.

As David Katz, M.D., founding director of Yale University’s Prevention Research Center, noted, this study was more of a comparison of low-carbohydrate diet to a high-carbohydrate diet than a comparison of a low-carbohydrate diet to a low-fat diet (4).

Another study actually showed that a Mediterranean diet, higher in fats with nuts or olive oil, when compared to a low-fat diet, showed a significant reduction in cardiovascular events — clinical end points not just biomarkers (5). However, both of these studies suffer from the same deficiency: comparing a low-carbohydrate diet to a low-fat diet that’s not really low fat.

Diet comparisons

Interestingly, in a meta-analysis (a group of 48 RCTs), the results showed that whether a low-carbohydrate diet (including the Atkins diet) or a low-fat diet (including the Ornish plant-based diet) was followed, there was a similar amount of weight loss compared to no intervention at all (6). Both diet types resulted in about 8 kg (17.6 lb) of weight loss at six months versus no change in diet. However, this meta-analysis did not make it clear whether results included body composition changes or weight loss alone.

In an accompanying editorial discussing the above meta-analysis, the author points out that it is unclear whether a low-carbohydrate/high-animal protein diet might result in adverse effects on the kidneys, loss of calcium from the bones, or other potential deleterious health risks. The author goes on to say that, for overall health and longevity and not just weight loss, micronutrients may be the most important factor, which are in nutrient-dense foods.

A Seventh-Day Adventist trial would attest to this emphasis on a micronutrient-rich, plant-based diet with limited animal protein. It resulted in significantly greater longevity compared to a macronutrient-rich animal protein diet (7).

Psyche

Finally, the type of motivator is important, whatever our endeavors. Weight loss goals are no exception. Let me elaborate.

A published study followed West Point cadets from school to many years after graduation and noted who reached their goals (8). The researchers found that internal motivators and instrumental (external) motivators were very important.

The soldiers who had an internal motivator, such as wanting to be a good soldier, were more successful than those who focused on instrumental motivators, such as wanting to become a general. Those who had both internal and instrumental motivators were not as successful as those with internal motivators alone. In other words, having internal motivators led to an instrumental consequence of advancing their careers.

When it comes to health, an instrumental motivator, such weight loss, may be far less effective than focusing on an internal motivator, such as increasing energy or decreasing pain, which ultimately could lead to an instrumental consequence of weight loss.

There is no question that dietary changes are most important to achieving sustained weight loss. However, we need to get our psyches in line for change. Hopefully, when we choose to improve our health, we don’t just focus on weight as a measure of success. Weight loss goals by themselves tend to lead us astray and to disappoint, for they are external motivators. Focus on improving your health by making lifestyle modifications. This tends to result in a successful instrumental consequence.

References: (1) Psychoneuroendocrinol. online 2014 April 12. (2) JAMA 2012;307:491-497. (3) Ann Intern Med. 2014;161(5):309-318. (4) Huffington Post. Sept 2, 2014. (5) N Engl J Med. 2014 Feb 27;370(9):886. (6) JAMA. 2014;312(9):923-933. (7) JAMA Intern Med. 2013;173:1230-1238. (8) Proc Natl Acad Sci U S A. 2014;111(30):10990-10995.

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.

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Walking may reduce the need for dialysis. METRO photo
Are activity and exercise the same?

By David Dunaief, M.D.

Dr. David Dunaief

Let’s begin with a pretest. I want to make it clear that a pretest is not to check whether you know the information but that you have an open mind and are willing to learn.

1) Which may have the most detrimental impact on your health?

a.   Smoking

b.   Obesity

c.   Inactivity

d.   A and C

e.   All have the same impact

2) People who exercise are considered active.

a.   True

b.   False

3) Inactivity may increase the risk of what? Select all that apply.

a.   Diabetes

b.   Heart disease

c.   Fibromyalgia

d.   Mortality

e.   Disability

With the recent wave of heat and humidity, who wants to think about exercise? Instead, it’s tempting to lounge by the pool or even inside with air conditioning instead.

First, let me delineate between exercise and inactivity; they are not complete opposites. When we consider exercise, studies tend to focus on moderate to intense activity. However, light activity and being sedentary, or inactive, tend to get clumped together. But there are differences between light activity and inactivity.

Light activity may involve cooking, writing, and strolling (1). Inactivity involves sitting, as in watching TV or in front of a computer screen. Inactivity utilizes between 1 and 1.5 metabolic equivalent units — better known as METS — a way of measuring energy. Light activity, however, requires greater than 1.5 METS. Thus, in order to avoid inactivity, we don’t have to exercise in the dreaded heat. We need to increase our movement.

