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Vitamin D

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Foods high in Vitamin D include egg yolks, beef, shiitake mushrooms, cheese, milk and cold-water fatty fish like salmon, above.
In most geographic locations, sun exposure will not correct vitamin D deficiencies

By David Dunaief, M.D.

Dr. David Dunaief

Vitamin D is one the most widely publicized and important supplements. We get vitamin D from the sun, food and supplements. With our days rapidly shortening here in the Northeast, I thought it would be worthwhile to explore what we know about vitamin D supplementation.

Vitamin D has been thought of as an elixir for life, but is it really? There is no question that, if you have low levels of vitamin D, replacing it is important. Previous studies have shown that it may be effective in a wide swath of chronic diseases, both in prevention and as part of the treatment paradigm. However, many questions remain. As more data come along, their meaning for vitamin D becomes murkier. For instance, is the sun the best source of vitamin D?

At the 70th annual American Academy of Dermatology meeting, Dr. Richard Gallo, who was involved with the Institute of Medicine recommendations, spoke about how, in most geographic locations, sun exposure will not correct vitamin D deficiencies. Interestingly, he emphasized getting more vitamin D from nutrition. Dietary sources include cold-water fatty fish, such as salmon, sardines and tuna.

We know its importance for bone health, but as of yet, we only have encouraging — but not yet definitive — data for other diseases. These include cardiovascular and autoimmune diseases and cancer.

There is no consensus on the ideal blood level for vitamin D. The Institute of Medicine recommends more than 20 ng/dl, and The Endocrine Society recommends at least 30 ng/dl. More experts and data lean toward the latter number.

Skin cancer

Vitamin D did not decrease nonmelanoma skin cancers (NMSCs), such as squamous cell and basal cell carcinoma. It may actually increase them, according to one study done at a single center by an HMO (1). The results may be confounded, or blurred, by UV radiation from the sun, so vitamin D is not necessarily the culprit. Most of the surfaces where skin cancer was found were sun exposed, but not all of them.

The good news is that, for postmenopausal women who have already had an NMSC bout, vitamin D plus calcium appears to reduce its recurrence, according to the Women’s Health Initiative study (2). In this high-risk population, the combination of supplements reduced risk by 57 percent. However, unlike the previous study, vitamin D did not increase the incidence of NMSC in the general population. NMSC occurs more frequently than breast, prostate, lung and colorectal cancers combined (3).

Cardiovascular mixed results

Several observational studies have shown benefits of vitamin D supplements with cardiovascular disease. For example, the Framingham Offspring Study showed that those patients with deficient levels were at increased risk of cardiovascular disease (4).

However, a small randomized controlled trial (RCT), the gold standard of studies, calls the cardioprotective effects of vitamin D into question (5). This study of postmenopausal women, using biomarkers such as endothelial function, inflammation or vascular stiffness, showed no difference between vitamin D treatment and placebo. The authors concluded there is no reason to give vitamin D for prevention of cardiovascular disease.

The vitamin D dose given to the treatment group was 2,500 IUs. Thus, one couldn’t argue that this dose was too low. Some of the weaknesses of the study were a very short duration of four months, its size — 114 participants — and the fact that cardiovascular events or deaths were not used as study end points. However, these results do make you think.

Weight benefit

There is good news, but not great news, on the weight front. It appears that vitamin D plays a role in reducing the amount of weight gain in women 65 years and older whose blood levels are more than 30 ng/dl, compared to those below this level, in the Study of Osteoporotic Fractures (6).

This association held true at baseline and after 4.5 years of observation. If the women dropped below 30 ng/dl in this time period, they were more likely to gain more weight, and they gained less if they kept levels above the target. There were 4,659 participants in the study. Unfortunately, vitamin D did not show statistical significance with weight loss.

Mortality decreased

In a meta-analysis of a group of eight studies, vitamin D with calcium reduced the mortality rate in the elderly, whereas vitamin D alone did not (7). The difference between the groups was statistically important, but clinically small: 9 percent reduction with vitamin D plus calcium and 7 percent with vitamin D alone.

One of the weaknesses of this analysis was that vitamin D in two of the studies was given in large amounts of 300,000 to 500,000 IUs once a year, rather than taken daily. This has different effects.

USPSTF recommendations

The U.S. Preventive Services Task Force recommends against giving “healthy” postmenopausal women the combination of vitamin D 400 IUs plus calcium 1,000 mg to prevent fractures (8). It does not seem to reduce fractures and increases the risk of kidney stones. There is also not enough data to recommend for or against vitamin D with or without calcium for cancer prevention.