What are the potential costs of inactivity? According to the World Health Organization, over 3 million people die annually from inactivity. This ranks inactivity in the top five of potential underlying mortality causes (2). The consequences of inactivity are estimated at 1 to 2.6 percent of health care dollars. This sounds small, but it translates into actual dollars spent in the U.S. of between $38 billion and $100 billion (3).

How much time do we spend inactive? Good question. In an observational study of over 7,000 women with a mean age of 71 years old, 9.7 waking hours were spent inactive or sedentary. These women wore an accelerometer to measure movements. Interestingly, as BMI and age increased, the amount of time spent sedentary also increased (4).

Inactivity may increase the risk of mortality and plays a role in increasing risks for diseases such as heart disease, diabetes and fibromyalgia. It can also increase the risk of disability in older adults.

Surprisingly, inactivity may be worse for us than smoking and obesity. For example, there can be a doubling of the risk for diabetes in those who sit for long periods of time, compared to those who sit the least (5).

By the way, the answers to the pretest are 1) e; 2) b; 3) a, b, c, d and e.

Let’s look at the evidence.

Does exercise trump inactivity?

We tend to think that exercise trumps all; if you exercise, you can eat what you want and, by definition, you’re not sedentary. Right? Not exactly. Diet is important, and you can still be sedentary, even if you exercise. In a meta-analysis — a group of 47 studies — results show that there is an increased risk of all-cause mortality with inactivity, even in those who exercised (6). In other words, even if you exercise, you can’t sit for the rest of the day. The risk for all-cause mortality was 24 percent overall.

However, those who exercised saw a blunted effect with all-cause mortality, making it significantly lower than those who were inactive and did very little exercise: 16 percent versus 46 percent increased risk of all-cause mortality. So, it isn’t that exercise is not important, it just may not be enough to reduce the risk of all-cause mortality if you are inactive for a significant part of the rest of the day.

In an earlier published study using the Women’s Health Initiative, results showed that those who were inactive most of the time had greater risk of cardiovascular disease (7). Even those who exercised moderately but sat most of the day were at increased risk of cardiovascular disease. Moderate exercise was defined as 150 minutes of exercise per week. Those at highest risk were women who did not exercise and sat at least 10 hours a day. This group had a 63 percent increased risk of cardiovascular disease (heart disease or stroke).

However, those who sat fewer than five hours a day had a significantly lower risk of cardiovascular events. And those who were in the highest group for regular exercise (walking seven hours/week or jogging/running four to five hours/week) did see more benefit in cardiovascular health, even if they were inactive the rest of the day. Sitting longer did not have a negative impact on the individuals in the high exercise level group.

Worse than obesity?

Obesity is a massive problem in this country; it has been declared a disease, itself, and it also contributes to other chronic diseases. But would you believe that inactivity has more of an impact than even obesity? In an observational study, using data from the EPIC trial, inactivity might be responsible for two times as many premature deaths as obesity (8). This was a study involving 330,000 men and women.

Interestingly, the researchers created an index that combined occupational activity with recreational activity. They found that the greatest reduction in premature deaths (in the range of 16 to 30 percent) was between two groups, the normal weight and moderately inactive group versus the normal weight and completely inactive group. The latter was defined as those having a desk job with no additional physical activity. To go from the completely inactive to moderately inactive, all it took, according to the study, was 20 minutes of brisk walking on a daily basis.

All is not lost!

In another study, which evaluated 56 participants, walking during lunchtime at work immediately improved mood (9). This small study clearly shows that by lunchtime activity changed mood for the better, increasing enthusiasm and reducing stress when compared to morning levels, before participants had walked. Participants had to walk at least 30 minutes three times a week for 10 weeks; pace was not important.

So what have we learned thus far about inactivity? It is all relative. If you are inactive, increasing your activity to be moderately inactive by briskly walking for 20 minutes a day may reduce your risk of premature death significantly. Even if you exercise the recommended 150 minutes a week, but are inactive the rest of the day, you may still be at risk for cardiovascular disease. You can potentially further reduce your risk of cardiovascular disease by increasing your activity with small additions throughout the day.

The underlying message is that we need to consciously move throughout the day, whether at work with a walk during lunch or at home with recreational activity. Those with desk jobs need to be most attuned to opportunities to increase activity. Simply setting a timer and standing or walking every 30 to 45 minutes may increase your activity levels and possibly reduce your risk.

References: (1) Exerc Sport Sci Rev. 2008;36(4):173-178. (2) WHO report: https://bit.ly/1z7TBAF. (3) forbes.com. (4) JAMA. 2013;310(23):2562-2563. (5) Diabetologia 2012; 55:2895-2905. (6) Ann Intern Med. 2015;162:123-132, 146-147. (7) J Am Coll Cardiol. 2013;61(23):2346-2354. (8) Am J Clin Nutr. online Jan. 24, 2015. (9) Scand J Med Sci Sports. Online Jan. 6, 2015.

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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Recent studies suggest that sleep deprivation results in weight gain. Stock photo
Even short-term sleep deprivation can negatively impact health

By David Dunaief, M.D.

Dr. David Dunaief

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

In this week’s column, we are going to focus on sleep deprivation, since it may impact our quality of life and influence concerns like weight gain and disorders that involve insulin resistance, kidney function and cognition. Even a short duration of inadequate sleep can have a surprising impact.

How much sleep do we need? Conventional wisdom has always been eight hours (1). However, it varies depending on the individual. About 26 percent of Americans get eight or more hours of sleep per night (2). During the workweek, approximately 30 percent of individuals in the U.S. get fewer than six hours of sleep. When you get down to five hours or less per night, the evidence suggests that most people get into trouble.

Weight gain

In a small, prospective (forward-looking) study, results showed that sleep deprivation results in weight gain. Why is this? You actually burn more calories (about 5 percent more) when you sleep fewer hours, but you consume significantly more calories than you metabolize (3). The individuals who were sleep restricted gained about two pounds. That may not sound like much, but the scary part is it occurred over a short time period — one workweek, or five days.

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

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

In another study, the results were similar (4). This one involved 225 healthy participants. Those who were sleep restricted gained about two pounds of weight over five days. Just like the previous study, participants were in a controlled laboratory where food was provided and their sleep monitored. In both studies, significant late-night eating was common.

In the Nurses’ Health Study, results showed that, for participants who regularly slept five hours or less, there was a 32 percent increased risk of gaining more than 30 pounds (5). This observational study involved approximately 68,000 women and was 16 years in duration.

Effects on aging

In a very small, but well-designed, randomized prospective study, adipocytes (fat cells) in sleep-deprived individuals became resistant or insensitive to ever-higher levels of insulin (6). This may be a precursor to increased risk of weight gain and diabetes. The sleep-deprived participants were allowed four-and-a-half hours of sleep per night over a period of four days compared to the control group, which was allowed eight-and-a-half hours per night. The most surprising effect found was that the fat cells of sleep-deprived individuals aged approximately two decades metabolically, so that participants in their 20s had fat cells that functioned similarly to those of people in their 40s.

Diabetes

In the Millennium Cohort Study, participants with inadequate sleep were at significantly greater risk of developing type 2 diabetes than those with sufficient sleep (7). In fact, participants who had five hours of sleep per night were at a 28 percent increased risk, and those who had fewer than five hours a night had a 52 percent greater risk. Adequate sleep was defined as at least seven hours. This was a prospective (forward-looking) observational study involving over 47,000 military personnel. The researchers brought up a good point: While sleep is on the decline, diabetes has been on the rise over the last three decades.

Cognition

Sleep deprivation’s impact on cognition may be immediate. In a study, healthy participants were subjected to sleep deprivation that resulted in decreased neurobehavorial functioning, or cognition, when compared to controls (8). Those in the sleep deprivation group were restricted for five days to four hours per night in bed, while those in the control group were allowed 10 hours per night. The sleep-deprived group was then allowed one night of 10 hours of sleep. While they recovered some neurobehavioral functioning, they didn’t reach their previous baseline levels. This study simulated the workweek followed by one day of recovery. The study was an in-laboratory, well-controlled study involving 159 healthy participants.

In the Familial Adult Children Study (FACS), presented at the prestigious 64th Annual American Academy of Neurology Meeting, participants with poor quality sleep were more likely to have high levels of amyloid beta plaques (9). The significance of these plaques is that they may be precursors to Alzheimer’s disease. The researchers discovered that participants who woke five times in each hour of sleep had a substantially greater risk of developing amyloid beta plaques. Thus, those with lesser sleep efficiency were more likely to have preclinical Alzheimer’s disease. None of the patients showed any symptomatic cognitive deficits, only early preclinical signs of Alzheimer’s. This is a very preliminary study that requires further prospective and randomized clinical trials.

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

References: (1) Sleep. 1995;18:908. (2) National Sleep Foundation, 2005. (3) Proc Natl Acad Sci USA. 2013;110:5695-5700. (4) Sleep. 2013;36:981-990. (5) Am. J. Epidemiol. 2006;164:947-954. (6) Ann Intern Med. 2012;157:549-557. (7) Diabetes Care Online. July 2013. (8) Sleep. 2010;33:1013-1026. (9) AAN Abstract 703.

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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Walking is an easy way to help you lose weight, which will help relieve pain and restore function in your joints. Stock photo
Walking can reduce the risk of functional decline

By David Dunaief, M.D.