Need for clinical trials

We need clinical trials to determine the effectiveness of vitamin D in many chronic diseases, since it may have beneficial effects in preventing or helping to treat them (9). Right now, there is a lack of large randomized clinical trials. Most are observational, which provides associations, but not links. The VITAL study is a large RCT looking at the effects of vitamin D and omega-3s on cardiovascular disease and cancer. It is a five-year trial, and the results should be available in 2018.

When to supplement?

It is important to supplement to optimal levels, especially since most of us living in the Northeast have insufficient to deficient levels. While vitamin D may not be a cure-all, it may play an integral role with many disorders.

References: (1) Arch Dermatol. 2011;147(12):1379-1384. (2) J Clin Oncol. 2011 Aug 1;29(22):3078-3084. (3) CA Cancer J Clin. 2009;59(4):225-249. (4) Circulation. 2008 Jan 29;117(4):503-511. (5) PLoS One. 2012;7(5):e36617. (6) J Women’s Health (Larchmt). 2012 Jun 25. (7) J Clin Endocrinol Metabol. online May 17, 2012. (8) AHRQ Publication No. 12-05163-EF-2. (9) Endocr Rev. 2012 Jun;33(3):456-492.

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

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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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By David Dunaief, M.D.

Autoimmune diseases are becoming increasingly common, affecting approximately 23.5 million Americans, with 78 percent of them women. These numbers are expected to continue rising. There are more than 80 conditions with autoimmunity implications (1). These diseases include rheumatoid arthritis (RA), lupus, thyroid (hypo and hyper), psoriasis, multiple sclerosis and inflammatory bowel disease, to mention just a few.

Dr. David Dunaief

Autoimmune diseases are defined by the immune system inappropriately attacking organs, cells and tissues of the body, causing chronic inflammation. Thus, inflammation is the main consequence of immune system dysfunction, and it is the underlying theme tying these diseases together. Unfortunately, autoimmune diseases tend to cluster (2). In other words, once you have one, you are much more likely to acquire others.

Drug treatments

The mainstay of treatment is immunosuppressives. For example, in RA where there is swelling of joints bilaterally, the typical drug regimen includes methotrexate and TNF (tumor necrosis factor) alpha inhibitors, like Remicade (infliximab). These therapies are thought to help reduce the underlying inflammation by suppressing the immune system and interfering with inflammatory factors, such as TNF-alpha. The disease-modifying antirheumatic drugs (DMARDs) may slow or stop the progression of joint destruction and increase physical functioning. Remicade reduces C-reactive protein (CRP), a biomarker of inflammation.

However, there are several concerning factors with these drugs. First, the side effect profile is substantial. It includes the risk of cancers, opportunistic infections and even death, according to black box warnings (the strongest warning by the FDA) (3). Opportunistic infections include diseases like tuberculosis and invasive fungal infections. It is no surprise that suppressing the immune system would result in increased infection rates. Nor is it surprising that cancer rates would increase, since the immune system helps to fend off malignancies. In fact, a study showed that after 10 years of therapy, the risk of cancer increased by approximately fourfold with the use of immunosuppressives (4).

Second, these drugs were tested and approved using short-term randomized clinical trials, but many patients are put on these therapies for 20 or more years. Remicade’s package insert was approved with approximately two years of data.

So what other methods are available to treat autoimmune diseases? These include medical nutrition therapy using bioactive compounds, which have immunomodulatory (regulation of the immune system) effects on inflammatory factors and on gene expression, and supplementation.

Nutrition and inflammation

Raising the level of beta-cryptoxanthin, a carotenoid bioactive food component, by a modest amount has a substantial impact in preventing RA. In one study, participants drank the equivalent of about one glass of freshly squeezed orange juice a day with a resultant 49 percent risk reduction in the development of RA (5).

While I have not found studies that specifically tested diet in RA treatment, there are dietary studies that have shown anti-inflammatory effects in other diseases, using biomarkers such as CRP and TNF-alpha. In a study that looked at the Mediterranean-type diet in 112 older patients, there was a significant decrease in inflammatory markers, including CRP (6).

In another study, participants showed a substantial reduction in CRP with increased flavonoid levels, an antioxidant, from vegetables and apples. Astaxanthin, a carotenoid found in fish, was shown to significantly reduce a host of inflammatory factors in mice, including TNF-alpha (7).