Dr. David Dunaief

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

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

It turns out that OA is not just caused by friction or age-related mechanical breakdown but rather by a multitude of factors. These include friction, but also local inflammation, genes and metabolic processes at the cellular level (3). Being a more complicated process means that we may be able to prevent and treat it better than we thought by using exercise, diet, medication, injections and possibly even supplements. Let’s look at some of the research.

How can exercise be beneficial?

In an older study, results showed that even a small 10-pound weight loss could result in an impressive 50 percent reduction of symptomatic knee OA over a 10-year period (4).

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

Actually, the patients in this study were a mean age of 67 and were obese, with a mean body mass index (BMI) of 31 kg/m2, and either had or were at risk of knee arthritis. In fact, the most interesting part of this study was that the researchers quantified the amount of walking needed to see a positive effect. The least amount of walking to see a benefit was between 3,250 and 3,750 steps per day, measured by an ankle pedometer. The best results were seen in those walking >6,000 steps per day, a relatively modest amount. This was random, unstructured exercise. In addition, for every 1,000 extra steps per day, there was a 16 to 18 percent reduced risk of functional decline two years later.

Walking is an easy way to help you lose weight, which will help relieve pain and restore function in your joints.

Where does vitamin D fit in?

For the last decade or so, we thought vitamin D was the potential elixir for chronic diseases. If it were low, that meant higher risk for disease, and we needed to replete the levels.

Well, a randomized controlled trial (RCT), the gold standard of studies, has shown that low vitamin D levels may indeed contribute to knee osteoarthritis (6). However, repleting levels of vitamin D did not seem to stem disease progression. In fact, it had no effect on the disease, to the bewilderment of the researchers. There was no change in joint space, knee pain, mobility or cartilage loss slowing. Hmm. The patients were supplemented with vitamin D 2,000 IU for two years.

There were 146 patients involved in the study. Blood levels of vitamin D were raised by 16.1 ng/ml in the treatment group to >36 ng/ml, which was significantly greater than the 2.1 ng/ml increase in the placebo group. Since the reasons for the results are unclear, work to maintain normal levels of vitamin D to possibly prevent OA, rather than wait to treat it later.

Acetaminophen may not live up to its popularity

Acetaminophen (e.g., Tylenol) is a popular initial go-to drug for the treatment of osteoarthritis, but what does the research say about its effectiveness? The answer might surprise you. Although acetaminophen doesn’t have anti-inflammatory properties, it does have analgesic properties. However, in a meta-analysis (involving 137 studies), acetaminophen did not reduce the pain for OA patients (7).

In this study, all other oral treatments were significantly better than acetaminophen including diclofenac, naproxen and ibuprofen as well as intra-articular (in the joint) injectables, such as hyaluronic acid and corticosteroids, except for an oral Cox-2 inhibitor, celecoxib, which was only marginally better.

What about NSAIDs?

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

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

Don’t forget about glucosamine and chondroitin

Study results for this supplement combination or its individual components for the treatment of OA have been mixed. In a double-blind RCT, the combination supplement improved joint space, narrowing and reducing the pain of knee OA over two years. However, pain was reduced no more than was seen in the placebo group (10). In a Cochrane meta-analysis review study (involving 43 RCTs) results showed that chondroitin, with or without glucosamine, reduced the symptom of pain modestly compared to placebo in short-term studies (11). However, the researchers stipulate that most of the studies were of low quality.

So, think twice before reaching for the Tylenol. If you are having symptomatic OA pain, NSAIDs such as diclofenac may be a better choice, especially with SoluMatrix fine-particle technology that uses a lower dose and thus means fewer side effects, hopefully. Even though results are mixed, there is no significant downside to giving glucosamine-chondroitin supplements a chance.

However, if it does not work after 12 weeks, it is unlikely to have a significant effect. Also, try increasing your walking step count gradually; this could improve your risk of functional decline. And above all else, if you need to lose weight and do, you will reduce your risk of OA significantly.

References: (1) Arthritis Rheum. 2008;58:26-35. (2) Popul Health Metr. 2006;4:11. (3) Lancet. 1997;350(9076):503. (4) Ann Intern Med.1992;116:535-539. (5) Arthritis Care Res (Hoboken). 2014;66(9):1328-1336. (6) JAMA. 2013;309:155-162. (7) Ann Intern Med. 2015;162:46-54. (8) FDA.gov. (9) ACR 2014 Annual Meeting: Abstract 249. (10) Ann Rheum Dis. Online Jan 6, 2014. (11) Cochrane Database Syst Rev. 2015 Jan 28;1:CD005614.

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

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