Vitamin D

Vitamin D is ubiquitous in helping to treat and prevent many chronic diseases — autoimmune diseases are no exception. Vitamin D affects over 200 genes, according to Wellcome Trust Centre for Human Genetics at University of Oxford. In the absence of vitamin D, T-cell response, part of the immune system, becomes dysfunctional and uncontrollable, resulting in an increase in multiple sclerosis (MS) and inflammatory bowel disease — Crohn’s and ulcerative colitis. However, when normal levels of vitamin D are conveyed to the vitamin D receptors, proper T-cell functioning is restored with no subsequent autoimmune disease, at least in animal studies (8).

Interestingly, multiple sclerosis patients are notoriously very low in vitamin D, and it is difficult to raise the levels. There was a small study proclaiming that MS patients may need as much as 50,000 IUs of vitamin D2 weekly, and that it was safe (9). I would check with a neurologist specializing in MS before taking such a high dose.

Fish oil

Fish oil helps your immune system by reducing inflammation and improving your blood chemistry.

If you think vitamin D is impressive, fish oil affects as many as 1,040 genes (10). In a randomized clinical study, 1.8 grams of eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) supplementation had anti-inflammatory affects, suppressing cell signals and transcription factors (proteins involved with gene expression) that are pro-inflammatory, such as NFkB.

In RA patients, fish oil helps suppress cartilage degradative enzymes, while also having an anti-inflammatory effect (11). When treating patients with autoimmune disease, I typically suggest about 2 grams of EPA plus DHA to help regulate their immune systems. Don’t take these high doses of fish oil without consulting your doctor, since fish oil may have blood thinning effects.

Probiotic supplements

The gut contains approximately 70 percent of your immune system. Probiotics, by populating the gut with live beneficial microorganisms, have immune-modulating effects that decrease inflammation and thus are appropriate for autoimmune diseases. Lactobacillus salvirus and Bifidobacterium longum infantis are two strains that were shown to have positive effects (12, 13).

In a study with Crohn’s disease patients, Lactobacillus casei and L. bulgaricus reduced the inflammatory factor, TNF-alpha (14). To provide balance, I recommend probiotics with Lactobacillus to my patients, especially with autoimmune diseases that affect the intestines, like Crohn’s and ulcerative colitis.

Fiber

Fiber has been shown to modulate inflammation by reducing biomarkers, such as CRP. In two separate clinical trials, fiber either reduced or prevented high CRP in patients. In one, a randomized clinical trial, 30 grams, or about 1 ounce, of fiber daily from either dietary sources or supplements reduced CRP significantly compared to placebo (15).

In the second trial, which was observational, participants who consumed the highest amount of dietary fiber (greater than 19.5 grams) had reductions in a vast number of inflammatory factors, including CRP, interleukin-1 (IL-1), interleukin-6 (IL-6) and TNF-alpha. (16).

Immune system regulation is complex and involves over a 1,000 genes, as well as many biomarkers. Dysfunction results in inflammation, and potentially autoimmune disease. We know the immune system is highly influenced by bioactive compounds found in high nutrient foods and supplements. Therefore, bioactive compounds may work in tandem with medications and/or may provide the ability to reset the immune system through immunomodulatory effects and thus treat and prevent autoimmune diseases.

References: (1) niaid.nih.gov. (2) J Autoimmun. 2007;29(1):1. (3) epocrates.com. (4) J Rheumatol 1999;26(8):1705-1714. (5) Am J Clin Nutr. 2005 Aug; 82(2):451-455. (6) Am J Clin Nutr. 2009 Jan;89(1):248-256. (7) Chem Biol Interact. 2011 May 20. (8) Prog Biophys Mol Biol. 2006 Sept;92(1):60-64. (9) Am J Clin Nutr. 2007 Sep;86(3):645-651. (10) Am J Clin Nutr. 2009 Aug;90(2):415-424. (11) Drugs. 2003;63(9):845-853. (12) Gut. 2003 Jul;52(7):975-980. (13) Antonie Van Leeuwenhoek 1999 Jul-Nov;76(1-4):279-292. (14) Gut. 2002;51(5):659. (15) Arch Intern Med. 2007;167(5):502-506. (16) Nutr Metab (Lond). 2010 May 13;7:42.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.

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Vitamin D levels may play an important role in the treatment of multiple sclerosis.

By David Dunaief, M.D.

David Dunaief, M.D.
David Dunaief, M.D.

Medicine has made great strides in the treatment of multiple sclerosis over the last few decades. Multiple sclerosis (MS) is an autoimmune disease where there is underlying inflammation and the immune system attacks its own tissue. This causes demyelination, or breakdown of the myelin sheath, a protective covering on the nerves in the central nervous system (CNS). The result is a number of debilitating effects, such as cognitive impairment, numbness and weakness in the limbs, fatigue, memory problems, inflammation of the optic nerve causing vision loss and eye pain (optic neuritis) and mobility difficulties.

There are several forms of MS. The two most common are relapsing-remitting and primary-progressive. Relapsing-remitting has intermittent flare-ups and occurs about 85 to 90 percent of the time. Primary-progressive (steady) occurs about 10 percent of the time. Relapsing-remitting may eventually become secondary-progressive MS, which is much harder to control, although dietary factors may play a role.

Diagnosis and progression

MS is diagnosed in several ways. The ophthalmologist may be the first to diagnose the disease with a retinal exam (looking at the back of the eye). If you have eye pain or sudden vision loss in one eye, it is important to see your ophthalmologist. Another tool in diagnosis is an MRI of the CNS. This looks for lesions caused by the breakdown of the myelin sheath. The MRI can also be used to determine the risk of progression from a solitary CNS lesion to a full-blown MS diagnosis. This is accomplished by examining the corpus callosum, a structure deep within the brain, according to a presentation at the European Neurologic Society (1). Approximately half of patients with one isolated lesion will progress to clinically definite MS within six years. An MRI may be able to predict changes in this portion of the brain within two years. Patients with a family history of MS should discuss this diagnostic with a neurologist.

Medication

Interferon beta is the mainstay of treatment for MS for good reason. Data shows that it reduces recurrence in relapsing-remitting MS and also the number of brain lesions.However, in a study, interferon beta failed to stop the progression to disability in the long term (2). Many MS patients will experience disability over 20 years. Ultimately, what does this mean? Patients should continue therapy; however, they should have realistic expectations. This study was retrospective, looking back at previously collected data — not the strongest of studies.

In an RCT, higher levels of vitamin D in the blood showed a trend toward reduced disability in timed tandem walking and in disability accumulation.

Vitamin D impact

Vitamin D may play a key role in reducing flare-ups in relapsing-remitting MS. There have been several studies that showed this benefit with vitamin D supplements and/or with interferon beta. In one study, interferon beta had very interesting results showing that it may help increase the absorption of vitamin D from the sun (3). This was a randomized controlled trial (RCT), the gold standard of studies, involving 178 patients. The study’s authors suggest that interferon beta’s effectiveness at reducing the frequency of relapsing-remitting MS flare-ups may have to do with its effect on the metabolizing of vitamin D. In those who did not have higher blood levels of vitamin D, interferon beta actually increased the risk of flare-ups.

Physicians should monitor blood levels of vitamin D to make sure they are adequate. It may be beneficial for MS patients to get 15 to 20 minutes of sun exposure without sunscreen per day. However, patients with a history of high risk of skin cancer should not be in the sun without protective clothing and sunscreen.

In a prospective (forward-looking) observational study, patients with higher levels of vitamin D, even in those without interferon beta treatment, had reduced risk of relapsing-remitting MS flare-ups (4). The patients with higher levels had 40 ng/ml, and those with lower levels had 20 ng/ml. Patients’ blood samples were assessed every eight weeks for a mean duration of 1.7 years. The relationship with vitamin D was linear — as the blood level increased two-fold, the risk of flare-ups decreased by 27 percent.

In an RCT, higher levels of vitamin D in the blood showed a trend toward reduced disability in timed tandem walking and in disability accumulation (5). The results did not reach statistical significance, but approached it. A much larger RCT needs to be performed to test for significance.

Diet and lifestyle

Interestingly, a study found that caffeine, alcohol and fish — fatty or lean — intake may result in delay of secondary progression of relapsing-remitting MS (6). This observational study involved 1,372 patients. The reduction in risk of disability was as follows: Moderate daily alcohol intake resulted in a 39 percent reduction; daily coffee consumption showed a 40 percent reduction; and fish two or more times a week showed a 40 percent reduction.

All of these results were compared to patients who did not consume these items. However, the same effect was not shown in primary-progressive MS patients: Fatty fish actually increased risk of progression, compared to lean fish. With MS, vitamin D blood levels may be critically important. They are one of the easier fixes, although it may take higher doses of vitamin D supplementation to reach sufficient levels, once low.

While food (fish with bones, for example) provides vitamin D, it falls short of the amount needed by an MS patient. Interferon beta and vitamin D supplementation may have added effects. Lifestyle changes or additions also have tantalizingly appealing possibilities.

References: (1) Abstract O-293; June 2012. (2) JAMA. 2012;308:247-256. (3) Neurology. 2012;79:208-210. (4) Neurology. 2012;79:254-260. (5) J Neurol Neurosurg Psychiatry. 2012;83(5):565-571. (6) Eur J Neurol. 2012 Apr;19(4):616-624.

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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